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To the Children:
So here are the notes we poured our blood, sweat, and tears into.
Couple of things:
1) Disclaimer: If there is anything in these files that offends you or anyone else, we dont apologize, well, because
you got it for free
2) Disclaimer: W e still dont know if a lot of the questions on these files are right or not. You will soon find in your
studies that some exact questions have different answers from different test years, so say a prayer and guess if
you get it on your test. So dont come tell us if you have found any errors or mistakes because, a) we dont care
anymore, and b) just fix it, make the files better, and help someone else benefit from your criticism.
3) Contents:
a. Entire 2004 dental decks, typed up, and searchable (Control F for those who have been living in a cave)
b. Every single question/answer from the USC CD will all the various test questions. All of these items will
be highlighted in green I believe they go up to 2002
c. Random remembered questions after 2002, but definitely not all and most are from 2003 to 2005. All of
these answers are listed in yellow highlights.
d. A ton of explanations from both Kaplan and USMLE First Aid books on a lot of the tough topics and topics
they constantly hit over and over again.
e. A ton of sweet images, charts, graphs, etc. courtesy of Google images, inc.
f. A bunch of comedic relief intermixed in the pneumonic devices that helped us on the test.


***Look to the book for eruption sequence
***Make a chart w/ # of canals by tooth start w/ 77 Q 97
79a Q44 confirm w/ correct eruption sequence, 85 review Pullinger
80 Q90 Bennett shift
Basically everything is from Ectomesenchyme except for Enamel, which is from Ectoderm
A quick review of Odontogenesis
Induction interaction between ectomesenchyme and epithelium
6th week
Formation of dental lamina
Bud Stage
Proliferation both dental lamina and underlying ectomesenchyme
8th week
Dental lamina into 10 buds per arch
Shape of tooth is evident
Enamel organ starts to form
Tooth buds of the Maxilla appear 1st!
Cap Stage
Proliferation and Differentiation
Morphodifferntiation change into other shapes
Histodifferentiation branch into different tissues
9-10th week
***NOW tooth germ is complete
Bell Stage
Differentiation of Odontoblasts
For the whom the BELL TOMES
Differentiation to its furthest extent resulting in 4 different cell types in the bell-shaped enamel organ (makes enamel
and Hertwigs root sheath)
OEE cuboidal
IEE columnar (Think I looks like a column)
Stellate reticulum network of star-shaped cells

Stratum intermedium flat to cuboidal

Dental papilla (makes dentin and dental pulp) differentiate into 2 layers
Outer cells
Central cells
Dental sac (makes Cementum, PDL, and alveolar bone proper) increases in collagen fibers
11-12 weeks
Remember enamel organ makes Enamel
Appositional Stage
Cells that were differentiated into specific tissue-forming cells begin to deposit the specific dental tissues (i.e. enamel,
dentin, cementum and pulp)
Maturation Stage
Mineralization begins at the DEJ and continues until total development accomplished, taking approximately 2 yrs to
Ectodermal Origin
4 Layers of Enamel Organ
Outer enamel epithelium
Outer cellular layer
Inner enamel epithelium (IEE)
Innermost layer
Cells will become ameloblasts
Essential for the initiation of dentin formation
*NOTE: In a developing tooth, the junction of the dental papilla and the IEE becomes the DEJ
Stratum Intermedium Think I is next to I
Lateral to inner enamel epithelium
Essential to enamel formation (nutrients for the ameloblasts of inner enamel epithelium) during calcification
Stellate Reticulum
Central core and fills bulk of organ
Contains lots of intercellular fluid (mucous type rich in albumin) which is lost prior to enamel deposition
After enamel formation, all 4 layers become 1 and form the Reduced Enamel Epithelium
What is the reduced enamel epithelium made from??? Attached epithelial cuff???
Very important in forming the dentogingival jxn, where the enamel and epithelium meet as tooth erupts
This forms initial junctional epithelium
96% inorganic, 1% organic, 3% water
Calcium and Phosphate
Fluoride and Zinc (Minor)
Optically clear
Protein rich in Proline
Brittle, but can endure 100,000 PSI of pressure
Yellow to grayish
Selectively permeable membrane (water and ions via osmosis)
Enamel Rods or Prism
Fundamental morphologic primary unit
Aligned perpendicularly to the DEJ (except in cervical regions of primaryteeth)
A chamfer or long bevel is commonly used as a gingival finish line in permanent tooth preparations because the
direction of the enamel rods in the region of the CEJ is such that the rods deviate from the horizontal in an apical
The direction of enamel rods in primary teeth is inclined in an occlusal direction in the cervical 1/3 of the crown
The direction of enamel rods in permanent teeth in the cervical 3rd of crown is apically
512 million per crown
Rods increase in diameter as they flare outward Tails (from 48 microns)
Begin at the future cusp and spread down the cusp slope
Oldest enamel is at DEJ under cusp or Cingulum
Good thermal insulator
They represent the path of a single ameloblast from CEJ to surface
Hunter Schreger bands??
Alternating light and dark bands seen in enamel that begin at DEJ and end before they hit the surface

Represent areas of enamel rods cut in x-section dispersed between areas of rods cut longitudinally
Lines of Retzius
As ameloblasts retreat in incremental steps, they create artifact lines
Where these lines terminate, they form tiny valleys on tooth surface called perikymata
The small ridges, perikymata, seen on facial surfaces of canines, are the result of normal development
Perikymata are the result of normal enamel apposition
A Neonatal line exists where enamel was formed before and after birth
Found in both perm and prim
Enamel tufts
Fan-shaped, hypocalcified structures of enamel rods that project from the DEJ into the enamel proper
Unknown fxn
Enamel Spindles
Elongated Odontoblastic processes (hair-like) that transverse the DEJ from the underlying odontoblast
They are parallel to rods and hypocalcified and arise from DEJ
Tomes fibers
May serve as pain receptors
Tomes processes are from Enamel at the DEJ
Tomes Granular Layer is found in radicular dentin and lies just beneath the cementum, and distinguishes root
dentin from crown dentin
Enamel lamellae
Defects in the enamel resembling cracks or fractures which transverse the entire length of the crown from the surface
to the DEJ
Contain mostly organic material and may be carious
Perikymata and lamellae are seen on the surface of enamel, where Tufts are not
Remnant of the onset of enamel formation from the junction of the dental papilla & IEE
Ameloblasts secrete enamel matrix as they retreat away from the DEJ, then matrix mineralizes
Odontoblasts begin dentin formation immediately before enamel formation, by laying down collagen matrix and then moving
from the DEJ inwards towards the pulp (newest dentin always closest to the pulp)
Area at which calcification begins
Morphology determined at Bell Stage
70% inorganic, 20% organic, and 10% water
Test Q says 20-30% organic
Mostly of collagen fibers, Type I
More mineralized than cementum or bone, but less than enamel
Hardsoft: enameldentincementum
Calcium Hydroxyapatite
Main cell is odontoblast derived from ectomesenchyme
More flexible than enamel
Forms the greatest amount of tooth structure
Along with pulp tissue, is formed by the dental papilla
The ectomesenchyme influences the oral epi to grow down into the ectomesenchyme
Elongation of inner enamel epithelium and differentiation into ameloblasts
(making it columnar, but outer is still cuboidal)
This triggers the mesenchymal cells to differentiate into odontoblasts
Differentiation of Odontoblasts
Deposition of first layer of dentin
Deposition of first layer of enamel
*Deposition of root dentin and cementum
Mantle Dentin

Peripheral or first layer of dentin adjacent to enamel or cementum

Consists of more coarse fibers (Korffs) Think Dorff on Golf
Peritubular Dentin (Intratubular Dentin)
Lines each dentinal tubule
More mineralized than intertubular dentin
Intertubular Dentin
This is the main bulk of dentin
Surrounds peritubular dentin
Less mineralized
Interglobular Dentin
Imperfectly calcified matrix of dentin situated between the calcified globules near the periphery of the dentin
**Each tubule contains a cytoplasmic process (Tomes fiber) of an odontoblast
Dead tracts are tubules with dead cytoplasmic fibers in them
Primary dentin
Layed down before apical foramen closure
Dentin laid down before birth???
Secondary dentin
Formed after foramen closure
Slower forming than primary, as functional stresses are placed on tooth
Following the initial period of functional activity, an appreciable alteration in the size of the pulp chamber is a
direct result of deposition of secondary dentin
Regular and uniform layer
**There is a sharp change in the direction of tubules at junction of primary and secondary
The tubules of secondary dentin are wavy
Reparative dentin
What indicates Trauma during Dentin Formation????
Forms in response to stimuli produced by carious penetration of a tooth
Formed very rapidly in response to irritants like attrition, abrasion, erosion, caries, etc.
The tubules of reparative dentin are twisted
Sclerotic dentin
From aging and slowly advancing dental caries
Tubules become obliterated, which blocks access of irritants
All the following are seen dentin except
Tomes granular layer, Odontoblastic processes, Stria of retzius, and contour lines of Owen
Odontoblasts are mesenchymal origin
Formed by cementoblasts from PDL, not from odontoblasts from pulp
Slightly softer and yellower
Most closely resembles bone, except no Haversian systems or blood vessels
Avascular, No innervation
Compensates for tooth loss
Protects from resorption
Reparative fxn
50% Inorganic, 40% Organic, and 10% Water
Has the Highest Organic Content
Collagen and protein
More resistant to resorption than alveolar bone (permits ortho movement of teeth w/o resorption)
2 Types
No cells
Coronal 2/3rds
Contains cementoblasts, cememtocytes, fibroblasts from PDL and cementoclasts
Apical 1/3rd
Thickest to compensate for attritional wear of the occlusal/incisal surface and passive eruption
Peripheral layer of developing cementum that is not calicified
From Dental Papilla

Vascular and noncalcified

Fibroblasts (Majority)
Q: What cell is most found in pulp of 62 year old?
Odontoblasts no cementoblasts or ameloblasts
Histiocytes fixed macrophages
Undifferentiated Mesenchymal cells (reparative fxn)
NOT Adipocytes
Loose CT (collagen and reticular fibers there are no elastic fibers in the pulp)
Blood vessels & nerves & lymph vessels
Blood flow is most like it is in the cranium
Ground Substance (water and long carbohydrate chains attached to protein backbones)
Large when tooth first erupts, then gets smaller (usually from progressive trauma)
The size of the pulp chambers of the maxillary first premolars usually decreases with age due to thermal shock; normal
physiological & masticatory functions; excessive attrition and abrasion
The size of the pulp cavity within a tooth is influenced by the age of the tooth, parafunctional activity of the tooth, &
history of the tooth (abrasion, erosion, caries, etc.)
NOT related to sex
NOT related to ability of Ameloblasts to form dentin (duh, they dont, odontoblasts do)
The primary function of the dental pulp is to form dentin
Transmission of pain stimuli
Production of a defensive reaction when tooth is exposed to irritation
Does not cause formation of the mesenchyme of the dental papilla
Does not innervate the enamel
Pulp does not have function of pressure
Anatomy of the pulp
Central zone Pulp proper or Pulp Chamber)
Pulp chamber
The space occupied by the dental pulp w/in the tooth crown
The pulp chamber of a mature tooth contains
Blood vessels and nerves
NOT Odontoblasts or enamel lining
Lined peripherally by a specialized odontogenic area which has the following zones (inner to outer):
Pulpal Core similar to cell rich zone
Cell-rich zone contains fibroblasts
Cell-free zone of Weil capillary and nerve plexus (Plexus of Raschkow)
Think Cell Free of Weil has to be next to odontoblasts for Sensory (Hydrodynamic)
Odontoblastic layer contains odontoblasts and lies next to predentin and mature dentin
Pulp canals
Radicular pulp is continuous with tissues of the periapical area via the apical foramen
Accessory Pulp canals
May be found in the cervical third of the root
Contain nervous and vascular tissues
May be found in furcation areas of molars
Allow the pulp tissue to communicate with the PDL space
All stimuli to the pulp result in pain sensation (heat, cold, chemicals, touch)
Free nerve ending is only type of nerve in pulp, so regardless of source, you get pain
Contains both myelinated and unmyelinated nerve fibers
Myelinated sensory
Unmyelinated Motor (regulate size of vessel lumen)
NOT to concerned with speed here
Afferent and sympathetic
Proprioception is NOT found in pulp
Pulp capping
More successful in young teeth because:
Apical foramen is large
More cells

Very vascular
Less fibrous elements
More tissue fluid
BUT young pulp does lack a collateral circulation
Old pulp is more likely to have denticle or pulp stone
True denticle complete with tubule and processes
False denticle amorphous in structure no dentin structure
Free denticle unattached to outer pulpal wall
Attached denticle attached at dentin-pulp interface
Clinical crown
Part that is visible in oral cavity occlusal to the gingival margins
Anatomic crown
Part that is covered by enamel coronal to the cervical line
A V-shaped incipient enamel extension coronoradicularly on a crown may be found in bifurcated areas of any
multirooted teeth and commonly on Eskimo teeth
May be smaller or larger than clinical crown
Larger than clinical crown in gingivitis
Smaller (shorter) than clinical crown in gingival recession
Occlusal surface
Chewing surface of posterior teeth
Incisal edge
Cutting of anterior
Point Angles (4)
3 come together
Line Angles
Anterior (6)
Not mesioincisal or distoincisal (because they are rounded)
Posterior (8)
Any linear elevation on the surface of a tooth
Oblique Mx M1s (& primary Mx M2s)
Labial Canines
Buccal PMs
Cervical Primary teeth
Marginal All teeth
The ridge that extends from the distoincisal angle to the cingulum is the distal marginal ridge
Triangular Posterior teeth
Transverse Union of a L triangular ridge of a B cusp & a B triangular ridge of a L cusp
Marginal ridges
Marginal ridges on adjacent teeth are usually at the same height
Occlusocervically, the height of the mesial marginal ridge of a perm Mn M1 is the same as the height of the distal
marginal ridge of a Mn PM2
NOT at the same height on the Distal of Mn PM1 and Mesial of Mx PM2
When restoring the marginal ridges of posterior teeth, their shape should be
Rounded to help form occlusal embrasures and improve food flow (decreases food impaction)
Wide enough for strength and to provide an occlusal platform when there are opposing cusps
The following marginal ridges have little or no contact in centric & eccentric relationships:
Mesial of Mx canine(I think Distal of Mx Canine is not getting a contact from the Mn PM1)
Mesial of Mn PM1
Distal of Mn PM2?????
Developmental grooves (Primary)
Sharply defined, shallow, linear depressions
Separate lobes or cusps
Buccal/lingual grooves
Separate cusp ridges from marginal ridges see Brand book, p.174, for an illustration
Pits are at the junction
Supplemental grooves (Secondary)
Small, less distinct, irregularly placed grooves
Do not demarcate major divisional parts of a tooth
The groove that extends from the mesial pit of Mx PMs towards the the MB line angle is the MB secondary groove

Elevation of mound of enamel
Mamelons (Sean thanks a lot)
Small, rounded projections on incisors
Indicative of malocclusion in teenagers & adults
Anterior open bite is likely in a 10-year-old pt
Usually 3 mamelons
Extra formation of enamel
Cusp of Carabelli (it is NOT formed by a lobe, but it is a tubercle)
What is the thing called between 2 cusp ridges on a cusp?? Tubercle? Only answer making any sense
Bulbous elevation of enamel, from a lingual lobe on anterior
12 cingula in a complete dentition
Lingual cusp of Mn PM1 similar to growth of Cingulum of a canine both done by lobes
Long depression or a V-shaped valley on occlusal surface of a posterior tooth between ridges and cusps
Irregular depression or concavity
Jxn of developmental grooves
Narrow channel or crevice
Sometimes deep
Depth of developmental groove
Embrasures (4 per contact)
Generally speaking:
Contacting surfaces have Bigger embrasure
Mx ant L > F
Mn ant F > L the oddball
Posteriors L > F (except for between Mx M1 and M2 molars)
Where is the smallest embrasure???
Incisal embrasure of Mn centrals, then Incisal of Mx centrals
Rounding of the mesiofacial & distofacial line angles contributes to the formation of facial embrasures
The deflective function of mesiofacial & distofacial line angles protects the facial part of the interdental papilla
Is the biggest embrasure of the PM1 and the canine is on the F or L I think????
Posterior embrasures are generally larger on the L than on the F w/ the contact w/ in the facial moiety, except between
Mx M1 & M2
The widest is found between Mx canine & PM1 (1979b)
The largest is found between Mx lateral & canine (with Mx canine & PM1 as an optionhmm) (1996)
This is the interproximal space
The apex of the triangular-shaped boundary of the IP space is the contact area of the adjacent teeth
Stimulate tissue
The largest incisal embrasure is between Mx lateral & canine (because canine-PM1 embrasure is not an incisal embrasure)
Posterior embrasures are generally larger on the lingual than on the facial, with the contact area within the facial moiety,
EXCEPT between maxillary M1 & M2
Arch stability
Cusps, root forms, contact areas, & periodontal fibers all contribute to arch stability
NOT Embrasures
Other contributors: Facial & occlusal embrasure, and horizontal & vertical overlap
One of the primary sections of formation in the development of the crown of a tooth

Represented by a cusp in posterior and mamelons and cingula in anteriors

Separated by developmental grooves or developmental depressions in anteriors
The minimum number of lobes any tooth can develop from is 4
3 labial, 1 lingual
The perm Mx central incisor has 3 mamelons & 4 developmental lobes
3 Buccal, 1 lingual
The lingual cusp of a Mx PM1 is formed entirely by the lingual lobe
Except for Mand 2nd PM (3 Buccal, 2 lingual)
1st Molars (Mn)
5 lobes (by each cusp)
2nd Molars (Mx M1)
4 lobes (cusp)
3rd Molars
At least 4 lobes (variations exist)
The movement of the tooth through the surrounding tissue so that the clinical crown gradually appears longer
NOT Exfoliation (Dont get clowned)
Tooth makes its appearance in the mouth when one-half of the root is completed
3 Stages of Dentition
Primary Dentition (6 ms to 6 yrs)
Mixed Dentition (6 yrs to 12 yrs)
Commences with the 1st Perm Molars
Permanent Dentition (12 yrs+)
Permanent Dental Formula
I 2/2 C1/1 B2/2 M3/3 = 16 x 2 = 32
An imaginary animal (I 2/2 C1/1 M2/2) has the same # of anterior teeth as are found in a humans permanent dentition
Deciduous Dental Formula
I 2/2 C1/1 M2/2 = 10 x 2 = 20
Succedaneous teeth
Centrals to 2nd PMs
When extracting a primary Mx incisor in which the root has been partially resorbed due to pressure from its developing
succedaneous tooth, the buccal aspect will usually be longest & attached most securely to the gingiva
The first evidence of root resorption on a primary incisor is seen on the lingual root surface
Primary Teeth
All 20 primary teeth in utero
Begin to form about 6 weeks in utero
Begin to calcify about 4-6 months in utero
Primary teeth show calcification in utero during the 2nd trimester
1st and 2nd molars show calcification during 5-6 months and completed by 3yrs
Primary roots are completed
14 months after emergence for Mn
Mn teeth erupt from 6-7 months to 20 months
15 months after emergence for Mx
Mx teeth erupt from 7 months to 24 months
Calcification of the roots is normally completed by 3-4 yrs old
Remember last tooth comes in at 24 months Primary Mx M2
At 1.5 yrs, roots are completed for Mn centrals and laterals and Mx Centrals???
Primary Calcification Initiation Sequence
(in weeks)
(in weeks)

Hypoplasia of primary teeth limited to the incisal thirds of incisors, incisal tips of canines, and occlusal portion of molars
indicates a metabolic disturbance during the prenatal period
If a women took tetracycline during the second trimester, what teeth would be affected???? (Week 13-27)
Primary teeth ONLY
Note Tetracycline affects teeth erupting 1-2 years after taking it
Eruption Sequence
Primary Eruption Sequence From the Tooth Bible
Mn central (6)
Mn laterals (7)
Mx central (7.5)
Mx lateral (9)
Mn M1 (12)
1 yr, you should have 10 teethUnless youre a girl then @13 months youll have 12 teeth!!!
Mx M1 (14)
Mn canine (16)
Mx canine (19)
Mn M2 (20)
Mx M2 (24)
Deciduous eruption sequence: Central, Lateral, M1, Canine, M2
The last primary tooth to erupt is the Mx M2
Also last to start and finish calcifying
The first primary teeth to erupt are the Mn R & L central incisors
At 1 year, a child is expected to have erupted prim Mx & Mn incisors & M1s
A parent notices a new primary tooth at 12 months, most likely a Mn M1 (12 month Molar)
Prim M2s are expected to erupt shortly after the childs 2nd birthday
Last anterior tooth to calcify
Most dramatic change to the Oral Flora occurs when primary teeth erupt
Exfoliation sequence for Primary Teeth
6-8 yrs
7-9 yrs
1st Molars
10-12 yrs
9-12 yrs (10-11 for Mx canine was the correct answer option)
2nd Molars
10-12 yrs
Primate Space
Occur in deciduous dentition
Mx: space between laterals & canines
Mn: space between canines & M1s
NOTE: Spacing always occurs, but these are most noticeable
The perm dentition differs from primary in that primary teeth develop arch diastemata
Occur in 50% of children
Spacing between anterior teeth in the dentition is most frequently caused by growth of the dental arches
Permanent teeth
Begin to form at 4 months in utero
Calcification Initiation Sequence
3-4 months
4-5 months
10-12 months
The Last Permanent Anterior Tooth of the Mx to initiate calcification is the Lateral @10 months
18-21 months
2-2.5 years
2.5-3 years
7-9 years
3-4 months

3-4 months
4-5 months
Dont get clowned, here its the Canine as the last anterior to initiate calcification
21-24 months
2-2.5 years
2.5-3 years
8-10 years
Mx & Mn M1s begin to calcify at birth
In development of the human permanent dentition, the first teeth to begin calcification are the Mn M1s
Initiation of calcification for the mandibular central incisors is 3-4 months
The incisal ridge is the 1st structure to begin to calcify in an anterior tooth
Perm M3s begin to calcify at 8-10 yrs of age
Active eruption of teeth occurs after of the root is formed (perm or primary)
50% of root calcification is complete at the time of eruption
The apex is usually fully developed by 2-3 years after eruption
Permanent Dentition Eruption Schedule
Permanent Dentition
Age (yrs)

6 to 7
6 to 7
6 to 7
7 to 8
7 to 8
8 to 9
9 to 10
10 to 12
10 to 12
10 to 12
10 to 12
11 to 12
11 to 13
12 to 13
17 to 21
17 to 21


1st molar

1st molar
central incisor
central incisor
lateral incisor
lateral incisor
1st premolar
1st premolar
2nd premolar
2nd premolar
2nd molar
2nd molar
3rd molar
3rd molar

3-4 mos
3-4 mos
3-4 mos
10 months
4-5 mos
1.75-2 yrs
1.5-1.75 yrs
2.25-2.5 yrs
2-2.5 yrs
4-5 mos
2.5-3 yrs
2.5 yrs
8-10 yrs
7-8 yrs

9-10 yrs
9-10 yrs
9 yrs
10 yrs
10 yrs
11 yrs
12-14 yrs
12-13 yrs
12-13 yrs
13-14 yrs
12-14 yrs
13-15 yrs
14-15 yrs
14-16 yrs
18-25 yrs
18-25 yrs

2.5-3 yrs
3-4 yrs
4-5 yrs
4-5 yrs
4-5 yrs
4-5 yrs
6-7 yrs
5-6 yrs
5-6 yrs
6-7 yrs
6-7 yrs
6-7 yrs
7-8 yrs
7-8 yrs
12-16 yrs
12-16 yrs

CRAP: The third pair of perm teeth to erupt in normal sequence is Mn lateral incisors (1996 Q53)???
UNLESS, they asked for 3rd pair of succedaneous!!!
(Looks like 5th pair to me, unless you go by molars centrals laterals, in which case, why specify Mn laterals?)
1st succedaneous to erupt is the Mn central incisor at 6-7 yrs old (dont get clowned Mn M1 is not succedaneous)
Permanent max centrals erupt just after at 7-8 yrs
Permanent max laterats erupt at 8-9 yrs
6 yr old
Presents with all 20 primary and 4 perm 1st molars
First sign of mixed dentition
Mn Molars at age 6
Ordinarily, a 6-year-old would have the following teeth clinically visible:
All primary teeth & permanent M1s
7 yr old (another Q said 6 year old)
Presents with 18 primary and 6 perm teeth
4 perm molars
2 mand perm central incisors
On a panoramic radiograph of a 7-year-old, the dentist will expect to see all of the following:
Primary Mx laterals w/ partially resorbed roots
Partially erupted Mx centrals w/ incomplete root closure at the apex
Partially erupted Mn laterals w/ incomplete root closure at the apex


Fully erupted Mn M1s w/ incomplete root formation & non-closure at the apex
Not fully erupted Mn centrals w/ complete root formation and closure at the apex (it takes 2-3 years)
At 8 years of age
The teeth normally present are perm central & lateral incisors, primary canines & molars, permanent first molars
The Perm Mx M1 has no distal contact (it does have a mesial contact with the primary Mx M2)
At 9 years of age,
12 primary teeth remain in the mouth (Primary C9 and 2 Molars per quadrant)
At 10 years of age
The perm teeth expected are central & lateral incisors, first premolars, and first molars (What about Mn Canines??)
One would expect the root of the perm M1s to be finished forming & calcifying
One would expect primary tooth H (primary Mx canine) to be mobile due to the erupting succedaneous tooth
BAD Q, hope you dont get it
CAREFUL, because J was also an option, which is the PM2 coming in to replace Primary M2
The first perm tooth to erupt is generally the Mn M1
The earliest indication of a mixed dentition consists of the primary dentition and the Mn M1s
The earliest indication is NOT the exfoliation of any primary tooth
The last perm incisors to erupt are the Mx laterals
Perm PM1 replaces primary M1
The earliest age by which the roots of the Mx PM1 are completely formed is 12-13 years
Typically eruption is 10, then 2-3 years for root completion
At age 26, the third molars are fully erupted with a complete root structure
The perm Mn arch is the only arch (prim or perm) in which the canine erupts before the tooth immediately distal to it
In Primary, Remember M1 is the distal tooth and it erupts at 12 months!!!!, canines in Mn at 16, Mx at 19 months
3 Cardinal Eruption Rules:
1) Girls teeth erupt BEFORE Boys
2) Mn erupt BEFORE Mx
3) Teeth of slender kids erupt BEFORE fat kids, (so much to get through)
Teeth usually erupt in pairs one on the left & one on the right
The follicles of the developing permanent incisors are in a position lingual to the deciduous roots
Eruption problems:
In cases of delayed resorption of primary incisors, the permanent incisors may be expected to erupt lingual to the normal arch


DENTAL ANOMALIES (new section ) see Ch 7 of book

Dens in dente
Occurs when enamel becomes invaginated
Most commonly found in permanent lateral and central incisors
Known for giving endo like symptoms, but no decay on crown, etc.
Retarded growth of a portion of a single tooth germ, or the proliferation of a segment of the odontogenic epithelium in
the dental papilla
Supernumerary teeth arising in the midline of the maxillae (most common supernumerary)
A small, calcified radiopaque mass between the roots of #8 & #9 is most likely due a mesiodens
Tooth appears mesial to both Mx central incisors
The cemental union of two fully formed teeth that were originally separate entities
Can be mistaken for Subgingival calculus


Union of 2 adjacent tooth buds

Upon examination, the dentist notices that there is an abnormally wide Mn incisor; further examination reveals that there are
only 3 Mn incisors present; most likely due to fusion
Incomplete splitting of a single tooth germ
A pt has an extremely wide, notched tooth in the Mn incisor position; clinical & radiographic exam reveals 28 teeth have
erupted (4 M3s unerupted); most likely due to gemination
Anterior Palatine Foramen
Radiolucent and circular in shape
Must Consider
Guiding (non-supporting) cusps are related to the Interproximal areas or developmental grooves
Supporting cusps are related to the marginal ridge and fossae
Supporting cusps are aligned with supporting cups of the same quadrant
Guiding (non-supporting) cusps overlap facial to mandibular teeth and lingual to maxillary teeth
Facets usually develop on
Linguoincisal of Mx centrals
Facioincisal of Mn canines
Attrition on a Mn Canine, what would the Mesial ridge look like?? M ridge would be shorter than D
Attrition of a Mx Canine, what would the Mesial ridge look like?? M ridge would be longer
Linguoincisal of Mx canines
Incisal edges of Mn laterals is done with Mx central AND lateral incisors, NOT Canines
Pt with Normal Class I, has wear facets on inner aspect of facial cusp of Mx PM2, these can only be caused by Mn PM2
LEAST likely spot for attrition is labioincisal area of Mx lateral incisor
Complete (usually with Ectodermal Dysplasia)
Usually 3rds (Max more) >Max laterals >Mand 2nd PMs
Rule: if only one or a few teeth are missing, the absent tooth will be the most distal (if molar, then 3 rd)
So if a premolar were missing, which primary tooth would most likely remain?
Mand. 2 molar
Many, but not all teeth
A developmental abnormality characterized by the presence of fewer than the usual number of teeth
Few gone
Old school classifications
Heterodont Human teeth, or several kinds of teeth, serving a variety of fxns
Diphyodont To produce 2 sets of teeth (perm/prim)
Monophyodont 1 set of teeth
Polyphyodont Teeth being replaced continually (amphibians)
Homodont teeth are all alike
A typical nonpoisonous reptile is a homodont (What a lame question!)
Hypsodont long teeth (High crowned)
Haplodont a primitive basic tooth form having a single conical crown and a single root
Selenodontic Longitudinal Mesiodistal Ridge formation (Grazing animals, along with Hypsodontic)
Teratogens affecting Dentofacial Development
Worse during first trimester
ASA, Valium, Dilantin, Cigarettes
Cleft Lip and Palate
CMV, Toxoplasma
Microcephaly, Hydrocephaly, Microphthalmia
Ethyl Alcohol
FAS Central mid-face discrepancy
Rubella Virus
Microphthalmia, Cataracts, Deafness
Vitamin D excess
Premature suture closure
Dental hypoplasia
If it occurs, it will be present when the teeth erupt
Tetracycline staining


A 5-year-old child is treated with large doses of tetracycline over a one year period. The perm teeth least likely to show
staining are lateral incisors, canines, and premolars. Perm centrals & M1s are more likely to stain.
Kaplan gives this explanation: Since the child is 5 years old, the teeth erupting at 6 or 7 will be MOST likely to show
staining, and those erupting later are less likely. On average, centrals erupt at 7, laterals at 8, canines at 11, PM1s at 9,
and M1s at 6.
So most likely stains teeth erupting 1-2 years after tetracycline usage
Excessive calcified tissue formation at the root apices
Fusion of the alveolar bone to a tooth
Also when different tooth obstructs
Dentin Islands
Most common in Mx 2nd PM and in Mn Canine
Caries/Dental decay
Areas susceptible to caries include pits & fissures, Facial surfaces cervical to the height of contour (Cervical Thirds), &
proximal surfaces
On molars, the L of Mx M1s & B of Mn M1s are most likely to develop caries (due to those fissured grooves)
Least likely to occur on cusp tips
Mandibular canine is most likely to resist invasion by caries
Periodontal Disease
The following morphologic variations tend to accelerate existing periodontal disease
Enamel projections, fused roots, and excessively short roots
Malpositioned teeth
If a Mn PM2 is linguoverted, there is an area of overcontour affecting the lingual gingival sulcus
Linguoversion means the tooth is lingual to the normal position
Tendency of teeth to erupt into an empty space; tends to follow extraction of opposing teeth
An extruded Mn R M3 (Mx M3 extracted) will most often impede a protrusive Mn movement
Anterior open bite
More common in African Americans
Can be caused by thumb sucking
Protrusion of max incisors
Constriction of max arch
Lingual inclination of mand incisors
Rotation of max laterals
Class II Malocclusions
Can be caused by abnormal swallowing (tongue Thrust)
Can be caused by mouth breathing
Presents with facial gingival of Max bleeding, edematous, and red
Midline affected the most
Mx arch is slightly longer than Mn
Mx diameter is 128mm
Mn diameter is 126mm
3rd1st molars innervated by PSA nerve (from V2)
1st molarPMs innervated by MSA nerve (V2)
Canines & incisors innervated by the ASA (V2)
A branch of the cranial nerve V to the tongue may be anesthetized during administration of an IA block (think sensory CN
V) -- the Lingual Nerve
Dryopithecus pattern
shows up most clearly in the mandibular first molar
Its the name of the ape they think we descended from, blah, blah
Maxillary Molar of early Primate
Had a trigon made up of 3 cusp MB, ML, DB
Heart shaped/triangular
Rodents (Rodentia)
Mammalian order with continuously erupting teeth in which apices never form
How many times do we swallow in one day?
2,000 times a day
When does a person swallow the most??
Daytime, when theyre NOT eating
PRIMARY TEETH (look at pictures)


Primary vs. Permanent Teeth

Fewer molars (2 vs. 3) and no premolars
Primary teeth have proportionately larger pulp cavities than perm teeth
Distinguished by long, pointed pulp horns
Crowns of primary incisors are shorter incisocervically compared with MD dimension
Roots of anteriors taper more rapidly
Are comparatively longer & slimmer than perm teeth
Are more divergent than perm teeth
Root trunks are less pronounced than perm teeth
Enamel ends abruptly
Are whiter than perm teeth
Are smaller than perm teeth
Crown : root Ratio is smaller than perm teeth meaning they have longer roots
Crowns are more bulbous & constricted than perm teeth appear shorter & fatter than perm teeth
Cervical ridges are more pronounced than perm teeth large facial buldge
No mamelons on primary teeth
Primary arch is more circular than the perm arch
Smoother occlusally (fewer pit/fissures)
Narrower occlusal table
1mm enamel (uniform thickness) on occlusal surface vs. 2.5mm of perm teeth
B and L surfaces are flatter than perm teeth (occlusal to the cervical ridge)
Leeway Space
The MD widths of the primary molars in any quadrant are greater than their perm successors (PMs) (by 2-4mm)
With respect to their permanent successors, the sum of the MD diameters of the deciduous M1 & M2 is generally
All Prim Molars
Differ the most from the perm teeth that replace them (among molars, canines, lateral incisors, central incisors)
Lack an identifiable root trunk
All Prim 1st Molars
In Max Teeth
Prim MB > ML
Perm ML > MB
In Mn Teeth
Prim ML > MB
Perm MB > ML
Dont get clowned They are opposites in Primary vs. Permanent
Distal surface is shorter than the mesial, occlusogingivally
Has a transverse ridge
Prominent mesial marginal ridge
Prominent MB cervical ridge
Present with the greatest morphologic deviations from permanent teeth (especially Mn M1)
All Prim 2nd Molars
Larger than M1s & resemble perm M1s
Show up after childs 2nd Birthday (20 months Mn, and 24 n=months Mx)
Individual Primary Teeth
Prim Mx Central
M/D view =
B/L view =
Occlusal =
MD dimension is wider than incisocervical dimension
Wider MD & shorter incisocervically than perm
Straighter incisal edge: SHARPER, more angled incisal edge
NO mamelons (same with laterals)
Prominent labial AND lingual cervical ridges!!!!! (This Q gave teeth A, F, J, L, & T I got clowned by L Mn M1)
Most damaged (with Mx laterals) by baby bottle tooth decay
Prim Mn Central
M/D view =


B/L view =
Occlusal =
Prominent cingulum
Often has a developmental groove on distal of root
Has the smallest FL dimension of any crown
Prim Mx Canine
M/D view =
B/L view = Pentagon
Occlusal =
4 lobes
3 facial, and 1 on the lingual
Widest primary anterior tooth
Appears wider and shorter than perm
Crown height is less than MD diameter
Diamond-shaped crown from facial aspect (Kaplan differs from the pentagonal outline mentioned above)???
Prominent cingulum
Cusp is much longer & sharper than perm canine
Cusp points distally
ODD BALL -- Mesial cusp ridge is longer than distal cusp ridge (opposite for perm Mx canines)
Opposite of what you think for Perm canines and Prim Mn Canines
Pulp chamber looks pointed at incisal tip
Prim Mn Canine
M/D view =
B/L view = Arrow-shaped from the facial
Occlusal =
Smooth labial surface
Longer distal incisal ridge than mesial incisal ridge
Prim Max 1st Molar
M/D view =
B/L view =
Occlusal = trapezoidal (peripheral); rectangular (table)
*Most atypical of all Mx molars*
Intermediate form between PM and Molar
Crown somewhat resembles a perm PM, but the root form is typical of a perm Molar
Of primary molars, prim Mx M1 bears the greatest resemblance to a perm PM
One Q gives resemblance to Mx PM2 as the correct answer
Smallest prim molar
Bicuspid (2 main cusps = MB & ML, 2 indistinct distals)
MB cusp > ML cusp
Cervical ridge in the MB area most prominent cervical ridge among primary Mx teeth!!!!!
The mesial surface is larger than the distal surface
From a facial view, BOTH Primary Mx M1 and M2 have a short root trunk
The cervical line on the mesial curves slightly toward the occlusal it does not have a straight cervical line
H-shaped occlusal pit-groove area
3 Roots (root structure corresponds to that of perm Mx M1)
Number and form of the roots corresponds to Mx M1
Short root trunk
Does the Prim Mx M1 has a lingual groove???

Prim Max 2nd molar

M/D view =
B/L view =
Occlusal =



Same characteristics as perm Mx M1 except:

MB cusp is almost same size as ML
MB pulp horn is longest and largest
Normally has a Cusp of Carabelli, just like Perm Mx M1
Most likely primary tooth to have an oblique ridge (looks like perm Mx M1)
Has the greatest FL dimension of all primary teeth!!!!!
The difference between Primary Mx M2 and Permanent Mx M1 is that the primary tooth has a much narrower
measurement at the CEJ compared to its contact area
They are similar in that both crowns converge to the distal and lingual
NOT that they both have well developed 4 cusps, oblique ridges, well developed marginal ridges, or rectangular outline
From a facial view, BOTH Primary Mx M1 and M2 have a short root trunk
Last Primary tooth to erupt
This is the primary molar that typically has a transverse ridge, oblique ridge, & a DL groove
3 Roots
Short root trunk
Primary Mx M2, roots are less curved than Permanent Mx M1

Prim Mand 1st Molar
M/D view =
B/L view =
Occlusal = Rhomboidal peripheral outline; Rectangular table (if you disregard the large MB ridge)
Unlike any other tooth
Both Prim Mn M1 and M2 have central and lingual grooves
Most normally exhibits a Distal Triangular Fossa
Based on morphology, a Class II MO prep would be the most difficult on a primary Mn M1 (of any teeth)
Because of HUGE MB pulp horn!!
4 cusps = 4 pulp horns (dont be thinking that it has 5 just because a Mn M1 has 5)
ML cusp is highest & sharpest!!!!!
MB and ML make up transverse ridge
Oval with MB expansion
Cervical ridge/Bulge in the MB area
Which primary tooth has a facial cervical ridge which is so distinctly prominent that it is uniquely different from ALL
other teeth? Primary Mn M1!!!!!
The CEJ is most apically positioned on the mesial 1/3 of the crown of a primary Mn M1
S Shaped cervical ridge
The Distal portion is shortest occlusogingivally
A prominent transverse ridge distinctly separates the mesial portion from the remainder of the occlusal table!!!!!

Prim Mand 2nd molar
M/D view =
B/L view =
Occlusal =
Closely resembles a perm Mn M1 occlusally
Same characteristics as perm Mn M1 except:
Has a more prominent facial cervical ridge
MB, DB, and D cusps of prim Mn M2 are about same size
The easiest way to distinguish between primary Mn M2 & perm Mn M1 is comparative size of D cusps
Not the widest in the cervical like the perm Mn M1 (primary teeth are constricted)
Has 3 occlusal fossae, like a perm Mn M1


5 cusps does not have 4 cusps (dont get clowned)

All 3 buccal cusps are the same size (unlike perm M1)

All Teeth:
CEJ (cervical line) curvature is greater on mesial than distal side
Facial height of contour is in cervical third
The only thing that all teeth have is M/D marginal ridges
Some All Rule, w/ exceptions:
All teeth have a M and a D marginal ridge
All teeth are wider FL than MD except:
Mx centrals & laterals
Mn molars
All teeth tilt facially EXCEPT Mn PM2 & Mn Ms (tilt lingually)
Mn PM1 is Straight up and down
All teeth tilt mesially EXCEPT Mx centrals & Mn centrals & laterals (ever so slightly tilted distally)
Mx canine has greatest tilt; PMs are the straightest
All Anterior Teeth:
Incisal edge or 1 cusp
Cingulum & lingual fossae 12 teeth have cingula (per dentition i.e. primary/permanent)
Cingula centered mesiodistally on: Mx lateral, Mx canine, Mn central
Cingula off-centered to the distal on: Mx central, Mn lateral, Mn canine
Both Facial and Lingual height of contour are in the Cervical 1/3 rd
Marginal ridges parallel to long axis
1 root
Triangular outline viewed from M or D (wedge-shaped from M or D aspect)
Trapezoidal outline viewed from B or L (longest uneven side toward the occlusal or incisal)
Contacts are centered faciolingually
Usually mesial edge is sharper than distal (Distal is rounded like letter D & Mesial is pointy like the letter M)
The incisal edges & incisal thirds of F surfaces of Mn anteriors generally oppose L surfaces of Mx anteriors w/in the incisal
Viewed from the sagittal plane and progressing anteriorly, the axial inclination of the anterior teeth inclines facially
All Posterior Teeth:
2 or more cusps
Occlusal table with ridges & grooves
Occlusal table makes up 55-65% of the BL dimension of the tooth
Marginal ridges perpendicular to long axis of the tooth
Facial height of contour in cervical third
Maybe except for Mandibular Molars which have them at the jxn of cervical and middle
Lingual height of contour in middle third
Except for the Mn PM2s, which have their height of contour in the occlusal 1/3 rd
Mesial marginal ridge more occlusal than distal except for Mn PM1s
Contacts in middle 1/3
Contacts in the Faciolingual direction are located in the Buccal side of the center
Are mesially inclined
All posterior teeth have rectangular occlusal tables, EXCEPT PM1s, which have trapezoidal occlusal tables
This is NOT the same as Occlusal outline (aka crown profile) see Kaplan p.549
All Maxillary Posterior Teeth:
Wider BL than MD
1st is larger than 2nd (& also 2nd larger than 3rd for molars)
Trapezoidal outline viewed from M or D (shortest, uneven side is towards the occlusal)
The B cusps of the Mx arch are B to the B cusps of the Mn arch
From a frontal plane view, axial inclination of Mx teeth is Buccally


Are progressively more buccally inclined as one moves posteriorly

From a frontal view, the plane of occlusion of the Mn arch is a concave curve
If a root goes into Mx sinus, it is usually from Mx M1
A more recent Q: The structure in the Mx alveolar bone that Mx premolar roots occasionally penetrate is the antrum (aka
maxillary sinus)
All Mandibular Posterior Teeth:
Lingual inclination of buccal surface
Rhomboidal outline viewed from M or D has a design flaw that encourages cusp fracture
Kaplan says: Because the crown is rhomboidal, the L surface leans lingually. The overhanging L cusp is not well
supported by underlying tooth structure and has a higher tendency to fracture.
Facial cusps of Mn posteriors oppose the central fossa line in the Mx dentition
IN a sagittal view, both anterior (yes, anterior) & posterior teeth are mesially inclined (other options were wrong 02Q44)
All Incisors:
Incisal edge
Marginal ridges run parallel to long axis of tooth
M & D contact areas are approximately centered faciolingually
Are 1st succedaneous teeth to erupt
Viewed incisally, the cingulum, lingual fossa, marginal ridges, & mesiofacial developmental depression are visible (not CEJ)
On the crown, the facial developmental depressions separate the labial lobes
All Maxillary Incisors:
Mesioincisal edge is sharp
Distoincisal edge is rounder
Distinguish Mx incisors from Mn incisors
Both larger than Mn incisors
Central is larger than lateral except root length which could be quite similar
Cervical line is greatest of all teeth on mesial side of max. centrals
Incisal edge is centered labiolingually
Embrasures: L > F
Have distinct lingual anatomy & may contain pits
Both Mx centrals & laterals are wider MD than LL
Mx incisor roots more frequently contain a single root canal than Mn incisors, Mx PM1s, Mx Ms (MB root), Mn Ms (M root)
Roots are more rounded than on Mn incisors
All Mandibular Incisors:
Laterals are larger than centrals; Centrals are smallest of all teeth
Incisal edges are lingual to root axis line (Lingual to the LL midpoint)
Indistinct cingula w/o grooves and pits
Smooth, continous convexity incisoapically
Wider LL than MD
Embrasures: F > L
Alveolar process is thinnest facial to Mn central incisors (good for infiltration injection)
In anesthesia of the Mn arch, local infiltration is likely to be effective in the incisor area
Proximal Contact
Contact occurs in the incisal third
Tends to occur equidistant from facial and lingual surfaces
All Canines:
1 cusp
Longest tooth in the mouth
Favorable crown-to-root ratio
Crown very bulky labiolingually
Transitional form between anterior & posterior teeth (mesial like incisors & distal like premolars)
Longevity (know why)
Labial ridge, developmental depressions, mesial & distal cusp slopes or ridges
The slight incisocervical concavity on the labial crown surface of the canines that is found in the incisal third, just mesial
to the labial ridge (whew!) is the mesiolabial developmental depression
Mesioincisal ridge shorter than distoincisal ridge
Lingual ridge
Viewed from the incisal, one expects to see:
Lingual fossa


Distal cusp ridge

Mesiofacial developmental depression (Labial Side)
Not the cervical line
Mesial contact is more incisal than distal contact
Crown form from labial aspect is pentagonal
Root has triangular cross section
Only cusped teeth which feature functional lingual surface rather than a functional occlusal surface
All Premolars:
1 buccal cusp
1 or 2 lingual cusps
Transitional between canines and molars in function
Enamel is thickest in the occlusal third
Have their long axis most perpendicular to the horizontal plane Mx & Mn PMs are the most nearly vertically aligned teeth
The union of the F & L triangular ridges forms a transverse ridge
All Maxillary Premolars:
B & L cusps of nearly EQUAL heights (but on Mx PM1, the B cusp is slightly larger)
The L cusp tip is located more mesially than the B cusp tip
Wider BL than MD (wider BL than Mn PMs, although MD dimension of all PMs is about the same)
Trapezoidal outline viewed from M or D
From occlusal view, more rectangle
Lingual height of contour is ~ midway between the CEJ & the L cusp tip (Dumb way of saying Middle 1/3rd)
1st is larger than 2nd
Roots are more flattened MD than Mn PMs
Roots have mesial concavities
In development, Mx PMs show crown completion at the same time
All Mandibular Premolars:
Large buccal cusp & very small lingual cusp(s)
Nearly equal MD & BL
1st PM is smaller than 2nd PM
From proximal view, crown tilts lingually in relation to the long axis of the tooth
Occlusal table is lingually displaced (Mx PM table is centered FL)
Rhomboid when viewed from the interproximal
Mn PM B cusps are more toward the FL midpoint than are Mx PM B cusps
From occlusal view, more square
Mn PMs compared to Mx PMs:
Mn have more rounded roots and seldom bifurcated
Mn crowns are tilted to the lingual
Have crowns much more rounded
Mn have less developed lingual cusps
In development, crown completion of Mn PM1 is 5-6 years; for Mn PM2, crown completion at 6-7 years
All Molars:
Largest and strongest teeth
At least 2 buccal cusps
1st, 2nd, 3rd, 6 year, 12 year, and wisdom tooth respectively
3 to 5 cusps
2 or 3 roots
Are NOT Succadaneous
DL cusp gets smaller as you go posterior in the arch
Root canals usually join the pulp chamber apical to the CEJ
3 Root Types:
Single or 1 Root
Max 2nd PM
Mand PMs
Bifurcating or 2 Roots
Max 1st PM (B/P)
Mand Molars (M/D)


Trifurcating or 3 Roots
Mx M1s & M2s (MB, DB, P)
Some M3s
All Maxillary Molars:
Wider BL than MD
Usually 4 cusps; ML > MB > DB > DL
2 lingual cusps of different size (again, ML > DL)
Oblique ridge extends between the ML & DB cusps
Formed by the union of distal cusp ridge of the ML cusp & the triangular ridge of the DB cusp
The transverse groove of the oblique ridge connects central & distal pits
The ridges that make up the oblique ridge meet near the center of the occlusal surface on a level w/ the marginal ridges
Slides through the angled sulcus (DB) found on the occlusal surface of Mn Molars
The three cusps that form the primary cusp triangle on a Mx molar are the MB, DB, & ML (not DL or Cusp of Carabelli)
Crowns are either rhomboidal or heart shaped
>Rhomboidal when viewed occlusal
The crown portion that differs the most in contour and size is the distolingual
Their arrangement and design allow room for the powerful masseter muscle
Distolingual Developmental Groove
Fissured groove usually exists on L of Max Molars prone to caries
As such, cavity preparations would most frequently have to be extended from the occlusal to the L of Mx
(more so than to the B of Mn molars dont get clowned)
3 roots (P, MB, DB)
Root length: P > MB > DB
All Mx roots are inclined distally & lingually EXCEPT the DB root of Mx M1 (inclined bucally)
Floor of pulp chamber is triangular (DB, MB, P)
The line connecting the MB and P is the longest
Apex is formed by the P canal
Considering the formation of root and pulp canals, the root canal instrument would be placed from the MB to DB in an
apical direction to gain access to the DB root of the perm Mx M1
Orifice location
MB: under the mesial slope of the MB cusp
DB: under the B groove
P: slightly distobuccal to the ML cusp tip
Distinguish between Mx & Mn molars by occlusal outline, arrangement of roots, & number of roots
NOT by # of cusps, # of developmental grooves, or size of the crowns
All Mandibular Molars:
Wider MD than BL
NO oblique ridge
Rectangular when viewed occlusally
Rhomboid when viewed from the interproximal
4 or 5 cusps with lingual cusps
L cups usually same height
Lingual cusps oppose grooves and embrasures only
Crowns inclined lingually from proximal view and a little distally relative to long axis of root (15-20% Lingual)
Mn molars have long axes positioned with their root apices facial and their crowns lingual
Height of contour is at the jxn of the cervical and middle thirds
2 roots (M or D)
M is very thin MD, wider BL and concave on both M and D
Pulp horn is higher on M than D
All Mn roots are inclined distally & facially
2 pulp canals almost always in M root
MB canal curves more than ML
Larger kidney shaped canal is found in the D root
Smaller more circular canals are found in M root, because there is 2 of them
Characteristics of Individual Teeth
Maxillary Central Incisor:


M/D view = Triangular
B/L view = Trapezoidal
Occlusal =
Longest and widest anterior crown
Longest of all Crowns Correction from old card
But not as thick labiolingually as the Mx canine
Average crown length is 10.5mm
Wider MD than FL (same with Mx lateral incisor)
Incisocervical & mesiodistal dimensions nearly equal
Mesioincisal is sharper
Narrowest incisal/occlusal embrasures of all Mx teeth
Of all teeth, the greatest incisal curvature of a cervical line is on the mesial surface of Mx centrals (more so than Mn
Anatomic features include cingulum, mamelons, marginal ridges & cervical ridges (not triangular ridges or cuspal ridges)
Incisal ridge of the crown is on line with the center of the root
Prominent cingulum located off-center toward distal
Different from Mx lateral in that
Has a shallow, broad lingual fossa on the incisal one-half of the lingual surface
The cervical outline of the facial surface is a broad curve, sometimes described as part of a semicircle
Has a distally located Cingulum (Mx lateral has central Cingulum)
3 Mamelons & 4 Developmental Lobes
Greatest axial inclination relative to occlusal plane (the Mx centrals vary the most from a vertical inclination) its a
28 tilt
Wear facets can develop in the linguoincisal area
M & D pulp horns are more likely to be found in Mx centrals (than Mn centrals??, Mn canines, Mx PM1s, or Mn PM1s)
A cross-section at the CEJ has a round form??? (Book says rounded triangular form)
Kaplan says: round on cross section, but may show some ligual convergence, with the mesial being longer than the distal
1 Root
Triangular pulp chamber in x-section, with the base of triangle located facially, apex located lingually, mesial side longer
than distal side: the tooth is most likely a Mx central
Length is 13mm
One root, one canal
Among choices of Mx central, Mx PM1, Mx PM2, Mn central, Mn lateral, and Mn PM1, Mx central is LEAST
likely to have a divided pulp canal!!!!!
Conical with blunt apex; lends itself well to rotation w/ extraction forceps during surgical removal

Maxillary Lateral Incisor:
M/D view = Triangular
B/L view =
Occlusal =
Smaller than central, and resembles it
MD measurement > FL (same with Mx Central incisor)
Different from Mx central in that
It has a DL groove
Diffentiate from Mn lateral by its more pronounced lingual fossa
Mx lateral is the incisor most likely to have a L groove that extends from enamel to cementum (Know your grooves)
This radicular groove is prone to decay
The DL groove of the Mx lateral is the anatomic feature most likely to complicate root planing
Lingual surface
Lingual surface is most concave of any of the incisors
Lingual surface has most distinct anatomy of all incisors
Lingual fossa is more pronounced on a Mx lateral than a Mn lateral
Marginal ridges are more prominent on the L surface of Mx lateral than other incisors


Mx lateral is most likely tooth to have a carious developmental pit on the lingual surface
Crest of the Cingulum is slightly distal to the faciolingual bisector mmmm, because Cingulum is supposed to be
Longer root relative to crown length
Root length is equal to or longer than that of Mx central (Only dimension like this)
Root is round to ovoid in x-section
Root usually deviates to the distal
More circular pulp outline in x-section
Incisal edges are a little more rounded than on central
Of the Mx incisors, the distoincisal angle of the lateral is the most convex incisal angle
Tooth most often in an abnormal relation and contact with adjacent teeth in the same arch
May be absent
LAST anterior to begin to calcify (10 months)
Among options of Mx canine, Mn canine, Mx central, and Mx lateral, a lingual pit is most common on a Mx lateral
M3s & Mx laterals have the greatest anatomic variation, variation in tooth mass, variation in crown size & form

Lingual view
Mandibular Central Incisor:
M/D view = Triangular
B/L view =
Occlusal =
Smallest permanent tooth
Smooth lingual surface
Flat facial surface
Sharp mesioincisal & distoincisal edges
Incisal Edge
Flat incisal edge
The incisal edge crosses the tooth parallel & slightly lingual to a plane bisecting the tooth into F & L halves
The Mx were just in the middle
Intersecting a plane bisecting the tooth into mesial and distal halves at a right angle to that plane
NOT considered to be wider MD than FL
Most symmetrical tooth
Mn central is usually bilaterally symmetric when viewed labially and incisally
Mesial and distal characteristics of the Mn central are most difficult to distinguish hardest tooth to distinguish R/L
Look at CEJ to determine M or D
Cingulum is centered
Contact Mx centrals during protrusion and lateral protrusion
First succedaneous teeth to erupt
In ideal ICP, the distoincisal aspect will contact with the Lingual fossa of Mx central, NOT distal marginal ridge
The lingual cervical line positioned more apically than facial cervical line
(Also same as Mn Laterals, NOT Mn Canines or Mx anteriors)
Shortest root of all Mn teeth
Thin MD & wide FL
Ovoid on x-section
Concavities on both M & D surfaces (this one gets used over & over again)
Also, B of Mn Molars and MB of Mx Molars
Most common lower anterior with multiple canals!!
(CAREFUL, Mandibular Canine is most likely anterior with multiple roots!! Or in other words Bifurcated)
Root canal:
A cross section at midroot of a perm Mn central is likely to show that the pulp cavity is flattened mesiodistally


Mandibular Lateral Incisor:
M/D view = Triangular
B/L view =
Occlusal =
Slightly larger than central incisor wider MD than Mn central
Mesioincisal edge sharper than distoincisal
Cingulum slightly off center to the distal
Mesial marginal ridge slightly larger
Distal contact area slightly cervical to level of mesial contact area (incisal 1/3)
Viewed incisally, the crown looks twisted on the root base so that the distal is curved toward the lingual
This is the feature that is the most reliable criterion for differentiating perm Mn centrals from laterals
The incisal edge follows the arch curvature in relation to the faciolingual axis
The lingual cervical line is positioned more apically than facial cervical line
Viewed proximally, the greatest curvature of both the F & L outlines will be in the cervical 1/3 of the crown
The greatest FL crown curvatures extend 0.5 mm F or L beyond the FL diameter of the root
Not a big step up from cementum to enamel
Wear facets on the incisal edges of Mn laterals are caused by occlusion w/ Mx centrals & laterals
Small % with 2 canals
Concavities on both M and D surfaces
Very narrow MD Ovoid root in x-section
Larger than central root in all directions

Lingual view of Right

Mesial View of Left Lateral
Maxillary Canine:
M/D view = Triangular
B/L view = Pentagonal
Occlusal = Diamond
Longest tooth; longest root
BUT Longest Crown is Mx central > Mn Canine > Mx Canine
Wider FL than MD has the largest FL dimension of all anterior teeth
The only ones wider MD are Mx centrals and laterals
Bulky crown w/ prominent ridges
Wider MD dimension of the crown on the facial than lingual
Mx canine has the greatest labial convexity of all anterior teeth
Least often extracted (along with Mn canine)
When viewed from incisal, mesial and distal outlines are asymmetrical
BOTH Canines have a longer Distal MR
Remember Primary Mx Canine is the only one with Longer MR
When viewed from incisal, cusp tip is Facial and Mesial
When viewed from incisal, There is a distal portion that exhibits some concavity in the facial outline
NOT thinner mesially!
Gingival pits/grooves, although not type traits, are common features
Incisal margin occupies at least one-third of the crown height
When viewed from the Facial, M and D margins are NOT parallel
THINK Mn Canine is more Parallel (i.e. Straight margins)
Intermediate form between anterior & posterior tooth
Sharp cusp tip (before wear)
The middle facial lobe (of the 4 developmental lobes) is the lobe that includes the cusp tip


In occlusion, the cusp tips do not make contact, because the tips line up with the facial embrasure
Mx cusp tip is more nearly centered over the root when viewed from the labial
NOTE: When viewed from the mesial, a line bisecting the root from the apex passes lingual to the cusp tip
In other words, Mx canine cusp tip is displaced Facially in a F/L direction, where Mn is Lingually
Again, Remember Buck tooth flare up top
OPPOSITE to Mn, which has its cusp tip displaced lingually
Mx crown shorter than Mn crown (but Mx still longer overall)
Mx cingulum more pronounced than Mn
Mx lingual anatomy is more distinct than Mn
BULKIER in Both Directions
Mx crown is wider MD than Mn
Mx crown is wider FL than Mn
Mn crown makes contacts more incisally than Mx!!!!!
Mn crown has a straighter mesial border (viewed from facial)
The cusp tip horizontally overlaps a Mn anterior & a posterior tooth
Mx canine is the only tooth with the potential to contact both anterior & posterior antagonists
Wear facets on the L surface of a perm Mx canine can be caused by contact with Mn canine & PM1
Enamel on the facial surface extends farther apically than the lingual
Normal lingual anatomy:
Cingulum, L ridge, M & D fossae, M & D marginal ridges
NOT prominent developmental grooves & NOT L cusp)!!!!!
There is some evidence of developmental grooves
Dont get clowned, Development Depressions are on the facial
The structure immediately mesial to the DL fossa is the lingual ridge
The structure immediately distal to the ML fossa is the lingual ridge (believe it or not)
The M & D fossae meet the proximal surfaces of the tooth at the M & D marginal ridges
The structure immediately mesial to the ML fossa is the M marginal ridge
The most likely anomaly of a Mx canine is a lingual tubercle??? (agenesis, dwarfed root, peg crown, root bifurcation)
Well developed lingual anatomy, ridges and fossa
Marginal ridges are heavy & prominent
Mesial & distal concavities/fossae are frequently found
Distal portion of the facial surface displays some concavity (viewed from incisal)
Cingulum is centered MD
Height of contour of both labial & lingual is in the cervical third
How to distinguish between R & L Mx canines:
The mesioincisal angle is less rounded than the distoincisal angle
The curvature of the cervical line (CEJ) is greater on the mesial than the distal
The mesial surface is straighter than the distal surface (distal surface is more convex than mesial)
Mesioincisal cusp ridge is shorter than distoincisal so, cusp tip is not centered over the root center (mesiodistally)
From a proximal view, the Mx canine tends to be positioned in the arch with its axis most nearly vertical
(This is from among answer choices Mx canine, Mx lateral, Mx central, Mn lateral, Mn central)
NOTE PMs were not an option, all incisors are flared (Look at the All PMs section for some clarity)
Pulp cavity has its widest dimension faciolingually in the cervical third of the crown (vs. middle third of the root, crown,
Another Q: In the cervical third of the root (vs. apical third of root, incisal third of crown, etc.)
In a MD x-section, the pulp cavity is pointed at its incisal limit
One root, one canal
Least likely tooth to have two roots (among Canines & PMs)
Root has M & D concavities D is more distinct
More oval pulp outline in x-section
Canine eminence making it the thickest in the cervical 1/3rd
Roots of Mx canines dictate alveolar wall morphology, although they are under bone


Mesial of Max Canine
Mandibular Canine:
M/D view = Triangular
B/L view = Pentagonal
Occlusal = Diamond
Long, narrow crown (the only larger dimension on Mn canine than Mx canine is incisocervical)
Longest crown of all perm teeth Toss up with Mx Central
Crown is distally inclined relative to the root
Its greatest FL measurement > its greatest MD measurement (Same as Mx canine)
Less sharp cusp tip (before wear)
Cusp is displaced lingually (differentiate from Max canine, when looking from incisal)
The mesial cusp ridge shorter than distal so, cusp tip is not centered over the root center (mesiodistally)
Has greater bulk distal to a BL bisecting plane than mesial to the plane its the transition tooth !!
The Mx Canine Does NOT have a difference in bulk (M or D)
Height of contour: cervical third for labial & lingual (at the level of the cingulum)
Labial and lingual ridges less developed, great for caries resistance
This is the tooth most likely to resist invasion by caries
Flatter labial surface than on Mx
Lingual surface
Relatively flat in the fossa area
Poorly developed in the marginal ridge area
Poorly developed in the cingulum area
The lingual crown surface is the narrowest MD (among labial or lingual crown surfaces of Mx/Mn canines)
Facial outline (viewed from proximal) is made up of one continuous arc & differs from the outline of a Mx canine
Remember Mx Canine has 3 facial planes
Mesial outline (viewed from facial), from the contact area to the root apex, relatively straight
Mesial axial surface is almost parallel to long axis of tooth
Wear facets are likely to develop incisal 1/3 of the labial surface of a Mn canine
Anterior tooth most likely to have a bifurcated root (facial & lingual)!!!
In x-section at the CEJ, the root is best described as ovoid, but wider mesiodistally at the labial
Irregularly oval
Developmental depression may appear on mesial root surface
Often has a divided pulp (2 canals) more often than Mx canine, Mx central, L root of Mx M1, DB root of Mx M2

Right Mn Canine
Maxillary 1st Premolars:
M/D view = Trapezoidal
B/L view = Pentagonal
Occlusal = Hexagonal
B surface has a prominent buccal ridge running axially
B surface is wider than L surface
L cusp is mesially displaced
B cusp is distally displaced
B cusp slightly to the distal
(BUT Mx PM2 has B cusp offset to the mesial!!!)
So, the mesial cusp ridge is longer than the distal cusp ridge the only PM w/ this feature
Largest of all PMs
Has a greater cervico-occlusal crown height than Mx PM2, Mn PM2, Mx M1or M2, Mn M2
Clinically, a Mx PM1 has four point angles with one point angle located at each of the four corners of the occlusal surface


Marked mesial concavity that progresses onto the root surface

Angular occlusal table
Steepest cusp inclines (well, steeper than Mn PM2, Mx M1, Mn M1 or M2)
Deep Sulcus, meaning steep cusp angles
Mesial contact is towards the mesiofacial line angle its with a Canine
Widest of all PMs, but still greater BL than MD
Mesial marginal developmental groove & mesial crown concavity on the cervical
REMEMBER, MesioLINGUAL developmental groove for Mn (because its by the tongue)
Mesiomarginal developmental groove for Mx
Among PMs, Mx PM1 is characterized by a deepened concavity on the mesial surface of the crown & root
The mesial surface has the deepest concavity of any posterior permanent tooth
The groove is the morphologic feature that presents the greatest difficulty in restorative dentistry
B cusp slightly longer than L cusp
BOTH Mx PM1 and Mx PM2 have L cusps offset to the mesial, but B cusps differ
In a CUSP TO FOSSA contacting relationship in ICP, Mx PM1 is most likely to articulate w/ Mn PM1
NOT both Mn PM1 and PM2 (Dont get clowned)
Picket Fence Pulls it into the Distal Fossa!!!
Occlusal pattern has deep sulcus and long central groove (relative to PM2), but fewer supplemental grooves (than PM2)
Think Biggest PM has to be stretched so it doesnt look wrinkled
2 roots! (The ONLY PM w/ 2 roots) as such, Mx PM1 has a bifurcation
Also has two pulp horns
When viewed from proximal, the axial inclination of roots appears MOST vertical
Cervical x-sections of root outline & pulp chamber floor outline are both kidney-shaped
Among PMs, Mx PM1 generally poses the greatest problem when root canal therapy, extraction or apicoectomy is being
Easiest to perforate
There are sharp demarcations between pulp chambers & pulp canals in Mx PM1s due to 2 roots
This is not the case for any anterior teeth or other premolars
More likely to present w/ 3 roots than Mn central, Mx canine, Mn canine, Mx PM2, or Mn PM2
If Mx PM1 has 3 roots, where would they be? 2 Buccal, 1 Lingual
CAREFUL, eventhough the Lingual is larger
Most common problemwhen extracting? Leaving a root tip
Mx PM1 differs from Mn PM2
It has 2 roots
Has a longer central developmental groove
Presence of a mesial marginal developmental groove
BUT it is the same in that both have a lower L cusp than B cusp (only slightly on Mx)

Crown Outline (Left)

OR Right



Max RIGHT 1st PM

(L canal is bigger)

Maxillary 2nd Premolar:

M/D view = Trapezoid
B/L view = Pentagonal
Occlusal = Rounded (Hexagon)
B cusp slightly to the mesial
(BUT Mx PM1 has B cusp offset to the distal so from the buccal both cusps merge together!!!)
L cusp inclined mesially, just like Mx PM1
Difficult to tell M from D
Crown is wider FL than MD
Less prominent buccal ridge
Smaller than 1st PM
More rounded occlusal table than PM1
Proximal contact with PM1 is Facial to mesiodistal line bisecting the crowns
B & L cusps nearly equal in size and are in-line
Both are offset to the mesial


Distal buccal cusp ridge is longer than mesial buccal ridge (opposite of PM1)
No mesial groove & concavity
Characterized by the presence of a short central groove has more supplemental grooves than PM1
Known as the wrinkled occlusal appearance when compared to PM1
(Good comparative features between Mx PM1 & PM2)
1 root

Mandibular 1st Premolar:
M/D view = Rhomboidal
B/L view = Pentagonal
Occlusal = Diamond (like the canine)
Smallest of all PMs
Most resembles a canine transitional tooth
2 cusps
But, Mn PM1 is the only PM that frequently only has one pulp horn (think of the weak-sauce L cusp)
Cusp may have varying forms (from person to person)
Long, sharp B cusp centered directly over the root
Mesial cusp ridge is shorter than the distal cusp ridge (So B cusp more mesial) Just like Canine
L cusp is also more mesial
Very small L cusp, non-functioning L cusp contacts no Mx tooth in ideal ICP
L cusp is ~2/3 the height of the B cusp
L cusp is similar in development to the cingulum of a canine
Only PM that has a B cusp w/ triangular ridge so uniquely prominent as to frequently separate its mesial pit from its distal pit
HENCE, need for 2 different Preps
Usually no central groove, but may have pits
May have a central pit (but Mn PM2 has one more often)
Both M & D marginal ridges have little or no contact in ICP
More prominent B ridge than 2nd PM
In the Mn arch, the greatest lingual inclination of a crown from its root is seen in Mn PM1!!!!!
Masticatory function similar to that of canine
Facial Masticatory mucosa (attached gingiva) is the smallest
Mesial lingual developmental groove makes mesial marginal ridge run at a 45 degree angle
REMEMBER, MesioLINGUAL developmental groove for Mn (because its by the tongue)
Mesiomarginal developmental groove for Mx
This makes it the only posterior tooth that has higher distal marginal ridge than mesial marginal ridge
More occlusal surfaces can be seen from the mesial than from the distal in a Mn PM1
The groove originates in an occlusal pit & extends onto a proximal surface
Mesial marginal ridge is same height as distal marginal ridge of Mn PM2
1 Root
Has a shorter and pointed apex
Shape of pulp chamber
oval, & wider facial-lingual than mesial-distal
Broader facially than lingually
Usually free of marked distal curvature
Frequently seen with slight concave areas on M & D surfaces
Not flattened faciolingually
If a 2nd pulp canal is present, it is most likely found lingual to the 1st canal
A bifurcation is the most common root anomaly on Mn PM1 (not dwarfing, elongation, concrescence or trifucation)
The pulp chamber morphology of the FACIAL makes it most susceptible to exposure
The Lingual Angulation of the crown forces us to make an angle prep, so we dont hit the chamber




Mesial Right

Mandibular 2nd Premolar:

M/D view = Rhomboidal
B/L view = Pentagonal
Occlusal = Pentagonal
CAREFUL Tests before 98 say Square (Maybe for the H version w/ only 2 cusps?????)
L Height of Contour is OCCLUSAL 1/3rd (THE ONLY ONE TO HAVE IT!!!!)
Most congenitally missing PM
May have 3 cusps; B > ML > DL
If Mn PM is not an option
Maybe Mx M2
B cusp is centered M/Distally
DIFFERENT THAN up top, where they converged
B cusp is shorter than for Mn PM1
L cusps are functional
Wider on L than B
L surface is wider MD than for Mn PM1
Frequently has central pit; other PMs do not
NO ML groove or transverse ridge
Differences between Mn PM2 & Mx PM2:
The tip of the L cusp of the Mn PM2 is closer to the lingual border of the crown Hence Occlusal HOC
The occlusal outline of the Mn PM2 is more nearly square
Mx PM2 is more rounded occlusally rounded hexagon, where this is a Pentagon
The root of the Mn PM2 is more circular in cross section
The B & L cusps of the Mx PM2 are more nearly the same height More so than Mx PM1
The Mx PM2 crown outline (viewed from mesial) is a trapezoid with the short parallel side at the cervix
Whereas Mn PM2 is Rhomboidal
Mental foramen is located most closely to Mn PM2
Another Q: Usually situated nearest the apices of Mn PM1 AND PM2
1 Root
Thicker and longer than PM1
Longer, with blunted apex
Rounded root; lends itself well to rotation w/ extraction forceps during surgical removal (also Max central incisor)
ONLY PM with NO mesial root depression
Occlusal schemes
Most common type
The PM w/ the occlusal groove pattern that may simulate the letter "Y" is Mn PM2
5 lobes, 3 cusps
2 L cusps & 1 facial cusp (F > ML > DL)
This means the Mn PM2 is the only PM that usually has 2 L cusps
Shorter and wider than PM1
Square occlusal
*Because of this scheme, the Mn PM2 frequently has a central pit (the other PMs do not)
The total # of pits (3) on the occlusal surface of Mx M1 is the same as is found on a Y-type Mn PM2
The only premolar that may exhibit 3 occlusal pits
4 lobes, 2 cusps
More common than U-type
4 lobes, 2 cusps
Central developmental groove can look like a U or crescent
So, Mn PM2 is the tooth most likely to possess a crescent-shaped central developmental groove
Central developmental groove that is crescent shaped and extends out as a mesial and distal developmental groove
Dens Evaginatus most commonly on Mn PM2
May contain a pulp Horn
Maxillary 1st Molars:
M/D view = Trapezoid


B/L view = Trapezoid

Occlusal = rhomboid
Cornerstone of Mx arch
Largest permanent tooth NOT Mn M1
Rhomboidal outline (obtuse ML and DB; acute MB and DL)
Broader lingually than buccally (unlike any other perm)
(Has a MD measurement greater lingually than facially)
This makes the lingual embrasures associated w/ the Mx M1 relatively small
Cusp of Carabelli on ML cusp (5th cusp)
The Carabelli or fifth cusp on a permanent Mx molar is found on the ML lobe of M1
ML > MB > DB > DL (same sequence for Mx M2)
ML cusp is the largest and longest?? cusp of perm Mx teeth!!!!!
DL cusp is largest DL cusp of max molars
The most significant difference in the occlusal surface anatomy of Mx M1, M2 & M3 is the DL cusp gets progressively
The ML cusp tip is located D to the MB cusp tip
The DB cusp tip is located L to the MB cusp tip
Central groove runs from mesial pit to central pit on the occlusal table
The central pit is formed at the bases of the triangular ridges of the ML, MB, and DB (not DL)
There are 3 pits in Mx M1 (Same as Mn PM2 Y type)
Oblique ridge
The occlusal surface is usually distinctly divided by a ridge from the ML to the DB cusp
Forms the distal boundary of the central fossa
Passes through the DF sulcus (or angular sulcus) of permanent Mn M1
Opposes the developmental groove between the DF and D cusps of Mn M1
Is at the level of the marginal ridges
Mesial contact area when viewed from the mesial is usually facial to the center of the crown F/Lingually
CAREFUL, distal contact is centered Just like anteriors
The M border is broader than the D border
Both Mx M1 and M2 have Mesial Inclination
Distal surface has pronounced cervical concavity hard to adapt a matrix band (Along with Mesial of Mx 1st PM)
There is also a Mesial concavity that requires special attention when removing calculus deposits (Mx PM1 has one, too)
2nd Perm to erupt after Mn M1s
From the distal aspect, one can see 4 cusps
Occlusal contact should be anticipated on the L slope of the F cusp, the F slope of the L cusp, and L slope of the L cusp (but
not the F slope of the F cusp)
Roots two facial, one lingual
Tripod splayed out, whereas Mx M2 are closer together
Triangle formed by the orifices of the canals, the line connecting the P (L) to the M is the Longest
Roots of Mx M1 are equal or longer than roots of Mx M2
All 3 visible from Buccal
Root length/size: P > MB > DB
Is the largest, longest and strongest
(3rd longest of Max after canine and 2nd PM root)
Wider MD, than BL
Often has concavities/depressions on facial and lingual surfaces of the root
Longitudinal depression on the lingual, Concave on the buccal
Viewed from B, in line with B groove
Viewed from L, in line with the midpoint of MD diameter
Usually has 1 root canal
The shortest and smallest root
Little thicker B/L than M/D
Sharp apex
More inclined distal than 2nd Max Molar
Inclined Buccally
Flattened MD and has root depressions on both its M & D surfaces
Thicker B/L than mesiodistally
Blunted apex


Often has MB1 and MB2 (60%)

If a Mx M1 has a 4th canal, it is located in the MB root MB root can have 2 canals
MB2 is just L to the orifice to the MB Canal
Pulp horns of MB (and ML, if present) usually higher than D or P
The pulp horns most likely to be accidentally exposed in a Class II prep are MB & ML
ML comes with a MB 2 canal
Distance from cervical line (from farthest to closest): D > F > M
Remember Mn Molars have Bifurcations (F/L) and Mx Molars have TRIfurcations (F/ML/D)
Has a B developmental groove, starting at furca and ending at CEJ
If a root goes into Mx sinus, it is usually from Mx M1

Distal view
Mesial View
Cervical Cross
Maxillary 2nd Molars:
M/D view =
B/L view =
Occlusal =
At cervical level = Irregularly Triangular
Parotid Duct (Stensons) opens opposite to Mx M2
Smaller than 1st
No Cusp of Carabelli
Smaller oblique ridge
DL cusp is smaller than Mx M1
DL can be absent this means that Mx M2 can have 3 cusps w/ a central pit (also Mn PM2 and Mx M3)
DL groove is shorter than on Mx M1
MB line angle is most acute (viewed from occlusal) due to rhomboidal shape (MB & DL are acute)
B broader than L Think you turned Heart Shaped
More angular than 1st Molar
Both Mx M1 and M2 have Mesial Inclination
B groove is shorter and does NOT have a pit
The most constant & valuable trait to differentiate among Mx M1, M2 & M3 is the relative position of the DL groove
Shorter than roots of Mx M1
Closer together (more potential for fusion)
Have a greater distal inclination and have longer root trunk
The axial inclination of the P root of Mx M2 is distal & lingual
P is straighter than P of Mx M1
Maxillary 3rd Molars:
M/D view =
B/L view =
Occlusal = Heart shaped (Most often)
Most often congenitally missing tooth (along w/ Mn M3s, of course)
3 or 4 cusps (small or sometimes missing DL cusp, making it heart shaped with the apex lingually)
Among options of Mx M1, Mx M3, Mn M1, & Mn M3Mn M3 most frequently has 3 cusps
No Cusp of Carabelli
THE 1 constant
Always have BL wider than MD
Roots fused
The Mx tooth exhibiting the greatest statistical variation in root alignment is M3
The MB is noticeably larger than the DB
Shortest permanent tooth
Oblique ridge is often absent
May have paramolar attached
Crown tapers more from B to L
Has a single antagonist in ICP (NOTE: Mn centrals also occlude with only 1 tooth)


In a normal dentition, maxillary teeth having single antagonists are the M3s
Strange & extra anatomy (usually undersized anomalies)
Maxillary tooth exhibiting the greatest statistical variation in root alignment

Left M3
Mandibular 1st Molars:
M/D view = Rhomboid
B/L view = Trapezoid
Occlusal = Pentagonal
Cornerstone of perm dentition
MD dimension > BL dimension (Only slightly says the answer)
Has the longest MD measurement of all perm molars
When viewed sagittally, Mn M1s have their long axes at an angle least perpendicular to the occlusal plane
DONT get clowned, because Mn M2 still has its roots set back most distally
Most often restored, extracted or replaced
5 cusps
3 buccal (MB, DB, D) & 2 lingual (ML, DL)
3 cusps can be seen from the buccal
Where is the Distal cusp located??? Distofacial
All about the same size: MB is the largest cusp & D is the smallest cusp
The distal pulp horn is the smallest on this tooth
The second largest Cusp is the ML
Lingual cusps are higher and more pointed
The position & height of L cusps of Mn M1 accommodate working movement
The L surface of each L cusp possesses a slightly convex shape in the occlusal third
5 cusps = 5 pulp horns
5 cusps = 5 triangular ridges (95% sure)
Distal cusp projects into the distal fossa of the Mx M1
The largest proximal crown surface of a Mn molar is the mesial of Mn M1
Buccal pits in the buccal groove common place for caries
Crooked central groove in MD course
4 Grooves on Mn M1
1 central, 2 Buccal grooves (B & DB); 1 Lingual groove
The developmental groove between the distofacial cusp & the fifth cusp of a perm Mn M1 is the distofacial
The Number of developmental grooves distinguishes Mn M1 from Mn M2 4 for M1 and 3 for M2
Of all molars, the mesial fossa of the Mn M1 is most distinctly separated from the remainder of the occlusal table by a
transverse ridge (not to be mistaken with the oblique ridge of Mx Ms)
Both marginal ridges have developmental grooves
2 Roots, usually 3 canals (2 mesial canals) 2 roots means Mn M1 has a bifurcation
Furcations are B and Lingual
Roots incline distally
Pulp chamber is wider MD than FL
Have Longitudinal grooves on Both M and Distal surfaces of Mesial root,
BUT no longitudinal groove on the Distal of the Distal root
What distinguishes Mn M1 mesial root from Distal root?
Larger, 2 canals, biconcave
Mesial root of Mn M1 is typically very thin MD, much wider FL, and concave on both M & D surfaces (also MF of Mx
Mesial root has a strong distal curvature in the apical 1/3rd
In a mid-root x-section, the mesial root of Mn M1 is larger than any other Mx or Mn M1 root
The distal is smaller than mesial (D before M!!)
Are strongly compressed in a MD direction
The root trunk of the perm Mn M1 is equal in length to the mesial furcation of Mx M1
Which was the shortest distance to furcation from CEJ


Right Mn M1
Mesial Root
Buccal of R
Distal of L
Mandibular 2nd Molars:
M/D view =
B/L view =
Occlusal = Rectangular
4 cusps
Cusps are of approximately equal size
CAN see the Lingual cusps from the Facial view as a little taller (SEE PIC BELOW)
Perm M2 differs from perm M1 in number of cusps
The DB cusp is the centric holding cusp of this tooth, and it occludes in the central fossa of Mx M2
Use height of contour to distinguish between B & L
Viewed from the occlusal, The greatest FL diameter of Mn M2 is located in the mesial 1/3 of the crown
More occlusal surface is visible from distal than mesial view
Normally the crown of Mn M2 inclines mesially & lingually
Facial has slight cervical dip, Lingual does not
3 developments grooves (from occlusal aspect) Central, Buccal, and Lingual
B & L developmental grooves
B groove extends half way down B surface Hello, buccal pit anyone?
L groove barely extends onto L surface
B & L grooves form right angles with central groove makes a + shaped occlusal surface
Central groove straight groove
More secondary grooves than Mn M1
1 B groove and 1 B pit no DB groove, as is present in Mn M1
Has large MB cervical expansion (like primary M1)
Viewed from the occlusal, the greatest FL diameter of a perm Mn M2 is located in the mesial third of the crown
2 roots (M & D) Distal is smaller again, D before M!
Closer together & inclined more distally than Mn M1 roots
Longer root trunk

Buccal view of R
Mandibular 3rd Molar:
M/D view =
B/L view =
Occlusal = Ovoid
4 or 5 cusps
Bulbous crowns that taper M to D
Calcification begins at 8-10 yrs
Extra grooves
MB cusps are wider/longer than DB
Rectangular form MD dimension of the crown is greater than the BL
Perm molar w/ shallowest central fossa
Oversized anomalies are more common, undersized more common in Max M3s
This Q comes from the 2001 Pilot:
Q: A radiograph of tooth #32 shows two well-formed roots. When sectioning this tooth to separate the roots & simplify
extraction, which of the following best describes how the cut should be made?
A: Bucco-lingually through the crown & furcation
Marked distal inclination of root trunk


Roots fused and shorter

Long root trunk

Virtually always have one root & one canal
Newly erupted have 3 pulp horns
Least likely to have divided pulp canal (among Mx PM1, Mn cent, Mn Lat, and Mn PM1)
Pulp outline is somewhat triangular at cervical level
Pulp chamber is wider M/Distally
Mesial and distal pulp horns are MOST likely
Mid-root is round
Newly erupted have either 0 or 2 pulp horns
Pulp outline is round for both sections
Root length is the only dimension that is the same or bigger than Mx central
Pulp chamber has the greatest faciolingual width of any anterior tooth
Longest root/Longest root canal
Least likely tooth to have two roots (among Canines & PMs)
F/L longitudinal section has the pulp cavity its widest dimension in the cervical third
Pulp cavity in M/D section is pointed at its incisal limit
Cervical cross section is ovoid, wider labiolingually
Mid-root is less ovoid to round
70% 2 canals
2 pulp horns, buccal is larger
Possibility of 3 Roots (2 Buccal/1 Lingual)
Sharp demarcation between chamber and canals
Lingual canal is slightly wider, even though lingual root is usually small
Cervical cross section is Kidney shaped with concave side on M
Mid-root is figure 8 shaped, lingual canal still slightly larger
30% 2 canals, usually just branches into 2 foramina in the apical third
2 horns, B is larger
Cervical cross section is oval
But remember, it still has a root depression MAND PM2 is only PM that DOES NOT have a mesial
root depression
Mid-root is ovoid and wider BL than MD
MB1&2, DB, Palatal
60% MB2 canal
Always assume there is an MB2, unless you dont find it (the root is so wide)
NO pulp horn for cusp of Carabelli
MB and ML pulp horns are most susceptible to exposure
Cervical cross section is rhomboid
Mid-root has 3 roots, M with 2 canals
Furcations (closest to the CEJ = Mesial more than Facial more than Distal is Farthest
P root has a buccal curvature
P root has a concave lingual surface
Often has concavities/depressions on facial and lingual surfaces of the root
Longitudinal depression on the lingual, Concave on the buccal
DL pulp horn is smaller than M1 to match DL cusp size decrease


When compared to M1, M2 roots are greater in distal inclination

The axial inclination of the P root of Mx M2 is distal & lingual
Opposite to Mandibular M1 and M2, where M1 has greater distal inclination
When crown is heart shaped, cervical cross section is more triangular
70-90% are normal
10-30% 1 canal with branching into 2 canals
1-2% 2 fully formed root canals
NO pulp horns
Cervical cross section is Thin M/D, Wide F/L, and Concave on both M/D surfaces (see both pics)
Mid-root is still ovoid, but canal is more constricted
60% 1 canal
40% 2 canals look for double PDL space
Often the canals join apically will usually heal if you seal off one canal
Very few of the two canal cases do not join apically
NO pulp horns
Cervical cross section is ovoid
Mid-root is still ovoid, but canal is more constricted
6% with 2 complete root canals
Occasionally 2 roots (Labially and Lingually)
Cervical cross section is ovoid (irregularly oval)
Ovoid and wider M/D on the labial
Another Q: Flattened in a M/D direction
Mid-root is ovoid
25% 2 canals (or more)
Fast-beak phenomenon: apically the canal space disappears means you have 2 canals
During Endo on #21, you suspect a second canal, MOST likely on LINGUAL just like Canine
2 pulp horns, large pointed B horn, small rounded L horn
Sometimes L is missing, and then would look like a canine
Broader facially than lingually
Usually free of marked distal curvature
Frequently seen with slight concave M/D
Cervical cross section is ovoid
Mid-root cross section is round
5% 2 canals
2-3 Pulp horns (Y type have 2 lingual pulp horns) with B a lot larger
Cervical cross section is ovoid
Mid-root cross section is ovoid
Always 2 mesial canals
70% have only 3 canals
30% have 2 distal canals, for a total of 4
4-5 Pulp Horns
Mesial 2 are about the same size, Distal 2 are about the same, but the MB is a lot bigger than the DB
Pulp horns likely to be exposed in newly erupted Mn M1 are BOTH MF and ML
D horn is sometimes large enough to detect (usually only in newly erupted)
Cervical cross section follows crown shape with 5 humps in the chamber (Pentagonal)
Mid-root is usually elongated kidney of M with 2 canals and concave toward Distal, then D root has 1
canal kidney shaped with concave toward M


Watch for C shaped canals in Distal root

Mesial root is very thin M/D, much wider F/Lingually and concave on BOTH M/D surfaces
Mesial root has the greatest mid-root cross section of any first molar root
Still usually 2 canals in M root
Usually just one canal per D root
Varies, but usually same as M2
All Rules
All embrasures are greater on the Lingual EXCEPT
Mx M1, M2
Mn anterior (to the mesial of the Canine)
Viewed from occlusal, all posteriors have contacts slightly buccal to the faciolingual midpoint
Also, slightly to the occlusal from the center of the proximal surface
Viewed labially, anterior teeth have contacts in the incisal to middle 1/3, except for the D contact of Mx canines
All permanent incisors have M and D contact areas approximately centered faciolingually
Viewed from facial, the proximal contacts are as follows:
Max teeth
IJ, JM, JM, MM, MM, MM, MM, M (all Ms except 1st 5 contacts IJJMJ) I Jump Jump Michael Jordan
Mand teeth
II, II, IM, MM, MM, MM, MM, M (all Ms except 1st 5 contacts be sure to count each one)
***I = Incisal 1/3rd
***J = Junction of Incisal/Middle 1/3rd
***M = Middle 1/3rd
NOTE: Mx centrals & laterals and Mn laterals (???) have distal contacts apical to their mesial contacts (so do Mx canines)
Maxillary central & lateral IP contact
The contact is centered faciolingually
NOT incisocervically
The lingual embrasure is wider/larger than the facial embrasure
There was a PBL type question that basically stated the orthodontist would want the distal proximal contact of the Mx
central and the lateral to be in the incisal 1/3rd, (IN reality, it should be Junction)
Mn incisor IP contact
Contact tends to occur equidistant from F & L surfaces
Contact occurs in the incisal third of the crown
Mn Canine and Mn PM1
Centered faciolingually
The facial embrasure is smaller than the lingual
In the incisal third
Mandibular posteriors
In the Mn posterior segment of the arch, the contacts of Mn PM2 & all 3 Mn molars are aligned in a straight line
This is not the case in the Mx arch
Proximal contact of posterior teeth creates wear patterns that eventually cause reduced IP embrasure spaces
The following anterior teeth have a distal contact area in a more apical position than the mesial:
Mx central incisors; Mx lateral incisors; Mn lateral incisors more apical, yet still in I
The following permanent teeth have mesial & distal contact areas at about the same level occlusocervically:
Mn central incisors, Mx PMs, Mx molars, Mn molars
The contact area DOES
prevent food impaction
form embrasures
stabilize the dental arch
protect the periodontium
It does NOT
distribute occlusal forces
protect mucosal tissues
provide better retention for the restoration
provide spillways, maybe the embrasure does
guide food toward the occlusal surface


guide food over the free margin of the gingiva

Loss of the contact area can result in drifting of teeth, food impaction, bone loss, damage to the interdental papilla, unfavorable
Contact areas between posterior teeth in normal alignment aid in preventing mesial and distal drift
NOT in preventing Rotation
When two proximal surfaces diverge from an area of contact, lingual, facial, occlusal & cervical embrasures are formed
A proximal surface is always next to an adjacent tooth (hence, proximal)
Occlusal table
Area of a tooth bordered facially & lingually by crests of the cuspal ridges of F & L cusps, and mesially & distally by crests
of the marginal ridges
Normally makes up 55-65% of B/L tooth dimension
Overbite (vertical overlap)
Is when incisal edges are w/in incisal third of mand incisors
Overjet (horizontal Overlap)
Pt with overjet has?? Decreased anterior disclusion??
Determinants of Occlusion
R/L TMJ and suspensory ligaments and condyles
Teeth (occlusal surfaces)
Neuromuscular system
Programmed by teeth and what nature/man do to them
4 Determinants of design for restoring complete and functional occlusal surface:
Amt of vertical overlap allows you to make the cusps bigger and fossa deeper
Contour of articular eminence
Amt & direction of lateral shift in working condyle
Position of tooth in arch
Equilibration (Occlusal Adjustment) Principles:
Maximum distribution of stress
Forces borne on long axis
Change surface to surface flat contacts to point-to-surface
We want DOTs not Smudges
Odonto-, Enamelo-, Coronoplasty
Relationship of bones of the upper and lower jaws w/o tooth contact
CO (ICP) is slightly anterior to CR
Ligament Guided
Relationship between Max and Man occlusal surfaces that provides the Maximum Inter-locked Position MILP
Tooth Guided
Determined by tooth contacts
The VDO is smallest in a position of maximum intercuspation
ICP supports the mouth during empty mouth swallowing
During non-masticatory swallowing, the teeth are usually in contact in ICP
Rinses the mouth of saliva and helps moisten oral structures
Masseter muscles contract and the tip of the tongue touches roof of mouth
Tooth contacts are longer duration during swallowing than chewing
When the Mn moves from ICP (MILP maximum interlocking position??) to a more posterior position, any tooth contact
that occurs is called a retrusive contact
Placing the Mn in a retruded path of closure usually results in: (meaning you stop at Retruded Contacts)
Increased VDO, increased horizontal overlap (of incisors?), and decreased vertical overlap
In a retruded contact position, the Mx central does not contact any tooth
Terminal Hinge Axis
The center of rotation for the mandible when it opens from retruded contact position
Rest (postural) position of Mn
Muscle guided occurs when muscles of mastication are in tonic equilibrium


Determined exclusively by the behavior of the mandibular musculature

Usually there is no teeth contact
Occurs the neuromuscular system has the least amount of activity
Usual reflex is the tonic stretch reflex of Mn elevators (myotatic reflex)
If the mandible were forced into CR from the rest position, the pts reflex neuromuscular defense would resist the
applied force
Freeway Space or Interocclusal distance
Results from Rest Position of the Mn
When mandible is at physiological rest, the space that exists between the teeth, (should be no contact)
Averages between 2-6mm
All 8 muscles of mastication plus supra and infrahyoids are in equilibrium
Angle Classes of Occlusion
*Determined by MB cusp of Mx M1
Class I (70%)
*MB of cusp line up with MB groove
In terms of cusp/fossa relationship, the DB cusp of the Mn M1 rests in the central fossa of Mx M1
Mx centrals overlap Mn centrals
Mx canine lies in embrasure between Mn canine and PM1
Mn posteriors are positioned more lingually & mesially than Mx posteriors
Mx posteriors are positioned more facially & distally than Mn posteriors (hey, it was a question)
Which may occur in class I pt
ANSWER was NONE of these:
Cross tooth balance
Bilateral tooth contacts in excursives
Posterior tooth contacts in protrusive movements
If you move from a postural position to ICP, you will be using the temporalis (last bit of closure)
Class II (25%)
*MB cusp between Mn M1 & PM2
Mn incisors occlude even more posterior
In a protrusive movement (in a Class II relationship), Mn canines articulate w/ canines, if you are thinking Class
II shift back
Mn PM1 lies between Mx PM1 & PM2
Mx canine is mesial to Mn canine
MB cusp of Mn M2 would articulate in the central fossa of the Mx M2, NOT the normal marginal ridge areas
Increase/Decrease Condylar Distance, OR Increase/Decrease of Bennett Angle
One of these 2, game time decision ???
Class III (<5%)
*MB cusp falls between Mn M1 & M2
Chin protrudes
Mn incisors overlap anterior to Mx incisors
A patient w/ a true or pseudo-Class III (Angle) occlusal relationship has no incisal guidance
As the Mn retrudes, the Mx laterals contact Mn canines & laterals
In a Class III malocclusion, the MB cusp of Mn M1 occludes in the mesial fossa of Mx PM2
Mx canine is distal to Mn canine
Often found when Mn arch is larger than Mx arch
Guiding cusps = Balancing = Non-supporting = Non-centric = Shearing
Mand Lingual, Max Buccal
Supporting cusps = Working = Stamp = Centric (NOTE: This changes with posterior crossbite pts)
Mn Buccal, Mx Lingual
Centric stops are areas of contact that a supporting cusp makes with opposing teeth
i.e. ML cusp of max molar with central fossa
5 Characteristics
Contact opposing in ICP
Support VDO of the face
Nearer to the faciolingual center of the tooth
Outer incline has potential for contact
Broader, more rounder cusp ridges
In centric occlusion, opposing contact may be expected at B slopes of L cusps of Mx posterior teeth
Posterior crossbite:
Mx facial & Mn lingual cusps are considered supporting cusps
In a working movement, the inner aspects of Mn L cusps may contact (inner means twd the tooth midline, not inner
as in toward the lingual)


Anterior crossbite:
When Mx & Mn incisors are in crossbite, the contacting surfaces are Mn lingual & Mx facial
Supporting cusps vs. Guiding cusps
Supporting cusps make fossa or marginal ridge contact
Supporting cusps of the same quadrant line up with each other
Guiding cusps are related to IP areas or developmental grooves
Guiding cusps overlap facial to Mn teeth & lingual to Mx teeth
NOTE: Mx F cusps & Mn L cusps (Guiding or non-supporting cusps) require sufficient occlusal length & horizontal
overlap for soft tissue protection
Horizontal & vertical overlapping of teeth afford some degree of protection for lips, cheeks & tongue
PICKET FENCE (get your incisal edge/cusp tip stuff down)
Teeth occluding only 1 tooth in opposite jaw:
Mn centrals
Mx M3s (Dont get clowned by Mn M3s in a question!)
Mx lateral opposes incisal edge of Mn lateral & canine; but, opposes no teeth at its incisal edge!!!!!
Cusp tip of Mx canine is in direct alignment w/ a facial embrasure of the Mn teeth
Mx posterior teeth oppose F & L inclines of F cusps, and F inclines of L cusps (not L inclines of L cusps)
L cusps of Mx posterior teeth oppose marginal ridges and central & distal fossae
B cusps of Mx posterior teeth oppose grooves & embrasures (meaning buccal grooves, not central grooves)
L cusps of Mx PMs contacts the distal fossa of respective PMs (Mx PM2 distal fossa of Mn PM2)
F cusps of Mx PMs oppose Mn PM & tooth distal to it
Mx PM1 opposes Mn PM1 & PM2
Distal marginal ridge of Mx PM1 is in contact w/ the mesial ridge of the F cusp of Mn PM2
In LEFT lateral movement, the L cusp of Mx RIGHT PM1 may appear to pass toward the tip of Mn PM2
Mx PM2 opposes Mn PM2 & M1
In a CUSP TO FOSSA contacting relationship in ICP, Mx PM1 is most likely to articulate w/ Mn PM1
(This is due to the lingual inclination of Mx PM1 Mn PM2 is not involved in a CUSP TO FOSSA manner)
ML of Mx molars goes to central fossa
ML cusp of the perm Mx M1 opposes the central fossa of Mn M1
ML cusp passes through the LINGUAL sulcus if its on the same side as the working movement
ML cusp of LEFT Mx M1 slides through the sulcus between DB and D cusps on Mn M1 during a RIGHT
working movement
DL goes to distal marginal ridge of same numbered Mn molar and mesial marginal ridge of tooth distal to it
DL cusp of Mx M1 opposes the mesial marginal ridge of Mn M2
DL cusp of Mx M2 opposes the mesial marginal ridge of Mn M3 & the distal marginal ridge of Mn M2
MB cusp of Mx M1 opposes the B groove of Mn M1
NOTE: its the triangular ridge of this cusp, not the cusp tip that opposes the groove DONT GET
But, in a more recent question, it was the tip of the MB cusp of Mx M2 that opposes the B groove of Mn M2
In left working movement, the MB cusp of Mx right M2 will pass through, NOTHING, its the buccal cusp
DB cusp of Mx M1 opposes DB developmental groove of Mn M1!!!!!
DB groove also serves as escape for ML in non-working
The DL cusp of Mx M2 has the potential to oppose the mesial portion of Mn M3
Oblique ridge of Mx M1 opposes the DB groove on Mn M1!!!!!
(The prior 3 lines work great together, since the DB cusp connects through the oblique ridge to the ML cusp)
Mn central opposes Mx central only distoincisal aspect of Mn central opposes the lingual fossa of Mx central
Mn centrals contact Mx centrals during protrusion and lateral protrusion
It is important to check protrusion when restoring the incisal edge of an anterior tooth
Mn lateral opposes the distal marginal ridge of a Mx central, mesial marginal ridge of Mx lateral, and maxillary lateral
incisor 2-3 mm cervically to the incisal edge
Mn canine (incisal 1/3 of facial surface) opposes a Mx lateral & Mx canine at the approximation of their marginal ridges
An older question gave opposes the incisal embrasure between Mx lateral & canine as the correct answer, but in
this question (1989Q63), that answer option was available and was incorrect
The mesial cusp ridge of a perm Mn canine opposes the distolingual of the Mx lateral
B cusp of Mn PM1 contacts the mesial marginal ridge area of the Mx PM1
L cusps of Mn molars oppose grooves & embrasures (meaning lingual grooves, not central grooves)
ML cusp of Mn molar opposes the lingual embrasure of the same numbered Mx molar and tooth mesial to it
ML cusp of Mn M2 opposes the embrasure between Mx M1 & M2
DL cusp tip of Mn M1 has no antagonist


***D cusp of Mn M1 projects into the distal fossa of Mx M1

DB cusp of Mn molar opposes the central fossa
The central fossa of Mx M2 would be contact with the DB cusp of Mn M2
MB cusp of Mn molar opposes the mesial marginal ridge of the same numbered Mx molar and the distal marginal ridge
of the tooth mesial to it
MB cusp of Mn M1 opposes the occlusal embrasure between Mx PM2 & M1
MB cusp of Mn M2 opposes the mesial marginal ridge of Mx M2
B cusp of PM1 lies directly below the contacting area of Mx canine & PM1
B cusp of PM2 opposes the mesial marginal ridge of the Mx PM2
Some teeth w/ little or no marginal ridge contact in ICP & eccentric relationships
M & D of Mn PM1, D of Mn PM2
Class II Picket Fence
In a patient with a Class II, Division I angle occlusal relationship in maximum ICP, the MB cusp of Mn M2 articulates
with the central fossa of Mx M2
3 Planes of Movement
Frontal (up/down)
Horizontal (side/side)
Sagittal (forwards and backwards)
5 Factors of Mandibular movement
Initiating Position (CR)
Most stable and most easily reproduced
Types of Motion
When the mouth is open to any given degree, there is more interocclusal
distance anteriorly than posteriorly because of the rotary nature of the
opening movement
1st ~20mm of opening is rotational; then translational
Occurs when the Mn moves from a maximum intercuspal position to a
maximum protruded position
***NOTE: When the mandible is opened beyond the point where the
condyle begins to translate, the meniscus glides downward and forward on
the articular eminence
Opening the mouth maximally from retruded position causes the Mn to
rotate, then translate
Direction of Motion
3 Planes
Degree of movement
Clinical significance of movements
Each pt may have different relationships
Mandible is a Class III lever like a shovel
Fulcrum Condyle
Force Muscles
Workload Teeth
Functional Occlusion
All contacts during chewing, swallowing, or normal actions
Those made outside normal range, may create wear facets or attrition
Bruxing, clenching, nail biting, thumb sucking, cheek biting
Jaw closure in parafunction varies from masticatory function in the following ways:
Teeth seldom, if ever, contact in mastication
Teeth are in tight contact during parafunction
Masticatory cycles are vertical and cyclic


Sagittal Plane Posselts Envelope (ABOVE)

The final movement of the Mn in tooth closure is directed by the cusp-fossa relationship of opposing teeth
The maximum intercuspal position is the most superior point #3
Postural or rest position is that black dot right under #3,4
Retruded contact position is #4
Terminal Hinge axis is #6F
Masticatory Cycle of mandibular central incisor is #5
Curve #7 is the pathway for a maximum opening both rotatory & translational (NOT a border movement)
From which point to which point is there the greatest change in anterior guidance? I think from 3 2 (OR from CR
(3) to Edge to Edge Contact (2)
Intercuspal position is determined almost exclusively by tooth contact
The maximum opening position is the most inferior
In a normal diagram in the sagittal plane, initial occlusal contact in RCP occurs at a more inferior position than ICP at #4
Mastication of food occurs primarily in lateral contacting movement
In 90% of the population, the average distance from 34 is ~1.25mm (ICP is anterior to RCP)
In the other 10%, 3=4 (RCP = ICP)
The left border above is the protrusive opening path
Frontal Plane
Viewed anteriorly, chewing stroke (masticatory movement) vertical & tear drop in appearance (RIGHT)
In Frontal Plane there is Posterior contacts only on A
Canines are cusp tip to cusp tip on B

Horizontal Plane (Gothic Arch)

This records the position of the Mn anterior teeth, in assessing condylar movement via the lateral pterygoids
The diamond shape results from 1) L lateral, 2) L lateral w/ protrusive, 3) R lateral, 4) R lateral w/ protrusive
Points 5 & 6 in the figure on the right (below) represent the R & L lateral contacting positions, respectively
The apex of the horizontal plane Gothic arch tracing represents CR (OR POINT 1 Below)
Diagram shows (1999 Q 197 SEE RIGHT)
Horizontal component of movement from retruded contact position (1) to ICP
Anterior component of movement from ICP (2) to maximum protrusive
position (4)
Lateral component of movement from retruded contact position (1) to ICP (2)
Mandibular movements occurring laterotrusively
This diagram does NOT show Vertical component of any of the


Centric Relation





Bennett Movement = Lateral shift = Immediate side shift
Best described as a bodily shift of the mandible in the direction of the working condyle
Occurs during the earliest stage of lateral movement
Influences the M/D position of the cusps on all molars
Thats how you know where to wax up your cusp tips
The greatest influence of Bennett movement is potentially on the working side teeth in lateral movement
Wrong answers include: on posterior teeth in RCP, ICP, or during protrusion
When an exaggerated Bennett component is present in lateral jaw movement, it will have its greatest potential for
interference with the MD positioning of cusp tips
Most influences the lingual concavity of the maxillary anterior teeth and the cusp height and groove direction of the
posterior teeth (2001 Test, but before we had Anterior Guidance, what gives???)
Bilateral Balanced Occlusion
The stable simultaneous contact of opposing upper and lower teeth in centric relation position with a smooth bilateral gliding
contact to any eccentric position within the normal range of mandibular function, developed to lessen or limit tipping or
rotation of the denture bases in relation to the supporting structures
Unilateral Balanced Occlusion AKA Group Protected or Group Function Occlusion
If you extract the mandibular canine, you then would have only posterior group fxn
The idea is to eliminate all Non-working contacts
*In unilateral balanced occlusion, contact between upper B & lower B cusps, along w/ simultaneous contact between upper L
& lower L cusps, will most likely occur in laterotrusive movement
Mutually Protected Occlusion (MPO)
Includes Anterior and Canine Guidance
None of the posterior teeth contact on the non-working side when the Mn moves laterally
Anterior teeth disclude all posterior teeth in eccentric movements
Condyles are in their most superoanterior position in closure
Axial loading of occlusal forces occurs in closure
Posterior teeth contact more heavily than anterior teeth
In mediotrusion, the posterior teeth disclude the anterior teeth; in protrusion, the anterior teeth disclude the
posterior teeth
Anterior Guidance (anterior coupling)
Results from both horizontal and vertical overlap
Provides protection in disclusion of posteriors
Plays the greatest role in disoccluding the posteriors in latero-protrusive movements
Anteriors have mechanical advantage because they are farther away from the fulcrum, so better leverage to offset the
closing musculature
Canine Protected Occlusion
Only canine is involved in MPO
Curve of Spee
Best described as the anterior-posterior curvature of the occlusal surfaces of the teeth, as seen in a facial view
Mx arch is convex; Mn arch is concave
Another: The line beginning at the tip of the canines & following the F cusps of posterior teeth (viewed from the facial)
Curve of Wilson
Tilting of the Mn posteriors lingually makes the Mn arch concave & the Mx arch convex, when viewed from the front
According to curve of Wilson which way do maxillary molar roots tilt?
Compensating Occlusal Curvature or Sphere of Monson
The 3D curvature of the occlusal plane, which is the combo of Wilson and Spee
The line beginning at the tip of the incisors and following the facial cusps of the posterior teeth as viewed from the facial
Axial Position
Which describes the relationship of the teeth with the vertical axis?
Spee, Wilson, Monson, or Axial inclination (Position)


Normally described in terms of the roots inclination, which means that the crown is normally inclined in the
opposite direction
Cusp Height Potential
Less vertical overlap, shorter the cusps must be
Greater vertical overlap, longer the cusps may be
Increased overlap allows for higher cusp ridges and deeper fossae
Less horizontal overlap of anteriors, longer the cusps may be
Greater horizontal overlap, shorter the cusps must be
Teeth articulation
The following are alterable factors in tooth articulation:
Incisal guidance, compensating curve, cusp-fossa relationship, & posterior tooth morphology (not postural position)
NOTE: Lateral movements are an asymmetrical Mn movement (retrusion, protrusion are symmetric movements)
Laterotrusion = Working movement
In a lateral excursion, the teeth that ideally provide the predominant guidance through the full movement are the canines
In a lateral excursion, the Mn canine cusp tip passes mesial to the Mx canine cusp tip
The lingual cusps of a Mn M1 must be restored to accommodate working movement
From R lateral relation to centric: DB cusp of Mn M2 moves through the buccal groove of R Mx M2
During a working movement, the F cusp ridges of the Mx PM1 on the working side oppose the distal cusp ridge of Mn
PM1 & the mesial cusp ridge of Mn PM2
In a R laterotrusive movement, the L cusp of R Mx PM2 passes through the embrasure between R Mx PM2 & M1
In a R lateral excursion, the ML cusp of the perm R Mx M1 passses between the L cusps of Mn M1
This ML cusp passes through the L groove of Mn M1
In a R working movement, the ML cusp of L Mx M1 moves through the sulcus between DB & D cusps of Mn M1
A broad, flat facet existing on the outer aspect of the ML cusp of a Mx M1, and running in a ML to DF direction, was
probably caused by a working movement??? I think NON working!
In a L working movement, MB cusp of L Mx M2 will pass through the B groove of L Mn M2
In a L working movement, MB cusp of R Mx M2 will pass through nothing (actually mediotrusion for this cusp)
Mediotrusion = Non-working = Balancing movement
On Mn M1, the DF groove serves as an escapeway for the ML cusp of the Mx M1 during non-working Mn movements
The non-working condyle moves downward, forward & medial
The non-working pathway of Mx cusps on Mn posterior teeth is toward the distofacial
In a patient with a left canine protection, the ML surface of the R Mx M1 contacts the DB surface of the R Mn
M1 during a left lateral excursion. This contact is a non-working side interference
On the non-working side in an ideal occlusion, interfering contacts on posterior teeth will be located on the inner incline
of Mx & Mn supporting cusps
When moving the Mn from ICP to a R lateral relation, the L cusp of L Mx PM1 movees through the F embrasure
between the L Mn PMs
If the L cusp of #5 breaks off during trauma, this is most likely due to a left mediotrusive movement
In a L lateral movement, The L cusp of the R Mx PM1 may appear to pass toward the B cusp of the Mn PM2
The most likely Mn movement that occurs in breaking a Mn central incisor is a protrusive movement??? (01 Pilot)
Dumb Q: In protrusion, which way do the Mx cusps go? Nowhere, but maybe it was posterior relative to the Mn cusps
Condylar movement
A bilaterally symmetrical condylar movement
Lateral pterygoids are primary movers
The condyle moves forward and carries the disk with it
The underside of the meniscus moves distally relative to the superior surface of the condyle
The disk tends to be tilted in a superior-inferior fashion on the condyle
Mn incisors
Make contact w/ Mx incisors in protrusive & lateral protrusive movements (but NOT working/nonworking)
Contacting surfaces are the lingual of the Mx & incisal edge of the Mn
In a protrusive contacting movement, Mx laterals contact the Mn laterals & canines
In a protrusive movement, the F cusp tip of Mn PM2 has the potential to contact the DF cuspal incline of Mx PM1
When a protrusive Mn movement (anterior teeth edge-to-edge) is achieved, the Mn M1 has the potential to contact Mx
Protrusive pathway
The protrusive pathway of Mn cusps on Mx posterior teeth is toward the mesial
Remember arrows on the Mx teeth tell exactly where the Mandible is going.
Arrows on the Mn teeth are in opposite to actual direction of mandibular movement
Lateral checkbite record


Using the lateral checkbite record to set a respective condylar inclination implies that:
The non-working side condyle has moved anteriorly & medially
TMJ structural elements:
Condylar process, articular disc, capsular ligament, & joint cavities (not sigmoid notch)
The TMJ has two synovial cavities
Dense avascular fibrous CT covers the articulating osseous structures of the TMJ
There are also a few elastic fibers present
Glenoid fossa an oval cavity/depression in the temporal bone, anterior to the auditory canal
The joint:
A bilateral (complex) diarthrosis between 1) the articular tubercle/eminence of the temporal bone & 2) the Mn condyle
One Q said: What type of joint is the TMJ? Ans: an atypical diarthroidal joint (atypical due to lack of hyaline
Oblong processes, wider mediolaterally than anteroposteriorly
Concave anterior aspect (fovea pterygoidea)
Articulating surface is the superoanterior aspect slightly convex
Retrusive both condyles move upward & back into the Mn fossa
Protrusive both condyles move forward & down the articular eminence
Lateral contacting mvmt:
Working side condyle merely rotates
In laterotrusion, the working condyle rotates along a vertical axis and translates laterally (a little,
Non-working side condyle moves downward, forward & medially
Lateral protrusive mvmt:
Working side condyle rotates, moves forward & downward
Non-working side condyle moves forward & downward & medially
***See p. 587 in Kaplan for pictures I think this could be a dont get clowned thing
The articular disc:
Is the tissue intervening between the articulating bones of the TMJ
Effectively divides the TMJ into two separately functioning compartments
The disc is attached laterally to the Mn condyle
Collateral Ligaments
The disc (meniscus) is moved forward principally by the lateral pterygoid muscle
Some fibers of the lateral pterygoid m. attach to the anterior border of the disc
Kaplan says: the medial & lateral corners of the articular disc are directly attached to the poles of the condyle via the
collateral ligaments
As the mouth is opened widely, the articular disc moves anteriorly in relation to the articular eminence, but distally in
relation to the condyle
In the sagittal plane, the posterior border is the thickest section of the articular disc

Joint spaces:
Upper compartment:
The space between the disc and the articular fossa & eminence
More recent Q: The superior joint cavity of the TMJ is bordered by the Mn fossa & the superior surface of the disc


Translation occurs here

Lower compartment:
Rotation of the condyle primarily occurs in the inferior joint space
Temporomandibular (lateral) ligament
Has an outer oblique portion which limits the extent of jaw opening and initiates translation of the condyle down the
articular eminence
With a fracture of the left condyle, the condylar head remains in the mandibular fossa due to the TM ligament (01)
Prevents posterior & inferior displacement of TMJ

Collateral ligament
Medial and lateral connectors from the disc to the condyle
Restricts the movement of the articular disc away from the condyle during function
Another Q: Discal ligaments (synonyms) restrict the movement of the disc away from the condyle during fxn
During lateral Mn movement, the articular disc is tightly attached to the condylar head by the collateral ligaments
When the cusp tips of left Mx & Mn canines are placed in contact, the right condyle is positioned down the slope of the
articular eminence
Ligaments associated w/ the TMJ serve to protect surrounding & supporting tissues from damages
During function and in traumatic situations, the TMJ is protected by the synovial fluid, durability of the fibrocartilage,
ligament suspension, and muscles of mastication
Whats under the fibrocartilage? Periosteum???
Undifferentiated Mesenchyme or Hyaline Cartilage??
A projection of the facial surfaces of Mn molars would be medial to the anterior border of the ascending ramus
The condyle on the working side generally rotates about a vertical axis and translates laterally (rotation is the 1 movement)
Innervated by PAM: Posterior deep temporal, auriculotemporal, masseteric
Mandible position
Mn ALWAYS deviates to the side of the injury
Lateral pterygoid muscle (mandible deviation)
Hypoglossal nerve (tongue deviation)
Mn postural position is determined almost exclusively by the behavior of the Mn musculature
So its not alterable
Primary Muscles of Mastication (4 Pairs)
Origin: Lateral surface of temporal bone
Insertion: Coronoid process of Mn
Anterior fibers elevate the Mn (close the mouth)
Q says masseter & medial pterygoid hold the condyle in most superior anterior position
Posterior fibers contraction retrude the mandible
Temporalis muscle is the principal retractor of the Mn
They are assisted by the anterior and posterior bellies of digastric muscle
Origin: Zygomatic arch
Insertion: Lateral side of angle of Mn
Closes the mouth (elevator of Mn)
The most powerful muscle of mastication??? (1999 Exam.pdf #177 & 02 #178 what about temporalis?)
Medial Pterygoid
Origin: Medial surface of lateral pterygoid plate, pyramidal process of palatine bone & tubercle of Maxilla
Insertion: Medial side of angle of Mn
Closes the mouth (elevator of Mn)


NOTE: the masseter & medial pterygoid position the condyle in the most superior anterior position
Lateral Pterygoid
Superior head:
Origin: Infratemporal surface of sphenoid bone
Insertion: TMJ capsule & disc [SUPERIOR HEAD];
Inferior head:
Origin: Lateral surface of lateral pterygoid plate
Insertion: Condyle of Mn
NOT an elevator of Mn
Simultaneous contraction: depress (open) & protrude the jaw
Unilateral contraction: side-to-side movement of Mn
The muscle of mastication primarily responsible for synchronizing the movement of the condyle & articular disc
Contraction results in moving the mandible in opposite direction of contracted muscle (working movement)
(right muscle contraction moves Mn to the left)
Contraction of both simultaneously results in protrusion
Lateral pterygoids are the prime movers to a protrusive position
Contraction produces a forward movement of the condyle from the articular fossa
Contraction also opens the jaw
Assisted by the anterior bellies of digastric and omohyoid
Brings the articular discs and condyles down and anterior
When the incisal edges of the anterior teeth are placed in end-to-end contact, the Mn condyles have moved
downward & forward
Subsidiary Muscles
Compresses the cheek holding food under the teeth
Suprahyoid Muscles (4)
Contract to raise the hyoid bone during swallowing
In swallowing, downward displacement of the Mn is prevented by contraction of the masticatory muscles
Also, teeth come into occlusal contact & the tip of the tongue touches the roof of the mouth
Assist lateral pterygoid in depressing the mandible (Opening the mouth)
Assist Posterior fibers of Temporalis during retraction
Pulls the hyoid superiorly and posteriorly during swallowing
Fixes the hyoid bone for infrahyoid action
Anterior belly
Opens mouth (depresses Mn)
Arises from trochlea of hyoid bone & inserts into digastric fossa of Mn
Innervated by mylohyoid branch of V3
Posterior belly
Fixes the hyoid bone for infrahyoid action
Arises from mastoid process & passes through trochlea of hyoid bone
Innervated by digastric branch of VII
Elevates the hyoid bone
Raises the floor of the mouth (for swallowing)
Depresses Mn when hyoid is fixed
Forms the floor of the mouth in the lingual vestibule
Inserts into the mylohyoid line on the medial side of the Mn
Moves in an upward slanting direction to the posterior
In the Mand M2/M3 area, the root apices are inferior to the mylohyoid line
Apices of Mand PM1/PM2 are superior to the mylohyoid line
Innervated by mylohyoid branch of V3
Depresses Mn
Can also help to retract Mn
Works with mylohyoid
**Both genio and mylohyoid form floor of the mouth
Innervated by C1 via CN XII


Infrahyoid Muscles (4) [Strap Muscles]

Depressors of the larynx and the hyoid bone
Lie between deep fascia and visceral fascia covering the thyroid gland, trachea, and esophagus
Innervated by ansa cervicalis (motor plexus from the Ventral rami of C1-3)
Pulls the hyoid downward and raises the larynx
Pulls the hyoid downward
Pullys the larynx downward
Pulls the hyoid downward
Extrinsic Tongue Muscles (4) pg 405 Netters H&N anatomy
Genial tubercle to dorsum of tongue
Protrudes the tongue and Depresses the tongue
The muscle fibers that extend into the lingual frenum are from the genioglossus
Also has inferior fibers that connect the tongue to the hyoid
Greater and lesser horn (cornu) of the hyoid bone to lateral aspects of the tongue
Depresses the lateral sides of the tongue
Styloid process to lateral aspects of the tongue
Retracts and elevates the tongue
Palatine aponeuroses to the side of the tongue
Elevates the posterior tongue and closes the oropharyngeal isthmus
(aiding in the initiation of swallowing)
Does not retract the tongue
Intrinsic Tongue Muscles (3)
Alter shape of tongue
Shortens tongue (curls tip)
Narrows tongue
Flattens and broadens tongue
Incision By incisors
Prehension (grasping) by the canines
Trituration by PMs and Ms
**The masticatory function of incisors & canines is primarily biting
Comprised of 2 functional units:
1) Gingival Unit
Free gingiva + attached gingiva + alveolar mucosa
Lined by masticatory mucosa
2) Attachment apparatus
= Cementum + PDL + Alveolar bone proper
NOTE: a question gives cementum, PDL & bundle bone as the correct answer (not lamina dura) see below
What protects the attachment apparatus
Anterior teeth might be responsible for disarticulating the posterior teeth in parafunctional grinding
Oral Mucosa is either keratinized or non-keratinized
Strata basale, spinosum, granulosum, corneum
Strata basala, spinosum


Lamina propria
Dense CT of variable thickness
CT papillae carry BVs & nerves
Epithelial rete pegs are found between the CT papillae
CT of variable thickness/density
Contains glands, BVs, nerves, adipose tissue
Types of Oral Mucosa
Masticatory Mucosa
Free gingiva (some), hard palate, attached gingiva, interdental gingiva, dorsum of tongue
The hard palate submucosa contains adipose tissue anteriorly & glands posteriorly
NOTE: the hard palate also has long rete pegs
Orthokeratinized true keratin, NO nuclei, Uneven surface --- Dentures??
Parakeratinized keratinized cells retain their nuclei Masticatory Gingiva??
Thick, dense, firm lamina propria
Of Mn teeth, the facial masticatory mucosa (attached gingiva) is narrowest on PM1
Non-masticatory Mucosa = Lining or Reflective Mucosa
Free gingiva (some), lips, cheek, vestibule, alveolar mucosa, floor of mouth, soft palate, ventral tongue
Thin, movable
Specialized Mucosa
Covers the dorsum of the tongue and taste buds
Vermilion border
Transition zone vs. Skin of the lip
Keratinization ends
Longer papillae carrying large capillary loops
Fewer sebaceous glands
No sweat glands
Sidenote: the # of melanocytes per unit area of mucosa does not vary between races; the difference is in cellular activity
Gingival fibers
Collagen fibers that provide support for the marginal gingiva including the interdental papilla
Found w/in the Free Gingiva
Continuous with the CT fibers and are often considered part of the ligament (PDL)
Types (5)
Circumferential (circular) fibers
Encircle the tooth around the most cervical part of the root and insert into the cementum and lamina propia
of the free gingival and the alveolar crest
Resist rotational forces
Transseptal fibers
Extend from tooth to tooth coronal to the alveolar crest & are embedded into cementum of adjacent tooth
Occurs through the Interproximal segment of the alveolus
NOT via the facial aspect of the alveolus
Not on the facial and no attachment to the alveolar crest
These are not PDL fibers (apical, oblique, principal, transverse, & interradicular fibers are PDL or
principal fibers)
Maintain dental arch integrity
Dentogingival fibers
From the cementum apical to the epithelial attachment and course laterally and coronally into the lamina
propia of the gingival
Dentoperiosteal fibers
From the cervical cementum over the alveolar crest to the periosteum of the cortical plates of bone
Alveologingival fibers
Insert in crest of alveolar process and spread out through the lamina propria into the free gingiva
Apical, Oblique, Horizontal & Alveologingival fibers are attached to bone
Gingival apparatus
Term used to describe the 5 gingival fiber types and the epithelial attachment
Gingival ligament
Includes the dentogingival, alveologingival, and circumferential fibers


Free Gingiva (aka Marginal gingiva)

Collar of tissue that is not attached to the tooth or alveolar bone
1-3mm wide and forms the soft tissue wall of the gingival sulcus next to the tooth
Described as forming the wall of the gingival sulcus
Extends from free gingival groove to gingival margin/crest
(The free gingival groove is what gives the gingival roll its appearance its the one Jake & Boom-Boom
overacccentuate separates the free gingiva from the attached gingiva)
The healthy free gingiva aids in the self-cleansing process by adhering closely to the tooth surface below the height
of contour of the cervical enamel
NOTE: If the cervical enamel ridge is too great, it will adversely affect the self-cleaning quality of a dentition
Gingival Margin
Top edge or crest
1mm band of gingiva that forms immediate collar around the base of the tooth
Hence Marginal Bleeding
Gingival Sulcus
Areas between the unattached gingiva and the tooth (Popcorn kernels)
Above jxnal epithelium, continuous with, but structurally different
Epithelium is non-keratinized (same w/ gingival col)
Then your PMNs couldnt get out!!
Healthy sulcus should NOT have rete pegs (rete pegs indicates inflammation)
Epithelial attachment (Junctional epithelium)
Joins the gingiva to the tooth
Normally follows curvature of CEJ
Does NOT normally stay at the same level throughout adult life
Inner layer of cells of junctional epithelium attaches gingiva to tooth
***Hemidesmosomes & Internal basal lamina are referred to as the epithelial attachment
The epithelial attachment in always an actual part of the tooths periodontium
The junctional epithelium is thin & non-keratinized
Susceptible to bacterial metabolite breakdown
Lymphocytes & plasma cells are routinely seen in the bottom of the gingival sulcus
Interdental Papilla
Portion of the free gingiva that fills the gingival embrasures (below contact area)
Consists of 2 papillae that are connected by the concave-shaped interdental col
Interdental col
Conforms to the shape of the contact area
Not present in teeth w/o contact
Small proximal contact areas with firm well-formed interdental papillae tend to decrease caries
susceptibility when occlusal and environmental factors are favorable
When restoring coronal structure, the creation of excessively round buccoproximal line angles tends to
create abnormal function with the interdental papilla
Deflective fxn of mesiofacial and distofacial line angles protects the interdental papilla
The interdental papilla between the Mand 2nd PM and 1st Molar is the shortest
(all other answer choices were anterior to this answer what about between the molars?)
Incisive Papilla
The elevation of gingival tissue directly lingual to embrasure between Mx central incisors
Free Gingival Groove
Separates the free gingiva from the attached gingiva
Attached Gingiva
Part of the gingiva that is attached to the underlying periosteum of the alveolar bone and to the cementum by CT
fibers and epithelial attachment
Present between the free gingiva and the more movable alveolar mucosa
Extends from Mucogingival jxn to free gingival groove
The attached gingiva on the facial of the Mand 1st PM is very narrow
Mucogingival Jxn
Separates the attached gingiva and the alveolar mucosa
Joins lining mucosa and masticatory mucosa
Separates Keratinized from Non keratinized


Attached Gingiva
Stippled, firm, thick
No separate Submucosa, hard palate?
No glands, except posterior of hard palate
Epithelial ridges high
Epithelium thick, keratinized

Alveolar Mucosa
Thin, loosely attached to periosteum
Well-defined submucosa
Many small glands present
Epithelial ridges low
Epithelium thin, non-keratinized


General Info:
0.2mm wide
Widest in the cervical region narrowest in the middle region
Thickness depends on:
Age (thickness decreases 0.1mm in old agefrom deposition of cementum and bone)
Stage of eruption
Fxn of the tooth
In loss of function:
PDL narrows it becomes taut like yarn
Regular arrangement is lost
PDL becomes a thin MB w/ irregularly arranged fibers
Cementum may become thicker
In occlusal trauma:
Alveolar bone is resorbed
PDL is widened (PDL space enlarges) -- inflammation
Tooth becomes loose
Health & ability of PDL to resist occlusal force depends on:
Anterior teeth have slight or no contact in ICP
The occlusal table is less than 60% of the overall FL width of the tooth
The occlusal table of the tooth is generally at right angles to the long axis of the tooth
Crowns of Mn molars are inclined about 20 toward the lingual
Derived from the dental sac
(which makes the entire attachment apparatus- cementum, PDL, and alveolar bone proper)
Forerunner of the PDL in mandibular development is the Dental Sac
Connects to cementum and alveolar bone (Directly adjacent)
Contains remnants of Hertwigs root sheath (Rests of Malassezcalled cementicles when calcified)
Sharpeys Fibers terminal portion
Diameter greater on bone side vs. cementum
PDL contains:
Blood vessels
Periosteal blood supply is the major source of blood to the PDL
Also gingival arteries & arteries of the periapical area
Extracellular substance of fibers (gingival and principal)
Mostly collagen
Type I & III
Ground substance
Mostly proteins and polysaccharides
Oxytalan fibers
Related to the microfibrillar component of elastic fibers
Run parallel to root surface
Fxn of PDL:
Attachment of tooth to bone via principal fibers
Formation of CT components by activities of CT cells (cemento-, fibro-, and osteoblasts)


By activities of CT cells (blast vs. clast of above cells)

Through blood vessels
By Trigeminal nerve
Proprioceptive and tactile sensitivity
DOES NOT help to maintain the epithelial attachment
If you bite on a popcorn kernel, what causes relaxation of the jaw???
Mechanoreceptors in the PDL (Mesencephalic Nucleus)
Principal Fibers (5)
Main structural elements w/in the PDL
There are NO elastic fibers in the PDL
Composed of Type I collagen
Collagenous ONLY
Classified as belonging to general group of alveolodental fibers
Offer initial resistance to tooth movement in occlusal direction
Alveolar crest fibers
From cervical cementum of the tooth to the alveolar crest
Fxn to counterbalance the occlusal forces on the more apical fibers and resist lateral movement
Oblique fibers (33%)
Insertions into the cementum and extend apically and obliquely into the alveolus
Most resistant fibers to forces along the long axis of the tooth (masticatory)
Protects tooth from apical pressure
Reduce the probability of forceful impaction into the alveolus because of a blow to the crown
Group of fibers most likely to be found in the middle 1/3rd of root
Horizontal Fibers
Perpendicular from alveolar bone to the cementum and resist lateral forces
Interradicularr fibers
Only in multi-rooted teeth
Extend from cementum in furca are to bone w/in furca area
Part of alveolar bone that houses teeth
2 Main Parts:
1) Alveolar Bone Proper
AKA Cribiform Plate, Tooth Socket, or Lamina Dura
Immediately surrounds root of the tooth to which the PDL fibers attach
Has minute openings for vascular and nerve components (called Cribiform plate or lamina dura)
2 layers of Bone:
Compact lamellar bone
Layer of bundle bone layer PDL fibers insert into this bone
Tooth attachment via Cementum, PDL, AND Bundle Bone
2) Supporting Alveolar Bone
Bone which surrounds the alveolar bone proper and gives support to the socket
2 Types of Bone
Cortical plate compact bone forms the outer and inner plates of alveolar process (thicker in Mn)
Spongy Bone fills in area between cortical plates,
NOT present in anterior or in radicular bone of maxillary posteriors as the cortical plate fuses
with the cribiform plate
IN SHORT From tooth
Cementum PDL Bundle Bone Lamellar Bone Cortical Plate Spongy Bone Cortical Plate
The ratio of organic to inorganic material is approximately the same in alveolar compact & spongy bone
Normal interosseous architecture is influenced to the greatest extent by the level of adjacent CEJs (because the level of
the CEJs determines the height at which the PDL attaches to cementum)
During eruption of perm teeth, alveolar bone is resorbed & deposited intermittently
In health, the height of the IP alveolar crest is related to the position of the cementoenamel lines of adjacent teeth!!!!!
Alveolar crest & interdental septum can be altered by:
Tooth rotation, drifting, tilting, or eruption
When viewed occlusally, the alveoli of R & L Mn central/lateral incisors tend to be aligned nearest to a straight line
What causes formation of the alveolar process?


Formation of teeth
W/o teeth there is no process
Retromolar pad
A slight elevation of gingival tissue, normally found posterior to the most posterior Mn molar tooth
Nasopalatine canal
Its opening is located at the anterior midline of the palate
Random stuff added from recent Files
Most important thing in checking excursive
Lateral checkbite
Most important in checking protrusion
Condylar inclination
whats most important when checking articulation of teeth!!!!!
bennet angle
condylar inclination
ICP contacts I put this
Horizontal angle
Lateral check bite
Whats most important thing in mounting maxilla to articulator
bennet angle
condylar inclination
ICP contacts
Horizontal angle
Lateral check bite
Facebow record I put this
Whats most important thing in checking excursives
bennet angle
condylar inclination
ICP contacts
Horizontal angle
Lateral check bite
Facebow record
Whats most important thing in checking protrusives
bennet angle
condylar inclination I put this
ICP contacts
Horizontal angle
Lateral check bite
Facebow record
You change the settings on the condyle of the articulator on BOTH sides, what movement does it affect?
Left lateroprotsive
Right lateroprotsive
Left medioprotusive
Right Medioprotusive
Right laterotrusive this is what I put because it was the only one different from all the rest as it wasnt
adjusting condyler angle on articulator directly effects what movement on the excursives: posterior guidance (closer to articular
eminence) or Ant guidance (protrusion)
Questions with pictures (not added to notes)
77 Q07, 66, 78, 84; 79a Q01-05, 07, 30, 64, 71, 78, 81, 82, 90-93; 79b Q01-04, 07, 25, 32-36; 80 Q01-06, 20, 86, 91-94; 81 Q01-10,
18, 22, 25-27, 80, 87, 92; 84 Q01-08, 15, 26, 33, 35, 56, 70; 86 Q01-09, 10?, 28, 38, 57, 63, 67, 73, 85; 88 Q02, 08, 11, 16, 20, 26, 29,
32, 41, 43, 48, 56-7, 62, 68, 72, 75-6; 89 Q02, 07-09, 13, 24, 25, 36, 37, 54, 62, 69; 96 Q14, 16, 28, 32-4, 41, 43, 45, 51, 66
USC messed up the following questions:
1977 Q41; 83
1979a Q49 (E should read 2-4mm)
1979b Q47 (no picture)
1980 Q 1,2 wrong pics, 96??
1984 Q39 (wrong Ans should be (e), (f), (g)); Q81 (poorly worded should say toward the incisal at the (A) mesial aspect)
1989 Q19 (no correct Ans would be E); Q39 (wrong Ans should be C)


1996 Q35 (no picture); Q81 (no correct answer option given the correct answer is C)
Lame questions:
1977 Q35 (Dryopethecus pattern); Q50 (teeth of grazing animals); Q70 (dentin islands); 88
1979a Q19 (fossil teeth see 79b Q ); Q97 (rodent teeth)
1979b Q28 (biochem about muscles); Q43; Q79 (anatomy section)
1980 Q96

Random Stuff all from 2007 so know this you dummy

Teeth with least amount of angulation? premolars


More detail on thoracic duct lots of 2007 questions from that.
Exocrine organs
USC messed up the following questions:
1979 Q79 (all of these structures pass through the diaphragm)
Questions I just didnt include:
1982 Q92

Components of cells
o Plasma MB:
Dynamic, selectively permeable MB enclosing the cytoplasm
Between cell wall & cytoplasm
Lipids (phospholipids, cholesterol, glycolipids)
o Cholesterol increases mechanical stability; also decreases MB fluidity, but prevents freezing
o Increasing unsaturated FAs increases fluidity
Proteins (integral MB proteins & peripheral MB proteins)
o All transport proteins are integral MB proteins
One layer of charged lipids on either side of a layer of neutral lipids
Cell coat and microfilaments are attached to the cell membrane (golgi complex is not)
o Cell Wall:
Protects the cell from changes in osmotic pressure
Anchors flagellae
Maintains shape
o Fluid stuff:
Viscous, translucent, watery material that is a primary component of animal cells
Contains large % water & inorganic ions (K+, Ca2+, Mg2+, Na+) & naturally occurring organic compounds (e.g., proteins)
o Irritability
Property of protoplasm responsible for cell being sensitive to a stimulus
Protoplasm of the cell nucleus plays part in reproduction
Communicates with the cytoplasm by way of nuclear pores
o Molecules < 40kD can diffuse freely between nucleoplasm & cytoplasm thru the pores
Protoplasm of the cell body that surrounds the nucleus, converts raw material into energy
Site of most synthesis activities
Contains cytosol (viscous, semitransparent fluid that is 70-90% water), organelles, and inclusions (metaplasm)
Name given to lifeless material stored in cytoplasm
EX: glycogen (an example of a cytoplasmic inclusion), fat deposits, pigment granulesincluding lipofuscin (yellowishbrown substance that in quantity as cells age), and melanin (abundant in epidermis of skin & retina)
o Lipofuscin is the wear & tear pigment
o Microtubules:
Specialized type of filament composed of polymerized tubulin (protein)
Cylindrical hollow structures in the cytoplasm of all eukaryotic cells
Provide support and assist in cellular locomotion
Flagella and cilia
o Flagella:
Present in humans only in the spermatozoa
Core composed of microtubules
9 double circumferential microtubules and 2 single centrally located microtubules
Much longer than cilia

Move w/ an undulating snake-like motion

Short, hair-like projection from the cell MB
Beat in coordinated waves
Core composed of microtubules
9 double circumferential microtubules and 2 single centrally located microtubules
9 + 2 arrangement of microtubules
o Similarities between Flagella and Cilia:
Nine sets of doublets, two singlets in center
Basal body
Essential to function of cilia and flagella
From the basal body, fibers project into the cytoplasm, possibly to anchor the basal body to the cell
Move by contraction of tubular proteins
o Axoneme: Inner core of the flagella or cillia
Characteristic 9+2 pattern
Peripheral pairs share common wall of 2-3 protofilaments
Central pair of tubules are separated from one another and are enclosed w/in a central (single) sheath. Doublets and
central sheath linked by nexins
o CenTRIoles:
Nine sets of triplets
The microtubule organizing center of the cell
o Centrosomes:
Contain centrioles
Much smaller than microtubules and have contactile and structure groups (a filament is much smaller than a tubule)
Contractile is made up of
o Double-stranded helices of polymerized actin
o Actin and myosin
Structural is made up of
o Tonofilaments support the cell and provide attachments for Desmosomes, which anchor contigous cells, and
terminal webs , which anchor microvilli
What layer are they found in???? are they used in hemidesmosomes at the basal layer = stratum germ/basale,
Im going with Spinosum?
They are found in ALL layers except for corneum This test Sucks!
If it said anything about desmesomes Id go with spinosum. Hemidesmisomes go w/ basale.
Involved in local movement, by sliding filament movement (as in muscle fiber microfilaments)
o Microvilli:
Think Microvillaments
Core of microfilaments
Primary purpose is to increase functional surface area (not flagella or cilia)
o ***Hey: Microvilli have microfilaments; Cilia have microtubules dont screw it up!!! Since flagella and cilia are
for movement, you need a TUBE rather than a little filament. Actin and Myosin (the filaments) are in the intestinal
o Stereocilia:
Long, nonmotile microvilli that cover the free surface of some of the pseudostratified columnar epithelium which
line the inside of the Epididymis
S for Sex and Stereocilia
Different from Cilia in that they are Nonmobile and have microvilli (microvillaments) NOT microtubules
Facilitate the passage of nutrients from the epithelium to the sperm by increasing the epitheliums surface area
Also present in the ductus (vas) deferens, which is also lined with pseudostratified epithelium
Intermediate filaments
Attachments between IFs are by DESMESOMES
Rope-like filaments that function in structural roles
Barr body: The unused X chromosome in the XX female or the XXY (abnormal) male
Sex chromatin body
Genetic activity of both X chromosines is essential only during the first weeks after conception
Later development only requires one functional X
Inactivated X chromosome appearing in dense chromatin mass attached to nuclear MB of normal female
Absent in normal males
If a male has a barr body, then he has Klinefelters (XXY)
Sex of embryo determined if Barr body present, as early as eight weeks





Important in recognition in epi cells because it tells us sex

Cytoskeletal elements:
Form network of protein structures
DNA is found principally in the nucleus
Feulgen Reaction test to distinguish beween DNA and RNA
Tells us what the Nucleus is FEUL (full) of
Nucleolus: located within the nucleus and NOT MEMBRANE BOUND
Site of rRNA synthesis (not DNA, tRNA, or mRNA) Assembles ribosome components
NOTE: rRNA is the most abundant RNA in the cell
NOT bound by a membrane (unlike nucleus, lysosome, mitochondrion, & pinocytotic vesicle)
Site of protein synthesis
All protein synthesis begins on free polysomes
Smooth ER (ribosomes are absent): Stores Ca++ in muscle cells
Steroid synthesis (vs. Protein Synthesis for RER)
The Q reads: Smooth ER predominates in steroid producing cells, but not in protein producing cells
Protein synthesis for use inside the cell not sure about this isnt this done by free ribosomes.
Intracellular transport
Detoxification reactions (hydroxylation & conjugation)
Glycogen degradation & gluconeogenesis (glucose-6-phosphatase is an integral MB protein of the SER)
Lipolysis begins in the SER
***Hepatocytes & steroid hormone producing cells of adrenal cortex are rich in SER
Rough ER (ribosomes are attached):
Protein synthesis for use outside the cell aka, site of synthesis of secretory proteins
Also site of N-linked oligosaccharide addition to many proteins
Think Osteoblasts
Associated with RNA repeated again & again & again on tests (rRNA)
*Cytoplasmic RNA is localized in granular endoplasmic reticulum
Has regions that are smooth in appearance called transitional elements
***Mucus-secreting goblet cells & Ab-secreting plasma cells are rich in RER
Active cells characterized by an abundance of rough ER (fibroblasts, osteoblasts)
Golgi apparatus:
Flat, membranous sacs or cisternae arranged in stacks (the stacks are called dicytosomes) w/ two poles
The cis face receives material
The trans face is for transportation function
Packages, stores, modifies & sorts products post-translational
Packages secretory material and forms lysosomes
Forms glycoproteins for extracellular use
Proteoglycan assembly from proteoglycan core proteins
Modifies N-oligosaccharides on asparagine
Adds O-oligosaccharides to serine & threonine residues
Procollagen filaments formed here from polymerization of amino acids!!!!! KNOW THIS
Polymerization of molecules into collagen fibrils occurs in the Golgi
Cytoplasmic MB-bound vesicles containing glycoprotein hydrolytic enzymes that digest & destroy exogenous material
Lysosomes deal w/ biochemical breakdown & phagocytosis in the oral region
Are formed in the Golgi apparatus (they bleb off of it)
Are called to action when the cell produces too much proteins
Contain oxidases, enzymes capable of reducing oxygen to hydrogen peroxide and hydrogen peroxide to water
Bile acid synthesis occurs in peroxisomes
Store & excrete various substances w/in the cytoplasm
Threadlike structures w/in the cytoplasm that provide ATP
Similar to bacteria in shape & size
Reproduce by dividing (also like bacteria)
The most important organelle or component of a cell for oxidative processes = mitochondrion
Contain a double MB (inner & outer MBs)
Outer MB:
o Smooth, continuous, permeable

o Contains a lot of porin (integral MB protein that forms channels in the outer MB)
Inner MB:
o Impermeable to small ions (due to high content of cardiolipin)
o Enzymes for ETC & Oxid Phos are embedded in the inner MB
Both mitochondria and nucleus have double-unit membrane (not lysosome, Golgi complex, or rough ER)
Maternal DNA Link
Contains cyclic DNA like bacteria
Crista of the Mitochondria folds of the inner membrane
Stores and provides more surface area for chemical reactions to occur (Protein NZs)
Embryonically early cell types/forms:
o Mesenchymal cells (mesoblastic cells)
Potential to proliferate & differentiate into diverse types of cells
Form a loosely woven tissue called mesenchyme or embryonic CT
o Mesectoderm (ectomesenchyme)
Derived from ectoderm, especially from the neural crest in the very young embryo
The primary source of cranial connective tissue cells is the ectomesenchyme
o Neural crest cells:
Give rise to spinal ganglia (dorsal root ganglia) and the ganglia of the ANS
Give rise to neurolemma cells (Schwann cells), cells of the meninges that cover the brain and spinal cord, pigment cells
(Melanocytes), chromaffin cells of adrenal medulla and several skeletal and muscular components of head
o Fetus Blood Cells
Developing fetus blood cells are found in the red bone marrow, liver, spleen, and lymph nodes
Important CellsFunction or Location
o Macrophagephagocytosis, defense against bacterial infection
Activated by gamma-IFN
Can function as APC
Kupffer cellliver
Histiocyteloose CT
o Mastmediators of inflammation on contact w/ antigen, same as Basophil in that it secretes Heparin & Histamine
Mediates allergic reaction involved in type I hypersensitivity reactions
o Schwannform myelin sheath around axons of PNS
Derived from neural crest cells
o Sertoliproduce testicular fluid (not testosterone)
o Leydigproduce testosterone Ley-dig cells produce testosterone for the Lay-ds.
o Fibroblastproduces collagen and reticular fibers, most common cell of CT
o Osteoblastforms bone matrix and gives rise to osteocytes
o Sustentacularinternal ear (organ of Corti), taste buds, olfactory epithelium susten-spec-tacular cells b/c involved in ear,
taste and smell!
o Pyramidalcerebral cortex (cerebrum)
The pyramids contain upper motor neuron fibers only
o Endotheliallining blood and lymph vessels, endocardium inner layer
o Ependymallining brain ventricles and spinal cord
o Ganglionicin the ganglion of peripheral to CNS
o Globulartransitional epithelium (kidney, ureter, bladder)
o Pricklestratum spinosum of epidermis spiny = prickly
o Chromaffinadrenal medulla and paraganglia of Symp NS
o Purkinjecerebellar cortex (cerebellum) info out of the cerebellum
o Claraterminal bronchioles
o Goblet cellsmucous MBs of female reproductive tract, respiratory tract, and intestines, colon No Goblet cells in stomach
o InterstitialCT of ovary and testis
o Isletpancreas
o Juxtaglomerularrenal corpuscle of kidney
o Hepatocyteliver
Cell replication:
o Chromosomes:
= DNA + protein (histones)
Appear as chromatin granules called chromatids, attached to centromeres when replicating
o Chromatin:
A complex of DNA & proteins (the proteins are either histone proteins or non-histone proteins)
Histone proteins:
o (+) charged proteins enriched w/ lysine & arginine


o Involved in DNA packaging

Non-histone proteins:
o Enzymes involved in nuclear functions such as replication, transcription, & DNA repair
Is the cell component that is genetically continuous from one generation to the next (not nuclear membrane or golgi
Euchromatin: (Eu means Good and Loose!!)
Loose form of DNA & transcriptionally active
Highly condensed & transcriptioinally inactive Heteros arent as kinky or sexually ACTIVE
Almost the entire inactive X chromosome somatic cells in a woman is in this form
Splitting of nucleus & cytoplasmtwo diploid (daughter) cells w/ identical genetic constitutions
Keeps the same 2N (diploid) the Q reads: The diploid number of chromosomes is perpetuated in somatic cells by a
process of mitosis
M phase mitosis (karyokinesis) division of the nuclear parts of cell (no protein synthesis)
See Below (PMAT)
Cytokinesis division of the cytoplasm, accompanies mitosis
Interphase (inactive phase) period between one mitosis and the next
o G1 phase 1st growth phase
By far the most variable cycle period timewise among different types of cells
o S phase when DNA is replicated
o G2 phase 2nd growth phase
Four active phases of Mitosis:
o Gradual coiling up of chromatin in nucleus
o Individualization of chromosomes, initiation of mitotic spindle w/ centriolar duplication
o Phosphorylation of the nuclear lamina during prophase initiates nuclear disassembly
o Disappearance of the nuclear envelope & nucleoli
o Chromosomes line up at the equatorial plate
o Spindle is complete
o The chromosomes split longitudinally and migrate to poles
o Beginning of cell division
o Nucleolar restitution w/ nuclear envelope formation
o End of cell division
o # of chromosomes after telophase???
46?? Only if youre counting PAIRS BEFORE Cytokinesis
There would be 46 PAIRS or 92, BEFORE cytokinesis. 23 pairs or 46 total afterward.
o Splitting of the cytoplasm
o Occurs right after telophase
o NOT essential for Mitosis to occur
Gametes genetic material between homologus chromosomes is intermixed
Two divisions separated by a resting phase
Total of 4 daughter cells, each w/ the original # of chromosomes
Goes to Haploid
Goes through meiosis I (where the reduction division happens) and then meiosis II (splitting of sister chromatids)

Epithelial tissue
CT Proper

Description & Function

May be one or several layers thick; lower surface bound to a supportive
basement MB of glycoprotein, mitotically active tissue; line all body
surfaces, cavities, and lumina and are adapted
Highly vascular (except cartilage); contain considerable intercellular
matrix; mitotically active tissue, support or bind other tissues and provide
metabolic needs
Limited mitotic activity; fibers are adapted to contract in response to
stimuli; movement of materials through the body, the movement of one
part of the body

Outer layer of skin, linings of GI tract,
urinary bladder, ducts and vessels; alveoli
of lungs; and covering of viscera and body
Tendons and ligaments; cartilage and bone,
adipose, blood
Smooth, skeletal, and cardiac muscle

Nervous tissue

Limited mitotic activity; respond to impulses to and from all body organs

Neurons and neuroglia

- CT in general:
o Derived from mesenchyme (mesoderm)
o Contains more intercellular material than cells
o Most common cells are the fibroblasts & macrophages
- CT Types:
o Dense CT provides tendons & ligaments w/ strong, flexible support; has high [fiber]
Dense regular: think more linear structures
Consists of tightly packed fibers arranged in consistant pattern EXs include tendons, ligaments, & aponeuroses,
&surrounding muscle fascia (NOT DEEP fascia though)
Dense irregular: think more lining structures
Consists of tightly packed fibers arranged in an inconsistent pattern
Found in dermis, submucosa of the GI tract, fibrous capsules, and deep fascia
o Loose CT (aka areolar CT) contains large spaces separating the fibers & cells, and contains a lot of intracellular fluid
Hypodermis is loose CT
- Collagen Types:
o Type I: most abundant found in dermis, bone, tendon, dentin, fibrous cartilage, fascias, late wound repair
o Type II: mainly in hyaline & elastic cartilage, vitreous body Type II for 2 eyes
o Type III: major component of reticular fibers (in skin, BVs, uterus, granulation tissue) think three on the (BV)
Three on the BeeVee for the RE-ticular fibers
o Type IV: found in basal lamina of basement MBs think fo on the flo
o Type V: present in fetal MBs Type Five to come Alive
o Type X: epiphyseal plate
- Tendons/ligaments:
o Ligament band of CT that binds bone to bone
o Tendon band of CT that attaches bone to muscle
More specifically, it secures the muscle fascia to periosteum
Aponeurosis = a sheet-like tendon
o ***When a tendon or ligament attaches to bone, the attaching fibers are called Sharpeys fibers (its not just in teeth)
These are the periosteal collagen fibers that penetrate the bone matrix, binding the periosteum to bone
- Fasciculus
o A bound group of individual muscle fibers
o Fasciculi are the bundles of muscle fibers composing the muscle
- Fascia
o Each muscle is surrounded by fascia, which secures the muscle to a tendon
o Composed of dense regular CT Linear
- Intercellular Junctions:
o Six major types of cell junctions in humans:
1) Tight junctions (zonula occludens)
Greatest resistance to substances moving between cells
o Think Keep it tight so nothing gets through
2) Intermediate junctions (zonula adherens)
Belt-like connects two neighboring cells
3) Desmosomes (macula adherens) (Think macules are spots)
Spot-like connects two neighboring cells
o Tonofibrils (tonofilaments) are found in the desmosome (spinosum???) Just not in the corneum
4) Hemidesmosomes
Spot-like connects plasma MB of an epithelial cell to the underlying basal lamina
o Epithelium anchored to the basal lamina and thus to the underlying CT
Common in stratified epithelium of skin and junctional epithelium of the epithelial attachment
Part of the oral cavity which is directly attached to the periosteum??
Hemidesmosomes to the CT
Junctional epithelium has hemidesmosomes & gap junctions
Bullous pemphigoid:
o Involves disruption of hemidesmosomes & consequent separation of the epithelium from the basal lamina
5) Focal contacts
Spot-like connects plasma MB of a fibroblast to the surrounding CT
6) Gap junctions
Specialized areas of cell MB connects neighboring cells
Communicating junctions

Organized collections of protein channels that allow ions/small molecules to passively traverse between connected cells
Separate from components of the junctional complex
Exist in all multicellular organisms and in almost all cell types
Some exceptions skeletal muscle (Because you want recruiting ability), RBCs, & freestanding cells such as circulating
- Classified according to cell shape & number/arrangement of cell layers
- Functions of Epithelium:
o Protection, absorption, excretion, and secretion
- Types of Epithelium:
o Simple squamous epithelium:
Found where diffusion & filtration occur
Endothelium lining BVs & mesothelium lining body cavities
Alveoli of the lungs
o Simple cuboidal epithelium:
Collecting ducts, as well as proximal & distal tubules of the kidney
Thyroid follicles
Respiratory Bronchioles
o Simple columnar epithelium:
Specialized for secretion or absorption
Lines the majority of the GI system
Small & large intestine, gallbladder, & stomach (epi associated with the tubular part of the GI tract)
There is a distinct epithelium change between the esophagus and the stomach
Uterine epithelium
Salivary gland striated ducts
o Stratified squamous epithelium:
Usually contains cuboidal cells in the deeper layers & squamous cells in the surface layer
This tissue is well adapted for abrasion and protection most resistant to trauma
Broadest classification of epithelium
Found on skin, linings of mouth, oropharynx, laryngopharynx, esophagus (usually not keratinized), anus, and vagina
When it thickens, rete pegs increase in size, and intercellular bridges become more evident
o Stratified cuboidal epithelium:
Ducts of the sweat glands
So simple cuboidal is kidneys, stratified cuboidal is for SWEAT!
o Stratified columnar epithelium:
Large ducts of salivary glands
Male urethra
o Specialized EXs:
Pseudostratified ciliated columnar epithelium:
Respiratory Mucous MB of nasal cavity, paranasal sinuses, nasopharynx, trachea, & bronchial tree
o Not the lining of the respiratory bronchioles, which lose their cilia and change to cuboidal and then to
Parts of the male reproductive tract
Transitional epithelium
Stratified tissue that lines the urinary bladder, ureter, and upper part of the urethra
Contains dome-shaped superficial cells that change form when contracted or stretched
When epithelium is damaged changes into transitional epithelium
When epithelial cells specialize so that a free border is characterized with the presence of microvilli, then the cell possesses
either a striated or brush border (not pseudopoda or cilia) (e.g. brush border of the small intestine)
Special stratified: transitional

Varies between cuboidal and squamous

Diffusion and filtration (Endo and mesothelium)
Secretion, excretion, or absorption (Kidney)
Absorption, secretion, and protection (GI)
Secretion and transport of particles out of air passages
(Respiratory/Mucus MB of nasal cavity)
Protection, prevents water loss (skin/esoph/anus/Vag)
Protection and secretion (sweat glands)
Protection (urethra)
Permits expansion (bladder, urethra)

Functions of skin:
o Prevention of body dehydration
o Synthesis of Vit D
o Prevention of pathogen entry
o Regulation of body temperature
o Epidermis (outer) consists of stratified squamous epithelium
Develops from embryonic ectoderm
Outer cells are dead, keratinized, & cornified
o SIDE BAR: Excessively thickened layer of the straum corneum composed of:
orthokeratin (hyperorthokeratosis): keratin layer without residual nuclei (Normal) and uneven surface (so you need ortho)
parakeratin (hyperparakeratosis): keratin layer with shrunken (pyknotic) residual nuclei (more even surface) para is with,
so WITH nuclei
In denture pt that continually wears them and eroded alveolar bone, the underlying alveolar mucosa is best described as
gingival mucosa becoming orthokeratinized mucosa
Basement MB:
o Thin structure that attaches epithelium to underlying CT in contact w/ the dividing layer of cells
o Consists of glycoprotein from the epithelial cells and a meshwork of collagenous and reticular fibers from the underlying CT
o Type IV collagen
o Contains Hemidesmosomes
o Consists of:
Basal lamina develops from epithelial cells
Basal epithelial cells are most likely to be in mitosis (stem cell layer)
Reticular lamina develops from CT
o Lamina Lucida/Densa??????
o Dermis (inner) deeper, thicker layer of the skin
Consists of dense irregular CT -sheetlike, layered. Not linear like dense regular.
Develops from embryonic mesoderm
BVs & lymphatics
5 types of nerve endings
o (one Q reads: The dermis contains a wider variety of nerve endings than does the epidermis)
Mitotic cells
Sebaceous glands
Associated with hair follicles and derived from ectoderm
Not found on palms of hands/soles of feet (Not found on glabrous skin)
Sweat/oil glands and hair follicles sheath which are in the basal layer
Papillary layer:
Thin & less fibrous
Has projections (papillae) that extend up toward the epidermal layer (rete pegs)
Finely constructed, thin, loose CT So most of dermis is dense irregular CT, but papillary layer is LOOSE!
Contains fibroblasts, mast cells, & macrophages
Elastic fibers are abundant and provide the skin tone
Reticular layer: (Deepest layer)
Thick, fibrous, dense irregular CT
Continuous w/ the hypodermis
Reticular fibers are abundant (Type III collagen)
Collagenous fibers & elastic fibers are also present
More fibers & fewer cells than in the papillary layer
o Tissue fluid reaches the epithelium in the skin through the ground substance of CT from capillaries
o Subcutaneous layer found beneath the dermis that binds skin to underlying structures
Connects dermis w/ underlying fascia of muscle:
o Composed of loose areolar CT, adipose tissue and BVs & and lymphatics
Major site of fat deposition (50% of body fat)
The Q actually asks: Where is fat found? & the answer is NOT dermis; submucosa or CT layers are options, which
works for the hard palate (submucosa), but maybe not the skin???
o My understanding: There is more fat found beneath the skin (the hypodermis) than in the oral cavity below the
mucosa (the submucosa.) CT layers is not specific enough

Good blood supply

Epidermis: (BiG Stars Give Lots of Charity)
o Outermost portion of skin develops from embryonic ectoderm
What cell junction type in epithelium Tight junctions (aka Zona Occludens) this resists substance passing through
o Layers from INSIDE TO OUT:
o 1) Stratum Basale (= Stratum Germinativum):
Least cytodifferentiated
Contains cuboidal or low columnar cells that exhibit lots of mitosis
Contains tonofibrils in the cytoplasm
Melanocytes are located here
Forms epithelial root sheath of hair follicle
o 2) Stratum Spinosum: aka PRICKLE LAYER
= prickle cell layer
Contains cells called Langerhans cells (unknown function perhaps immune response) Arent they Antigen Presenting
Cells? THINK SO!
Cell junction type in stratum Spinosum desmosomes (aka Macula adherens)
Malpighian layer denotes the stratum basale and stratum spinosum together
In the prickle cell layer of sulcular epithelium, the space in between cells is occupied by a small amount of tissue fluid,
NOT keratin or capillaries. Keratin is intracellular, and there is no blood supply to the epithelium!
THICKEST LAYER??, except for Thick Skin YES it is look at histo x-sections.
The following 3 Layers are NOT present in NON-Keratinized Oral Epithelium hmm. Check this out not sure about that line.
o 3) Stratum Granulosum:
Contain keratohyaline granules in the cytoplasm (not melanin or keratin granules)
o 4*) Stratum Lucidum:
Clear band of cells containing eleidin which is transformed into keratin as this layer becomes part of the stratum corneum
Most prominent in thick skin (palms & soles)
Absent in the thin skin and (orthokeratinized oral mucosa, which is thin skin)
NOT present in the oral cavity
o 5) Stratum Corneum:
Composed of closely packed dead cells filled w/ keratin
Thickest stratum corneum is found in the palm
Some cells of epithelium
o Keratinocyte:
Cell type most common in epidermis of skin
Specialized to produce keratin (a protective protein)
Tonofibrils & desmosomes are especially well developed in keratinocytes anchor to one another
o Melanocytes: produce melanin.
In basal layer
o Langerhans cells: antigen presenting cells, part of immune system
In spiny layer
o Merkel cells: associated w/ nerve endings
o Inflammatory cells: lymphocytes, monocytes, neutrophils
Cutaneous appendages: (see Kaplan in Integument chapter for all the details on these)
o Eccrine (merocrine) sweat glands normal, clear sweat producing
o Apocrine sweat glands smelly
o Sebaceous glands waxy
o Hairs
o Nails
Oral epithelium:
o Some structures found in the oral mucous membrane:
Basal lamina, lamina propria, keratohyaline granules (deeply stained granules in cytoplasm), stratified squamous epithelium
o Covered w/ stratified squamous epithelium
Areas of oral stratified squamous keratinized: gingiva, hard palate (are of mechanical stress)
o Permeabilities of oral mucosa:
Sublingual > buccal > palatal
Is based on relative thickness & degree of keratinzation
EX: sublingual mucosa is relatively thin & non-keratizined and thin lamina propia (great for meds)
o Sublingual musosa is the thinnest epithelium of the oral cavity
o Oral cavity is highly acceptable for systemic drug delivery
Mucosa is relative permeable w/ a rich blood supply
Virtual lack of Langerhans cells makes the mucosa tolerant to potential allergens
Route also bypasses the first-pass-effect & avoids pre-systemic elimination in the GI tract

EX nitroglycerin tablets given sublingually for rapid absorption

NOTE: alveolar mucosa is similar to sublingual mucosa appears red due to the numerous BVs & thin epithelial covering
o CT of oral cavity (referred to as lamina propria): synonymous with dermis layer in skin
Forms mechanical support & carries BVs & nerves
Two layers:
Papillary layer directly under epithelial layer, more cells, tone
Reticular layer dense, fibrous layer located under papillary layer
Oral mucosa of the cheek has a thinner lamina propria then the outer surface of the lip non keratinized vs. keratinized
o Submucosa:
Located between CT and muscle tissue
Present only in areas requiring a high degree of compressibility & flexibility (cheeks, soft palate)
Kaplan states that it is defined Submucosa, but immovable because it is tightly bound to underlying periosteum
The Anterior part contains much adipose tissue, and posterior part of the hard palate is full of glands
o NOTE: the most outstanding difference between the gingiva and the mucosa of the hard palate is the presence of glands
- Cartilage is avascular heals slowly after injury
- No calcium salts are present cartilage doesnt appear on x-rays
- Can support great weight, yet it is flexible & somewhat elastic
o Firmness of cartilage depends on:
Electrostatic bonds between collagen fibers & GAG side chains of matrix glycoproteins
Binding of water to the (-) charged proteoglycan complexes
- Cartilage has a preponderance of amorphous ground substance over fibers
- Chondrogenic cells = undifferentiated mesenchymal cells important to growth & development of cartilage
- Chondrocytes:
o Reside in depressions in matrix called Howships lacunae
o The only blood supply is provided by BVs entering cartilage through the perichondrium
o Secrete a hard, rubbery matrix around themselves
- Three subtypes:
o Hyaline
Most common type
Matrix contains many, closely packed, fine collagenous fibers
Has a capsule around the chondrocytes which represents the youngest layer of intercellular substance
Covers & protects bone
Precursor to bone in long bones, hyaline provides a region for bone to grow in length
Found where strong support & some flexibility are needed
Forms nearly all of fetal skeleton Most common type think were ALL fetuses
May grow interstitially, where bone only can grow appositionally
In adults:
Articular cartilage smooth and slippery, it lines movable joints Except TMJ!!!
Costal cartilages at the sternal ends of the ribs
Respiratory cartilages movable external nose and septum, larynx, trachea, and the bronchial walls
Auditory cartilages external auditory meatus and pharyngotympanic tube
o Think HYdraulics on the ACuRA.
Ground substance of hyaline cartilage is basophilic because it contains sulfated proteoglycans called
glycosaminoglycans (GAGs are highly negative)Like DNA, negative charged, so will bind to basic basophilic die. (vs.
GAGs can readily bind & hold water allows tissue to assume a gelatinous nature resistant to compression and also
permit some degree of diffusion
Most abundant GAG is hyaluronic acid
o Fibrocartilage
Most closely resembles dense, irregular CT
Matrix contains dense collagenous fibers
Withstands tension & compression
Found in intervertebral discs (vertebra), knee joint, TMJ, & symphysis pubis
o Elastic
Matrix contains collagenous & elastic fibers
Similar to hyaline cartilage but the fibers are not as closely packed
More importantly, elastic cartilage contains many elastic fibers (elastin)
Forms the external ear (pinna) and is also found in the epiglottis, the auditory meatus, & larynx
- Tropocollagen
o Protein molecule in BOTH collagen and reticular fibers
- Perichondrium:


o Consists of a fibrous outer layer (connective tissue MB) and a chondroblastic inner layer
o Very important to cartilage growth Only vascular part associated with cartillage
Cartilage growth:
o Interstitial chondrocytes divide w/in cartilage occurs in epiphyseal plates & articular cartilages
o Appositional where surface perichondrium lays down new layers results from differentiation of perichondrial cells
Mineralization of Bone
o All of the following are contributors to the mineralization of bone:
Holes or pores in collagen fibers
Release of matrix vesicles by osteoblasts
Alkaline phosphatase activity in osteoblasts and matrix vesicles
Degradation of matrix pyrophosphate to release an inorganic phosphate group
NOT Release of acid phosphatase by osteocytes trapped in lacunae
Bone growth:
o Appositional below the periosteum is a fibrous outer layer & a cellular inner layer of osteoblasts, which lay down bone
Because of bones rigid structure, interstitial growth is NOT possible
o Bone increases in size by way of appositional growth by osteoblasts (Not interstitial)
o Do not confuse bone growth w/ bone formation
Bone forms by either endochondral ossification or intramembranous ossification
Endochondral bone formation: (Think ENDO like long bones (files, etc.))
o Cartilage is precursor for bone in this type of growth
o The epiphyseal plate (disc) is a wedge of hyaline cartilage accounting for this increase
The plate is found between the epiphysis & diaphysis at each end of a bone
Cartilage cells of the epiphyseal plate form layers of compact bone tissue, adding to the bone length (by interstitial
growth in the cartilaginous epiphyseal plate) NOTE: Interstitial growth in bones, but of CARTILLAGE, NOT BONE!
The disc becomes inactive in most individuals by late teens/early 20s
o 1 ossification center near the middle of the diaphysis
o 2 ossification center in the epiphysis; forms later note: epi = on top ends of bone.
o Metaphysis the region between the 1 & 2 ossification centers
o The Diaphysis shaft
o Here are the steps, all concise-like:
1) chondrocytes proliferate in epiphyseal plate
2) chondrocytes hypertrophy on diaphyseal side of the area
3) matrix calcifies
4) chondrocytes die
5) osteoblasts lay down layer of primary bone along the bone spicules
Zones of the Epiphyseal Plate
o Zone of resting cartilage
Nearest to the epiphysis
Chondrocytes are disordered and are not dividing rapidly
o Zone of Proliferation
New cartilage is produced by interstitial growth
Multiple chondrocytes stack up forming columns
o Zone of Hypertrophy
Chondrocytes Mature and Enlarge Lacunae also appear swollen
More mature ones are at the diaphysis end and less mature are at the epiphysis end
o Zone of calcification
Thin layer of mineralized matrix
Death of hypertrophied chondrocytes occurs and the lacunae are invaded by blood vessels
Osteoblasts from the endosteum, travel with the connective tissue of blood vessels and aggregate on the calcified cartilage
New bone matrix is deposited by appositional bone growth, then remodeled


o *The width of the epiphyseal plate remains constant because as the bone elongates, there is remodeling inside the metaphysis
o Bones fuse between 12 and 25 depending on bone and leave an epiphyseal line
o Plate closes at age 18?? 24??
Bone Repair picture here? More text to explain at least!
o Blood Clot forms
o Bridging callus forms
o Periosteal callus forms
o New endochondral bone forms
o NOT new osteons grown across the callus

General Embryology
- Cleavage
o Begins w/in 24 hours of zygote formation
o With each division, the daughter cells (blastomeres) become smaller (no cell growth)
o Compaction begins w/ the 8-cell stage blastomeres flatten & are held together by tight junctions
o Morula by day 3 or 4, consists of the 16-32 cells, Solid Mass
The First solid ball of cells to form in the embryo
- Blastocyst formation Hollow ball of cells with inter blastocele layer
o Blastocele
Fluid begins to accumulate in the intercellular space & forms a central cavity known as the blastocele
o Blastocyst
In what stage do the cells start to have an inner cell mass?
Is the zygote, now free of its zona pellucida
Embryoblast inner cell mass projects into the cavity gives rise to the embryo proper
Which cells turn into the inner layer of the fetus?
I think Embryoblast
Trophoblast outer cell mass forms outer epithelial layer gives rise to the fetal portion of the placenta
Think Troph i.e. has affinity to travel to uterine wall!
- 1st Week: Implantation
o Begins by the end of the 1st week
o Upon implantation, the trophoblast produces hCG, a hormone that maintains the corpus luteum (which secretes
Excessive growth of the trophoblast results in hydatiform moles (hCG) which can fill the uterus and result in fetal
Also, the trophoblast can form the highly
malignant chorionepithelioma, a tumor of
the chorionic villi
o Ectopic pregnancy implantation outside the uterus
- 2nd Week: Bilaminar disc
o Epiblast primary ectoderm High columnar cells,
during 3rd week forms ectoderm and mesoderm
form the amniotic cavity On top
o Hypoblast primary endoderm Low cuboidal cells
contributes to primary yolk sac (or remaining
Blastocyst) On the bottom


3rd Week: Trilaminar disc Pic to Right

o Primitive streak
Linear thickening of the ectoderm cells
Defines the cephalocaudal axis of the embryo
Delimited rostrally by the primitive node
o Epiblast cells invaginate between epiblast & hypoblast(epiblast cells go
through the primitive streak) forms the intraembryonic mesoderm
o Notochord formation: (Get your Honda acCORD on your 16th birth
Day 16 cells of the primitive streak migrate rostrally & form the
tube-like notochordal process
The notochord is a rod-shaped body found in embryos of all
Composed of cells derived from mesoderm and defines the primitive
axis of the embryo
Found on the ventral surface of the neural tube
The notochord induces the the thickening of the ectoderm to form the neural plate
Turns in to the Nucleus Propulsus
o Neural plate begins to form
o Buccopharyngeal Membrane Ruptures
What causes the infolding of the head thing in embryology?
o Neural cells growing OR branchial arch formation?? Im 100% sure its from neural cells growing!
4th 8th Weeks: Embryonic Period
o Week 4
For the 4 chambers of the heart begins to beat; upper/lower limb buds begin to form for the 4 limbs, and 4 Visible
Branchial Arches
Neural Plate
The neural plate increases in length as the primitive knot and primitive streak move caudally
Invagination of the neural plate at day 18 forms the neural groove
The edge of each fold is known as the neural crest
Neural tube is formed when the crests fuse, starting at the 4th somite region (neck) and proceeding in cephalic and caudal
The cephalic end of the neural tube will eventually dilate to form the forebrain, midbrain, and hindbrain
o The spinal cord is formed from the remainder of the neural tube
o Neurelation sequence pictures below

Neural crest cells (Ectomesenchyme) Mostly peripheral nerve associated structures

Form Posterior root ganglia, sensory ganglia of the cranial nerves, autonomic ganglia, meninges, Schwann cells,
suprarenal cells, and Melanocytes
Head and Tail Folds Picture of folding to RIGHT
The entoderm (endo) germ layer gives rise to the GI and depends on BOTH the cephalocaudal folding and the lateral
folding of the embryonic disc in a tubelike fashion
Rapid longitudinal growth of the CNS causes the cephalic and caudal ends to bend and form head and tail folds
o As a result the brain comes to lie cranial to the cardiogenic area and septum transversum, which contributes to the
formation of the diaphragm.
o Part of the yolk sac becomes incorporated into the embryo as the foregut




This cavity opens into the midgut via the anterior intestinal
portal and is bounded anteriorly by the prochordal plate,
which is known at this stage as the buccopharyngeal
This membrane forms the back of the stomodeum and
ruptures at the end of the 3rd week to establish
communication between the amniotic cavity and the
primitive gut
o Blah, blah
Lateral Folds
The continued growth of the somites causes the expanding lateral
margins of the embryonic disc to bend ventrally, forming lateral folds
o As a result, part of the yolk sac is taken into the embryo to form the
o In addition, this folding constricts the initially wide communication
between embryo and yolk sac to a narrow, long vitelline duct,
which eventually lies w/in the umbilical cord
What causes the infolding of the head thing in embryology?
Neural cells growing OR branchial arch formation?? Im
100% sure its form neural cells growing!
THIS is why I think the answer to the above yellow
question is neural cells growth
3rd-8th week fetus most susceptible to teratogens
Ectodermal derivatives:
Surface ectoderm
Otic placode & lens placode
Hair & nails
Subcutaneous glands
Anterior pituitary gland
Mammary glands
Hair, enamel, sweat glands & salivary glands are all derived from ectoderm (dentin is not)
Neuroectoderm: CNS STUFF
Posterior pituitary gland
CNS neurons
Oligodendrocytes & astrocytes
Pineal gland
Neural crest:
ANS (e.g., autonomic ganglia)
Sensory ganglia of CNs
Schwann cells
Adrenal medulla (chromaffin cells)
Mesenchymal (mesodermal) derivatives:
CT (bone, cartilage)
Urogenital system
Adrenal cortex
Serous MBs lining the pericardial, pleural & peritoneal cavities
Endodermal derivatives: Liver, lungs, GI, pancreas, thymus and thyroids are all spongy like
GI system

Lining of respiratory tract, bladder & urethra
- 10 Week:
o Genitalia have M/F characteristics
Head & Neck Embryology
- Stomodeum = stomatodeum:
o Slight depression on the surface ectoderm
o Represents the primitive oral cavity
o Separated from primitive pharynx by buccopharyngeal MB (oropharyngeal MB)
Composed of ectoderm externally & endoderm internally (no mesoderm)
Covers the stomatodeum
Ruptures at 3 weeks (forming max palatal shelves)
o Prochordal Plate Look up more context here!
Consists of the endoderm of the roof of the yolk sac and embryonic ectoderm
Does NOT contain mesoderm
- Branchial Arches = pharyngeal visceral arches
o General features:
A series of rounded mesodermal (mesoderm cuz cartilage and muscle
from mesoderm) ridges on each side of head & neck of embryo at 4
Develop in the 4th week as neural crest cells that proliferate & migrate
into the future head & neck region
By end of the 4th week, FOUR well-defined pairs of branchial arches
are visible externally
o The 5th & 6th are small & cannot be seen on the embryo surface
Each branchial arch contains a cartilaginous bar or rod, a muscular
component, an artery, & a nerve
1st-3rd arch play role in formation of face & oral cavity
1st arch develops into Mn & large part of Mx
1st, 2nd & 3rd arches play role in tongue development
Contain striated muscle, not from somites
Branchial arches (are SVE special because they are striated, but not developed from body wall or somites)

From the above picture, the facial process indicated w/ the letter A gives rise to the secondary palate

Cartilages of each arch:

1st arch cartilage (M: Meckels, Mandible, Malleus, Muscles of Mastication, Mylohyoid)
1st arch develops into Mn & large part of Mx
A model for the Mn but does not form any part of Mn Meckels cartilage is scaffold only!
o What forms the Mn?? Intramembranous ossification of Meckels WHAT!?!?
o Fate is dissolution with minor contribution to ossification
Closely related to development of the middle ear
o Ossifies to form the malleus & incus
All 8 muscles innervated by V3 (4 mastication, 2 tensors, anterior belly of digastric, and mylohyoid)
NOTE: CN V supplies the muscles derived from the 1st pair of branchial arches
2 arch cartilage (Reicherts)
Closely related to development of the middle ear
o Ossifies to form the Stapes (Second = Stapes)
Think S Second, Stapes, Styloid Process, Stylohyoid, Seven (VII), Smiling (Muscles of facial expression)
Forms part of the hyoid bone
Also forms Styloid process of the temporal bone
Also forms the stylohyoid ligament
Stylohyoid muscle is from the 2nd arch
All facial expression muscles innervated by CN VII
3rd arch cartilage
Ossifies to form part of the hyoid bone hyoid is second and third branchial arches!
Stylopharyngeus muscle
Derivatives of the 3rd arch are innervated by CN IX
Think Pharynx: stylopharyngeus & glosspharyngeal nerve
4th & 6th arch cartilages:



Fuse to form laryngeal cartilages (except for the epiglottis)

All other pharyngeal and laryngeal muscles
XI via X:
o Spinal part of XI
Goes to SCM and trapezius
o Cranial part of XI
Joins X
Goes to pharyngeal muscles from vagal branches except stylopharyngeus
Goes to laryngeal muscles via recurrent laryngeal
NOTE: CN XII provides GSE fibers derived from the Occipital somites, not any arches
4th arch:
o Most pharyngeal constrictors, Except Cricopharyngeus
o THE EXCEPTION Cricothyroid which you would think is the area of 6th arch
o Levator veli palatini
o Innervated by superior laryngeal branch of CN X
6th arch:
o All intrinsic laryngeal muscles (except cricothyroid) superior laryngeal branch of X
o The EXCEPTION Cricopharyngeus which you would think is the area of 4th arch
o Innervated by recurrent laryngeal branch of CN X
5th arch
Absent (short-lived or not developed)
A little more about the arches: (yup, I know, I suck & youre pissed)
1st Arch:
Divides at 4 weeks embryonic development to form Mn & Mx processes
Mn (except condyles) & Mx are mostly formed by intramembranous ossification Condyles are endochondral!
Develops into two prominences or processes:
1) Mn process (larger) forms the Mn & lower lip
o Mn forms by merging of medial ends of Mn processes during the 4th week (Mn forms before Mx)
2) Mx process (smaller) forms the Mx, zygomatic bone, squamous part of the temporal bone, most of upper lip
o Mx forms by merging of Mx processes What about nasopalatine process?
o The upper lip is formed from the Mx processes and medial nasal processes
o The medial nasal process form the center of the nose and lateral nasal processes form the ala of the nose
o Maxillary teeth are developed from Arch I and a globular process
o NOTE: the intermaxillary arch is NOT a derivative of the 1st Arch what is the intermaxillary arch?
o The palatine shelf is a medial extension of the Mx process
o Lateral palatine processes of Mx process secondary palate (hard and soft palate)
What makes up the Maxillary Palate (hard and soft)/
The secondary palate; fusion of the maxillary processes ???
o Primary Palate is formed by the medial nasal processes and join the secondary palate at the jxn of the nasopalatine
Lateral cleft lip results from failed fusion of Max & medial nasas processes
May be unilateral or bilateral
o ***Cleft palate failure of fusion of the lateral palatine processes, nasal septum &/or median palatine process
Most common in Asians
Corners of the mouth
Formed by fusion of Mx & Mn processes
Tuberculum impar: (median tongue bud)
Median, triangular elevation which appears in the floor of pharynx just rostral to foramen cecum
Forms from 1st branchial arch
Gives first indication of tongue development in embryo at 4 weeks
Lateral lingual swellings (two distal tongue buds):
Develop on each side of median tongue bud
Elevations are the result of proliferation of mesenchyme of 1st arch
Swellings fuse to form the anterior 2/3 of tongue (mucosa and all)
o Delineated by circumvallate papilla??
Bifid tongue:
Results from lack of fusion of distal tongue buds (or lateral swellings)
Common in South American infants
2nd Arch:
Copula (helps to form posterior 1/3rd)
3 Arch:



Posterior 1/3 of tongue is formed by two elevations: the copula (2nd arch) & the hypobranchial eminence (3rd arch)
o Bifid uvula:
Results from failure of complete fusion of palatine shelves
Pharyngeal pouches: (NOT ARCHES) (PIC TO RIGHT)
o Paired evaginations of pharyngeal endoderm lining the inner aspects of the branchial arches in the neck region
NOTE: the parotid gland is NOT a derivative of a pharyngeal pouch
Messed up development of 3rd & 4th pouchesDiGeorge syndromeleads to T-cell deficiency & hypocalcemia
Pharyngeal Pouch

Structures Derived
Tympanic MB, audtitory tube, and middle ear cavity, mastoid air cells
Lymphatic nodules and palatine tonsils
Inferior parathyroid gland, thymus gland (Hassalls Corpuscles)
Superior parathyroid gland, ultimobranchial body which gives rise to parafollicular cells (C cells)
of the thyroid gland (produce calcitonin)
Rudimentary structure, becomes part of the fourth pouch

Vestibular lamina
o Separates lips & cheeks externally & the jaw structures internally in the developing embryo
o Outer lamina of the 2 epithelial lamina in embryo that separate the palate from the lip!!!!!
Frontal nasal process (prominence):
o Produced by the growth of the forebrain
o Develops the forehead and nose
Nasal placodes
o Thickened areas of specialized ectoderm that form on each side of the frontal nasal process
o Elevations form at the margin of these placodes
o What makes up the nose? Medial and lateral nasal processes
Two lateral nasal processes form the sides (alae) of the nose
Two medial nasal processes form the bridge of nose, nostrils, philtrum (upper lip), & primary palate (anterior to incisive
o Philtrum
What forms the philtrum? Medial Nasal Processes with Maxillary processes
See pics to right
o Derived from Mn, Mx, & Medial Nasal processes
o Derived from 1st, 2nd, and 3rd branchial arches
Anterior 2/3
1st Arch
Ectoderm (Mucosa)
Tuberculum impar (median tongue bud of first arch)
Lateral Lingual Swellings primary developmental source of mucosa of the
anterior 2/3 of the tongue
Posterior 1/3
2nd and 3rd Arch
Copula (2nd)
Hypobranchial eminence (3rd)
Tongue NOT formed from macula What is macula? Its in the eye asshole!
o At the jxn of the body and root of the tongue is:
Foramen Cecum
Lies at the base of the V of the sulcus terminalis
Sulcus Terminalis
V-shaped demarcation that separates anterior 2/3 from posterior 1/3
Circumvallate Papilla located in the back center or laterally though?
NOT Lingual raphe
o Taste in tongue:
All innervation is from the solitary nucleus
Anterior 2/3: CN VII
Posterior 1/3: CN IX


Extreme posterior and soft palate: CN X



Exocrine glands classified according to:
o 1) Type of secretion:
Mucous (water & mucin)buccal glands, glands of esophagus, cardiac & pyloric glands of stomach, palatine glands
Serous (enzymes)parotid, von Ebners glands (ONLY), pancreas & uterine glands
Mixedsubmand. & sublingual glands, glands of nasal cavity, paranasal sinuses, nasopharynx, larynx, trachea, and bronchi
o 2) Mode of secretion:
Merocrineonly the cell secretory product is released from MB-bound secretory granules EX: pancreatic acinar cells
Apocrinesecretion of product plus small portion of cytoplasm EX: fat droplet secretion by mammary gland
Holocrineentire cell w/ secretory product EX: sebaceous glands of skin & nose (Think Hol = Whole)
o 3) Structure of duct system:
Unbranchedsimple glands EX: sweat glands
Branchedcompound glands EX: pancreas
o 4) Shape of secretory unit:
Tubularcylindrical lumen surrounded by secretory cells EX: sweat glands
Acinar (alveolar)dilated sac-like secretory unit EX: sebaceous & mammary glands
Tubuloacinar (tubuloalveolar)intermediate in shape or has tubular & alveolar secretory units EX: major salivary glands
o NOTE: Salivary, sweat, sebaceous, and von Ebner's glands are all exocrine glands
Pituitary Gland (hypophysis cerebri):
o Master endocrine gland because it controls many other glands through release of tropic hormones
Tropic hormones = hormones that effect the activity of another endocrine gland
o Origin:
1) Upgrowth from ectoderm of the stomodeum roof of mouth (anterior pituitary, glandular portion from oral ectoderm)
Rathkes pouch diverticulum developing at 3 wks from the roof of stomodeum (primitive mouth) grows
toward brain
o The anterior lobe of the hypophysis develops from Rathkes pouch Think Antero = Adeno, not neuro origin
2) Downgrowth from the neuroectoderm of diencephalonfloor of brain (posterior pituitary, nervous portion) posterior,
or NEURO hypophysis, is of NEURO origin
o Positioned in the sella turcica of the sphenoid bone directly above the sphenoid sinuses
o Structure:
Adenohypophysis = Anterior Pituitary
Pars tuberalis, pars distalis, and pars intermedia the distal, intermediate, tube. DIT.
Pars intermedia is an avascular zone lying between the lobes but is considered part of anterior pituitary
Pars intermedia & tuberalis have no proven function in mammals Distalis Does the Damage
NO innervation
Contains alpha & beta cells
Hypothalamic-hypophyseal portal blood system not neural, so has the portal system
Neurohypophysis = Posterior Pituitary
Pituicytes Primary cell -Glial cells -of posterior pituitary, fusiform cell closely related to neuroglia Name says it all
Median eminence, infundibulum and pars nervosa The nervous, eminent, infundibulum. Nervous = Neuro-hypoph.
Infundibulum carries important nerve tracts from hypothalamus & substances to act on posterior pituitary
o The infundibular contains the hypothalamic-hypophyseal tract, which carries axons to the posterior pituitary
If you cut this stalk, lose the function of ADH (vasopressin) and oxytocin
Consists mainly of unmyelinated nerve fibers Doesnt need to go far, doesnt need the myelin to speed up cond.

Blood supply
From right & left superior and inferior hypophyseal arteries
Sinusoidal blood arrangement (sinusoidal arrangement of BVs also found in Liver and Spleen)
Forms a rich vascular portal system
Portal has two capillary beds
***Three portal systems in the body:
o 1) Hepatic portal system 1st capillary bed in intestines & 2nd in the sinusoids of liver
o 2) Renal portal system 1st capillary bed in glomerulus & ????
o 3) Hypothalamus-Hypophyseal portal system 1st bed in HTh & 2nd in Anterior Pituitary
Carries the Releasing Hormones produced in the hypothalamus to the anterior pit and have them release further
Synthesized peptide hormones:
Anterior Pituitary = pars distalis: FLAT PeG
The following tissues would be affected if the anterior lobe of the hypophysis were destroyed:
o Thyroid epithelium, zona fasciculata of adrenal gland, interstitial cells of testis, spermatogenic epithelium of testis
NOT adrenal medulla Affected by nerves that go straight here not hormones
B/C anterior lobe releases, TSH, ACTH, FSH/LH,
Hormones released from:
o Alpha cells GH & Prolactin (regular hormones) Alpha for acidic or Eosionophilic pEg
o Beta cells FSH, LH, ACTH, TSH (all tropic hormones)- meaning they act on other endocrine glands
Sidenote: The hypophysis is characterized by an anterior lobe w/ alpha & beta cells
Follicle stimulating hormone (FSH):
o Development of graafian follicles & estrogens in the ovary
o Promotes spermatogenesis in males
Luteinizing hormone (LH): L for LH for corpus Luteum and for Leydig cells
o Stimulates formation of corpus luteum & progesterone secretion
o Stimulates interstitial cells (Leydig cells) of testes to secrete testosterone
Corticotropin (ACTH):
o Controls secretion of adrenocortical hormones (glucocorticoids), which affect glucose, protein, & fat metabolism
Thyroid stimulating hormone (TSH):
o Controls secretion of thyroxine by thyroid, uptake of iodine, and synthesis
**Melanin Stimulating Hormone (MSH) and Beta-Lipotropin What is the deal with this MSH secretion, etc
o Secreted from the pars intermedia
Prolactin (Lactotropin):
o Promotes mammary gland development & milk production, breast development
The mammary glands are under direct control from the hypophysis
o Triggered by rising estrogen levels Need the estrogen
prolactin milk
Growth hormone (GH) aka somatotropin: Athletes take it cuz they want PTN building (muscles) and not fat/carb
o Growth in general; particularly skeletal system by stimulating aa uptake, protein synthesis, & CHO/fat breakdown
o Most plentiful of AP hormones



o Fusion of long bone epiphyses determines if excess GH will result in gigantism (children) or acromegaly (adults)
o Produced by acidophils in the anterior pituitary (pEg)
Posterior Pituitary Neurohypophysis or pars nervosa:
Consists of unmyelinated nerve fibers
Consists of 100,000 axons of the supraoptic and paraventricular nuclei of hypothalamus pg. 484 of blue neuroscience
Secretes ADH & oxytocin
Hormones are synthesized in hypothalamus & transported in axons to the poster lobe for storage and secretion
o Transport occurs via hypothalamo-hypophyseal tract
Antidiuretic hormone (ADH) aka vasopressin:
o Controls rate of water excretion into urine
o Helps to deliver milk from glands in breasts to nipples during nursing milk letdown and uterine contraction
Thyroid gland: LOOK AT MILLER POWERPOINTS FOR CLARIFICATION pg. 444 of Netter Head and neck anatomy book
o H-shaped structure two parts joined by a thin isthmus
The isthmus runs in front of the trachea and contacts it posteriorly
o It has rings of epithelial cells surrounding a space filled with colloid
o Characterized by the fact that it functions as the controller of general body metabolism
o In adults, the site of origin is seen as the foramen cecum
o Blood supply
External carotid superior thyroid artery (supplies thyroid gland) superior
laryngeal (enters thyrohyoid membrane) (top artery in pic)
Enters membrane with the internal branch of the superior laryngeal nerve (from the
inferior thyroid artery from thyrocervical trunk) (Bottom artery in pic) (pg. 123 & 129
Netters H&N anatomy)
SIDENOTE: Vagus, has both the superior laryngeal nerve and the recurrent laryngeal
nerve (BOTH do sensory and muscle)
Pharyngeal branch Innervates the pharyngeal constrictors except the
Cricopharyngeus (VI arch)
THINK Cricos are the ODD balls
Recurrent Laryngeal Sensory/PS: Everything from the folds down
MOTOR: All the motors of the Larynx except Cricothyroid (IV
Superior Laryngeal Sensory/PS: (Internal branch) above the folds
MOTOR: (External branch) to the Cricothyroid
o Nerve supply glandular branches of cervical ganglia of sympathetic trunk
o Cell types:
Follicle cells:
Synthesize thryoglubulin (from tyrosine), which is stored in colloid of each follicle, and is a precursor to T3 & T4
When pituitary gland secretes thyrotropin (aka TSH), the colloid becomes active & thyroglobulin molecules are
released and taken back into the follicular cells where they become T3 & T4
Remain inactive at times of low thyroid hormone need can be activated when necessary for mobilization of colloid
found in thryroid
Colloid in the usual thyroid follicle stains acidophilic (PINK)
Metabolically active follicular colloid stains BASOPHILIC
Parafollicular cells: (C cells)
Produce calcitonin lowers calcium & phosphate levels in blood tones down the calcium
Thyroglossal duct a narrow canal connecting the thyroid gland to the tongue during development
Disappears but persists as the foramen cecum
An upward extension of the thyroid gland could be a remnant of the thyroglossal duct, a pyramidal lobe, or a muscular slip
question answer was all of the above
Cervical cysts in the midline of the neck is from Thyroglossal duct
Parathyroid gland:
o Four glands two superior (superior thyroid artery from external carotid) and two inferior (inferior thyroid artery from
thryocervical trunk) pairs of glands on posterior (dorsum) of thyroid gland
o Develops from 3rd & 4th pharyngeal pouches 4th is superior and 3rd is inferior!
o Blood supply is mostly from inferior thyroid artery (with contribution from the superior thyroid artery to the superior glands
o Controlled by blood levels of calicum NOT TSH
o Cell types:
Principal cells (chief cells) secrete PTH, have clear cytoplasm

Oxyphil cells (acid secreting cells) granules in cytoplasm, unknown function

Regulates calcium & phosphate metabolism
Innervention by superior cervical ganglion (sympathetic)
Low PTH leads to tetany & muscle weakness duel to lack of Ca 2+
Pineal gland:
o Located in the epithalamus of brain and releases the hormone melatonin
o Thought to play role in regulation of sleep-wake cycle, body temperature regulation, and appetite circadian rhythms
Adrenal gland:
o Aka suprarenal gland
o Embedded in adipose tissue above kidneys
o Adrenal Medulla:
Secretes Epi and Norepi
Secretion of Adrenal medulla is NOT ESSENTIAL FOR LIFE (unlike those of Parathyroids, Adrenal cortex, Anterior
pituitary, Pancreatic islets (Langerhans) Just think fight/flight not necessary
From neuroectoderm (neural crest cells which differentiate into medullary cells called chromaffin cells)
Same embryologic origin as sympathetic ganglia (neurocrest)
So, chromaffin cells of adrenal medulla secrete catecholamine (NE and E)
So, the adrenal medulla is an endocrine gland of ectodermal origin in the abdomen
Is composed of many cells containing MB-bound osmiophilic granules
Has an intrinsic stroma consisting primarily of reticular fibers***
NOT separated from the cortex by a capsule of collagen fibers what separates it then?
o Adrenal Cortex:
Outside to In: Zona GlomerulosaZona FasiculataZona Reticularis (GFR like Glomerular Filtration Rate)
Also outsidein: SaltSugarSex (aldosteroneglucocorticoidsandrogens) life gets sweeter
Each Zone of the cortex has endocrine cells:
Zona Glomerulosa
o Thin layer, clusters of cells beneath CT capsule
o Secretes mineralocorticoids, primarily aldosterone Affects minerals i.e. Na+
Zona Fasiculata
o Thick middle layer, cells arranged in parallel columns that run at right angles to surface
o Secretes glucocorticoids, primarily cortisol; also small amounts of estrogenic & androgenic-like substances
Zona Reticularis
o Inner layer, cells arranged in interconnecting cords
o Secretes small amounts of cortisol & Dehydoropiandrosterone (DHEA)
Derived from the mesoderm Weird because the outside is from Mesoderm and the Inside is from Ectoderm
Q was what is not derived from neural crest? all were correct except adrenal cortex
Endocrine Glands that are ESSENTIAL FOR LIFE: parathyroid, adrenal cortex, anterior pituitary, pancreatic islets (Langerhans)

o Major gland of immune system
o Two soft, pinkish-gray lobes lying in a bib-like fashion below the thyroid gland and above the heart
o From 3rd branchial pouch
o Primary lymphoid organ (just like bone marrow. Secondary lymph tissue is: spleen, tonsils, lymph nodes, & Peyers
o Site of T-cell maturation/education
o Outer cortex contains primarily lymphocytes
o Inner medulla contains T-lymphocytes & Hassalls corpuscles (thought to be vestiges of epithelium unknown function)
Are Mature in the Medulla
o The thymus is the immune system organ most isolated from blood Important to regulate blood b/c important lymphocyte
education is occuring
o Master organ in immunogenesis in the young some believe it monitors total lymphoid system throughout life
o Requires zinc most critical involved in all aspects of immunity: Vit B6, Vit C, carbonic anhydrase, & others
o No afferent lymphatics of lymphatic nodules
o Blood from the internal thoracic & inferior thyroid arteries
o Innervated by vagus & phrenic nerves
o Has double embryologic origin:
Lymphocytes derived from hematopoietic stem cells (mesenchyme)
Hassalls corpuscles (epithelium) derived from endoderm of 3 rd pharyngeal pouch
o Produces thymopoietin & thymosin



Both are thymic lymphopoeitic factors confer immunological competence on thymus-dependent cells & induce
Also produces thymic humoral factor (THF) & thymic factor (TF)
Important in normal development of immune systemproliferation & maturation of T lymphocytes
o Has both exocrine & endocrine function
o Retroperitoneal organ, except for small portion of tail which lies in the lienorenal ligament
o Head & neck nestle in the curve of the duodenum; body is behind stomach; tail extends to spleen***
o Characterized by groups of special cells scattered among glandular alveoli
o Endocrine (pancreatic islets Islets of Langerhans)
Endocrine glands secrete products (hormones) into interstitial fluid to diffuse into capillariesbloodstream
*Alpha cellsglucagon
*Beta cellsinsulin, carb metabs, most abundant (80% of cells)
Degeneration of Islets of Langerhans leads to diabetes mellitus
*Delta cellssomatostatin acts locally w/in islets of Langerhans to depress secretion of insulin & glucagon
o Exocrine (acini):
Exocrine glands secrete products into ducts, Trypsinogen
Centroacinar cellspancreatic juices lipases, carbohydrases & proteases (to digest fats, CHOs, & proteins)
Centroacinar cells are ONLY found in the Pancreas
o Duct of Wirsung:
Main excretory duct begins at tail & joins common bile duct to form hepatopancreatic ampulla (ampulla of Vater)
Ampulla opens into duodenum (into descending portion [2nd part] of duodenum)
o Accessory pancreatic duct (Santorinis duct) opens separately into duodenum (when present)
Wolffian duct: (mesonephric duct) embryonic duct that develops in the male into the deferent duct, in the female it is obliterated Wolf
are strong and manly, why its obliterated in females
Major salivary glands are compound tubuloalveolar glands***
By way of General Visceral Efferents from both the salivatory nuclei & the lateral horns of the spinal cord
o Adenomere: part of developing salivary gland destined to become responsible for function
Composed of:
Intercalated ducts transport saliva to larger ducts
Striated ducts think striated like muscle, does work (transport), needs mitochondria
o contain mitochondria for electrolyte & water transport; simple, low columnar epithelium
o Striations of salivary glands are related to a combo of foldings of basal cell MBs & radially arranged mitochondria
And maybe by the striated ducts?
Glandular cells synthesize glycoproteins
o Serous demilunes:
A muctous tubuloalveolar secretory unit that contains lysozyme (degrades bacterial cell walls)
Serous demilune cells: associated w/ mucous acini of the sublingual & submandibular glands (Mixed serous)
Secrete into intercellular canaliculi, not into striated ducts
o Mucus cells: clear granules mostly everywhere
Function to protect & lubricate for transportation
Characterized by large, clear secretory granules that occupy most of the cell & a flattened nucleus-containing, condensed
chromatin at cell base
o Serous cells: nucleus and rER at the bottom, clear zymogen granules at the apex
Rounded euchromatic nucleus surrounded by rough ER in the basal third of the cell w/ zymogen granules (clearly visible &
easily stained secretory granules) at cell apex
NOTE: there is an abundance of zymogen granules in the apical cytoplasm (NOT ribosomes or mitochondria)
Apical granules in the parenchyma of the salivary gland cells represents secretion precursors
Serous cells are found in acinar cells of pancreas, parotid, gastric chief cells and intestinal paneth cells (found at base of vili
in intestines)
What is common among the pancreas and parotid?
They both have serous secretory cells
o Ducts:
Parotid Stensons duct
Submandibular Whartons duct
Sublingual gland Rivian ducts (Bartholin duct -- See below)
o Parotid gland:
Largest salivary gland
High in amylase activity
Distinguished by having serous acini only, realtively long secretory ducts, and long intercalated ducts

No serous demilunes b/c these associated with Mucous, not serous

Divided by Mn ramus into deep & superficial lobes
PS secretomotor from CN IX by way of lesser petrosal nerve, the otic ganglion, & auriculotemporal nerve (branch of
Diminished salivation due to middle ear involvement most likely involves the lesser petrosal nerve
Lymphatics superior deep cervical nodes
Stensons duct crosses over masseter m., pierces buccinator m. & opens into vestibule opposite Mx M2
Things that PASS through the Parotid Gland
Facial Nerve (NOT Artery OR Vein)
Retromandibular vein
External Carotid artery
Superficial temporal artery
Branches of the great auricular nerve
o Sensory loss in the skin overlying the parotid gland could be caused by damage to the great auricular nerve
Surgical excision of the parotid gland endangers the facial nerve, auriculotemporal nerve, & external carotid artery
Submandibular gland: (formerly submaxillary gland)
Mixed serous & mucous
Located in the submandibular triangle (digastric triangle)
Superficial part rests on mylohyoid muscle
To expose, you only need to cut the mucous membrane
Deep part is located around the posterior border of mylohyoid between the mylohyoid m. & hyoglossus m.
Whartons duct
Arises from deep portion of gland & crosses lingual nerve in the region of the sublingual gland
Runs anteriorly immediately deep to the mylohyoid muscle
Terminates on the sublingual caruncle (papilla) adjacent to the base to the base of the sublingual frenulum
o Sublingual caruncles are elevations that lie on either side of the lingual frenum
SIDENOTE: The lingual frenum is attached to the genioglossus
Facial artery enters the submandibular triangle deep to the posterior digastric & passes under to supply submandibular gland
Gives off submental branch as it emerges beneath the gland
PS secretomotor fibers leave CN VII in chorda tympani
Carries pre-G fibers to lingual nerve from which the submandibular ganglion is suspended
Fibers leave lingual nerve & synapse in ganglion w/ post-G
Also supply sublingual, lingual, von Ebners & inferior labial glands & glands of inferior portion of buccal mucosa
Post-G sympathetic fibers are from superior cervical ganglion
They gain access via the adventitia of the facial & lingual arteries
o Submandibular & sublingual lymph drainage is to the deep cervical lymph nodes look up all lymph drainage
o Sublingual gland:
Contains mostly mucous w/ some serous demilunes
Bartholins Duct major sublingual duct opens on sublingual papilla in floor of mouth (accompanies
submandibular duct)
Mylohyoid muscle supports the glands inferiorly
Innervated by PS of CN VII w/ chorda tympani from submandibular ganglion
Blood from sublingual artery (from lingual a. from external carotid a.)
o Von Ebners glands:
Located around the circumvallate papillae of the tongue
Function rinse food away from papilla after it has been tasted
o Parotid & Von Ebners are the only adult salivary glands that are purely serous
o Mucus-secreting glands
Palatine gland and Buccal glands (PURELY MUCOUS)
Submandibular (submax)
Sublingual NOT purely mucous
Mucus of the trachea
Glands of the esophagus
NOT parotid gland or mucosa of ureter
Parasympathetic innervation controlling salivation originated ONLY with VII and IX
Fordyces Granule
o Aberrant sebaceous glands ectopic (?)


Foregut esophagus, stomach, duodenum, liver, gallbaldder, pancreas

Celiac artery
o Midgut jejunoileum, cecum, ascending colon, transverse colon
o Hindgut descending colon, sigmoid colon, superior 1/3 of rectum
o Single sheet of simple squamous mesothelium that lines the abdominopelvic cavity and covers the abdominal and pelvic organs
o Parietal layer portion on the cavity wall
o Visceral layer portion on the organ
o Some of the organs are suspended from the body wall by a double fold of peritoneum called a mesentery
o Some organs are moved to or develop behind the peritoneum, hence retroperitoneal
Intraperitoneal structures:
o Usually have a mesentery or peritoneum
Stomach, jejunum, ileum, appendix, transverse & sigmoid colon, spleen, liver, and gallbladder
Retroperitoneal structures:
o Organs do not have mesenteries
o Structures on posterior abdominal wall are retroperitoneal:
Think all Vertical Organs and the Pancreas SAD PUCKER. (Suprarenal glands, Aorta, Duodenum, Pancreas, Ureter,
Colon, Kidney, Esophagus, Rectum
Duodenum, ascending & descending colon, rectum, kidney & ureters, pancreas, suprarenal glands, IVC, and abdominal aorta
NOT liver, spleen, other shit above
Parts of the large intestine in sequential order alternate between intra- & retroperitoneal:
o Ascending colon (retro)transverse (intra)descending (retro)sigmoid (intra)rectum (retro)
Vagus nerve innervates ascending colon and transverse (?) (but does not innervate the descending colon, sigmoid colon,
rectum or anus)
o 10 inches, behind trachea in thorax, empties in cardiac portion of stomach through cardiac orifice
o Upper 1/3 has skeletal , Middle 1/3rd has skeletal + smooth muscle; lower 1/3 has smooth muscle only
What type of muscle is present in lower 1/3rd Smooth
Divided into 3 portions on basis of muscularis externa
o Receives blood from inferior thyroid artery, branches of descending thoracic aorta, and left gastric artery
o PS from esophageal branches of CN X
o Motor fibers from recurrent laryngeal of CN X & S innervation from esophageal plexus
Abdomen divided into 9 regions by 4 imaginary planes (Hollywood Squares, Tic-tac-toe):
o 1 Epigastricmidline region above umbilical region (contains most of stomach)
2 Hypochondriacregion to R & L of epigastric region. Located beneath the cartilage of the rib cage (spleen here)
o 1 Umbilicallocated centrally, surrounds the umbilicus
2 Lumbarareas to the R & L of umbilical region
o 1 Hypogastric (pubic)midline region directly below the umbilical region
2 Iliac (inguinal)regions on R & L of hypogstric region
o In upper part of abdomen, extending below the left costal margin into epigastric & umbilical regions, protected by lower ribs
o Connects w/ esophagus via cardiac sphincter & to small intestine via pyloric sphincter
The purpose of the Gastroesophageal sphincter is to prevent reflux of stomach contents
o 1.0 L capacity
o Receives blood from all 3 branches of celiac artery (L & R gastric, short gastric, and L & R gastroepiploic a.)
o Venous Drainage from the Portal vein & Splenic Vein
o Stomach regions:
Cardiaclies near junction of stomach & esophagus
Fundusenlarged portion above and left of esophageal opening into stomach dome
Bodymiddle or main portion of stomach
Pylorislower portion, lying near small intestines
o Rugae transient folds of the mucosa & submucosa present in an empty stomach but smoothen out in a distended stomach
o Gastric glands of stomach in the lamina propria:
Parietal (oxyntic)in fundus & body, secretes 0.16 M HCl and Gastric Intrinsic Factor (Dont want at cardiac or pyloris)
pH of stomach is <2, due to HCl secretion
Chief (zymogenic)in fundus & body, secretes pepsin Dont want pepsin at ends (cardiac or pyloris)
Enteroendocrinepresent throughout stomach; produce gastrin, serotonin??? (1989 Q26)
The G cell is an enteroendocrine cell that produce gastrin
o Lesser & greater omentum mesenteries that connect the stomach to other viscera (Lesserliver; Greater Guts (small


Greater Omentum
Connects transverse colon to the stomach
Lesser Omentum
A peritoneal fold connecting the lesser curvature of the stomach & the first part of the duodenum to the liver
Connects Liver to the stomach (Lesser = Liver)
Contains the common bile duct, hepatic artery, & the portal vein the hepatic triad makes sense cuz Lesser = Liver
o No Goblet cells in stomach (rest of GI tract below stomach were other options)
Trachea, small int & large intestine DO have goblet cells
Small intestine (D J I)
o Small intestine secrete:
Malatase, sucrase, lactase converts disaccs to monosaccs
Aminopeptidase & dipeptidase converts polypeptides to individual aa
Enterokinase converts trypsinogen to trypsin
o Small intestine mucosa:
Plicae circulares = tranverse folds of mucous MB increasing surface area of jejunum (aka valves of Kerckring)
Villi (numerous in entire small intestine) absorb via microvilli projections on the free surface of the cells lining villi
Each villus consists of a lamina propria that has vessels, nerves, and lacteals goes straight up into villus
The central lacteal absorbs chylomicrons into the lymphatic circulation through junctional gaps
Epithelial cells lining villi:
Show surface modification known as the striated border (or brush border) -- microvilli
o Disaccharidases & dipeptidases carry out their activity at the striated (brush) border aka brush border NZs
o Lactose intolerance is caused by deficiency of the disaccharidase lactase
Goblet cellsmostly in the ileum (become more numerous as one proceeds distally along the small intestine)
Absorptive cellssimple columnar cells w/ microvilli
Villi, microvilli, brush border, and circular folds all increase surface area in small intestine (NOT rugae stomach)
Enteroendocrine cellssecrete enterogastrones (secretin & CCK) into bloodstream found in duodenum
Paneth cells(stain red) found at bases of villi of tubular intestinal glands (crypts of Lieberkuhn) & secrete digestive
enzymes, lysosymes (Pan for gold at the base of the villi)
o Duodenum:
One foot longshortest but widest in small intestine, horseshoe-shaped curves around head of pancreas
Brunners glands (submucosal glands) secrete alkaline mucus Neutralizes acidic chyme
Small, branched, coiled, tubular glands in submucosa that secrete alkaline mucus to neutralize gastric acid (histologically
differentiates stomach & duodenum)
Retroperitoneal in the latter parts
Receives common bile duct & pancreatic ducts at the ampulla of Vater (small rounded elevation in wall of duodenum)
Duct of Wirsung:
Main excretory duct begins at tail & joins common bile duct to form hepatopacreatic ampulla (ampulla of Vater)
o Ampulla opens into duodenum (in descending portion [2nd part] of duodenum)
Accessory pancreatic duct (Santorinis duct) opens separately into duodenum (when present)
Blood supply superior pancreaticoduodenal artery (arises from gastroduodenal artery & inferior pancreaticoduodenal
arising from superior mesenteric)
Pre-G PS are in dorsal motor nucleus of CN X
o Jejunum Think WORKER of the intestine
Thicker muscular wall for more active peristalisis, mucosal inner lining of greater diameter for absorption
Has more plicae circulares (valves of Kerckring) & more villi for absorption
Plicae circulares are most characteristic of the jejunum
Tall columnar epithelium (like the rest of the GI tract!!!)
o Ileum: Think immune system and more individual functions
More mesenteric fat, more lymphoid tissue (Peyers patches), more complex vascularity, more goblet cells
Lymphoid tisse (Peyers Patches MALT for Ag presentation & secretory IgA) to handle waste and destroy bacteria
Preferred site for Vit B12 absorption
Ileocecal valve joins small & large intestines

Gastric inhibitory polypeptide

Major activities
Stimulates gastric acid secretion
Stimulating secretion of pancreatic enzymes, and
contraction and emptying of the gall bladder
Stimulates secretion of water and bicarbonate from
the pancreas and bile ducts
Inhibits gastric acid secretion (HCl) and motility
and potentiates release of insulin form beta cells

Stimuli for release

Presence of peptides and amino acids in gastric
lumen. Distension of stomach
Presence of fatty acids and amino acids in the
small intestine
Acidic pH in the lumen of the small intestine
Presence of fat and glucose in the small intestine


in response to elevated blood glucose



Large intestine:
o Three Parts:
1) Cecum vermiform appendix extends downward from cecum (appendix contains large amt of lymphoid tissue )
Infection at the vermiform appendix would spread by entering the bloodstream via the Brachiocephalic Vein
2) Colon ascending (shortest), transverse, descending, & sigmoid
3) Rectum no teniae coli
o Teniae coli:
Three thick, longitudinal bands of smooth muscle fibers that extend the entire length of colon
Function for peristalsis
Shorter than the large intestine therefore cause it to form small pouches called Haustra
o Epiploic appendages (appendices epiploicae) small areas of fat-filled peritoneum lacking in the small intestine
o Function of large intestines (colon):
Remove water from material entering it
Water removed by absorption
Large intestines do not secrete enzymes into lumen
o Colon epithelium: Yes microvilli, no regular villi
Simple columnar w/ border of microvilli to increase surface area for absorption of water from lumen
Goblet cells lubricate dehydrating fecal mass w/ mucous
Crypts of Lieberkuhn (intestinal glandsin stomach they are called rugae) invade lamina propria (L for L) (not same
as goblet cells)
o Note: Lieberkuhn are in Lamina Propia, but Brunners are in Submucosa
No villa formed in large intestines (no surface area increase) Distinguishes it from Small Intestine
o Colon muscularis externa: inner circle smooth muscle layer
o Innervation
Vagus nerve supplies PS to ascending & transverse colon
Pelvic splanchnic nerves to descending & sigmoid colon w/ rectum & anus (Think where you get SPANCHED)
o Anal canal:
Rectal columns of Morgagni = vertical folds, produced by the infolding of the mucous MB around the submucosa
The columns is separated by furrow-like rectal sinuses, which end distally in small valve-like folds called anal valves
Internal = smooth muscle; External = skeletal muscle
Epithelium (from valves to opening):
Simple cuboidalstratified cuboidalstratified squamouskeratinized stratified squamous
Liver: (picture)
o Largest & most active organ, largest gland of the body
o Lies under right side of diaphragm
o Blood flow:
Blood supply hepatic artery & portal vein
The central hilus, or portal hepatis:
o Receives venous blood from the portal vein & arterial blood from
the hepatic artery
o Also transmits the common bile duct
o ***Portal Triad = Portal vein + hepatic artery + bile ducts (sometimes
lymph vessels) (3 things together at corners of hexagonal
The central vein lies outside the portal triangle (Central vein in
middle of hepatocytes)
Blood eventually drains via the three hepatic veins into the IVC which is
transported to heart
Esophageal veins serve as an important collateral circulatory unit to the
hepatic portal system
Cirrhosis esophageal varices Death
o Sinusoids: (Represented by straight black radial lines in the picture)
Irregular capillaries w/ round pores 100-200 nm in diameter. No basement MB
Allow macromolecules of plasma full access to the surface of liver cells through the space of Disse
o Autonomic nerve fibers from celiac plexus
o Divided into large right lobe & small left lobe by attachment of peritoneum of falciform ligament (PICTURE)
Right lobe of liver is further subdivided into quadrate lobe and caudate lobe by presence of gallbladder, fissure for
ligamentum teres (umbilical vein remnant), IVC, and fissure for ligamentum venosum


Coronary ligaments attatch liver to underside of diaphragm

Liver cells (hepatocytes): Are involved in:
Protein synthesis, storage
Transformation of carbs
Synthesis of cholesterol, bile salts, phospholids, and detoxification
Modification of endogenous & exogenous substances
Encircle a central vein and radiate outward (pic above)
Produce & excrete bile, excrete bilirubin (major end product of hemoglobin decomposition)
Contain large number of mitochondria and smooth ER
Contain lots of glycogen clustered near SER
20-30 micron polyhedral eosinophilic cells
6 or more surfaces may either contact another cell to form gap jxns and bile caniliculi or form a free surface with microvilli
exposed to the perisinusoidal Space of Disse
Bile canaliculi
o Tubular spaces limited by the plasma membrane of several hepatocytes
o Form a network that progresses along the plates of the liver lobule in the direction of the portal canals
o At the periphery of the lobule, these ducts empty into the Herings canals, which are small ducts of cuboidal cells
o Then these ductules terminate in the cuboidal or columnar lined bile ducts, which go on to form the right and left
hepatic ducts, which together constitute the common hepatic duct
o BILE FLOW: Bile Canaliculi Bile ductules (Herings) Right and left hepatic ducts
Common Hepatic
Produces prothrombin, fibrinogen, albumin etc.
Stores lipid and carbohydrates & vitamins
Converts lipids and amino acids into glucose via the enzymatic process of gluconeogenesis
Detoxifies and inactivates drugs by oxidation, methylation, and conjugation
Liver regeneration can be as much as 90% in about 2 weeks
Does NOT deal w/ phagocytosis of particulate matter Kupfer cells do this I guess not a function of the liver?
Secrete bile into common hepatic duct, joined by short cystic duct of gallbladder to form common bile duct
Bile is conducted away from the liver and into the cystic duct by the common hepatic duct
Kupffer cells:
Reticuloendothelial macrophages which line sinusoids of the liver. Come from monocyte lineage
Function to filter bacteria or small foreign particles out of blood
Originate from the mononuclear phagocyte system
Remove bacteria and toxins entering blood through the intestinal capillaries.
Have vacuoles, lysosomes, and granular ER

o Pouch-like organ that stores & concentrates bile by absorbing water & salts (bile continuously produces in liver)
o When small intestine is empty, sphincter of ampulla (Oddi) constricts forcing bile up the cystic duct to gallbladder
With food (particularly fats), CCK relaxes ampulla for bile to mix w/ chyme



Bile emulsifies neutral fats & absorbs FAs, cholesterol, & certain vitamins
Gallbladder has Simple Columnar Epithelium
Gallbladder does NOT contain a submucosa***
Colon, stomach, jejunum, & duodenum do have a submucosa present
Receives blood from cystic artery of the right hepatic artery
Is innervated by vagal fibers from celiac plexus
Lymph from gallbladder drains into a cystic lymph node, then into the hepatic nodes and then into celiac nodes




Eye Structure pg. 505 in Netters H&N anatomy book

o As if I were a ray of light, I would pass through:
Anterior Chamber (filled with aqueous humor)
Pupil (made from the Iris which contains the sphincter muscles)
Lens (which is made more or less ovoid by the ciliary muscles in the ciliary bodies found at the periphery of the iris)
Vitreous body
Made of Type II Collagen Think type II for 2 eyeballs
3 Layers of back wall
o Rods (night visionuse your rod at night!) and Cones (C for Color)
o Continues all the way to just below the Ciliary Bodies
o Macula
Fovea centralis in the Macula
Avascular region that contains ONLY cones for most acute vision (What a perfect placeonly Cones)
o In other words, 3 layers to the eye
External Fibrous Layer
Sclera and Cornea
Middle Vascular Pigmented Layer
Uvea (consists of choroid, ciliary body, & iris)
Internal Neural Layer
Lacrimal Apparatus (Flow of drainage)

Lacrimal glands
In a picture is located on the Lateral side
o Lacrimal ducts
Superior and Inferior Fornix
Lacrimal puncta (tear duct)
o Lacrimal Canaliculi
o Lacrimal Sac
o Nasolacrimal Duct
Drains into the inferior nasal meatus behind the inferior nasal concha (I want my $50 dollars,..$50 dollars)
- Tears (Parasympathetic pathway)
o Under PS control:
CN VII the Greater Petrosal nerve which came to the Pterygopalatine ganglion then hopped a ride on the
zygomaticofacial branch of V2 then on the Lacrimal branch of V1 to the lacrimal gland
- Ear consist of:
o External ear:
Receives sound waves
Auricle & external auditory canal
Innervation is Auriculotemporal does anterior part of external auditory meatus; Auricular branch of vagus does back of
auricle and posterior part of external meatus; Great Auricular does posterior part of auricle; Lesser Occipital does behind the
o Middle ear (tympanic cavity):
Air to bone conduction
Ossicles malleus (hammer) stapes (stirrup) and incus (anvil)
A stapedectomy surgery will improve hearing
Two muscles stapedius muscle (smallest skeletal muscle in the body) (att.
To stapes in pic) & tensor tympani muscle (cut in pic)
Medial wall oval & round windows
Lateral wall tympanic membrane left wall
Middle ear communicates posteriorly w/ the mastoid air cells and the mastoid
antrum through the aditus and antrum
Eustachian tube serves to equalize air pressures between the tympanic cavity
(middle ear) & the nasopharynx (anterior wall not shown in pic)
Middle ear infections (otitis media) are quite prevalent and may become
extensive due to connection to both the mastoid air cells and the nasopharynx by
way of Eustachian tube
Pt is clinically deaf but a tuning fork on mastoid process causes hearing there is
a problem of disarticulation of ossicles Just not a nerve problem!
NOT caused by a laceration of auriculotem, laceration of cn 8, or problem w stapedius muscle
o You would have no hearing ever if it was a nerve problem, and stapedius
dampens the sound.
o Inner ear: (PIC TO RIGHT) pg. 483 Netters H&N anatomy
Located in the Petrous Part of the Temporal Bone
Transmits to the nerves
Bony labyrinth
3 cavities: vestibule, semicircular canals, cochlea
Filled w/ perilymph (Na+ rich) Just like a regular extracellular environment
Membranous labyrinth
3 parts:
o Cochlear duct base of the cochlea = high frequency; apex = low frequency
o Saccule & utricle both contain maculae for sensing linear acceleration
o Semicircular canals contain ampullae for sensing angular acceleration Think ampitheatres(ampulla) are round,
Filled w/ endolymph (K+ rich) Just like an intracellular environment
Hair cells are found in both the cochlear & vestibular apparatus

Urinary system:
o 2 kidneys, 2 ureters, 1 urinary bladder & 1 urethra
o Removes nitrogenous waste as urea from blood
Urea is produced when foods containing protein are broken down
o Lined w/ transitional epithelium
o Genital & urinary systems are supplied w/ PS fibers from pelvic splanchnic nerve



o Kidneys, ureters, & urinary bladder all located retroperitioneally (behind the peritoneum) All vertical organs!
Kidneys: pg. 246 of Clementes anatomy book, or pg. 65 of USMLE Kaplan vol.1
o Epithelium
Bladder and Ureters Transitional
Tubules Simple cuboidal
o Contain extensive vascularity & millions of nephrons w/in renal cortex & medulla
o Filter blood & regulate volume & composition of body fluids during urine formation
o Located retroperitoneally
Can be approached surgically w/o violating the continuity of the peritoneum (ovary, spleen, & gallbladder can not)
o Right kidney lies slightly lower than the left due to large size of the right lobe of liver
Right kidney is close to the Colon, Liver, and Duodenum (CLOSEST to Colon)
o Left kidney is in visceral contact anteriorly with the stomach
o Each is surrounded by a fibrous renal capsule & is supported by an adipose capsule
o Each has an indentation the hilum on its medial border through which the ureters, renal vessels, & nerves enter/leave
Point of entry/exit for renal artery, renal vein & ureter
o Divided into outer dark-brown renal cortex & inner light-brown renal medulla
o Derived from mesoderm of the intermediate cell mass 1994Q58
Intermediate cell mass into both kidneys & gonads
o Horseshoe kidney: when the inferior poles of both kidneys fuse
Bloodflow through the kidney:
o Renal arteryinterlobar arteriesarcuate arteriesinterlobular arteriesafferent arterioles
Internal features of kidneys:
o Cortex outer layer (glomeruli are located here)
o Medulla inner layer, consists of renal pyramids separated by renal columns
2-3 pyramids may unite to form a papilla
o Renal columns found between pyramids; cortical tissue
o Renal papilla apex of pyramids; the collecting ducts pour into minor calyces here
A renal papilla projects directly into the minor calyx
o Minor calyces unite to form major calyces, which then unite to form renal pelvis
o Functional unit of excretory system
Smallest unit of the kidney that makes urine
o Subunit of kidney that purifies blood & maintains safe balance of solutes & water
o >1 million nephrons per kidney
o Made up of a renal corpuscle, proximal convoluted tubule, loop of Henle, & distal convoluted tubule
Renal corpuscle aka Malpeeeeegian Corupuscle
Consists of a glomerulus (network of parallel capillaries) & the surrounding Bowmans capsule
Site of filtration (passage of plasma substances from glomerulus into Bowmans capsule)
o BP forces fluid into Bowmans capsule
Bowmans capsule has simple squamous epithelium (parietal layer)
Also has a visceral layer formed by podocytes
Where do you find podocytes? Glomerular epithelium
Between the layers is the urinary space
Renal tubule
Four regions:
o 1) Proximal convoluted tubule in cortex
o 2) Loop of Henle in medulla Thin part has thinner cells, and thick part has thicker cells!
Thin limb Simple squamous
Thick limb Simple cuboidal
o 3) Distal convoluted tubule in cortex
o 4) Collecting duct in medulla (Technically not part of the nephron)
After filtration, the tubules handle tubular reabsorption & tubular secretion
o Water, glucose & sodium are reabsorbed into blood
o Waste products are retained & emptied into collecting tubuleureters
Juxtaglomerular apparatus:
o JG cells
Modified smooth muscle of afferent arteriole
Secrete renin in response to low renal Blood flow, & BP, low Na+, & high sympathetic tone
Renin converts circulating angiotensinogen into AT I, which is then converted into AT II by ACE
Also secrete erythropoietin
o Macula densa
Na+ sensor

Part of distal convoluted tubule

o Afferent arteriole
o Polkissen cells
o Long, slender, muscular tubes that transport urine from renal pelvis to base of the urinary bladder
o Fibro-muscular tube that carries urine from urinary bladder to outside of the body
o In males it carries semen as well as urine (if youre lucky)
Urinary bladder:
o Distensible sac situated in pelvic cavity posterior to the symphysis pubis
o Slightly lower in females than in males
o Concentrates urine & serves as a reservoir
o Tonically Contracted
o Adults pass ~1.5 quarts of urine each day
o Volume of urine formed at night that formed during day
o Normal urine is sterile contains fluids, salts, & waste products, but is free of bacteria, viruses & fungi
o Bladder tissues are isolated from urine & toxic substances by a coating that discourages bacterial attachment & growth on walls

I knowits HOT.

Mineral content


Formative cell

Translucent yellow
Epithelial (ectoderm)
NOT mesenchyme
No replacement, some


Wear, staining, caries

Cells in mature tissue


Comparison of Tooth Tissues

Light yellow

Light yellow

None, except denticles or
pulp stones
Blood red
Dental papilla

reparative 2dentin
Increased 2 & sclerotic
Yes, only as pain
Cytoplasmic extensions
from odontoblasts

New cementum

Can recover from mild


Increased amount w/
age (apex)

Reduces in size; may be

Odontoblasts & other types


Hardest tissue in body
Richest in calcium highly mineralized
Secreted by ameloblasts totally acellular
Enamel has no possibility of self-repair because its formative cells are lost once it is completely formed
96% inorganic minerals of calcium and phosphorous as hydroxyapatite (HA)
1% (or 2%) organic material (protein which is rich in proline) for calcium sequestering?
3% water
Maturation of enamel is characterized by an increase in inorganic content & a decrease of BOTH water & organic material
Ectodermal origin (NOT ectomesenchymal)
ALL other tooth components are derived from ectomesenchyme (neurocrest cells)
PICTURE: Forming enamel/dentin layers

PICTURE: Shows tomes processes and odontoblast processes in picket fence arrangement in forming teeth

Enamel rod or prism:

Fundamental morphologic unit of enamel
Bound together by an interprismatic substance (interrod substance)
Each is formed in increments by a single ameloblast An enamel rod is the pathway of a single ameloblast from the DEJ to
the surface
At the time enamel matrix is first formed in a tooth, the nuclei of ameloblasts move to the non-secreting end of the
cell (Reverse polarization)
Ameloblasts have short extensions towards the DEJ called Tomes process when they are in their Secretory stage
These Tomes processes give the ameloblasts at the DEJ a picket-fence appearance
The Tomes processes from the enamel are picketed with enamel spindles of the dentin (odontoblastic processes)
CAREFUL, Odonotblastic processes are Called Tomes FIBERS
During Calcification, Ameloblasts get their nutrients from the Stellate Intermedium see pic above
The interface between pre-ameloblasts and pre-odontoblasts is most like the interface between Epi and Dermis???
Look at other answers here see if one is better.
Rods begin at DEJ & extend to outer surface
Rods normally diverge radially away from the DEJ
Exception: in the cervical portion of primary teeth, the rods diverge toward the occlusal
Enamel rods converge toward the surface in the area of fissures although they are still diverging from the DEJ
5-12 million rods per crown
Rods increase in diameter (4 up to 8 microns) as they flare outward from DEJ


Oldest enamel in a fully erupted tooth is located at DEJ underlying a cusp tip or cingulum
Is a good thermal insulator
Organic matrix decreases as tooth matures and inorganic increases (F & Zn are minor constituents)
Optically clear in a demineralized histologic section of a adult tooth due to low organic (high inorganic) content
Extremely brittle, but very strong in compression can endure crushing pressure of ~100,000 psi
Coupled w/ dentin has cushioning property
Semitransluscent yellow to grayish-white
Selectively permeamble MB allows water & certain ions to pass via osmosis (Remember Bleaching!)
Crystals (Inorganic)
Have their long axes parallel to the rods in the bodies of the rods & deviating increasingly in their tails
Their tails are at the surface, heads at the DEJ

The degree of calcification in C, compared to that of D, islower

This would be opposite for a x-section of dentinal tubule
Fluoride Topical Application
Acid solubility of the surface enamel is reduced by fluoride
Enamel Caries
Are thought to penetrate along the route of the rod sheath
Spreads parallel to enamel rods
Hunter-Schreger bands: (Everyones TIGER hunting riffles are pointed in
different directions)
Refers to alternating light & dark lines seen in dental enamel that begin at the
DEJ & end before they reach enamel surface
They represent areas of enamel rods cut in cross-section dispersed between
areas of rods cut longitudinally

Lines of Retzius: (Stria) (A) (Think Age Bands like a tree) pg. 186 in dental
histology book
Artifacts in enamel (not found in dentin) created by incremental steps of
Analogous with with Contour Lines of Owen in Dentin
Have increased organic content and are indicative of the rhythmic
variation in the calcification of the enamel matrix
They follow the appositional growth pattern
Neonatal line: 1985 Q87
One of the lines of Retzius is accentuated
Marks the division between enamel formed before & after birth
Found in decidous teeth and cusps of permanent 1st molars
Found in enamel of primary incisors, permanent canines, and
permanent 1st molars???
Found in dentin of permanent mandibular incisors and
permanent first molars??? (Check Calcification ages)
Perikymata: (Peri KY jelly) mata
Where lines of Retzius terminate on the tooth surface making a
small valley traveling circumferentially around tooth
Ribbed surface of the tooth (for her pleasure)
Imbrication Lines of Pickerill:


Depression or grooves formed when growth rings (lines of Retzius) are incomplete at the enamel surface
Enamel tufts: (B)
Fan-shaped, hypocalcified structures of enamel rods that project from the DEJ into the enamel proper (unknown function)
Never found at the outer surface of enamel (perikymata, enamel matrix, & enamel lamellae are) makes sense bc they come
from the CEJ
Enamel lamellae: (C)
Defects in the enamel resembling cracks or fractures which traverse the entire length of crown from surface to DEJ
Contain mostly organic material & may provide pathway for bacteria to enter
Hypomineralized structures extending from the DEJ to the surface of the enamel

A = Stria of Retzius; B = Enamel Tuft; C = Enamel Lamella; D = DEJ

For Pic above

Gnarled Enamel: (A) Right

Found most frequently in cusps, (pits and fissures?)
Enamel spindles: (B?)Right
Careful, its not enamel, ITS a dentinal process
Elongated odontoblastic processes (hair-like) that traverse the DEJ from the
underlying odontoblasts they go up in the enamel and get trapped there
May serve as pain receptors
In a ground section of a permanent lateral incisor, the enamel spindle is the first
formed (other options were: perikymata, gnarled enamel, granular layer of Tomes)
Odontoblast is formed before the enamel and enamel defects
Enamel spindle (dentin) formation happens BEFORE Granular layer of
Tomes pg. 200 in Bibbs book
Serve as the counterparts to the Picket-Fence DEJ from the odontoblast side (Tomes
processes from ameloblastic side)
Primary Enamel Cuticle (aka Nasmyths MB) (Think Cellophane wrapping)
Delicate MB covering the crown of a newly erupted tooth
Produced by the ameloblast after it produces the enamel rods
Worn away by mastication and cleaning
Replaced by an organic deposit called the pellicle
Pellicle formed by salivary glycoproteins & invaded by bacteria to form plaque
**In a newly erupted tooth, the junction between the tooth surface and crevicular epi is a Basal lamina-like structure between
the enamel and the epithelium
During the early stage of eruption, the enamel matures
During eruption, the epithelial covering of the enamel unites with the oral epithelium and then degenerates
70% inorganic (calcium hydroxyapetite), 20% organic (primarily Type I collagen), 10% water
More mineralized than regular bone, but less than enamel
The apatite crystal is oriented parallel to the collagen fibers in the dentin matrix (not parallel to dentinal tubules)???
Purposes of Dentin:
Nutritivekeeps organic components of the surround mineralized tissue supplied w/ moisture and nutrients
Sensoryextremes in temperature, pressure, or trauma to the dentin or pulp are perceived as pain
Pain originates in the pulp due to free nerve endings about the odontoblastic cells
*NOTE: in peripheral organs, the free nerve endings are receptors stimulated by pain (not touch, pressure,
Tactile receptors in tooth free nerve endings (A-delta & C fibers)
Protectiveformation of reparative(tertiary) or secondary dentin
Theory of Pain
Hydrodynamic phenomena involving fluid influx into the tubules which then stimulate receptors in the pulp
Formed from the dental papilla (so is dental pulp) (see picture- tooth formation in Cap Stage)
Mesenchymal dental papilla adjacent to the IEE differentiates into odontoblasts
Main cell is the Odontoblast, derived from ectomesenchyme


Cell body is in the pulp cavity Process goes into

dentinal tubules
**Ectomesenchyme is the primary source of
cranial connective tissue
Odontoblasts begin dentin formation before enamel
formation by the ameloblasts
Preameloblast differentiation
Odontoblast differentiation
Predentin secretion
Ameloblast differentiation
Enamel matrix secretion
Dentin mineralization
Enamel mineralization

During the last part of active eruption the

odontoblasts are still functioning actively (ameloblasts are not) at this point they are now considered Reduced
Enamel Epithelium
Incremental lines of von Ebner (aka contour lines of Owen): pg 199 in Bibbs book
Lines in dentin that correspond to lines of Retzius in enamel
Also have a neonatal line which marks the transition between dentin formed before & after birth
Types: pg. 197 of Bibbs book
Mantle dentin
The 1st formed portion of the dentin thus closest to the CEJ
The peripheral portion of dentin adjacent to enamel (DEJ) or cementum (CEJ), consisting mostly of coarse fibers
(Korffs fibers)
Circumpulpal dentin the remaining dentin
During the lifespan of a multirooted tooth, dentin forms most rapidly on the floor and roof of the pulp chamber
Peritubular dentin (AKA intratubular dentin): intra meaning within the tubule
Lines each dentinal tubule most mineralized dentin; more than intertubular dentin ( inorganic salt content)
Intertubular dentin: (in between tubules)
Surrounds the peritubular dentin, less mineralized (has content of inorganic salts)
Interglobular dentin:
Imperfectly calcified matrix of dentin situated between the calcified globules near the periphery of the dentin
Primary dentin:
Dentin forming the initial tooth shape
Deposited before completion of the apical foramen
shouldn't it be
Secondary dentin:
Dentin formed after completion of the apical foramen
Formed at a slower rate than primary dentin as functional stresses are placed on a tooth
Does not contain cells (primary cementum & cancellous bone BOTH do) cells are in the pulp!
A regular & somewhat uniform layer of dentin around the pulp cavity
Junction between 1 & 2 dentin is characterized by a sharp change in direction of dentinal tubules
Reparative dentin (Tertiary dentin):
Formed very rapidly in response to irritants such as attrition, abrasion, erosion, moderately advancing dental caries,
Forms at the pulp interface of the dentin in response to caries
Sclerotic dentin:
Results from aging & slowly advancing dental caries
The dentin tubules become calcified & obliterated, which blocks access of irritants to the pulp by way of tubules
On a histological Slide:
Dentin tubules appear dark/black due to air when sectioning
Dentinal Tubules
Dentinal tubules are S-shaped in the crown due to crowding of the odontoblasts
Each dentinal tubule contains the cytoplasmic cells of an odontoblast
Primary curvatures of the dentinal tubules is LESS in root dentin than in crown dentin More in CROWn due to
increased CROWding
Tomes fibers: (AKA Odontoblastic Fiber)
CAREFUL, Ameloblasts give off Tomes Processes
Long, slender, cytoplasmic extension arising from each odontoblast
Occupy the dentinal tubules
Dentin sensitivity is mediated by these fibers
Because of these fibers, odontoblasts are considered living tissue


Dead tracts:
Groups of dead, coagulated cytoplasmic processes of the dentinal tubules
Attributed to aging, caries, erosion, cavity preparation, or odontoblastic crowding
Shows up dark on ground section of tooth
A dead tract can form if odontoblastic processes disintegrate & leave open dentinal tubules
Morphology of DEJ determined at the Bell stage Enamel Organ has also differentiated into four layers (oee, Iee, stellate
reticulum and stratum intermedium)
For whom, the BELL TOMES!
Interface between dentin & enamel
Where calcification of a tooth begins
Oldest dentin is next to DEJ Same with oldest enamel!
Slightly softer & lighter in color (yellow) than dentin
Avascular and not innervated but does have cells
Cementum is formed by cementoblasts from the PDL, as opposed to dentin which is formed from odontoblasts of the pulp
In order for cementum to form during root development, the epithelial root sheath (Hertwigs) must be fenestrated or
the continuity must be broken
Lines the apical foramen of a fully developed permanent tooth (Important for ENDO, dont perf the cementum)
50% inorganic (HA), 40% organic (collagen/protein), & 10% water
Similar to bone in the degree of mineralization
Collagen fibers formed from BOTH cementoblasts AND fibroblasts
Most closely resembles bone (more so than dentin) except there are no Haversian systems or BVs
Distinguished from enamel by presence of collagen fibers and the cellular component in mature tissue
Distinguished from dentin in that dentin was made by pulp cells and cementum by PDL cells
Similar to bone in that both contain cells in lacunae with canaliculi extending toward nutritional source
Secondary dentin does not contain cells
Cementum does NOT contain blood vessels
Important in orthodontics:
More resistant to resorption than alveolar bone, permitting orthodontic movement of teeth w/out root resorption
Two types of cementum (no functional difference)
Acellular cementum:
Usually predominates in the coronal 2/3 of the root. Thinnest at the CEJ
Cellular cementum: (Think C for laCunae)
Contains cementoblasts, inactive cementocytes, fibroblasts from the PDL, and cementoclasts
Occurs more frequently on the apical 1/3 of the root
Remember you need active Cementoblasts for attrition wear replacement
Usually the thickest to compensate for attritional wear of the occlusal/incisal surface & passive tooth eruption
Best differentiated from acellular cementum by the presence of lacunae (not by any functional difference) Makes
sense if its gonna have cells, gotta have a place for the cells to be- lacunae
Peripheral layer of developing cementum (uncalcified)
Calcified bodies sometimes found lying free w/in the PDL or fused w/ the cementum of the tooth
Primary cementum
Possesses lamellae (not lacunae, canaliculi, or cementocytes) so no cells, just rings in primary cementum
Main function provides rough surface for attachment of Sharpeys fibers (PDL)
Compensates for loss of tooth surface due to occlusal wear by apical deposition of cementum throughout life (apposition of
apical cementum)
Protects the root surface from resorption during vertical eruption & tooth movement
Reparative function of cementum allows reattachment of CT following periodontal treatment
Replaces resorbed dentin or cementum
Mature Pulp is composed of primarily Loose CT
In mature pulp, which cells predominate? Fibroblasts!
25 yr old has pulp characterized as Loose CT
Derived from Dental Papilla (mesoderm) Pic above of dental papilla
After the tooth is formed, the dental papilla remains as the dental pulp


Coronal pulp
Located in the pulp chamber and pulp horns
Radicular pulp
Located in pulp canals
Apical foramen
Communicates w/ the PDL
Local resorption/deposition of cementum & local resorption of dentin may change the position/shape of apical foramen
Accessory canals
Extend from pulp canals through root dentin to PDL
Formed by a break in the (Hertwig) epithelial root sheath from blood vessel trapped, etc.
Central Zone (pulp proper)lined peripherally by specialized odontogenic area which has these zones (inner to outer):
Pulpal core similar to cell-rich zone
Cell-rich zone contains fibroblasts (most abundant cell type in the pulp)
Cell-free zone (of Weil) Capillary and Nerve plexus (Plexus of Raschkow)
Odotoblastic layer contains odonotblasts and lies next to the predentin and mature dentin
Nerve Fibers
Principle types of nerves in the pulp are sympathetic & afferent fibers Sympathetic control blood, afferent tranmit the
pain from free nerve endings
Age changes in pulp:
Decrease in:
Intercellular substance, water, & cells
Size of pulp cavity due to secondary &/or tertiary dentin
Number of reticulin fibers
Increase in:
Number of collagen fibers
Calcifications w/in pulp (called denticles or pulp stones)
True: complete w/ tubule and processes
False: amorphous in structure
Free: unattached to outer pulpal wall
Attached: attached at dentin-pulp interface
Pulp capping
More successful in young teeth because:
Apical foramen of a young pulp is large
Contains more cells
Is very vascular
Has fewer fibrous elements
More tissue fluid
Does lack collateral circulation
Alveolar Process
Alveolar bone proper: (aka: cribriform plate or lamina dura) (SOCKET)
Part of alveolar process which immediately surrounds root of tooth & to which the fibers of PDL are attached
Has minute openings which provide passage for vascular nerve components NOT for attachment of sharpeys!
During growth and development of the alveolar process, osteoblasts, osteoclasts, and osteoid are present
Resorbs when subjected to pressure - thus orthodontics is possible
What causes alveolar bone development?
Tooth Growth, w/o teeth it wont grow
Consists of:
1) Compact lamellar bone
2) A layer of bundle bone
Sharpeys fibers insert into this layer
Supporting alveolar bone:
Surrounds the alveolar bone proper & gives support to the socket
Consists of:
Cortical plate (compact lamellar bone)
Lamellar bone has more what than woven bone? Collagen, (not cells, water, ground substance)
Forms outer & inner plates of the alveolar processes
Thicker in Mn than Mx Why we cant give infiltration injections in Mn
Spongy bone (cancellated bone):
Fills in area between cortical plates of bone
This type of bone is not present in anterior region of mouth here the cortical plate is fused to the cribriform plate


This is also true over the radicular buccal bone of the maxillary posteriors
NOTE: Alveolar bone proper is the only essential part of the bone socket supporting alveolar bone is not always present
Growth is appositional like all bone!
Bone can only grow appositionally, but cartilage can grow appositionally or interstitially
Causes the formation of resting lines during growth of Mn B/C it grows appositionally
During active tooth eruption there is apposition of bone on all surfaces of the alveolar crest and on all walls of the bony socket???
The bone formed at the base of the socket is usually in the form of horizontal trabeculae See this on radiographs
The best theory describing the force needed for active eruption is from the cells and fibers of the PDL pulling the tooth out
Permanent teeth move occlusally and buccally when erupting
Break in the mandible from a baseball at the mental foramen, which way will the muscles
pull the fragments
Large anterior and superior Small Inferior and Posterior
When you open your mouth, the buccal vestibule is squashed by the Coronoid process
Apical abscesses
Mn M2s & M3s have a marked tendency to produce cervical spread of infection most
Attachment of muscles may determine the route that an infection will take, channeling the
infection into certain tissue spaces
Mandibular Teeth
Infections perforate below the buccinator
Swelling of the lower of the face
Infection will spread medially (lingually) from the Mn into the submandibular space & masticatory spaces
It pushes the tongue forward and upward
Further spread cervically may involve the visceral space and lead to edema of the vocal cords and airway obstruction
Molar abscess will reach the floor of the mouth by continuous spread until the lingual attachment of the mylohyoid m.
Swelling at the angle of the mandible is from the deflection of exudates from the mylohyoid m.
Tooth #32 is infectedinfection spreads to parotid, buccopharyngeal, & masseteric fasical spaces, NOT the temporal
In Hep C pt, Tooth #28 needs to be extractedWhich is a life-threatening sequelae of that txLudwigs Angina -Life
threatening sequellae from infection nothing to do with heart Angina means Strangeling in greek!
Alpha delta fibers are responsible for sharp pain C fibers are for dull pain
Maxillary teeth
Perforate the bone above the buccinator attachment
Cause swelling of the upper of the face (which will eventually spread to the entire face)
Lingual spread
From infected Mn premolar or molar teeth into floor of mouth when above the level of attachment of the
mylohyoid m.
This is due to the mylohyoid line position relative to roots of premolars & molars search it in the Dental Anat file
Below the mylohyoid, it would drain into the submaxillary/submandibular space
Ludwigs Angina
Cellulitis, usually of odontogenic origin, bilaterally involving the submaxillary, sublingual, and submental spaces, resulting
in painful swelling of the floor of the mouth, elevation of the tongue, dysphasia, dysphonia, and (at times) compromise of the
airway hence the life-threatening part
Mesial Drift (or in mesial tilting during orthodontic movement):
Coronal half of the Mesial root wall shows resorption from osteoclastic activity
Coronal half of the Distal wall of the root shows deposition from osteoblastic activity
Similar situation: loosening & tightening of primary tooth before its lost
Alternate resorption (clasts) and apposition (blasts) of cementum and bone
First sign of tooth development (seen in histo sections) occurs in 6th week in utero (pictures)
Tooth development appears to be initiated by the mesenchymes inductive influence on the overlying ectoderm
In 6th week there is a thickening of the oral epithelium (derivative of the surface ectoderm)
These thickenings or U shaped bands are called the dental lamina and follow the curve of the primitive jaws (20)
At certain point on dental lamina, the ectodermal cells proliferate and produce swellings which become the enamel organ
Inside the depression of the enamel organ is an area of condensed mesenchyme becomes the dental papilla
Surrounding both the enamel organ and dental papilla is a capsule-like structure of mesenchyme called the dental sac
Enamel organ separates from the dental lamina AFTER the layer of dentin is deposited
Each tooth is the product of two tissues that interact during tooth development 1) oral epithelium & 2) underlying ectomesenchyme
The epithelium grows down into the underlying ectomesenchyme to form small areas of condensed mesenchyme, which become
tooth germs
Sequence of Tooth Histogenesis


The ectomesenchyme influences the oral epithelium to grow down into the ectomesenchyme
Elongation of inner enamel epithelium
This triggers the mesenchymal cells to differentiate into odontoblasts
Differentiation of odontoblasts
Deposition of first layer of dentin
Deposition of first layer of enamel
Deposition of root dentin and cementum
Stages of Histogenesis
Initiation (Bud Stage):
Initial interaction between oral epithelium and mesenchyme (ectomesenchyme), formation of dental lamina
Congenitally absence of teeth results from an interruption in this phase
Fused or geminated teeth occur during initiation and proliferation stages of tooth development
Proliferation (Cap stage):
Shape of tooth becomes evident, enamel organ is formed
Differentiation (Bell Stage):
Final shaping of tooth; cells differentiate into specific tissue-forming cells (amelo-, odonto-, cemento-, & fibroblasts) in
emanel organ I think this also means: IEE, OEE, Stellate Reticulum and stratum Intermedium
Histodifferentiation and mophodifferentiation occur during this stage ^^^^^
DEJ determined at this stage For whom the BELL TOMES
Forms the DEJ (the 1st structure formed by tooth but that remains in the fully developed tooth not IEE)
Cells that were differentiated into specific tissue forming cells begin to deposit the specific dental tissue
**Dentinogenesis imperfecta & amelogenesis imperfecta occur during histodifferentiation
Terms of Dentinogenesis
From Top of Diagram to bottom
Oral Epithelium
Epithelial layer on top
Dental Lamina
Stem connecting the Oral Epithelium to the Enamel Organ
Tooth Germ
Enamel Organ, Dental Papilla, Dental Sac (not successional lamina)
Enamel Organ
Derived from ectoderm
Gives rise to enamel and Hertwigs Root Sheath
4 Layers of Enamel Organ (not in order):
1) Outer enamel epithelium (OEE)
Outer cellular layer
Outlines the shape of future enamel organ
2) Inner enamel epithelium (IEE)
Innermost layer
Cells will become ameloblasts
Essential for the initiation of dentin formation (ameloblasts stimulate dentin formation)
1st formed in a partially erupted central incisor (among 1/2 cuticles, stellate reticulum, stratum intermedium)
3) Stratum Intermedium
Lateral to IEE
Essential to enamel formation (nutrients for the ameloblasts of IEE), but does not actually secrete the
Ameloblasts will only form enamel when stratum intermedium is present
4) Stellate Reticulum
Central core and fills bulk of organ
Contains lots of intercellular fluid (mucous type rich in albumin) which is lost prior to enamel deposition
Disturbances during morphodifferentiation of the enamel organ affect the shape of the tooth
IEE & OEE of enamel organ come together in the neck region and form Hertwigs root sheath
After enamel formation, all 4 layers become 1 and form the Reduced Enamel Epithelium
The reduced enamel epithelium & oral epithelium fuse to form the initial junctional epithelium
Very important in forming the dentogingival junction, where the enamel & epithelium meet as tooth erupts
This forms initial junctional epithelium (attached epithelium joining gingiva to tooth)


Dental Sac (aka Dental Follicle) Dental Sac Pic above a few pages
Derived from mesenchyme (derived from neural crest cells) NOT from oral epithelium
Gives rise to the cementum, PDL, and alveolar bone proper (aka attachment apparatus)
The embryonic precursor to cementoblasts
Surrounds the tooth germ (enamel organ/dental papilla)
Dental Papilla
Derived from mesenchyme (derived from neural crest cells)
Gives rise to the dentin and pulp
Triangular shaped inside the bell stage under the enamel organ
Peripheral cells of dental papilla differentiate into odontoblasts which produce predentin (calcifies to become dentin)
Center of dental papilla will become dental pulp
Epithelial Diaphragm
Multiple root formation follows unequal proliferation of the epithelial diaphragm okay
Hertwigs Epithelial Root Sheath
Sheath is formed by the joining of the IEE & OEE
After crown formation, the root sheath grows down
It shapes the root of the tooth & induces formation of root dentin (stimulates differentiation of odontoblasts)
Uniform growth of this sheath will result in the formation of a single rooted tooth
Medial outgrowths or evaginations of this sheath will produce multi-rooted teeth
???OLD TEST (1987) The # of roots formed is determined by the number of medial ingrowths of the cervical loop
Hertwigs epithelial root sheath is characterized by:
1) The formation of cell rests (rests of Malassez) in the PDL when the sheaths functions have been accomplished
2) The absence of stellate reticulum and a stratum intermedium IEE and OEE only!
After first root dentin is deposited, the cervical portion of Herwigs root sheath breaks down
This new dentin comes in contact w/ the dental sac
This communication stimulates cells fibroblast cells from the dental sac to differentiate into cementoblasts which
produce cementum
Accessory root canals are formed by a break or perforation in the rooth sheath BEFORE the root dentin is deposited
Epithelial Rests of Malassez
Are remnants of Hertwigs epithelial root sheath
Some degenerate and others calcify or become cementicles
Persistent rests can be found as groups of epithelial cells in the PDL
Continuity of Hertwigs epithelial rooth sheath must be broken in order for cementum to be deposited during tooth development

Tomes Granular Layer

Formed by odontoblasts that produce an organic matrix
Found in radicular dentin and lies just beneath the cementum
So, the granular layer (Tomes) makes the root dentin readily distinguished from crown dentin
**Interglobular dentin differs from Tomes granular layer in that interglobular dentin usually occurs a short distance
inside the DEJ and represents uncalcified areas?????


Partial Anodontia (Hypodontia)

Radiograph of 10 year pt where 2 succedaneous teeth are missing
PDL pg. 225 in Bibbs book
0.2mm wide
Thickness depends on:
Age (decrease 0.1mm in old agedue to deposition of cementum & bone)
Stage of eruption
Function of the tooth
(PDL is thin and irregular principle fibers on teeth that lose their function) Like skel muscle use it or lose it!
Vital to the functional life of a tooth because it:
Contains nervous and vascular elements
Allows for physiologic movement of the tooth
Provides a cellular source for new cementurn and bone
Derived from the dental sac!!!!!
Connects cementum to alveolar bone
Contains remnants of Hertwigs root sheath (Rests of Malassezcalled cementicles when calcified)
Sharpeys Fibers terminal portion
Diameter greater on bone side vs. cementum
Only consist of Collagenous fibers, NOT reticular or elastic
Insert into Bundle Bone and Cementum
Function of PDL:
Attachment of tooth to bone via principal fibers
Formation of CT components by activities of CT cells (cemento-, fibro-, and osteoblasts)
By activities of CT cells (blast vs. clast of above cells)
Through BVs
Proprioceptive & tactile sensitivity
PDL and its hard tissue anchorage in terms of resisting occlusal force:
Anterior teeth have slight or no contact in the ICP
Occlusal table is < 60% of the overall faciolingual width of the tooth
Occlusal table of the tooth is generally at right angles to long axis
Crowns of Mn molars are 15-20 lingually inclined
Hence roots are positioned more facially for these teeth
Following loss of tooth function:
One may expect a reduction in width & loss of regular arrangement of principal fibers???
Like pulling a yarn taut???
PDL & nerves
2 Types
Free, unmyelinated endings convey PAIN think cold test takes a long time to react
Encapsulated, myelinated convey PRESSURE Think fast jaw jerk reflex
PDL contains:
Osteoblasts, fibroblasts, Macrophages, Cementoblasts, etc. And the various -clasts
Extracellular substance of fibers (gingival and principal)
The principal fibrous elements of the PDL in adults is chiefly collagen And only
collagen in sharpeys fibers.
Ground substance
Mostly proteins and polysaccharides
Oxytalan fibers Like elastin, are part of elastic fibers
Related to the microfibrillar component of elastic fibers
Run parallel to root surface
Gingival fibers (5) (picture) name tells it all for these guys.
General features:


Collagen fibers that provide support for the marginal gingival including the interdental papilla
Found w/in the free gingiva
Continuous w/ the CT fibers and are often considered part of the ligament (PDL)
Circumferential (circular) fibers (A)
Encircle the tooth around the most cervical part of the root
Insert into cementum & lamina propia of the free gingiva & alveolar crest
Resist rotational forces
Transseptal fibers (BELOW A)
Extend from tooth to tooth (cementum to cementum), coronal to alveolar crest
Are embedded into the cementum of adjacent teeth
Not on the facial and no attachment to the alveolar crest
Maintain dental arch integrity
Classified w/ principal fibers of PDL (AKA collagenous fibers).
Are included in the Interdental Ligament pg. 228 of Bibbs book
Dentogingival fibers (B)
From the cementum apical to the epithelial attachment; course laterally & coronally
into gingival lamina propria
Dentoperiosteal fibers (C)
From the cervical cementum over the alveolar crest to the periosteum of the cortical
plates of bone
Alveologingival fibers (D)
Insert in crest of alveolar process and spread out through the lamina propria into the free
Principal Fibers of the PDL(5) (picture) pg. 226 in Bibbs book
General features:
Composed of Type I collagen
Sometimes classified as belonging to general group of alveolodental fibers
Connect the cementum to the alveolar bone
Never found in contact w/ enamel
Alveolar crest fibers (B)
From cervical cementum to the alveolar crest
Function to counterbalance the occlusal forces on the more apical fibers and resist
lateral movement
Horizontal Fibers (C)
Perpendicular from alveolar bone to cementum
Resist lateral forces
Oblique fibers (33%) (D)
Most numerous
Insert into cementum and extend apically and obliquely into the alveolus I think this is backwards: Alveolus apical into
Resistant to forces along the long axis of the tooth (masticatory)
Found usually in middle 1/3 of root
Apical (E)
Offer initial resistance to tooth movement in occlusal direction extrusive movements
Interradicular fibers (F)
Only in multi-rooted teeth
Extend from cementum in furca are to bone w/in furca area
Gingival apparatus
Term used to describe the 5 gingival fiber types and the epithelial attachment
Gingival Ligament
Includes the dentogingival, alveologingival, and circumferential fibers
The gingiva offers protection against bacterial invasion, the most important factor in this protection being that the surface
epithelium is highly impervious
Free Gingiva (aka marginal gingiva)
Collar of tissue that is not attached to the tooth or alveolar bone
1-3mm wide & forms the soft tissue wall of the gingival sulcus next to the tooth
Extends from free gingival groove to gingival margin
Structures: pg. 153 in Bibbs book
Gingival Margin


1mm band of gingiva that forms immediate collar around the base of the tooth
Gingival Sulcus
Areas between the unattached gingiva and the tooth (where popcorn kernels go)
Above junctional epithelium (JE) continuous w/ JE, but structurally different
Epithelium is non-keratinized (same w/ gingival col)
Most vulnerable to inflammation
Healthy sulcus should NOT have rete pegs (rete pegs indicate inflammation)
Cells of the sulcular epi are joined TO EACH OTHER by desmosomes
Epithelial attachment (Junctional epithelium)
As supragingival plaque/calculus continues apically, it first would disrupt the attachment of the junctional epithelium
Joins the gingiva to the tooth
Inner layer of cells of JE attach gingiva to tooth
Cells of the epithelial cuff attach to enamel or cementum by means of hemidesmosomes
Internal basal lamina (**Basal lamina like structure)
Does NOT contain rete pegs as the superior apex of the free gingiva does
**Dentojunctional epithelium
Gingival epithelium that faces the tooth
Includes both Sulcular and Junctional
Interdental Papilla
Portion of the free gingiva that fills the IP embrasures below contact area
Consists of 2 papillae that are connected by the concave-shaped interdental col
Interdental col
Conforms to the shape of the contact area
Not present in teeth w/o contact
Non-keratinized Just as the rest of the free gingival/papilla is not keratinized as well
Blood vessels of the interdental papilla anastomose freely with BOTH periodontal & interalveolar vessels
Attached Gingiva
Part of the gingiva that is attached to the underlying periosteum of alveolar bone & to cementum by CT fibers & epithelial
NO submucosa
Present between the free gingiva & the more movable alveolar mucosa
Parakeratinized (means tissue with nuclear remnants in stratum corneum)
Masticatory Mucosa is Parakeratinized except with Dentures
Soft palate, skin of lips, floor of mouth & ventral tongue are NOT parakeratinized
Extends from the mucogingival junction to free gingival groove
Mucogingival Junction pg. 139 in bibbs book
Separates the attached gingiva and the alveolar mucosa
Joins lining mucosa & masticatory mucosa
Free Gingival Groove pg. 153 in bibbs book
Separates the free gingiva from the attached gingiva
Is related to the arrangement of the supraalveolar fibers (not probe depth measurement, alveolar crest, or degree of PD health)
Oral Mucosa
Covers all oral surfaces except the teeth
2 Layers:
Stratified squamous epithelium
Lamina Propria
CT that supports the epithelium
2 Layers
Attached to the periosteum or interposed over the submucosa (glands, BVs, nerves)
In the hard palate & gingiva, the lamina propria attaches directly to bone without an intervening submucosa
(not so for the soft palate) pg 153 in Bibbs book
Gingiva differs from alveolar mucosa in that it has high connective tissue papillae Makes sense more wear n tear, more
Specialized Mucosa
Covers the dorsum of the tongue and taste buds


Non-keratinized (most of the dorsum of the tongue is keratinized, right?)

Masticatory Mucosa No Sub mucosa???
Free gingiva, hard palate, attached gingiva, interdental gingiva
Beneath lies the lamina propria (dense, thick, firm CT containing collagenous fibers)
Lining or Reflective Mucosa
Inside of lips, cheek (buccal mucosa), vestibule, lateral surface of alveolar process, floor of the mouth, soft palate, ventral tongue
Thin, movable
Nonkeratinized, stratified squamous epi
Lamina Propia no glands in the lamina propria of the floor of the mouth
2 functional units:
Gingival unit
Free gingiva, attached gingiva, and alveolar mucosa
Attachment apparatus
Cementum, PDL, and alveolar bone proper
TMJ pg. 325 in Bibbs book
A diarthrodial joint that has a fibrous CT (fibrocartilage) on its articular surfaces (NOT hyaline)
Most diarthrodial joints are covered by hyaline cartilage
The articular surface of the condyle AND the posterior slope of the articular eminence have the same fibrous CT covering
Joint cavity is lined by a synovial MB & enclosed by a fibrous capsule So everything else is normal, just the fibrocartillage
Divided into two compartments by an articular disc
The TMJ of a child contains Undifferentiated Mesenchyme cells, then Cartilage layer under the Fibrocartilage
TMJ Nutrients
Hyaluronic acid of the Synovial fluid, feeding the articular cartilage
12 weeks condylar cartilage is present at the most superior aspect of the ramus
The condylar cartilage persists as the cartilage zone of the mature condyle, contributing to its adaptation potential
12 weeks The embryonic CT (Mesenchymal) between the growing condyle and temporal bone condenses to form the articular
13 weeks Cavitation forms the lower joint compartment then the upper compartment
14 weeks Joint development complete
Articular Surface of temporal bone
Articular fossa (or glenoid fossa or mandibular fossa) concave
In older people is covered with Fibrous CT with Chondrocytes chondrocytes for fibroCARTILAGE
In young adults the articular zone has
Articular zone of Fibrous CT
Proliferation zone of undifferentiated Mesenchymal cells UM
Cartilage zone
Articular Eminence convex
Is the anterior surface/boundary of the Mandibular (glenoid) fossa
42 yr old female with Hx of hyperPTHism, bilateral pain in TMJ, ears clogged and ringing
The region of the articular surface that is most likely missing is the Proliferative zone (I have no idea why!)
See 2001 Pilot Q 366

Posterior aspect of the condyle is rounded & convex, whereas the anteroinferior aspect is concave
Posterior aspect of the condyle can be palpated by way of the external auditory meatus


Growth of the condyle allows for the space needed for erupting teeth It grows upward and backwards
Condyle is broken through the pt. fovea?, there is no necrosis, what artery is supplying the tissue?
Temporal artery
Articular disc (meniscus) pg 326 in Bibbs book
Consists of fibrocartilagenous tissue, which resembles dense, irregular CT that may be associated w/ chondrocytes,
capable of providing smooth articulating surface
Meniscus is a biconcave oval plate
Divides the joint into two spaces:
Superior joint space bounded by articular fossa & articular eminence
Sliding Motion occurs between the disks & articular eminences in upper jt space, only disc and eminence
(thus the sliding cant rotate)
Upper compartment of the TMJ does
Translational movement
Inferior joint space bounded below by the condyle
Rotational Motion condyle rotates, and its on bottom.
Meniscus varies in thickness, the thinner, central intermedia zone separates the thicker anterior & posterior bands
Posteriorly, the meniscus is continuous w/ the posterior attachment tissues called the bilaminar zone which is vascular,
innervated tissue that plays an important role in allowing the condyle to move forward
NOTE: the bilaminar zone is the most vascular portion of the articular disc (NOT the posterior band)
Posterior-inferior lamina of bilaminar zone has a very dense collection of elastic fibers (1999Q23 confirmed
JC?) Pg. 258 in Netters H&N Anatomy
Retrodiscal Pad Area
Elastic fibers
Venous plexus well-vascularized structure of the TMJ
Collagen fibers
Loose connective tissue
NOT Hyaline Cartilage No hyaline cartilage there!
Nonarticular surfaces of the TMJ are covered w/ synovium or periosteum (dont get clowned by the non part)
Articular capsule
Surrounds the joint
Attached above to the articular eminence (tubercle)
Attached at margins of the mandibular fossa & below the neck of the Mn
Synovial MB lines the capsule in the superior & inferior spaces of the joint
It does not cover the articular surfaces of articular discs
Innervated by the auriculotemporal, the masseteric, and the posterior deep temporal (ALL V3)
Anterior portion is innervated by masseteric nerve ?? Netters H&N pg. 262 says
post. deep temporal innervates anterior part of TMJ
Ligaments (picture) pg. 259 Netter H&N anatomy
Temporomandibular ligament not pictured
Runs from articular eminence to the Mn condyle
Provides lateral reinforcements for the capsule
Is the only ligament that gives direct support to the capsule of the TMJ
Aka: lateral ligament
Prevents posterior & inferior displacement of the condyle
Sphenomandibular & stylomandibular ligaments
Are considered accessory ligaments responsible for limiting Mn movement
Sphenomandibular ligament attached to the lingula of the Mn and the spine of the sphenoid bone
Most often ligament damaged in an IA nerve block (tested again & again)- makes perfect sense since it attaches to
the lingula
Stylomandibular ligament attached at angle of the Mn
Lateral pterygoid muscle: pg. 246 Netter H&N Anatomy
Superior head:
Origin: Infratemporal surface of sphenoid bone
Insertion: TMJ capsule & articular disc
Inferior head:
Origin: Lateral surface of pterygoid plate pterygoid plate is the inferior part of the sphenoid bone makes sense!
Insertion: Neck of the Mn condyle
Protrude, depress (open), laterally move Mn depresses with superior head of lateral pterygoid
Auriculotemporal nerve, Masseteric, and Posterior Deep Temporal in the capsule and around the periphery of the disc


NOTE: the auriculotemporal nerve carries pain, touch, temperature, & proprioceptive modalities to the TMJ
The TMJ, as w/ all joints, receives no motor innervation
The muscles that move the joint receive the motor innervations
Branchiometric motor fibers innervate the temporalis, pterygoids, anterior belly of digastric, mylohyoid, & tensors
TMJ should be evaluated for tenderness and noise
The joint is palpated laterally (in front of the external auditory meatus) w/ the Mn in closed and open position
The joint is palpated posteriorly (through the external auditory meatus) w/ the Mn in closed and open position
Things to note:
Tenderness and sensitivity
Joint noises
Mn range of motion
Normal range of movement of adult Mn ~50 mm opening & ~10 mm protrusively & laterally
Magnetic resonance imaging (MRI):
Best imaging modality for identifying position of articular disc of the TMJ
Gold standard for soft tissue, especially the position of the articular disc
Utilizes magnetic field to alter energy levels of primarily the water molecules of soft tissue
Results in good visualization of various soft tissues, including articular disc
Major advantage of MRI is that there is no radiation involved
No harmful effects have been demonstrated
Panoramic, CT, & lateral transcranial radiographs are used to evaluate the bony structures of the TMJ
Dislocation (luxation)
May occur w/ one or both condyles
Relaxation of the supporting ligaments occasionally allows condyle to extend anteriorly beyond normal open position
May be manifested by true luxation that requires assistance for reduction
Or, it may be merely an overextended excursion anteriorly that is self-reducing (subluxation)
TMJ can only be dislocated anteriorly The post glenoid tubercle posterioly wont let it displace backward!
Anteromedial most common direction in which the articular disc in the TMJ can be displaced
A click sound is usually demonstrated when this happens
Articular disc is seated on condyle & held in place by collateral ligaments (attached to medial & lateral poles of the condyles)
Muscle fibers from the lateral pterygoid muscle are attached to the anterior portion of the articular disc
Reduction of the dislocation
Is done by standing behind pt w/ thumbs inside mouth and the index fingers below chin
Thumbs depress the back of the jaw, and the chin is elevated by the index fingers
The head of the condyle will then slide back into the articular fossa
42 yr old female with Hx of hyperPTHism, bilateral pain in TMJ, ears clogged and ringing
The region of the articular surface that is most likely missing is the Proliferative zone (I have no idea why!)
Click best describes sound associated w/ a disc displacement w/ reduction
Crepitation sound (crepitus) usually associated w/ a degenerative process (osteoarthritis) of the condyle
Dull thud usually associated w/ self-reducing subluxation of the condyle
Tinnitus ear ringing


Fluids in general:
o Extracellular fluid (Na-142; K-4) vs intracellular (Na-10 K-140) KIN Potassium is in
o Fluid: 50-60% of body weight
Intracellular fluid (w/in cells) = 35-40% of body weight
Extracellular fluid (outside the cells) = 15-20% of body weight
Blood plasma = 4-5% of body weight
Interstitial fluid = 11-15% of boby weight. Most of extracellular fluid is interstitial fluid
o Transcellular fluids: CSF, intraocular, synovial, pericardial, pleural, peritoneal
o Tissue (interstitial) fluid contains a small % of plasma proteins of low MW that pass through the capillary walls as a consequence
of hydrostatic pressure of blood. This fluid bathes the cells
o 8% of total body weight
o Volume = 4-6 liters
o Temp = 38C
o pH = 7.35-7.45
Blood composition
o 55% plasma:

91% water
7 % protein
Albumins 55% Albumin is the most prevalent plasma protein
Globulins 38% Igs
Fibrinogen 7% Clotting ptns
2% other solutes
Metabolic end products, food materials, respiratory gases, hormones, ions
45% formed elements:
1) Erythrocytes 4.3-5.8 million/mm3
Proerythroblast erythroblast normoblast reticulocyte erythrocyte
o What increases when a proerythroblast becomes an erythrocyte? cytoplasmic acidophilia
Biconcave, enucleated discs 7-8m in diameter
o Contain heme (an endogenous pigment)
o Biconcave shape increases surface area 20-30%
o High surface area : volume ratio
No MB-bound organelles
Energy source is glucose
o 90% from anaerobic metabolism degraded to lactate no mitochondria
o 10% from HMP shunt
Function = O2 & CO2 transport
o Oxyhemoglobin = hemoglobin molecule + O2
o Carbaminohemoglobin = hemoglobin + CO2 (~70% of CO2 is transported as bicarbonate ions) Not this
Remember Carboxyhemoglobin is CO
RBC MB contains chloride-bicarbonate antiport allows transport of CO2 to lungs for elimination
Hematocrit = proportion of erythrocytes in a blood sample
o 46%, for males, 40% for females
Formed via erythropoiesis stimulated by erythropoietin produced in kidney
o In erythropoiesis, the cytoplasmic acidophilia increases (Duh, they become more red )
o In erythropoiesis, cells trend toward:
A progressively smaller size
A progressive loss of organelles
A progressive increase in cytoplasmic Hemoglobin concentration
Average life span = 120 days
o Normoblast is a developmental stage of the erythrocyte (not monocyte, lymphocyte, or eosinophil)
Shrink and crenate in hypertonic solution
Become ghost cells in hypotonic solution Become bigger probably whiter like a ghost!
Erythrocytosis = polycythemia = # of RBCs
Anisocytosis = varying sizes
Poikilocytosis = varying shapes
2) Platelets 250-400k/mm3
Cytoplasmic fragments of cells that promote clotting (as part of hemostasis)
o Thrombopoietin stimulates megakaryocytes to give rise to platelets
Minute, irregularly shaped, disk-like cytoplasmic bodies found in blood plasma
No nucleus, DNA or hemoglobin
Life span is 5-9 days removed in spleen & liver
Stop blood loss by forming a platelet plug
Contain secretory vesicles (granules), which release ADP & others chemicals when platelets adhere to collagen
o Induces changes that make platelet surface sticky
o Additional platelets adhere to original platelets to form plug
Thromboxane A directly promotes platelet Aggregation
o Where PGI inhibits Platelet grouping
3) Leukocytes 5-10k/mm3
Neutrophils 60-70% [of leukocytes] in a differential blood count
o More recent #s say 40-75%
o Lobed nucleus, fine granules
o Large, spherical azuriphilic 1 granules (lysosomes)
Contain hydrolytic enzymes, lysosyme, myeloperoxidase, & lactoferrin
o Function = phagocytosis (they love to ingest bacteria)
o Nucleus becomes more hyperchromatic during the development in the red bone marrow
o Neutrophils w/ > 5 lobes are called hypersegmented
Lymphocytes 20-30% (agranulocytes)




Round nucleus, little cytoplasm

Function = produce Ab, destroy specific target cells
T cells:
Differentiate in the thymus
Account for 70-80% of circulating lymphocytes
Produces cell-mediated immunity
Interact w/ specific antigen, become sensitized & differentiate into several types of daughter cells:
Helper T cell (CD4)helps activate other T lymphocytes and B cells
Cytotoxic T cell (CD8)combines w/ Ag on surface of foreign cell causing lysis & cytokine release
Suppressor T cellsuppresses activation of immune system maintains hemostasis & tolerance to self
Memory T cellremains inactive until 2nd exposure to same Ag then reproduce to mount a faster
o Aka delayed hypersensitivity T cell
o B cells:
Differentiate in bone marrow
20-30% of circulating lymphocytes
Antibody immunity
Once activated by/sensitized to Agdaughter cells that either make Ab/s or become memory cells
Memory B cellsplasma cells (after 2nd exposure to Ag)
Can function as an APC (to T cells) via MCH Class II
o Plasma cells:
Differentiated from B-cells
Found in bone marrow, CT and sometimes blood
Off-center nucleus & clock-face chromatin distribution
Short 5-10 day life
Specific immunity
Aid in the immunologic defense of the body (NOT mast cells, neutrophils, giant cells)
Plasma cells (NOT T-cells or B-cells) produce most of the bodys Ab/s
Contain large amount of rough ER & well-developed Golgi apparatus (Same with Mucous secreting Goblets)
Are found in the inner medullary center of lymph nodes (aka Medullary Cords) Maybe get a pic of this
Monocytes 2-6% (agranulocytes)
o Kidney-shaped nucleus (Crescent Moon shaped)
o Differentiates into macrophages in tissues
o Function = phagocytosis
Eosinophils 1-4%
o Lobed nucleus, red or yellow granules
o Function = may phagocytize Ab-Ag complexes
o Contain histimase, acid phosphatase, and aurosulfurnimase
Basophils 0-1% Never Let Monkeys Eat Bananas Neutrophils, Lymphocytes, monocytes, Eosinophils, basophils
o Obscured nucleus, purple granules purple or blue BASOphils
o Function = release histamine, heparin, serotonin, & SRS-A (slow reacting substance of anaphylaxis)
o Similar to mast cells w/ coarse cytoplasmic granules
Granules contain heparin (anticoagulant), histamine (vasodilator) and bradykinin, serotonin, & SRS-A (slow
reacting substance of anaphylaxis)
Heparin can prevent blood coagulation & can speed the removal of fat particles from blood after a fatty meal
Occur in most loose CT, especially along the path of BVs
NOTE: serum = blood plasma w/o fibrinogen

Bone marrow
o Produces WBCs, RBCs & platelets by hematopoiesis
o Red marrow:
Cavities of cranial bone, vertebrae, ribs, sternum, & ends of long bones
Prior to birth, other areas produce blood elements: liver, spleen, lymph nodes
Hemacytoblasts (pluripotent stem cells):
So, the principal site of granulocytic hemopoiesis in the adult human is red bone marrow
o Yellow marrow:
Found only in cancellous (spongy) tissue of certain bones:
Flat skull bones, ribs, sternum, vertebrae, portions of ossa coxae & proximal epiphyses of humerus & femur
Minor location of fat storage
Blood vessel walls:
Tunica intima
Innermost layer
Consists of simple squamous epithelium (endothelium) and a thin CT basement MB
ONLY layer present in all vessels
In atherscletotic pt, this is the layer involved in the hypertrophy
Tunica Media
Middle Layer
Usually very thick in arteries (smooth muscle w/ some elastic fibers)
What keeps blood flowing during diastole
energy stored in elastic fibers of arteries
Tunica Externa (Adventitia)
Outer layer of CT w/ elastic & collagenous fibers
The tunica adventitia of the medium sized artery has mostly what?
collagen and elastin
In larger vessels, infiltrated w/ tiny BVs called vasa vasorum (vessels of the vessels) that nourish external tissues of BV
Highest BP found here
Greatest drop/change/gradient in BP is from the arteries to the arterioles
There are more elastic membranes in a large artery than there are in a medium-sized artery
Very small diameter (<0.5mm)
Small lumen, thick tunica media almost entirely of smooth muscle, little elastic tissue
Has the greatest proportion of smooth muscle thickness when compared to the size of the lumen Makes sense most
muscle = biggest pressure drop
Other choices: large arteries (dont get clowned), capillaries, veins
Smooth muscle (fibers, with single, centrally-placed nuclei) dilation/constriction is caused by neurochemical stimuli & has
profound impact on peripheral resistance


Can empty in toSinusoids in certain tissues (liver, spleen, pituitary, adrenal, carotid body, pancreas, parathyroid not in
kidneys, they just have a portal system
Sinusoids are wider & more irregular than capillaries
Walls consist of phagocytic cells, from part of reticuloendothelial systemdeal w/ phagocytosis & Ab formation
Exchange occurs here
Endothelium only (no tunica media or adventitia)
Which is seen continuously throughout Circulatory system?
Constant lumen & complete endothelial lining (unlike sinusoids)
NO elastic fibers
One RBC at a time
Velocity of blood is slowest here
Aorta: pg. 133 in Clemente anatomy
Tunica media is composed primarily of elastic fibers (distinguishing factor between aorta & arteries)
Has four parts:
1) Ascending aorta:
Beginning portion, R & L coronary arteries branch from it (to supply heart muscle)
Syphilis aneurysm occurs here
2) Arch of Aorta:
Gives rise to 3 Branches that supply all of the blood to the head, neck, and
upper limbs:
Extremely short
1st branch of aorta
At the neck it divides into the Right Common Carotid and right
Subclavian artery pg. 155 Clemente anat.
***Only 1 Brachiocephalic artery, BUT 2 Brachiocephalic
Left common carotid
Along w/ right common carotid, supplies head and neck
Left Subclavian
Along w/ right subclavian, supplies upper limbs
3) Thoracic portion: pg 152 in Clemente anatomy
From T4T12 (lies in the posterior mediastinum)
All of the arterial branches from this part are small
Posterior Intercostals (pic to lower right arteries coming of aorta)
Supply intercostal, serratus anterior, and pectoral muscles
Anastomoses w/ Anterior Cutaneous Arteries which arise from the Internal Thoracic (which is from the
At the mid-axillary line, give rise to Lateral Cutaneous artery
Supply the thorax & the diaphragm
Pericardial braches
Mediastinal branches
Esophageal branches
Bronchial branches
Superior Phrenic (at the level of the diaphragm)
4) Abdominal portion: (SEE BELOW) pg 152 in Clemente anatomy
Most common location for an atherosclerotic-induced aneurysm
From T12L4
Branches to:
Celiac Trunk
Superior Mesenteric
Inferior Mesenteric
NOTE: Spleen, stomach, pancreas & appendix are supplied by the 3 unpaired aortic branches (not
(Paired) (makes sense all structures above are unpaired, where Kidney, gonads, adrenals, are paired!)
If the renal artery is occluded, you are likely to get 2ndary HTN


Suprarenal NOT From upaired

Terminates w/ branching of:
Right Common Iliac arteries
Left Common Iliac arteries
Small Middle Sacral artery
Supply abdomen, pelvic region & lower limbs
Common Carotid: (FROM ABOVE)
Supplies head & neck
Branches into ICA & ECA at superior border of thyroid cartilage pg. 490 Clemente anatomy
Another Q: Branches at the level of C4 or the Hyoid bone
Carotid Sinus
Spindle-shaped dilation located at junction of ICA & ECA
Has baroreceptors for pressure when stimulated causes vasodilation, HR, & BP
Innervated by carotid sinus branch of CN IX (only 1 because its just a sinus, not a whole body) Sinus Ninus
Carotid sinus syndrome: temporary loss of consciousness accompanying convulsive seizures
Due to intensity of carotid sinus reflex when pressure builds in one or both carotid sinuses
Carotid body:
Lies posterior to the bifurcation of the Common Carotid
Innervated by CN IX & CN X (2 because its a whole body) Has X, because there are hot bodies in Vagus!
Sensitive to CO2 & O2 tension in blood BODY needs O2 in and CO2 out BODY doesnt like pressure
Carotid Sheath: pg. 479 Clemente anatomy
In it runs:
Common Carotid
Internal Jugular Vein
Vagus Nerve
NOT ansa cervicalis
NOT phrenic nerve
Branches of Common Carotid (2)
Internal Carotid: (3 Branches) pg. 490 & 524 Clemente anatomy
Inside the cranial cavity
Branches to:
Ophthalmic: pg. 526 Netters H&N anatomy
Supplies orbit & eye through optic foramen w/ optic nerve
Branches to:
Anterior ethmoidalSupplies the nasal cavity
Dorsal NasalAnastomoses w/ Angular branch (Facial)
Anterior Cerebral:
Great cerebral circle of Willis
Medial surfaces of hemispheres
Anterior & superior portions of frontal & parietal
Anterior portions of basal ganglia, internal capsule, corpus
Middle Cerebral: pg 526 Clemente anatomy
Great cerebral circle of Willis
Largest branch of ICA
Branches include Lenticulostriate Arteries
These are Arteries of Stroke (not the middle
Thin-walled, frequently rupture to cause cerebral
hemorrhage Makes Perfect sense!
Supply internal capsule, caudate, putamen
Lateral surface of the cerebral hemisphere
Posterior limb of the internal capsule & part of the basal
NOTE: Circle of Willis: (aka cerebral arterial circle)
Rupture of a vessel in the circle of Willis causes
subarachnoid hemorrhage


The Basilar artery emits into 2 posterior cerebral arteries (Basilar artery is formed by both vertebrals joining)
Then posterior cerebral arteries emits posterior communicating artery
Then posterior communicating artery joins middle cerebral artery
Then middle cerebral artery emits anterior cerebral artery (Mid. cerebral is term. branch of int. carotid)
Finally anterior cerebral arteries joined by anterior communicating artery
From Front to Back
Ant. CommunicatingAnt. CerebralMiddle CerebralPost. CommunicatingPost. CerebralBasilar
Anterior Communicating:
Most common circle of Willis aneurysm may cause visual field defects
Posterior Communicating:
Common area of aneurysm causes CN III palsy
The basilar & anterior communicating arteries are the unpaired vessels of the Circle of Willis
Forms an important means of collateral circulation in case of obstruction
If the internal carotid is blocked, blood will still get to the brain via the vertebral arteries/Basilar
NOTE: Stroke warning signs
Sudden weakness; paralysis; numbness of the face, arm, & leg on one/both sides of body
Loss of speech or difficulty speaking or understanding speech
Dimness or loss of vision, particularly in only one eye
Unexplained dizziness, unsteadiness, & sudden falls
Sudden severe headache & loss of consciousness
SIDENOTE: Branches of the Vertebral Artery (these have nothing to do w/ the carotid arteries)
Meningeal branches
Anterior & posterior spinal
Posterior inferior cerebellar (see diagram above)
Medullary branches
The Superior Cerebellar artery is not part of the vertebral artery
Basilar artery:
Formed by the union of the two vertebral arteries
Gives several insignificant (to Boards studying) branches
Significant branches: Posterior cerebral arteries
Occipital pole
Inferomedial temporal lobes
Subthalamic nucleus
External Carotid: (8 Branches) pg 506 clemente anatomy
From the level of the superior border of the thyroid cartilage (or C4) to the neck of the Mn into the parotid
Supplies the muscles of the neck, face, thyroid gland, salivary glands, scalp, tongue, jaws, and teeth
Branches from Inferior to Superior SALFO PMS (Some Angry Lady Figured Out PMS)
Superior thyroid
Ascending Pharyngeal
Posterior auricular
Superficial Temporal
Terminal Branches
Maxillary and Superficial Temporal the most superior branch
Superior Thyroid:
Supplies thyroid gland
Originates just below the level of the hyoid bones greater cornu
Branches to:
Superior laryngeal artery pg 453 netters H&N anatomy
Pierces thyrohyoid MB w/ the internal laryngeal nerve (aka internal branch of superior laryngeal n.)
CAREFUL (the artery is the superior thyroid, but then turns into superior laryngeal, whereas the nerve is
internal branch of superior laryngeal, then internal and external branches) pg 453 & 456 netters H&N anat
Lingual: (little Stub in picture near angle of Mn) pg 492 clemente anat or pg 374 & 414 H&N anatomy


Supplies tongue & floor of the mouth and tip of the tongue
Tongue also receives blood from Tonsillar branch (Facial) and Ascending Pharyngeal
Lingual artery does not follow the lingual nerve
Lingual artery does NOT pass between the medial pterygoid & the ramus of the Mn
Branches at the level of the tip of the greater horn of the hyoid bone in the carotid triangle
Passes Medial (deep) to the hyoglossus muscle and Superior to the Mylohyoid (Deep from the neck aspect)to enter
the oral cavity
So NOT between Hyoglossus and Mylohyoid
It passes between the Hyoglossus and the Genioglossus
Branches to: Which one supplies the dorsum of the tongue? Dorsal Lingual?
Dorsal Lingual
Deep Lingual
The terminal branch that supplies the anterior 1/3 of the tongue (tip)
Ascends between the genioglossus and the inferior longitudinal muscles
If you pierce the tip of the tongue with a bur, you most likely hit the Deep Lingual Artery You could also
hit lingual artery, or deep lingual vein
Facial: pg. 177, 289, netters H&N anatomy
Supplies face, tonsils, palate, labial glands, muscles of lips, ala and dorsum of the nose, muscles of facial expression,
and submandibular gland
Branches to: (8)
Cervical: (4) Facial to tonsils and to SubMn gland
a) Tonsillarto tonsils & some supply to the tongue pg. 433 & 434 Netters H&N anatomy
b) Ascending Pharyngealto pharyngeal wall & some supply to the tongue?????
c) Glandularto submandibular gland
d) Submentalto area below chin
Facial portion: (4) (can see these branches on pic above)
a) Inferior labialto the lower lip
b) Superior labialto the upper lip and vestibule of the nose
c) Lateral nasalto outer side of lateral nose (lateral wall)
c) Angularmedial side of eye
Terminal branch of facial artery
Anastomoses w/ the dorsal nasal branch of ophthalmic
Maxillary artery: (picture) pg 375 netters H&N anatomy & Infratemporal Fossa anatomy powerpoint
Supplies ALL teeth, muscles of mastication, hard/soft palate, and most of nasal cavity (NOT skin of forehead)
Branches from ECA at the posterior border of the Mn ramus
Terminal branch of ECA to region of infratemporal fossa and nasal cavity
Lateral pterygoid muscle divides maxillary artery into 3 parts: pg. 247 netters H&N anatomy
1) Mandibular portion before muscle (Doug And Mike Arent Inferior)
Gives rise to branches supplying the tympanic cavity and membrane, dura, and mandibular teeth
Deep Auricularto external auditory meatus
Anterior Tympanicto eardrum
Middle Meningealto cranial cavity (damage to this artery results in epidural hematoma/hemorrhage)
Accessory Meningealto cranial cavity
Inferior Alveolarto chin & Mn teeth (runs along w/ vein & nerve and lingual nerve in the
pterygomandibular spacebetween the pterygoid muscle and the ramus of Mn (lingual artery does not)
3rd Branch of Mx artery???Other Answer was Middle Meningeal,
IN Netters, they both come off at the same level!!! I
hate this test
2) Pterygoid portion passing over/under muscle (And Doug Poked
Mikes Behind)
Gives rise to branches that supply the muscles of mastication
Anterior Temporal
Deep Temporal aka Posterior Deep Temporal
Pterygoidmedial and lateral
3) Pterygopalatine portion crossing muscle Sahand And Dave Popped
In, Played, Ate
Gives rise to branches that supply the max teeth, portions of
the face, orbit, palate, and nasal cavity


Sphenopalatine pg 299 & 301 netters H&N anatomy

Terminal branch of maxillary artery
Enters the nasal cavity through the sphenopalatine foramen along w/ the nasopalatine branch of the
maxillary nerve
Principal artery to the nasal cavity, conchae, meatus, and paranasal sinuses
Damage results in epistaxis (nosebleed)
Nasopalatine (Comes off the Sphenopalatine- which came through the Sphenopalatine
Formamen with the Nasopalatine Nerve)
Comes through incisive foramen
Supplies anterior hard palate
Anastomoses w/ Greater Palatine artery of the Descending Palatine
Artery of the pterygoid canal
Descending palatinegreater and lesser palatine
Branches to:
Greater Palatine Arterypasses to the palate through the greater palatine foramen
Supplies mucosa of hard palate posterior to maxillary canine
Supplies Maxillary M2
A laceration of the palatal mucosa in the area of Mx M1 is most likely to damage the G. P. artery
Anastomoses w/ nasopalatine artery
Lesser Palatine ArterySupplies soft palate & tonsils after emerging from the lesser palatine foramen
Infraorbitalcanine and incisor, Part of the 3rd Part of the Maxillary Artery pg 177 & 301 Netter H&N anat
Careful, the Infraorbital NERVE comes out from V2, but this is the artery
Posterior Superior Alveolar (Dental)maxillary molars and premolar
PSA is a direct branch off of Mx artery
Anterior and Middle Superior Alveolar Maxillary anteriors
POSTERIOR BRANCHES of External Carotid (4):
Ascending Pharyngeal
Supplies the pharyngeal constrictor muscles
Supplies the tongue!!!
Occipital pg 139 Netters H&N anatomy
Pharynx and suboccipital triangle
Hooks CN XII Landmark for finding XII
Posterior Auricular
Back of scalp
Superficial Temporal does supply the temporalis muscle (along w/ the maxillary
Supplies the TMJ
Transverse Facial does NOT supply the temporalis (it branches off too early)
The Scapular Anastomosis
subclavian a.
( 1st part )

thyrocervical trunk

transverse cervical a.
suprascapular a.
axillary a.

scapular a.

( 3rd part )
humeral a.

subscapular a.

scapular a.

Subclavian (FROM ABOVE)

Divided in 3 parts by the scalene muscles pg 137-138 Netters H&N anatomy
1st Part Medial to the scalene m.
Vertebral (foramen magnum) Not pictured
FIRST BRANCH seems like it should be the third branch. See pg 16 Clementes anat. Then see pg. 138 Netters H&N
**If internal carotid becomes blocked, blood still reaches the brain via the vertebral arteries
Branches from vertebral artery found in section on circle of Willis


ThyroCERVical Trunk (3) comes off subclavian

Transverse cervical
Inferior thyroid
Internal Thoracic: (mammary)
Descends directly behind the 1st 6 costal cartilages, just lateral to the sternum
Branches to:
Upper Anterior Intercostalswhich anastomose w/ the Posterior Intercostals (Thoracic Aorta)
This network provides muscular branches to the intercostal, serratus anterior, and pectoral muscles
MusculophrenicSupplies the diaphragm and lower intercostal spaces anteriorly
Superior EpigastricEnters the rectus sheath and supplies rectus muscles are far as the umbilicus
***NOTE: The inferior epigastric artery (External Iliac) anastomes w/ the Superior Epigastric in the
rectus sheath in the area of umbilicus
2nd Part Behind the scalene m.
Costocervical (2):
Supreme intercostal (High Intercostal)
Deep cervical
3rd Part Lateral to the scalene m.
Dorsal Scapular:
Supplies the back
Axillary Artery pg. 293-296 Essential clinical anatomy
Continuation of the Subclavian
Begins at the 1st rib and ends at the margin of the teres major
m., then turns into the Brachial artery (runs with Median
Nerve), then turns into the Radial and Ulnar arteries at the
Cubital fossa
Brachial Artery
Supplies the Posterior Compartment of the arm
Supplies the latissimus dorsi m.
Divided into 3 Sections by the tendon of the pectoralis minor
m. (Screw The Lawyer Save A Patient)
1st Part (MEDIAL)
Supreme Thoracic artery
2nd Part (DEEP)
Thoraco-acromial -artery branches off the axillary
Lateral thoracic artery
3rd Part (LATERAL)
Subscapular artery
Posterior circumflex humeral artery
Anterior circumflex humeral artery
Abdominal portion of descending aorta: (FROM ABOVE)
From T12L4
Branches to:
CSI pg 138 essential clinical anatomy
1) Celiac Trunk pg. 102 Essential clinical anatomy
Hepatic (Common) the common hepatic artery is a branch of the celiac artery
Liver, upper pancreas, duodenum, and gallbladder
Branches to:
Right Hepaticto right lobe of liver
Cysticto gall bladder
Left Hepatic
Right Gastriclesser curvature of the stomach (ALL Gastrics go to lesser curvature)
Gatroduodenalpancreas and duodenum
***[SEE Hepatic Circulation BELOW]
Left Gastriclesser curvature of the stomach and inferior part of the esophagus
Splenic spleen, stomach, and omentum
Branches to:


Left Gastroepiploicto greater curvature of the stomach (Epiploic appedanges of Greater omenum)
Short Gastricto ??lesser?? curvature of the stomach
**Stomach supplied by: R & L Gastric, Gastroepiploic & Short Gastric artery
2) Superior Mesentericsmall intestine (duodenum and jejunum), pancreas, cecum, ascending and transverse colons
Supplies the GI tract from the middle of the 2nd part of the duodenum to the distal 1/3 of the transverse colon
Supplies the right colic flexure
3) Inferior Mesenterictransverse, descending, & sigmoid colons and rectum
1) Suprarenaladrenal gland, Adrenals are not supplied by one of the 3 upaired branches
2) Renalkidneys
3) Gonadal
4) Lumbarepaxial muscles of lumbar region -This is the only one that isnt obviously going to 2 paired structures
Terminates w/ branching of:
Right Common Iliac
Left Common Iliac
Small Middle Sacral

Cardiac Blood Supply

1st branch of the aorta is R/L coronary arteries
Right Coronary
Supplies right atrium, most of right ventricle, diaphragmatic surface of the left ventricle, part of AV septum, SA node
(60% of the time), and AV node (80% of the time)
Posterior interventricular (Aka posterior descending a)
Along with middle cardiac vein
Left Coronary
Supplies left atrium, most of left ventricle, some of the right ventricle, most of the IV septum, the SA node (40%), and
the AV node (20%)
Branches from the ascending aorta immediately above the anterior left cusp of the aortic valve
Anterior interventricular
Along with great cardiac vein
Necrosis on the anterior heart wall over both ventricles is likely due to occlusion of the ant.
interventricular a. (AKA L. Ant Descending)
Circumflex branch
Coronary Sinus pg 67 essential clinical anatomy


Great, Middle, and Small Cardiac veins

Hepatic Circulation
Hepatic portal vein
Brings food-laden blood from the abdominal viscera
Formed by union of Superior Mesenteric Vein & Splenic Vein
Blood from liver eventually drains into the hepatic veins and then to IVC
**Liver has mixture of arterial (hepatic) and venous blood (portal)
Blood supply to nose:
Sphenopalatine branch of maxillary artery
Anterior ethmoidal branch of ophthalmic artery to the dorsal nasal
Septal branch of superior labial branch of facial artery
Veins vs. Arteries:
Less muscle, lower pressure, less elastic tissue, same general structure, larger diameter
>70% of blood is found in the venous system at any one time
Valves in veins of arms & legs prevent backflow
Veins & arteries have pulse present, none in capillaries
Veins have larger tunica adventitia when compared to arteries
Artery: Media is thickest layer
Vein: Adventitia is thickest layer
CapsVenulesVeinsVena Cava
Venules have very thin tunica adventitia
Larger veins have thicker tunica adventitia
Drainage from Brain to Right Atrium
Superficial region of head & neck drains into External Jugular Vein (EJV)
EJV Subclavian Vein (coming from the Axillary Vein of the shoulder)
Subclavian Vein joins the IJV (coming from the Sigmoid Sinus of the brain)
IJV & SCV join to form the Left Brachiocephalic Vein
The Left Brachiocephalic Vein then receives the Vertebral Vein from the posterior portion of the head
Left Brachiocephalic Vein meets the Right Brachiocephalic Vein to form the Superior Vena Cava Right Atrium
Veins (Individual Facts)
Superior Vena Cava (SVC):
Union of two Brachiocephalic Veins, has no valves, blood from head, neck, upper limbs, & chest; empties into Right Atrium
Inferior Vena Cava (IVC):
Larger than SVC
Guarded by a rudimentary non-functioning valve
When IVC gets slowly occluded, there are collateral routes through BOTH epigastric veins AND the total azygos
Brachiocephalic Veins:
Formed at the base of the neck from the joining of the IJV & SCV
Present on both sides of the neck
The R & L Brachiocephalics meet in the superior mediastinum to form SVC
Azygos vein (right side) joins the posterior aspect of the SVC just before it pierces the pericardium (thats why its collateral
Infection of lower lip would first enter bloodstream at the Brachiocephalic Vein
Internal jugular vein (IJV):
Begins at jugular foramen as a continuation of the Sigmoid Sinus
Descends in the carotid sheath w/ common carotid and vagus nerve
Descends behind sternoclavicular joint w/ SCV to form Brachiocephalic Vein
Drain the venous sinuses of the skull
External jugular (EJV):
Drains the skin, parotid, & muscles of the face & neck
Formed by union of the Posterior Auricular Vein & the posterior branch of the Retromandibular Vein
Crosses the SCM vertically, under the platysma, and ends in the SCV (DIFFERENT than Artery)
Subclavian Vein (SCV):
Continuation of the Axillary Vein at the inferior margin of the 1st rib
Passes medially to join the IJV to form Brachiocephalic Vein
Crosses 1st rib anterior to the anterior scalene muscle (Subclavian goes Posterior)
So does the Phrenic
Subclavian tributaries are:
EJV on the left side at the angle of its junction w/ IJV


Lymphatics from the Thoracic Duct

On the right side it receives the Right Lymphatic Duct at the same location
Axillary Vein:
Begins at the lower border of the teres major muscle as the continuation of the Basilic Vein
Located in the Deltopectoral Triangle
(Think ABCs) Axillary Vein is really the union of the Cephalic (radial side) & the Basilic (medial side formed after
the Median Cubital Vein shoots off of the Cephalic Vein)
Brachial Veindrains venous blood from deep antebrachial regions and brachial regions to Axillary Vein
Cephalic Veindrains venous from radial side to the antebrachium and brachium into Axillary Vein
Superiorly the vein passes between the deltoid and the pectoralis major muscles and enters the deltopectoral triangle
where it joins to be the axillary vein
Damage in deltoid triangle damages cephalic vein
Becomes the SCV as it ascends to the inferior margin of the 1st rib
Basilic + Cephalic = AxillarySubclavian (receives EJV)Subclavian + IJV (Jxn for thoracic duct = Brachiocephalic
Id say this is a good thing to know!!!
Vertebral Vein:
Drains posterior portion of head
Then empties into the Left Brachiocephalic before it forms the Superior Vena Cava
Azygos Vein: (right side)
Drains posterior abdominal and thoracic body wall
Usually formed by union of the Right Ascending Lumbar and Right Subcostal Vein
Ascends through the aortic orifice of the diaphragm (A for A)
Lies in the posterior mediastinum & empties into the SVC at the junction of the 2 Brachiocephalic Veins
The Right Vagus nerve lies just posterior to the arch of the azygos
The Va-goose is most posterior
Azygos vein leaves an impression on the right lung as it arches over the root/hilum
Right Superior Intercostal Vein drains into Azygos vein
NOTE: the 2nd, 3rd & 4th R posterior intercostal veins drain from the R superior intercostal vein into the azygos vein
Left Superior Intercostal Vein drains into the Left Brachiocephalic Vein at level of ????
Hemiazygos Vein: (left side)
Formed by union of the Left Ascending Lumbar Vein & Left Subcostal Vein
Empties into the Azygos Vein
Ascends on the left side of the vertebral body behind the thoracic aorta, receiving the lower four Posterior Intercostal Veins
Accessory Hemiazygos Vein:
Formed by union of 4th -8th Intercostal Veins
Empties into Azygos Vein, sometimes meets up with the Hemiazygos first then crosses and joins the azygos
Face: Veins


Main Menu

maxillary v.

temporal v.
facial v.

retromandibular v.
jugular v.
jugular v.

superior labial v.
inferior labial v.
common facial v.
The veins of the face generally
follow the same pattern as the
arteries. The facial vein is the
major source of venous drainage for
superficial facial structures (or the
same areas that are supplied by the
facial artery).

subclavian v.
Superficial Temporal Vein: PIC
Drains the scalp & side of head
Descends anterior to the ear and plunges into the substances of the parotid gland
Maxillary Vein pg. 181 Netters H&N anatomy
Forms from the Pterygoid Plexus of Veins
Joins the Superficial Temporal Vein w/in the parotid gland to form the Retromandibular Vein
Retromandibular Vein: (Think Terminal Branches of Arterials)
Formed by union of Superficial Temporal & Maxillary vein w/in parotid pg. 204
Divides at the angle of Mn into:
Anterior Branch joins Facial Vein to form Common Facial Vein, which then drains into the IJV
Posterior Branch joins Posterior Auricular Vein (occipital) from behind ear to form EJV


Veins of Cervical Triangle: Retromandibular Vein, EJV & IJV

Facial Vein pg 528 Netters H&N anatomy
Begins as Angular Vein by the confluence of the Supraorbital and Supratrochlear Veins
Communicates w/ Superior Ophthalmic via the Supratrochlear and Supraorbital allowing infection from face to the Cranial
Dural Sinus
Drains directly into the IJV or joins the Anterior Branch of the Retromandibular Vein to form Common Facial Vein which
also enters IJV
The Facial Vein anastamoses w/ Retromandibular Vein below the border of the Mn & empties into the IJV, usually through
the Common Facial Vein
Angular Vein
Continues at the lower border of the orbital margin into the Facial Vein
Receives the Infraorbital and the Deep Facial Veins
Deep Facial Vein communicates between Facial Vein and the Pterygoid Plexus (which also becomes Max
Superior Ophthalmic Vein is a communication between the Facial Vein & Cavernous Sinus
Deep Facial Vein (most inferior vein in pic to right shows communication with facial v (anterior) and pterygoid plexus
Communication between the Facial Vein & Pterygoid Plexus
Superior Ophthalmic Vein Top vein in pic going from facial vein (anterior)to cav sinus (posterior)
Communication between the Facial Vein & Cavernous Sinus
Inferior Ophthalmic Vein Middle v. in pic, shows splitting to cav sinus and pterygoid plexus.
Divides into two terminal branches
One to the Pterygoid Plexus
One to the Superior Ophthalmic Vein to the Cavernous Sinus
Pterygoid Plexus of Veins:
The pterygoid plexus is in between the temporal and pterygoid muscles
The pterygoid plexus and its tributaries are the venous parallel of the maxillary
Infection that spreads posterior to Mx sinus enters here
Terminates posteriorly in the Maxillary Vein
Terminates anteriorly in the Deep Facial Vein (drains into Facial Vein)
The pterygoid plexus drains into the retromandibular vein
Retromandibular splits into Anterior and Posterior divisions:
Anterior joins Facial Vein to form Common Facial Vein and then
dumps into internal jugular vein Anterior to Internal!!!
Posterior receives the posterior auricular veins and forms the
external jugular vein, which then drains directly into the subclavian
Direct communications of the Pterygoid Plexus:
Maxillary vein (cut in pic)
Deep Facial vein can see
Posterior Superior Alveolar vein cut?
Infraorbital vein Can see its the inferior infraorbital
NOT VertebralDuh! This drains into left
Brachiocephalic vein
Surrounds the maxillary artery occupying the infratemporal fossa
associated w/ pterygoid muscles
Receives veins that correspond to the maxillary artery

Dural Venous Sinuses. Pg. 528 Netters H&N anatomy

View is with the skull cap removed and the cranial cavity exposed.
A. Sphenoparietal at junction of sphenoid and parietal bones
B. Intercavernous
C. Sigmoid
D. Occipital
E. Confluence
F. Basilar
G. Transverse
H. Superior Petrosal


I. Inferior Petrosal
J. Cavernous
K. Superior Sagittal
The Cavernous Sinuses:
Paired, irregularly shaped Venous Dural Sinuses
Created by drainage of Superior & Inferior Ophthalmic Veins, the Cerebral Veins, & the Sphenoparietal Sinus
Located on either side of the sella turcica of sphenoid bone in middle cranial fossa
Empty by way of Superior Petrosal Sinuses into the Transverse Sinuses which become the Sigmoid Sinuses
The Sigmoid Sinuses then empty into the Jugular Foramen by becoming the IJV
These veins do not have valves and so can also drain anteriorly into Ophthalmic Vein
Internal Carotid Artery and abducens (CN VI) nerve pass through the Cavernous Sinuses (CN VI is free-floating)
All of the others are embedded in lateral wall of the Cavernous Sinuses: Pg. 528 Netters H&N anatomy
Oculomotor (CN III), Trochlear nerve (CN IV), Ophthalmic nerve (CN V1), Maxillary nerve (CN V2)
Think Cavernous s-EYE-nuses (III, IV, VI are eye movers, & V1/V2 are above & below the eye on the face)
The Sinuses
Superior Sagittal above picture is weak, look at pic to lower right = giant sinus at top of skull
At the top of the falx cerebri
CSF flows into the arachnoid villi then into the superior sagittal sinus
Which dura divides cerebrum sagitally?
Falx Cerebri
Inferior Sagittal pictured on right: in mid sagital plane, below the superior sag sinut
At the bottom of the falx cerebri
Straight sinus pictured right: from inferior sagital sinus to confluens
When the great cerebral vein meets the inferior sagittal sinus, they form the straight
sinus which takes them down to the Confluence
In the falx cerebelli
Confluence of sinuses
Where the Superior Sagittal, Straight, Occipital, and both Transverse Sinuses meet in
the back
Transverse sinus
The 2 lateral sinuses that connect the Confluence to the Sigmoid Sinuses
Connects to the Internal Jugular Vein via the jugular foramen of the skull
Also collects the Superior Petrosal Vein
Cavernous sinuses
Anterior and Posterior intercavernous sinuses surround the Infundibular stalk of pituitary
Drain the valveless ophthalamic & paranasal sinuses danger of infection
Sella turcica
Lies directly above the sphenoid sinuses
Middle cranial fossa
Diaphragma sellae
The tentorium cerebelli forms the roof of the posterior fossa (Perpendicular to falx cerebri- it runs
horizontal in picture to right)
Danger triangle of face:
Covers the nose and maxilla and goes up to the region of the eye
Superficial veins communicate w/ the Dural Sinuses
Facial Vein has no valves and backflow of infection can get into the sinuses via the Deep Facial Vein (via Pterygoid Plexus) and
Superior Ophthalmic Vein (via Cavernous Sinus)
Veins of the Skull:
Direct tributaries to the Dural Sinuses (Cerebral Sinuses, or the sinuses of dura mater)
Various venous channels located in the dura mater and lined w/ endothelium
Emissary Veins: (THINK you have to go THROUGH the checkpoint to get to the COMMISSARY on BASE (of skull)
Valveless, connect the dural sinuses w/ the veins of scalp
Differently worded: emissary veins connect the venous sinuses of the dura mater w/ the extracranial veins
Diploic Veins:
Lie in channels in the diploe of the skull & communicate w/ Dural Sinuses, the veins of the scalp, and Meningeal Vein
Lie w/in the bone of the calverium and join as tributaries to the Emissary Vein
Portal Vein (aka: Hepatic Portal Vein):
Formed by the union of the Splenic and the Superior Mesenteric Veins (splenic behind pancreas in pic, SMV in front of
duodenum) Note: Also shows duodenum going around heat of pancreas.
Tributaries are R & L Gastric Veins & the Cystic Vein


Anterior to the epiploic foramen in the free edge of the lesser omentum
Epiploic foramen is bounded anteriorly by the free border of the lesser omentum
Greater peritoneal sac communicates with lesser peritoneal sac by means of the epiploic foramen
Posterior to the bile duct and the Proper Hepatic Artery
Ascends in front of IVC
Divides into R & L branches before entering liver
Carries 2x as much blood as the Hepatic Artery
Drains stomach, intestines, spleen, pancreas, and gallbladder
Drains into Hepatic Sinusoids, which then drains into the Center Vein
Here the blood travels through the hepatic portal system & makes it possible for
the liver to perform many functions, (like remove substances from blood,
metabolize, detox)
After leaving liver, blood travels through Hepatic Vein to IVC
Splenic vein: Shown to right
Drains spleen
Receives tributaries from:
Stomach = R & L Gastroepiploic Veins and R & L Gastric Veins
Pancreas = Pancreatic Vein
Gallbladder = Cystic Vein
Joins the Superior Mesenteric to form the Portal Vein
2 abdominal anastomeses
Superficial epigastric to the Lateral thoracic (off of subclavian)
Inferior epigastric from the external iliac to the Internal thoracic
Superior Mesenteric drains:
Small intestine, cecum, and ascending & transverse colon
Joins Splenic Vein behind the neck of the pancreas to form the Portal Vein
Inferior Mesenteric:
Drains rectum, descending colon of the large intestine
Usually joins the Splenic Vein behind the neck of the pancreas
Fetal vessels and their remnants:
One Q reads: Ligamentous remnants of the fetal circulatory system persisting in the adult include the ligamentum venosum,
ligamentum arteriosum, ligamentum teres of the liver (not ligamentum nuchae or ligamentum teres of the uterus)
Umbilical Vein (1) Ligamentum teres (aka: Round ligament of the liver):
Placenta to liver, forms major portion of umbilical cord, nutrient-rich blood from placenta to fetus
Forms the round ligament of the liver after birth (ligamentum teres)
Umbilical Arteries (2)Medial Umbilical Ligaments:
Arise from Internal Iliac arteries associated w/ umbilical cord
Transports blood from fetus to placenta, becomes adult medial umbilical ligament
AllantoisMedian Umbilical Ligament
Ductus ArteriosumLigmentum Arteriosum: (Ductus)
Between pulmonary trunk (left pulmonary artery) & aortic arch to bypass pulmonary circuitry
R to L shunt, we dont care about pulmonary circ. On way to lungs (pulm. Artery) gets shunted straight to aorta!
Does not carry fully oxygenated blood
Closes shortly after birth, atrophies, & becomes the ligamentum arteriosum
Ductus VenosusLigamentum Venosum
After Umbilical vein reaches the liver, then the Ductos venosus takes the blood to the IVC
Right Atrium foramen ovale
Carries Umblicial vein (O2 rich from momma) to the IVC (Just distal to where the bad blood was sent out in the iliac
Only fetal vein to carry O2-rich blood and nutrients
Foramen OvaleFossa Ovalis:
Opening between R & L atria to shunt blood passed the pulmonary circuitry, closes at birth and becomes the fossa ovalis, a
depression in the interatrial septum
Notochord Nucleus Pulposus kinda in a pretty random spot, no?
NOTE: The following are immediate changes that occur in the cardiovascular system at birth:
Closure of foramen ovale
Closure of the ductus venosus
Constriction of the ductus arteriosus
Constriction of the umbilical arteries
Not closure of the interventricular foramen
Since were thinking about the umbilical cord:


Contains 2 umbilical arteries de-O2d blood FROM fetus

Contains 1 umbilical vein O2d blood TO fetus (from placenta)


o Transparent, usually slightly yellow, often opalescent liquid found in lymphatic vessels
o Contains a liquid portion resembling plasma, as well as WBCs (mostly lymphocytes) & a few RBCs
o Absorbed from tissue spaces by lymphatic capillaries
o Flows through the filtering system (lymph nodes)
o Is eventually returned to venous circulation by lymphatic vessels
Functions of Lymphatic System:
o 1) Collect & return tissue fluids back to bloodstream
Fluid entering lymph capillaries is called lymph
Fluid enters due to differing osmotic pressure across capillary MB
Lymph is returned to venous system via 1) thoracic duct & 2) right lymphatic duct
Lymphatic system depends on:
Skeletal muscle contraction, presence of valves in lymphatic vessels, breathing & gravity to move fluid
Lymph vs. Veins
Walls of lymph vessels are thinner
Muscle layer is less developed
o 2) Transport absorbed fats
Lacteals transport fat products in small intestines from GI into circulatory system
Lacteals are lymph capillaries w/in villi of small intestine
o 3) Provide immunologic defense against disease-causing agents
Lymph filters through lymph nodes
Lymph nodes filter out microorganisms & foreign substances
Basic framework of all lymphoid tissues (EXCEPT Thymus) is primarily reticular fibers and lesser amount of collagen fibers
In the upper limb, the hallmark of lymph vessels is that they CONTAIN Valves Sean you got clowned Sean would get clowned, but
I never would because lymph needs valves to work! Idiots
Bone marrow is part of lymph system
Chief characteristic of lymphatic organ is presence of lymphocyte
Lymph nodes:
o Small, oval/round bodies of lymphatic tissue permeated by lymphatic channels
o Contains both afferent & efferent vessels (spleen, thymus, tonsils do not have both)
Contains numerous afferent lymphatic channels (spleen, thymus, palatine/pharyngeal tonsils do not)
The spleen, thymus, palatine & pharyngeal tonsils do not have numerous afferent vessels entering them as do lymph nodes
But wait, do spleen, thymus, tonsils, etc have afferent vessels?
o Primary function act as filters that remove & destroy Ag/s circulating in blood & lymph
Contain a lot of macrophages
o Lymphoid tissue in nodes produces Ab/s & stores lymphocytes
o Generally occur in clusters, particularly in armpits, groin, lower abdomen, & sides of neck
o Each node is enclosed in a fibrous capsules w/ internal trabeculae (CT) supporting lymphoid tissue & lymph sinuses
Trabeculae are specialized bands of CT that divide the lymph node
o Outer cortical region:
Contains separate masses of lymphoid tissue (called germinal centers, nodules)
source of lymphocytes
NOTE: The germinal center of a lymph nodule represents the area of
proliferation of lymphocytes
Also contains subscapular & cortical sinuses
Outer cortex B cells & nodules
Inner cortex T cells & NO nodules
o Inner medullary region:
Lymphoid tissue here is arranged in medullary cords source of plasma cells
What is not found within a medullary cord? Mast Cells. (macrophages, t-cells,
b-cells, plasma cells are found there)
Travel of lymph through nodes:
o Afferent lymphatic vessels carry lymph into node vessels enter on convex surface
of the node
Lymph is cleansed by macrophages, lymphocytes & plasma cells as it
circulates through cortical sinuses
o Efferent lymphatic vessels carry filtered lymph through the concave hilus region
into efferect collecting vessels

Collecting vessels converge into larger vessels lymph trunks (five in the body)
There are fewer efferents than afferents
o Lymph trunks empty into the thoracic duct or right lymphatic duct
Thoracic duct
Drains most of the body
Empties into junction of the LEFT internal jugular & LEFT subclavian veins (which becomes the L brachiocephalic v.)
Right lymphatic duct
Drains right side of head & neck, right upper limb, & right side of thorax
Empties into junction of RIGHT internal jugular & RIGHT subclavain vein
Deep cervical lymph nodes:
o Eventually receive all lymph of head & neck
o Form a chain along the internal jugular vein, from skull to root of neck
o Efferent vessels join to form the jugular lymph trunk then drain to thoracic duct or right lymphatic duct
o Mandibular 3rd Molars initially???
o Carcinoma of the larynx would most likely affect?
Deep cervical lymph nodes
Anterior cervical lymph nodes
o Drains internal structures of throat as well as post pharynx, tonsils, and thyroid
o What doesnt drain into ant cerv lymph nodes scalp, skin of neck and arm, thorax, axillary nodes
Parotid lymph nodes:
o Strip of scalp above parotid salivary glands
o Anterior wall of external auditory meatus
o Lateral parts of eye lids & middle ear
o **Drain into deep cervical lymph nodes
Submandibular lymph nodes:
o Lymph from most of the dental and periodontal tissues drains initially into the submandibular lymph nodes
o Front of scalp
o Nose & adjacent cheek
o Upper & lower lips (except center part)
o Drain the Oral Cavity
o Mx & Mn teeth (except Mn incisors) (dont get clowned by infraorbital lymph
node for drainage of Mx teeth)
o Anterior 2/3 of tongue (except the tip)
o Floor of mouth & vestibule & gingiva
o Angle of the mouth
o **Drain into deep cervical lymph nodes
Submental lymph nodes:
o Tip of tongue
o Anterior floor of mouth (beneath tip of the tongue)
o Mn incisors & associated gingiva
o Center part of lower lip & skin over chin
NOT Mn molars, upper lip, lateral portion of lower lip
o **Drain into submandibular & deep cervical lymph nodes
***NOTE: The primary lymph nodes draining the mandible are the submandibular
& submental nodes
Thoracic duct:
o Conveys lymph from lower limbs, pelvic & abdominal cavities, left side of
thorax, & left side of head, neck & left arm
o Begins below the abdomen as dilated sac the cisterna chyli
o Ascends through aortic opening in diaphragm, on the right side of the
descending aorta
o Empties into junction of the left internal jugular & left subclavian veins
o Contains valves & ascends between the aorta & azygos vein in the thorax (Azy goose and Thoracic DUCK touch)
How is it related to the esophagus and sympathetic chain?
Right lymphatic duct:
o Drains the right side of the head & neck, right upper limb, & right side of the thorax
o Empties into junction of the right internal jugular & right subclavian veins
Virchows node is a left supraclavicular node that gets lymph from most of the body via the thoracic duct
o Largest single mass of lymphoid tissue in body
o Ovoid organ ~size of a fist
o Develops from mesenchymal cells of the mesentery attached to primitive stomach weird
o Found in closest relation to the inferior surface of the diaphragm Spleen


Lies in left hypochondrium of abdominal cavity between stomach & diaphragm

Important blood reservoir
Filters blood ONLY (No afferent lymphatics)
Phagocytosis of undesirable blood particles
Manufactures mononuclear leukocytes
White pulp
One card says: Contains lymphatic nodules & lymphocytes, like a lymph node
Another card: Contains compact masses of lymphocytes surrounding branches of the splenic artery
o Red pulp
Consists of a network of blood-filled sinusoids, along w/ lymphocytes, macrophages, plasma cells, monocytes & RBCs
Contains: splenic cords, numerous erythrocytes and blood vascular sinusoids
o PALS is the center zone of the spleen, surrounding the Central arteriole
*USMLE says: T cells are found in the PALS & the red pulp. B cells are found in follicles w/in the white pulp.
The B cells in the white pulp are analogous with the B cell outer cortical germinal centers in the lymph node
PALS is the most analogous the paracortex in the medulla of the lymph node blah blah
o Site of erythropoiesis in fetus & infant not in adults!!!
Fetal erythropoiesis takes place in the Yolk sac, Liver, Spleen, Bone marrow (Young Liver Synthesizes Blood)
o Travel of blood through spleen:
Enters at the hilum through the splenic artery
Drained by the splenic vein joins lesser mesenteric vein to form hepatic portal vein to the liver w/ greater mesenteric vein
*Nerves to spleen accompany the splenic artery & are derived from the celiac plexus
o Bilobed lymphoid organ located in the superior mediastinum has no lymphatics
o Main function to develop immature T-cells into immunocompetent T-cells
Tests new T cells for ability to recognize self-MHC molecules & self-epitopes these T cells are destroyed
o Thymus large in newborns, grows until puberty & then regresses in adults
o In the adult thymus blood supply is isolated from parenchyma blood thymus barriersupply is MOST isolated from the
parenchyma of the thymus (more than the other options: spleen, lymph node, Peyers patch, pharyngeal tonsil)
o In the childs thymus blood supply is NOT isolated from parenchyma
o Hassels corpuscle are characteristic of the thymus histologically Its a HASSEL for blood to get to parenchyma in thymus
Pharyngeal tonsils:
o When inflamed, they are called adenoids
o Collection of lymphatic tissue located in posterior wall & roof of nasopharynx
o No lymph, sinuses or crypts
o Surrounded partly by CT & partly by epithelium, which forms deep infoldings (which arent crypts??)
o Characteristically covered by ciliated pseudostratified columnar like respiratory epithelium
This is the distinguishing feature histologically from the palatine tonsils
Palatine tonsils:
o Two masses of lymphoid tissue one mass on each side of oropharynx
o Reach maximum size during childhood & diminish considerably after puberty
o Contain many crypts & lymphoid follicles no sinuses
Think Crypts are in between your Arch CAVES
o Surrounded partly by CT and epithelium
o Found between palatoglossus and palatopharygeus
Lingual tonsils:
o Found on posterior portion of dorsum of tongue
o Smaller & more numerous each has single crypt
Peyers Patches:
o Follicular-associated epithelium
Enterocytes & M cells
o Germinal center
IgA positive B cells, CD4 T cells & APCs
o Intestinal tonsils, similar in structure & function to tonsils
o Located in the lamina propria & submucosa of the ileum
o Destroy bacteria
o No Goblet cells
o USMLE: M cells take up Ag. Stimulated B cells leave Peyers patch & travel thru lymph & blood to lamina propria of
intestine, where they differentiate into IgA-secreting plasma cells. The IgA is transported across the epithelium to deal w/
intraluminal Ag
Peyers patches & tonsils considered subepithelial & nonencapsulated lymphoid tissue (not thymus, lymph nodes)
Lymph from lungs, bronchi, and trachea drain into the mediastinal lymph nodes
The spleen, thymus, & lymph nodes are similar in that they all contain lymphocytes



Not all three filter blood, have a medulla and a cortex, serve as filters for tissue fluid, have afferent & efferent lymphatic vessels

Function of bone:
o Support
o Protection
o Body movement
o Hemopoiesis
o Mineral storage
Inorganic bone matrix is composed primarily of minerals Ca & P
Give bone its rigidity & account for ~2/3 of its weight
95% of calcium & 90% of phosphorous in body is deposited in bone/teeth
In mineralization of bone inorganic material increases, water content decreases, but little change in collagen
Different than enamel, because bone has a DECREASE in Organic content (collagen, son)
o Not fat storage
Nutrition of bone reaches cells of compact bone via caniliculi, capillaries, & Volkmanns canals (not osseous matrix or lamellae)
Bone formation:
o 1st evidence of bone ossification 8th week of prenatal development
o Endochondral ossification: (ENDO think long bones, condyles Long like FILES)
Most long bones are endochondral derived
Begins as a hyaline cartilage model this doesnt happen in flat bones
Know Fxn of Hyaline Cartilage in bone growth
Calcified cartilage is replace by bone (dont get clowned: hyaline cartilage is not transformed into bone)
Bone replaces cartilage osteocytes replace chondrocytes
Short & long bones (bones of extremities & weight bearing bones)
Mandibular condyles
The list includes ethmoid, sphenoid, & temporal bones
Cranial Base portions of the occipital, sphenoid, temporal, and ethmoid
o Intramembranous:
Bone formed directly no cartilage precursor
Takes place w/in MBs of CT
Flat bones of skull (cranial vault) & face (e.g., nasal bone), & clavicle
Mandible (except condyles), Maxilla
In ORTHO tx, the type of new alveolar bone formation is intramembranous
Contributes to growth of short bones & thickening of long bones
Involves transformation of osteoblasts to osteocytes
o Once formed, bone grows by appositional growth
o A disturbance in cartilage formation in a fetus results in deformities of the axial skeleton and the base of the skull
Bones grow NOT formed by
o Appositional
Cells of bone formation & resorption:
o Osteoblasts:
Synthesize collagenous fibers, bone matrix & promote mineralization during ossification
Become trapped in their own matrix & develop into osteocytes
Derived from mesenchyme (fibroblasts)
Have high RNA content & stain intensely with basic dyes (blue) makes sense constantly transcribing/translating
o Osteoclasts:
Large, multinucleated Giant Cells containing lysosomes & phagocytic vacuoles
Reversal Lines:
o Seen on the Cribiform plate (aka alveolar bone proper) of the alveolar process
o Indicates cessation of osteoclastic activity
Originates from Mononuclear-phagocyte family (MONOCYTE)
Form Howships Lacunae The evil, bone destrying Osteoclasts of the Monocyte galaxy fly in on their How-SHIPs!!!
o Osteoid:
Newly formed organic bone matrix that has not undergone calcification
Differs from bone in that it has no mineralized matrix
o Osteocytes:
Maintain the bone tissue
Bone properties:
o Hard due to calcification of extracellular matrix
o Elastic due to presence of organic fibers
o Strong due to collagenous fibrils


Bone components:
o Diaphysis
Cylindrical shaft of durable compact bone
o Epiphysis
Caps diaphysis
Location of secondary ossification center
Primary center is diaphysis
Spongy bone surrounded by compact bone
Contains red bone marrow
Erythropoiesis takes place mainly in the epiphysis says Sean
o Epiphyseal plate
Between epiphysis & diaphysis
Region of mitotic activity responsible for elongation of bone
o Medullary cavity
Centrally positioned space w/in diaphysis
Contains fatty yellow bone marrow (everywhere else)
NOTE: Red marrow = Blood cell formation
Cranial, vertebrate, ribs, sternum, epiphysis of long bones
o Nutrient foramen
Opening into diaphysis
Provides site for nutrient vessels to enter/exit medullary cavity
o Articular cartilage
Hyaline cartilage caps of each epiphysis
Facilitates joint movement
o Endosteum
Lines medullary cavity
Consists of supportive dense regular CT
o Periosteum
Dense regular CT covering surface of bone
Site for ligament & tendon-muscle attachment
Responsible for diametric bone growth
Has an outer fibrous layer and an inner osteogenic layer
o Compact bone (Lamellar)
Hard, outer layer of bone tissue
Covered by periosteum
Serves for muscle attachment
Provides protection & gives durable strength to bone
The component of bone tissue that gives a bone tensile strength is the collagenous fibrils of matrix
Consists of:
Matrix of compact bone is collagen plus salts of calcium & phosphorus
Osteocytes bone cells
Osteon a cylinder of compact bone composed of concentric lamellae (HENCE, lamellar or compact bone)
o The oldest lamella of the osteon is the most peripheral lamella
o Osteon canals are oriented parallel to the predominant direction of force like when you stand on an aluminum can
Lacunae depressions in the matrix where an osteocyte is located
Lamellae circular layers of osteocytes located in lacunae
Canaliculi processes connecting lacunae each
canaliculus resembles a miniature canal
Haversian canal central canal around which
concentric lamellae are located
o Contains BVs & nerves that serve the
o Exchange of substances between central canals
& osteocytes occurs along canaliculi
o Which part is the oldest? most peripheral
Haversian system = Haversian canal + surrounding
o Repeating system is found in compact bone of
diaphyses of long bones
Volkmanns canal = connects 2 Harversian canals, runs perpendicular to haversian canals


Cancellous (spongy or trabecular)

Porous, highly vascular, inner layer of bone tissue branching network of trabeculae
Makes bone lighter & provides spaces for marrow
Seen as spicules or trabeculae
o Immature bone (woven bone, nonlamellar bone, or bundle bone)
Laid down fast
Bundle bone receives the Sharpeys fibers in the alveolar bone proper
Surface features of bone:
o Fissure
Sharp, narrow, cleft-like opening (groove) between parts of a bone that allows passage of BVs & nerves
o Sulcus
Shallow, wide groove on bone surface that allows passage of BVs, nerves, tendons
A shallower & less abrupt cleft/groove than a fissure
o Incisure (notch)
Deep indentation on the border of a bone
o Fovea
Small, very shallow depression
o Fossa
Shallow depression may or may not be an articulationg surface (e.g., glenoid fossa & subscapular fossa, respectively)
o Foramen
Opening through which BVs, nerves, or ligaments pass
o Meatus (canal)
Tube-like passage running through a bone
o Process
Bone projection that serves for attachment of other structures
o Epicondyle
Projection or swelling on a condyle
o Spine
Sharp, slender projecting process
o Tubercle
Small, rounded process
o Tuberosity
Large, rounded, roughened process
o Trochanter
Large blunt projection for muscle attachments on femur
o Crest
Prominent elevated right or border of a bone
o Linea (line)
Small crest, usually somewhat straighter than a crest
o Ramus
Major branch or division of the main body of a bone
o Neck
Slight narrowing of the body of bone that supports the head
o Lamina
Very thin layer of bone
Unpaired bones ethmoid, frontal, occipital, & sphenoid
Ethmoid bone:
o Sieve-like bone at base of skull, behind bridge of nose (behind septal cartilage)
o Straddles mid-sagittal plane & aids to connect the cranial skeleton to the facial skeleton
o Each sinus divided into anterior, middle & posterior air ethmoidal cells
o Horizontal plate (cribriform plate)
Perforated (olfactory foramina) on either side of crista galli for passage of olfactory
nerve bundles
Crista galli sharp, upward, midline projection for attachment of falx cerebri
o Lateral masses (right & left)
Project downward from horizontal plate
Contain ethmoid sinuses & lamina orbitalis (lamina papyracea located in the
orbital medial wall)
The thinnest portion of the orbit is the Medial wall
The roof of the orbit is made from the Frontal bone
Superior & middle conchae are curved plates of bone that form the medial surfaces of the lateral masses
o Perpendicular plate
Downward projection from midline on the undersurface of horizontal plate



Forms upper portion of the nasal septum

Sphenoid bone: Pink bone in pic to right pg 35 Netters H&N anatomy
o Single bone that runs through the mid-sagittal plane
o Aids in connecting cranial skeleton to facial skeleton
o Consists of a hollow body & 3 pairs of projections:
Hollow body
Contains the sella turcica (houses pituitary gland) & sphenoid sinuses
Greater wing forms lateral wall of orbit (bottom pic) & roof of the infratemporal fossa (top pic)
Foramina in greater wing provide access to both pterygopalatine & infratemporal fossa
o Foramen ovale transmits V3
o Foramen spinosum transmits middle meningeal vessels & nerves to tissue covering brain
Lesser wing helps to form superior orbital fissure & roof of orbit
Contains optic canal (optic foramen) & ophthalmic artery
Superior Orbital Fissure
S.O.F. is located between greater and lesser wings of the sphenoid
o Left & right pterygoid processes Yellow bone to right, lateral pterygoid plates hanging down
Project downward from near junction of each of the greater wings w/in body of sphenoid bone
Run along posterior portion of nasal passage
Each proccess consists of a medial & lateral pterygoid plate
Lateral pterygoid plate
o Provides origin for both lateral & medial pterygoid muscles
Medial pterygoid muscle originates from medial surface
Inferior head of lateral pterygoid originates from the lateral surface
o ***Forms medial wall of infratemporal fossa
Medial pterygoid plate
o Forms posterior limit of lateral wall of nasal cavity
o Ends inferiorly as the hamulus (haMElus) for Medial pg 354 Netters H&N anatomy
Hamulus = small, slender hook acting as a pulley for tensor veli palatine tendon (from vertical to horizontal)
What is located directly behind Mx 3rd Molar?? Hamular notch, or Mx tuberosity Its gotta be!
TMJ components:
o Mandibular fossa
Oval depression in inferior surface of base of zygomatic process of the temporal bone
Articulates w/ condyle of Mn to form TMJ
o Articular eminence
Rounded bar of bone forming the anterior part of the Mn fossa
Posterior slope of eminence is lined by fibrous CT
o TMJ cavity
Divided into upper & lower compartment by articular disc
Upper disc glides forward on articular tubercle
Lower condyle rotates beneath the disc like a hinge
o This contains the condyle and capsule
Alveolar bone:
o Exists only to support teeth if tooth never erupts, it never forms if tooth is extracted, alveolus resorbs
o In children, it increases in height & length to accommodate developing dentition
o Position of tooth, not the functional load placed on it, determines the shape of the alveolar ridge
o Alternate loosening and tightening of primary tooth about to shed is from alternate resorption and apposition of cementum and
o The primary mineral component of alveolar bone in the periodontium is Hydroxyapatite
Mandibular condyles:
o Provides space for erupting molars
o Major site of growth
Soft tissue development carries the Mn forward & downward
Condylar growth fills in the resultant space to maintain contact w/ the base of the skull
o Long axes of Mn condyles intersect at foramen magnum, which indicates that axes are directed posteromedially
o Growth at the mandibular condyles provides the space between the jaws into which the teeth erupt
Hard palate:
o Anterior 2/3 formed by palatine processes of maxilla
o Posterior 1/3 by the horizontal plates of palatine bones
o The portion of hard palate located directly posterior to the Mx central is derived from the medial nasal processes
o Forms the roof of the oral caviy & floor of nasal cavity
If you over-implanted Teeth #710, you would penetrate the nasal cavity
o Covered w/ a mucous MB beneath these are palatal salivary glands


Submucosa of anterolateral is characterized by adipose tissue, where posterolateral contains nests of mucous salivary
glands - this is the glandular tissue we compress with the posterior palatal seal in dentures!
Roof of the oral cavity formed by the maxilla & the palatine bones; specifically the palatine processes of the maxilla & horizontal
plates of the palatine bones. Same as the floor of the nasal cavity
Soft palate:
o Posterior to & continuous w/ hard palate
o Contains
Lamina propia of loose fibrous CT
Tough fibrous CT sheet the palatal aponeurosis
Salivary acini deep to the mucous membrane
Shallow, blunt rete pegs *this is only one not obvious
o Posteriorly, soft palate is suspended in the oropharynx ends in the midline uvula
o Most palatal muscles receive innervation from pharygeal nerve plexus
o Motor branchers of CN V3 to tensor mucles of palate
o Sensory innervation provided by CN V2
Nasal cavity:
o Bridge of nose is formed by two nasal bones
o Lateral walls formed by superior, middle, & inferior conchae
o Bony floor formed by palatine process of Mx & horizontal plate of palatine bone =hard palate
o Roof formed by nasal, frontal, body of sphenoid & cribiform plate of ethmoid
o Medial wall or nasal septum formed by the perpendicular plate of ethmoid bone, vomer bone, & septal cartilage (pic above)
o The rest of the framework for bone consists of several cartilage plates
Specifically, the lateral nasal cartilage and greater & lesser ala cartilage
These are held together by fibrous CT
o Opens on face through nares
o Communicates w/ nasopharynx through choanae (posterior openings of nasal cavity to nasopharynx)
o Nasal conchae: See pic on right they are cut in pic to left to show meatus
Three pairs of scroll-like delicate shelves or projections, which hang into nasal cavity from lateral walls
Increase surface area w/in nasal cavity & expose the olfactory nerve to inhaled odors
Superior & middle conchae part of ethmoid bone (yellow bone)
Inferior conchae separate bone (aka inferior turbinates)
o Meatus of the Conchae:
Space below & lateral to each concha
Superior meatus
Receives openings of the posterior ethmoidal sinuses
(Two dots most superior)
(also drains posteriorly into sphenoethmoidal recess)
Middle meatus
Receives the openings of:
o Frontal sinus drains into infundibulum of middle meatus (Straw going
from frontal bone/sinus)
o Middle ethmoidal sinuses drain onto ethmoidal bulla (rounded prominence
on lateral wall of middle meatus) (round thing in pic)
o Anterior ethmoidal & maxillary sinuses drain into middle meatus via
the hiatus semilunaris (just below ethmoid bulla)
Hiatus semiluminares groove on lateral wall continuous w/ the infundibulum
NOTE: the maxillary sinus must drain upwards against gravity makes
maxillary sinus infections hard to treat
Inferior meatus:
Receives the opening of nasolacrimal duct drains lacrimal fluid from eye
surface of into meatus for evaporation
(tiny little hole just posterior to nose)
Cranial fossae:
o Anterior cranial fossa
Formed by frontal & ethmoid bones white and yellow. Also lesser wings of
sphenoid, pink.
Frontal lobes of cerebrum
Cribriform plate
Foramen cecum (contains emissary vein in fetal life)
Crista galli
o Middle cranial fossa



Formed by sphenoid (greater wings), temporal, & parietal bones

Temporal lobes of cerebrum
Hypophysis cerebri (pituitary gland)
Optic & carotid canal
Superior orbital fissure
Trigeminal impression for trigeminal ganglion
Separates the middle ear cavity & sphenoid sinus
Which foramen is not in the middle cranial fossa
o Posterior cranial fossa
Formed by occipital & temporal bones
Occipital lobes
Cerebellum, pons, & medulla oblongata
Internal auditory meatus
Jugular, condyloid, & mastoid foramen
Foramen magnum
Hypoglossal canal
o Petrous portion of the temporal bone:
Forms the floor of the middle cranial fossa
Separates the middle cranial fossa from the posterior cranial fossa
Zygomatic bone
o NOT part of the calvarium, because it comes from the 1 st Branchial arch
o Aka cheekbone, malar bone or zygoma
o Forms prominence of cheek & part of the lateral wall & floor of the orbital cavity
o NOT part of the calvarium (Temporal, Occipital, Parietal, Frontal all are)
o Anteriorly articulates w/ maxilla
o Posteriorly articulates w/ zygomatic process of temporal bone to form the zygomatic arch
Temporal fossa
o Shallow depression on side of cranium bounded by temporal lines
o Terminating below level of zygomatic arch
o Area above zygomatic arch, filled w/ temporalis muscle
o Lower margin is masseter muscle
Infratemporal fossa
o Lies posterior to maxilla (Green), between pharynx & ramus of mandible,
below infratemporal crest of greater wing of sphenoid bone (yellow)
o Boundaries of Infratemporal fossa:
Anterior wall posterior surface of maxilla
Posterior wall tympanic part & styloid process of temporal bone (pink)
Medial wall lateral pterygoid plate of the sphenoid bone (yellow)
Lateral wall ramus of the mandible
Roof (see lower pic) infratemporal surface of greater wing of sphenoid bone
Contains foramen ovale transmits V3 (in sphenoid bone yellow!)
Floor point where medial pterygoid muscle inserts into medial aspect of the Mn near the
o Communicates w/ pterygopalatine fossa (medial- between pterydoid plates and posterior
maxilla) via pterygomaxillary fissure (IN, UP, BACK Just like PSA block)
o Other openings communicating w/ the infratemporal fossa: foramen ovale, foramen spinosum
(not foramen rotundum)
o CONTENTS of infratemporal fossa: lots of Qs on this stuff
See 1999Q04 I dont like this one
Temporalis muscle (lower portion)
Temporalis muscle passes medial to the zygomatic arch & inserts into coronoid
Medial & lateral pterygoid muscles (cut, sandwiching the inferiorly running
inferior alveolar and lingual nerves)
Between them runs the:
o IA nerve and artery
o Lingual nerve
NOT the nerve to the masseter (little tiny one piercing superior head
of lat pterygoid)
Maxillary artery & most branches (including middle meningeal artery)

MAJOR artery of the infratemporal fossa drawing on bottom right

Pterygoid plexus of veins
Mandibular nerve & branches including lingual nerve
Chorda tympani shown joining the lingual nerve, just deep to IA nerve in pic
Otic ganglion (PS ganglion associated w/ glossopharyngeal nerve)
Sphenomandibular ligament Think about it Mn to sphenoid gonna be in this space!
o In a fractured condyle, muscular contractions may result in displacement of the condyle into the
infratemporal fossa
*Temporal & infratemporal fossae communicate w/ each other deep to zygomatic arch
Infratemporal crest of greater wing of sphenoid bone
o Separates the temporal fossa from the infratemporal fossa below it
Pterygopalatine fossa (Think Sphenopalatine Fossa)
o Communicates laterally w/ infratemporal fossa by way of pterygopalatine fissure
o Formed by the sphenoid (posterior/superiorly), palatine (medially), and maxillary bones (anteriorly) (not temporal)
Infection in Maxillary Sinus that spreads posteriorly spreads to pterygopalatine fossa ??? Confirm this
o Pterygopalatine ganglion:
Lies in the pterygopalatine fossa just below CN V2
Receives preG PS fibers from facial nerve by way of greater petrosal nerve
Also receives PostG fibers via the deep petrosal - Sympathetic
Sends postG PS fibers to lacrimal gland & glands in palate & nose (NOT to parotid gland- otic)
o CN V2 & pterygopalatine portion of maxillary artery pass through the fossa
Pterygopalatine fissure communicates:
o 1) Medially w/ nasal cavity through sphenopalatine foramen
The Sphenopalatine foramen connets the pterygopalatine fissure with the nasal cavity
o 2) Posteriorly w/ middle cranial cavity through pterygoid canal and (3) the foramen rotundum
o 4) Posteriorly w/ the pharynx through the pharyngeal canal
o 5) Anteriorly w/ orbit through the inferior orbital fissure
o 6) Inferiorly w/ oral cavity via the Greater Palatine canal
NO communication with Facial Canal
o Ribs
True 1-7
False 8-12
Floating 11-12
Articulate with the spine at the superior articular process of the vertebrae of the same number and the inferior facet for one
number lower (higher on the spine) in a synovial joint and are surrounded by a radiate ligament
When the arched shaft of the ribs is elevated, transverse diameter of the pleural cavity is increased Think about it
when elevated, you are breathing in, so the cavity is gonna increase in size
o Sternum
Has 3 parts:
The manubrium (top), the body (middle), the xiphoid process (bottom)
Sternal angle (inbetween manubrium and body)
The bottom of the sternal shield (bottom of manubrium)
Used to locate 2nd rib
Level of the branching of the trachea (where it passes behind the aortic arch)
Same plane as T5
Body of sternum articulates directly w/ manubrium & xiphoid process (not clavicle, 1st rib,
11th rib)
Hip bone
o Formed by fusion of ileum, ischium, pubis
o Articulates w/ the sacrum at sacroiliac joint to form pelvic girdle
o Two hip bones articulate w/ one another anteriorly at the symphsysis pubis
o Ilium:
Upper flattened part of hipbone
Iliac crest ends in front at anterior superior iliac spine & behind at
posterior superior ilac spine
Greater sciatic notch a large notch call
o Ischium:
L-shaped w/ upper thicker part (body) & lower thinner part (ramus)
Bears weight of body when person is upright & seated
Ischial spine & ischial tuberosity
Obturator foramen formed by ramus & pubis



Body, superior ramus, & inferior ramus
Bodies of the two pubic bones articulate in the midline at symphysis pubis
Medial to symphysis is pubic tubercle
Inguinal ligament connects the pubic tubercle to anterior superior iliac spine
Cup-shaped cavity on lateral side of hip bone
Receives the head of femur
Formed superiorly by ilium, posteroinferiorly by ischium & anteromedially by pubis

Three main classes of joints (articulations):
o Synarthroses: Think : these joints think it is a Syn to move!
Immovable joints (fibrous joints) EX: sutures
In a newborn, intervals between bones in the middle of the cranial base is Hyaline cartilage (see spheno-occipital15 lines)
o Diarthroses: These joints would rather sin (move) and DIE, than be still.
Freely movable joints (synovial joints)
Aneural & avascular
Covered in hyaline cartilage or fibrocartilage (TMJ)
o Amphiarthroses: amphi both.
Slightly movable articulations in which the contiguous bony surfaces are either connected by broad, flattened disks of
fibrocartilage or are united by interosseous ligaments (cartilaginous joints) EX: pubic symphysis, vertebrates
Joints can also be classified based on the associated CT type:
o Fibrousjoined by fibrous CT
1) Sutures
2) Syndesmoses between radius & ulna
3) Gomphosis tooth socket a synarthrosis joint that binds teeth to alveolar socket via the PDL
o Cartilaginousjoined by fibrocartilage or hyaline cartilage
1) Synchondroses epiphyseal plates w/in long bones
NOTE: The spheno-occipital synchondrosis in the midline of the cranial base of a newborn consists of hyaline
2) Symphysis mental symphsis
o *Synovialjoint capsule containg a synovial MB that secretes a synovial fluid
Lined with either Hyaline cartilage or fibrocartilage
Most joints are synovial such as TMJ
*Synovial joints:
o Freely movable (diarthrodial) joints
o Limited by one joint surface, ligaments, muscles, or tendons
o Have 5 distinguishing features:
1) Articular cartilage:
Thin layer of hyaline cartilage that covers the smooth articular surfaces
Contains no BVs or nerves
NOTE: TMJ contains fibrocartilage not hyaline cartilage
2) Synovial cavity:
Small fluid-filled space separation the ends of adjoining bones
3) Articular capsule:
Double-layered capsule
o Outer layer fibrous CT encloses the joint.
o Inner layer thin, vascular synovial MB (because it needs blood supply to produce synovia)
4) Synovial fluid:
Clear, thick fluid secreted by synovial MB
Provides nutrition
Fills joint capsule & lubricates articular cartilage at the articulations
5) Supporting ligaments:
Capsular, extracapsular, & intracapsular ligaments
Maintain normal bone positioning
o Some synovial joints have articular discs (i.e., TMJ & sternoclavicular joint) that divide the cavity into two separate cavities
o Fluid filled sac lined w/ a synovial MB
o Function = reduce friction
o May be located between tendon & bone to reduce friction during muscle contraction
o Bursitis inflammation of lining of a bursa

Subacromial bursa
Large synovial membrane which is adherent to undersurface of coracoacromial ligament, acromion, & deltoid laterally, &
floor is adherent to rotator cuff & greater tuberosity;
It envelops proximal humerus, & facilitates gliding of proximal humerus under coracoacromial arch
Atlanto-axial joint:
o Allows for maximum rotational movement of head about its vertical axis
o Synovial articulation between:
1) the inferior & articulating facets of the atlas (1st cervical vertebra)
2) the superior articulating facets of the axis (2nd cervical vertebra)
o Movement of head in saying NO
Atlanto-occipital joint: (the upper one)
o Synovial articulation between:
1) the superior articulating facets of the atlas
2) the occipital condyles of the skull
o Pemits rocking & nodding movement in saying YES


Muscle fibers:
o Sarcoplasm cytoplasm of muscle cells
Contains many parallel, threadlike structures called
o Myofibrils
Large, multinucleated skeletal muscle cells
Each is comprised of smaller strands called myofilaments
that contain contractile proteins: actin & myosin
An increase in #s of additional myofibrils causes muscle
fibers to hypertrophy
This is caused by progressively greater numbers of
both actin & myosin filaments in the myofibrils
The # of muscle fibers does not increase, the size of
each fiber increases
I Band
Gets smaller with contraction
Only Actin
o Z line
Separates adjacent sarcomeres
Where the T tubules lie
Desmin is also found at the Z lines
It aligns adjacent myofibrils in the myocyte, giving muscle its striated appearance
A Band (A for Alpha Male -- myosin, meaning it makes everyone come to it)
Doesnt change size with contraction
Both actin and myosin, but Myosin dictates borders this is because myosin (thick) is only present in the A Band
o H zone (Think HOT zone, where the ACTIoN is coming)
Gets smaller with contraction
Only Myosin
o M line Middle
o Sarcomere: (see figure)
Repeating contractile unit in the myofibril
Each sarcomere is enclosed between two Z lines (Think End of the alphabet)
Characterized by dark & light striations due to the arrangement of thick (myosin) & thin (actin) filaments
Dark bands = A bands (Anisotropic)
Contain myosin filaments throughout
o In normal light microscopy of striated muscle, the dark portion of the striation is caused by the presence of myosin
Outer regions contain both actin & myosin
H band central area of A band w/o actin/myosin overlap
Light bands = I bands (isotropic)
Bisected by dark Z lines, where actin filaments of adjacent sarcomeres join
o Sarcoplasmic reticulum:
Network of membranous channels, tubules & sacs in skeletal muscles
Analogous to endoplasmic reticulum of other cells
Extends throughout the sarcoplasm


The organelles that releases & sequesters/stores Ca2+ during muscle contraction & relaxation
o Fibrous CT covering of muscle:
The CT layer enveloping the entire skeletal muscle
Continuation of the outer fascia, dividing the interior of the muscle into bundles of muscle cells
Fasciculus = bundle of cells surrounded by each perimysium
The CT layer surrounding each muscle fiber
What immediately covers myofibrils?
o Endomysium or Sarcolemma?????
o Above it says sarcoplasm contains myofibrils so Id say sarcolemma is the answer for this one (if above is correct)
The 3 levels of fascia are interconnected, allowing vessels & nerves to reach individual fibers & cells
o Muscle-tendon junction
The union is made by a continuity of CT sheaths of the muscle with those of the tendon
Motor unit
o Def: alpha motor neuron + muscle fibers it innervates
o Axon of motor unit is highly branchedone motor neuron innervates numerous muscle fibers
o When a motor neuron transmits an impulse, all fibers it innervates contract simultaneously
Muscle contraction
o Tension develops because of interaction between actin & myosin filaments (see figure)
o Actin filaments (thin myofilaments, 5-8 nm diameter); composed of:
Actin globular actin (G-actin) molecules are arranged into double spherical chains called fibrous actin (F-actin)
*Tropomyosin (Like ROPE-Omyosin)long, threadlike molecules, lie along surface of F-actin strands & physically cover
actin binding sites during resting state
*Troponin (LIKE TRIP, i.e. tripped the SWITCH) a small oval-shaped molecule attached to each tropomyosin
o Myosin Filaments: (thick myofilaments, 12-18 nm diameter); composed of:
Light meromyosin (LMM) makes up rod-like backbone of myosin filaments
Heavy meromyosin (HMM) forms shorter globular lateral cross-bridges, which link to actin binding sites during
- Smooth muscle:
o Responsible for involuntary movements of internal
o Much smaller than skeletal muscle fibers
o Composed of uninucleate, elongated, spindle-shaped
cells (fusiform cells)
Do not possess regularly ordered myofibrils & are
therefore NOT striated (myofibrils lack transverse
Nuclei are found in the widest part of each fiber
o Do NOT possess T-tubules & sarcoplasmic reticulum
is poorly developed
o Contraction process is slow & not subject to voluntary
Types of Smooth muscle
Single unit
Has numerous gap junctions (electrical synapses) between adjacent fibers
These fibers contract spontaneously
EX muscular tunica of GI tract, uterus, ureters, & arterioles
Lacks gap junctions
Individual fibers are autonomically innervated
EX: ciliary muscle & smooth muscle of iris, ductus deferens & arteries
Skeletal muscle:
o Responsible for voluntary body movement
o Composed of bundles of very long, cylindrical, multinucleated cells
Possess regularly ordered myofibrils responsible for striated appearance (myofibrils have distinct transverse striations)
Striations consist primarily of actin & myosin proteins
Each fiber is innervated by an axon & motor neuron at a motor end plate
o Enlarges with prolonged activity as result of increase in sarcoplasm and in the number of myofibrils of existing muscle fibers


Not from differentiation of myoblasts or mitotic division of muscle fibers

Nuclei are either slender ovoid or elongated & are situated peripherally
Only skeletal muscle has peripherally located nuclei
o Contain transverse tubules (T-tubules -- at the Z line) & the sarcoplasmic reticulum is very well developed
o Contraction is quick, forceful, & usually under voluntary control
o Myofibrils (actin & myosin) are the contractile element
o Triad consists of terminal cisternae and fingerlike invagination of sarcolemma
Cardiac muscle fibers:
o Make up thick, middle layer of heart known as the myocardium
o Have larger T-tubules & less-developed sarcoplasmic reticulum as compared to skeletal fibers
o Short, branched, & single or binucleated
o Have more mitochondria between myofibrils; richer in myoglobin than most skeletal muscles
o Contain large, oval, centrally placed nuclei
o Characteristic feature presence of intercalated discs
Strong, thin unions between fibers
Provide low resistance for current flow
Within the discs, desmosomes attach cells & gap junctions allow electrical impulses to spread from cell to cell
o Can contract spontaneously w/o nerve stimulation
o Respond to increased demand by increasing fiber size known as compensatory hypertrophy



Sternum; clavicle


Inferior border of mandible;

mastoid groove

(Know how to
pick out of a

Mylohyoid line of mandible

** the mylohyoid ridge/line is
located on the body of the
**The mylohyoid is the muscle
responsible for displacing
denture when extended too far
Styloid process of temporal


Body and greater horn of hyoid



Thyroid cartilage


Superior border of scapula

Muscles of Anterior Neck

Mastoid process of
Turns head to side; flexes
temporal bone
neck & head
Hyoid bone (sling)
Opens jaw;
elevated hyoid bone
Does move the mandible
(one Q asked about
aiding in protrusion)
BUT is NOT a muscle of
Median raphe
Elevates hyoid bone &
(It must attach to hyoid
floor of mouth
NOTE: in the submental
region, the mylohyoid is
the 1st muscle to be
penetrated from the skin
NOT involved in
Body of the hyoid
Elevates & retracks
(gotta have style for the
hyoid bone
Lateral and dorsal tongue Raises the hyoid, retracts
the tongue to the
Body of hyoid
Depresses hyoid
Greater cornu of hyoid
Depresses hyoid;
elevates thyroid cart.
Clavicle; body of hyoid
Depresses hyoid

Accessory nerve CNXI
Ant belly (V3)
Post belly (VII)

Trigeminal V3

Hypoglossal n.
Ansa cervicalis
C1 via hypoglossal n.
Ansa cervicalis

Mandibular Movements and the muscles that make them! (courtesy of Dr. Millers PwrPts)
Lateral Pterygoids (1 )
Q reads The lat pterygoids, suprahyoid, & post digastric contract, what happens? Mandible opens
Lateral Pterygoid



Medial Pterygoid
Medial Pterygoid (2 )
Temporalis (Posterior Fibers)
All four muscles of mastication- Moving at different times in a complex fashion

Only 3 muscles Depress the Hyoid TOS, Thyrohyoid, Omohyoid, and Sternohyoid
Superficial Muscles of the Neck???
o Platysma
o Sternohyoid
o Maybe Splenius Muscles???
Muscles of the Deep Neck pg 113 Netters anatomy
o Often called the lateral vertebral muscles
o Form a large portion of the floor of the posterior cervical triangle

Longus Capitus pg 134

Anterior Tubercles of
C3-C6 vertebral
transverse processes

Longus Colli

Bodies of T1-T3, bodies

of C4-7, and transverse
processes of C3-C6


Anterior: Anterior
tubercles of transverse
processes of C3-C6
Middle: Posterior
tubercles of the
transverse processes of
Posterior: Posterior
tubercles of the
transverse processes of

Anterior tubercle of the

atlas (C1), bodies of C24, and transverse
processes of C5-C6
Anterior: Scalene
tubercle of 1st rib
Middle: Superior surface
of 1st rib
Posterior: External
border of 2nd rib

Flexes the neck
**In front of the cervical
vertebrae and are often
called prevertebral ms.
Flexes the neck (weakly),
and slightly rotates and
laterally bends the neck

C1-C3 ventral rami

Anterior and Middle:

Elevate the 1st rib, when
the 1st rib is fixed, they
flex the neck forward and
laterally rotate it to the
opposite side

Anterior: C5-C7 ventral


Posterior: Raises the 2nd

rib and flexes and
slightly rotates the neck

C2-C6 ventral rami

Middle: C3-C8 ventral

Posterior: C6-C8 ventral

Suboccipital Triangle
o Deep in the triangle passes the vertebral artery and the Suboccipital nerve (aka dorsal ramus of C1)
o Posterior Neck/Head Nerves
Greater occipital nerve (dorsal ramus of C2 spinal nerve)
Great auricular nerve (cervical plexus C2,3)
Lesser occipital nerve (cervical plexus C2,3)
Least occipital nerve (dorsal ramus of C3 spinal nerve)
Suboccipital nerve (aka dorsal ramus of C1)

Rectus Capitus Posterior
Rectus Capitus Posterior
Obliquus Capitus


Muscles of Deep Neck

Basilar portion of the
occipital bone

Muscles of Suboccipital Triangle

Arises from the tubercle
Medial part of the
Extends the head
of the posterior arch of
inferior nuchal line
the atlas
Arises from the spinous
Lateral portion of the
Extends head and rotates
process of the axis
inferior nuchal line
it to the same side
From the transverse
Occipital bone between
Extends the head and
process of the atlas
the superior and inferior
bends it laterally

Suboccipital nerve (aka
dorsal ramus of C1)
Suboccipital nerve (aka
dorsal ramus of C1)
Suboccipital nerve (aka
dorsal ramus of C1)

Obliquus Capitus Inferior

Spinous process of the


Anterior (there are two!)

Carotid (Superior) pg 120

Submandibular (Digastric, Submaxillary)
Pg 118 H&N
Submental pg 124
Muscular (or inferior carotid) Omotracheal
Posterior (THINK Os)
THE SCM divides the anterior and posterior
triangles, Pic Above
Omoclavicular (Subclavian)

nuchal lines
Inferior and dorsal
portions of the transverse
process of the atlas

Rotates the atlas, turning

the face towards the
same side

Location & Contents of the Triangles of

the Neck
SCM muscle, medial line of neck, inferior
border of mandible
Jugular notch also a boundry, not
omoclavicular space
SCM (posterior), posterior digastric
(superior), & omohyoid muscle (anterior)
Superior border is the posterior digastric
Digastric muscle, inferior border of
***NOTE: mylohyoid makes up the floor
Digastric, hyoid bone (only unpaired
triangle of neck)
Floor = Mylohyoid
SCM & omohyoid muscles, midline of neck
SCM & trapezius muscles; clavicle

SCM, trapezius, & omohyoid muscles

SCM, & omohyoid muscles, clavicle

Suboccipital nerve (aka

dorsal ramus of C1)

Four lesser triangles, salivary glands,
larynx, trachea, thyroid glands, various
vessels & nerves.
Carotid Sheath (Carotid arteries, internal
jugular vein, vagus nerve,) CN XII (where
the IJV originates from) , Ansa Cervicalis
Salivary glands, CN XII
Muscles of the floor of the mouth, salivary
glands & ducts
Larynx, trachea, thyroid gland,
Floor: Medial and Posterior Scalenes,
Splenius capitus, Levator scapulae, Nerves
& vessels, Anterior belly of Omohyoid
(NOT sternohyoid)
Cervical plexus, accessory nerve
Brachial plexus, Subclavian artery

o Anterior Triangle
Not Omohyoid
o Posterior Triangle
Occipital and Omoclavicular
o CN XII (Hypoglossal) travels from the Carotid triangle into the subMandibular triangle
Muscles that pass:


Medial scalene
Splenius capitis
Levator scapulae

Hyoid Bone
o Attached by muscles or ligaments to the mandible, clavicle, and tongue
Sternocleidomastoid (SCM)
o Origin
2 heads of origin
Sternal head arises from the anterior surface of the manubrium of the sternum
Clavicular head arises from the superior surface of the medial third of the clavicle
o ***Clavicle is first bone to calcify and is the most commonly broken
o Insertion
To the lateral surface of the mastoid process and the lateral half of the superior nuchal line
o Action
Tilts head to one side, flexes the neck, rotates the neck so the face points superiorly to the opposite side, both together flex
the neck
o Innervation
Spinal root of XI (and C2, C3)
Only Traps are also innervated by XI
o Sternocleidomastoid separates the anterior & posterior triangles of the neck
o Innervated by CN VII Its so superficial, its almost a facial muscle so its innervated by facial nerve!!!

Muscle of Mastication
Floor of the temporal bone
Coronoid process of Mn
Elevates & retracts Mn
Zygomatic arch
Lateral ramus of the Mn
Elevates Mn to occlude teeth
Medial surface of the Lateral
Medial surface of angle of Mn
Elevates Mn & moves Mn
pterygoid plate & tuberosity of Mx &
pyramidal process of palatine bone
Lateral pterygoid
Superior head: Greater wing of the
Superior head: Articular disc & capsule Opens, protrudes, & moves Mn
sphenoid bone
Inferior head: Condylar neck of Mn
Inferior head: Lateral surface of
lateral pterygoid plate
- Muscles of mastication
o Two groups based on function:
Masseter, temporalis, medial pterygoid elevate Mn to close mouth
In the temporalis, most elevation is from the anterior fibers, but the posterior fibers do contribute to elevation of Mn
Lateral pterygoid depresses Mn to open mouth, translates jaw (side-to-side) & protrudes Mn
What about mylohyoid as an elevator of Mn see 2000 Q01
Kaplan says mylohyoid also depresses the Mn (bad Q!!!) Elevates the hyoid not Mn tho
o All receive blood supply from pterygoid portion of the Mx artery
o Innervated by trigeminal nerve (V3)
o Masseter & medial pterygoid form sling around angle of Mn
Superificial head of masseter inserts on lateral surface of angle & medial pterygoid inserts on medial surface of angle
Primary closing muscles provide lateral stabilization of Mn
Both muscles exert similar forces upon Mn
Nerve to the masseter passes through the mandibular notch, BUT does not reach the muscle by passing through the
mandibular foramen Uhhh No SHIT! Why would it pass through the mandibular foramen?
o Medial pterygoid muscle:
The lingual nerve, inferior alveolar nerve, & IA artery all pass between medial pterygoid & Mn ramus (not lingual artery)
If needle lies below mandibular foramen during IA block, it will pierce the Medial Pterygoid muscle
A diffuse swelling at the angle of the Mn & lateral neck of the condyle constrains the following muscle (NOT the medial
Digastric, mylohyoid, lateral pterygoid, geniohyoid
o Lateral pterygoid muscle:
Condylar fracture or injury to lateral pterygoid results in deviation toward affected side
Damage to the articular disc of TMJ would result in paralysis of the lateral pterygoid muscle, which inserts on the articular
disc, joint capsule, & neck of the Mn. The patient would be unable to open his/her mouth
o Temporalis muscle:
Fan-shaped muscle originating from 1) the bony floor of the temporal fossa & 2) the deep surface of the temporal fascia
Inserts on the coronoid process of the mandible & the anterior border of the ramus of the mandible
Medial pterygoid


Anterior & superior fibers elevate Mn; posterior fibers retract Mn (these fibers also contribute to elevation of Mn)
Primary function of the temporalis muscle is to elevate & retrude the Mn
Innervated by deep temporal nerves (branches of V3)
Arterial supply by the maxillary & superficial temporal arteries
Passes medially (downward & deep) to zygomatic arch as a thick tendon before inserting
Posterior fibers retract Mn & maintain resting position of closure of mouth
o In a double vertical fracture at the mental foramina, muscle action will cause the small fragment to move inferiorly &
The small fragment would be the anterior part
Buccinator muscle:
o Does not move the jaw
o Innervated by CN VII
o Complex origin:
Maxilla along alveolar process superior to alveolar margin between 1 st & 3rd molars
Mandible along oblique line of Mn between 1st & 3rd molars
Pterygomaxillary ligament
Pterygomandibular raphe thin, fibrous band running from the hamulus of the medial pterygoid plate down to the Mn
(Along with Superior pharyngeal constrictor)
Marks the posterior border of the vestibular side of the cheek (posterior border of buccinator)
Connects the buccinator (ANTERIORLY) and the superior pharyngeal constrictor (POSTERIORLY)
o Inserts:
Orbicularis oris & skin at angle of mouth
o Pierced by the parotid duct
Parotid duct crosses the massetter and pierces the buccinator
o Proprioceptive fibers are derived from the buccal branch of V3
o Muscle innervation from the buccal branch of VII
o Actions:
Assists with mastication but NOT innervated by V3
Move boluses of food out of vestibules & back towards molar teeth
Tense the cheeks during blowing & whistling
Assist w/ closure of mouth
o Blood supply facial & maxillary arteries
IA nerve block injection
o Needle passes through mucous MB & buccinator muscle & lies lateral to medial pterygoid
o If needle passes posteriorly at level of Mn foramen penetrates parotid facial paralysis
o If needle passes well below Mn foramen penetrate medial pterygoid


Superior genial spine of


Styloid process of
temporal bone

Muscles of Tongue
Dorsum of tongue
Lateral side & dorsum of
tongue (some fibers go
into the hyoglossus m.)
Side of tongue
Side of tongue

Protrudes apex of tongue
through mouth
Depresses ALSO
Elevates & retracts
tongue (during swallow)

C1 via ansa cervicalis
via Hypoglossal nerve

Hyoid bone
Depresses side of tongue XII
Palatine aponeurosis
Pulls tongue upward &
XI via X (oddball alert!)
(Anterior Fauces)
- Muscles of Tongue
o All muscles of tongue are innervated by CN XII (except palatoglossus muscle pharyngeal plexus [CN XI via X])
Damage to what CN leads to movement of the tongue toward the side of the damage?
o Blood supply lingual artery; venous drainage into internal jugular vein
o Extrinsic muscles:
Anchor tongue to skeleton
Control protrusion, retraction, & lateral movements of tongue
Genioglossus, Hyoglossus, Styloglossus, Palatoglossus (Decks say
Palato IS an extrinsic, Netters doesntGo with Decks)
Lingual nerve, hypoglossal nerve, & submandibular duct are all
superficial to the hyoglossus (lingual artery is not)
o Intrinsic muscles:


Lie entirely w/in tongue itself

Named according to spatial plane: longitudinal, transverse, vertical
Fibers contract to squeeze, fold, & curl the tongue
NOTE the Exceptions C1 via XII Genioglossus (should be just XII)
for the extrinsic tongue muscles
Thyrohyoid (should be just ansa cervicalis) for the strap muscles
Taste buds: pg 402 Netters H&N anatomy
o Associated w/ peg-like projections on the tongue mucosa called lingual papillae
o Contain a cluster of 40-60 gustatory cells as well as many more supporting cells
o Each gustatory cell is innervated by a sensory neuron
o Have a turnover rate of 30 days, and are located on ventral and dorsum of the tongue??
o Kinds of Lingual papilla:
Filiform: (think MILI, like Millions)
Most numerous, small cones arranged in V-shaped rows paralleling the sulcus terminalis on anterior 2/3 of tongue
Characterized by absence of taste buds & increased keratinzation (DONT Taste, just like MILI didnt sing)
o Filiform papillae are the lingual papillae with the thickest keratin (think Mili Vanilli wore lots of Makeup)
Fungiform:, FUNGUS are on the Tip and SIDES
Mushroom-shaped, found on tip & sides of tongue
Most likely to be damaged by a tongue laceration
Taste buds innervated by CN VII (taste to anterior 2/3rds)
Largest but fewest in number (7-12), arranged in an inverted V-shaped row on back of tongue
Associated w/ ducts of Von Ebners glands
Have many taste buds, which are innervated by CN IX
Found on lateral margins as 3-4 vertical folds
Taste buds innervated by both CN VII & CN IX
Where are the taste buds found on the dorsum of the tongue?


Longitudinal Muscles of Pharynx

Styloid process
Posterior and superior margins of Thyroid
cartilage & muscles of pharynx
(Passes between the superior and middle
pharyngeal constrictors)
Hard palate; aponeurosis of soft palate
Thyroid cartilage & muscles of pharynx
Cartilage of auditory tube
Muscles of pharynx

Elevates pharynx & larynx

Elevates pharynx
Elevates nasopharynx??,
Pg 431
opens auditory tube
- Stylopharyngues innervated by the glossopharyngeal nerve (the other two are innervated by CN XI via X -- pharyngeal plexus)
- Soft palate:
o Blood supply lesser palatine artery/vein
o All muscles of soft palate (except one) are innervated by CN IX & X (pharyngeal plexus)
Exception: tensor veli palati m. innervated by nerve to the medial pterygoid, a branch of V3
o Anterior zone of the palatal submucosa contains fat
o Posterior zone contains mucous glands
o Attached inferolaterally to tongue by the glossopalatine archs
o Connected to lateral wall of pharynx by the pharyngopalatine arches
o Palatal salivary glands found beneath mucous MB of the hard & soft palate (mostly mucous)
o Five paired skeletal muscles of the soft palate:
1) Palatoglossus closes oropharyngeal isthmus
2) Palatopharyngeus
Elevates pharynx
Contraction during swallowing causes a fold in the posterior wall of the pharynx
3) Levator veli palatini pg 425 & 429 Netters H&N anatomy
Elevates soft palate during swallowing & yawning puts the soft palate against the oropharynx during swallowing
Innervated by X (XI via X)
Extrinsic muscle of the soft palate
Inserts in a palatine aponeurosis
From cartilage of Eustachian tube and petrous portion of temporal bone to the palatine aponeurosis of soft palate
4) Tensor veli palati


Tenses palate & opens mouth of the auditory tube during swallowing & yawning
Curves around the hamulus (if hamulus is fractured, actions of this muscle are affected)
From the scaphoid fossa of the medial pterygoid plate, spine of the sphenoid bone, and cartilage of Eustachian tube to the
palatine aponeurosis of the soft palate
Innervated by V3 its double weird in that its innervated by V3, and that it uses the hamuls as a pully
5) Uvular raises & shortens the uvula to help seal oropharynx from nasopharynx
o Uvula suspended from the soft palate
Innervated by pharyngeal nerve plexus (XI via X)
Unilateral nerve damage causes uvula to deviate to the opposite side (THE ODD BALL in that rule)
When uvular muscle contracts, the muscle on the intact side pulls the uvula toward that side
Bifid uvula:
Results from failure of complete fusion of palatine shelves
- Pharyngeal Constrictors (Circular Muscles)
o Superior Pharyngeal constrictor
From pterygoid hamulus, pterygomandibular raphe, posterior portion of the mylohyoid line and side of the tongue
All attach to the median raphe of the pharynx and the pharyngeal tubercle of the occipital bone
Constricts the wall of the upper pharynx during swallowing
Innervated by X
Forms the Fold of Passavant during swallowing
Lateral wall of the Oropharynx
Behind the Mandible
Superior and Middle Constrictors are split by CN IX (glossopharyngeal) and the
Stylopharyngeus musclepg 432 Netters H&N anatomy
o Middle Pharyngeal Constrictor
From the stylohyoid ligament and the greater & lesser horns of the hyoid bone to the median
raphe of the pharynx
Constricts during swallowing
Innervated by X
Behind the Hyoid bone
o Inferior Pharyngeal Constrictor pg 456
Arises from the oblique line of the thyroid cartilage and side of cricoid cartilage to the median raphe of the
Constricts during swallowing
Innervated by X
Behind the Thyroid and Cricoid cartilages
The lower end is referred to as the cricopharyngeal muscle, which is continuous with the esophageal muscle fibers
Circular Muscles of Pharynx
Superior constrictor
Medial pterygoid plate, pterygoid hamulus,
Median raphe & pharyngeal Constricts upper pharynx
pterygomandibular raphe; mylohyoid line of mandible, tubercle of skull
side of tongue
Middle constrictor
Greater & lesser horns of hyoid; stylohyoid ligament
Median raphe
Constricts lower pharynx
Inferior constrictor
Arch of cricoid & oblique line of thyroid cartilages
Median raphe of pharynx
Constricts lower pharynx

Styloid Process Muscles

o Stylohyoid
Innervated by VII
Perforated near its insertion at the hyoid bone by the tendon of the 2 bellies of the digastric bone
Elevates and retracts the hyoid bone that elongates the floor of the mouth
o Stylopharyngeus
Innervated by IX (only muscle IX hooks up)
Passes between superior and middle constrictors
Elevates the larynx and pharynx during swallowing and speaking
o Styloglossus
Innervated by XII
Some fibers interdigitate with hyoglossus muscle
Elevates and retracts the tongue during swallowing
One of the 4 Extrinsic muscles of the tongue
o Anterior pillars form the glossopalatine arch (aka palatoglossal arch)
The arch attaches the soft palate laterally to the tongue
Within the arch palatoglossus muscle elevates tongue & narrows the isthmus of the fauces


Posterior pillars form the pharyngopalatine arch (aka palatopharyngeal arch)

The arch attaches the soft palate to the lateral wall of the pharynx
Within the arch palatopharyngues muscle elevates pharynx, helps close nasopharynx, narrows the isthmus of the fauces,
& aids in swallowing
o Palatine tonsils:
Consist predominantly of lymphoid tissue
Found between the two arches in an area called the isthmus of the fauces
- Retropharyngeal or Prevertebral space pg 424 Netters H&N anat
o Lateral boundary at level of oropharynx is the carotid sheath (not pterygomand. raphe, medial pterygoid, or stylopharyngeus m)
o NOTE: retropharyngeal space lies between buccopharyngeal fascia & prevertebral fascia
Infection can spread from pharynx to mediastinum
- Strap Muscles (Infrahyoid Muscles)
o Depressors of larynx & hyoid after they have been drawn up w/ pharynx to swallow (deglutition)
o Lie between deep fascia & visceral fascia over the thyroid gland, trachea, & esophagus
o Innervated by ansa cervicalis (aka cervical plexus) from C1,2,3 (except thyrohyoid C1 fibers via CN XII)
o Sternothyroid
o Sternohyoid
o Thyrohyoid ***Boards ? said it WAS innervated by ansa cervicalis, and Geniohyoid was only one not
Anatomy notes say Infrahyoids, EXCEPT thyrohyoid (C1 via CN XII)
Maybe that one Q thinks that C1 (via CN XII) counts as part of ansa cervicalis
o Omohyoid
Manubrium of the
Body of the hyoid
Depresses the hyoid after C1, C2, C3
(ansa cervicalis)
C2, C3
manubrium of the
thyroid cartilage
after swallowing
(ansa cervicalis)
Inferior Belly: Superior
Superior Belly: Inferior
Depress the hyoid bone
C1, C2, C3
border of the scapula
border of the hyoid bone after the bone has been
(ansa cervicalis)
near the suprascapular
elevated. Retracts and
steadies the bone
* Then goes through a
fibrous attachment of the
Oblique line of the
Inferior border of the
Depresses the hyoid bone C1 via XII
**Does not raise the
lamina of the thyroid
body and the greater horn and if the hyoid is fixed,
(also to the Geniohyoid,
hyoid (its infrahyoid,
of the hyoid
draws the thyroid
and to the
cartilage superiorly

Suprahyoid muscles:
o Raise the hyoid during swallowing
o Assist lateral pterygoid in depressing Mn
o Assists posterior fibers of temporalis in retraction of Mn
Posterior Belly
Both bellies end in an
(Longest): Mastoid
intermediate tendon that
notch of the temporal
perforates the stylohyoid
muscles and is connected
Anterior Belly: Digastric to the horn of the hyoid
fossa of the mandible
Styloid process
Body of the hyoid
(Perforated by the
digastric intermediate
Mylohyoid line of
Median fibrous raphe
and the body of the hyoid
**If fall on nail in
submental region, first
muscle penetrated


Elevates the hyoid and
helps lateral pterygoids
open the mouth by
depressing the mandible

Anterior Belly: V3
(Mylohyoid n. branch)
Posterior Belly: VII
(SAME AS Stylohyoid)

Elevates and retracts the

hyoid to elongate the
floor of the mouth


Elevates hyoid and raises

floor of mouth during
swallowing, pushes
tongue upward or
**Can help depress the
mandible or open the

Mylohyoid n. branch

**Sublingual gland is
located superior to the
mylohyoid muscle

Mental spine (Genial


Body of the hyoid

Elevates and draws the

hyoid forward shortening
the floor of the mouth
When hyoid is fixed, also
helps retract and depress
the mandible

C1 via XII
(also to the
**C1 Ventral primary
ramus contributes to the
superior root of the ansa
cervicalis, which then
jumps on XII to get to
the geniohyoid
(thyrohyoid also)

Muscles of the Larynx pg 451 Netters H&N anatomy

o ALL (but the cricothyroid) of the intrinsic muscles of the larynx receive their innervation from the inferior (recurrent) laryngeal
nerve (of CN X)
o Posterior cricoarytenoid
Helps maintain a wide airway through the larynx
Pics from left to right: 1) POSTERIOR VIEW. oblique and transverse arytenoids (superior) and posterior cricoarytenoid (inferior). 2)
Lateral Cricoarytenoid (inferior), Thyroarytenoid (just above- in middle). 3) Cricothyroid (both straps below thyroid cartilage)


Anteriolateral part of
cricoid cartilage

Inferior aspect and
inferior horn of the
thyroid cartilage

Stretches and tenses
vocal cords


Posterior surface of the

laminae of the cricoid

Attaches to the muscular

process of the arytenoid

Oblique Arytenoids

Arytenoid cartilages

Transverse Arytenoid

Arytenoid cartilages

Attach to opposite
arytenoid cartilage
**(Some fibers continue
superiorly as the
Aryepiglottic muscle)
Attach to opposite
arytenoid cartilage

ONLY muscle that

ABDUCTS the vocal
folds and widens the
rima glottidis (space
between the vocal folds)
Close the inlet of the
larynx by adducting the
rima glottidis


Close the inlet of the

larynx by adducting the
rima glottidis

External branch of
superior laryngeal nerve
of X
(**Superior laryngeal
continues as internal
branch that pierces
thyrohyoid membrane
and does sensory above
the vocal cords)
Recurrent laryngeal
nerve of the vagus
(Inferior Laryngeal)
Recurrent laryngeal
nerve of the vagus
(Inferior) This does
evrythin below vocal
Recurrent laryngeal
nerve of the vagus
Recurrent laryngeal
nerve of the vagus
Recurrent laryngeal
nerve of the vagus


Recurrent laryngeal
nerve of the vagus
Recurrent laryngeal
nerve of the vagus
Recurrent laryngeal
nerve of the vagus

Lateral Cricoarytenoid

Derived from the

Thyroaryteniod muscle
Pulls on the True
**Located in the vocal
(cords?) and changes
folds themselves
- ALSO in the Larynx
o Conus Elasticus
Most superior portion is thickened and forms the vocal ligament
o Vocal Ligament
- The cricoid cartilage is cut twice in a sagittal plane (splits the body in left and right halves) is only one that forms a complete ring!
o Which cartilage would not be cut if larynx was cut in a sagittal plane? Arytenoids
o The thyroid cartilage, arytenoid cartilage, epiglottis & 2nd tracheal cartilages would not be cut twice
- Axilla
o Boundaries: (Pyramid)
Medial wall upper 4-5 ribs & their intercostal muscles, and the serratus anterior muscle
Lateral wall humerus (specifically the coracobrachialis & bicep muscles in the biciptial groove)
Posterior wall scapula, subscapularis, teres major, & latissimus dorsi muscles
Anterior wall pectoris major, minor, & subclavius muscles
Base axillary fascia or skin
o Contents:
Axillary vessels
Branches of the brachial plexus
Both heads of the biceps brachii
Muscles of the Axilla
Nerve Innervation
Pectoris major
Medial & lateral pectoral nerve from brachial plexus Flexes, adducts, & medially rotates arm
Pectoris minor
Medial pectoral nerve
Depresses the scapula
Latissiums dorsi
Thoracodorsal nerve from brachial plexus
Adduct, extends & medially rotates the arm
Axillary nerve (C5-C6)
Abducts arm, post. Fibers extend & anterior fibers flex
Teres major
Lower subscapular nerve from brachial plexus
Adducts, extends & medially rotates the arm
(medially rotates due to attchmnt on lateral humerus)
Teres minor
Branch of Axillary nerve
Rotates the arm laterally

Serratus anterior

Outer surface and
superior borders of
first 8 to 9 ribs

Pectoralis minor

Ribs 3-5


Rib 1


Occipital bone and

vertebrae C7-T12

Levator scapulae
Rhomboideus major
Rhomboideus minor

Muscles of the Shoulder

Insert on the ventral
Pulls scapula forward &
aspect of the vertebral
downward preventing winging
border of the scapula
Also rotates scapula upward to
abduct the arm above 90 degrees
Coracoid Process of
Pulls scapula forward &
Ventral surface of
Draws clavicle downward
Inserts into the upper
Elevates scapula, draws head
and medial border of
back, adducts scapula, braces
the Spine of the
shoulder, draws scapula
Scapula, and Clavicle
Elevates & draws scapula
Elevates & retracts scapula
Elevates & retracts scapula
Muscle of the Arm


Long thoracic nerve
(C5, C6, C7)
Medial pectoral nerve
Nerve to subclavius, C5,
Accessory nerve

Dorsal scapular nerve

Dorsal scapular nerve
Dorsal scapular nerve

Triceps Brachii

Scapula & humerus

Ulna (olecranon process)

Nerve Innervation

Biceps Brachii

Scapula (coracoid
process & supraglenoid

Ulna (coronoid process

Radius (styloid process)
Radius (tuberosity)


Primary Extensor of the
Flexes the forearm
Flexes the forearm
MEDIAL rotates the arm
Flexes the forearm &
arm, supinates the
**Primary supinator at
the radio-ulnar joint
**Flexion at the glenohumeral joint
**Flexion at the humeroulnar joint

Radial nerve is most commonly injured in a mid-humeral shaft fracture, because it runs in the radial (spiral) groove of the humerus
Coracoid Process
o A break would affect the biceps brachii and the pectoralis minor muscles (Pec major inserts into arm)
And one more factoid:
o The pronator quadratus m. is the primary pronator of the forearm (assisted by the pronator teres m.)
Triangle of auscultation
o Bounded by the upper border of the latissimus dorsi, the lower border of the trapezius, & the medial margin of the scapula
o Site where breathing sounds can be heard most clearly
o Floor is formed by the rhomboid major


Transversus abdominis
Internal abdominal
**Along with the
aponeuroses of the
transverses, forms the

Muscles of Anterior Abdominal Wall -- (TIRE from Deep to Superficial)

Compresses abdomen
Lateral half of the
inguinal ligament, the
iliac crest, and the
thoracolumbar fascia

Inferior borders of the

cartilages of the last 3
to 4 ribs, the linea alba,
pubic crest, and
pectineal line

Compresses abdomen; lateral

rotation, acting alone it bends
the vertebral column laterally
and rotates it to bring the
shoulder of the opposite side

Lower intercostal,
iliohypogastric &
ilioinguinal nerves
Lower intercostals (T7T11), subcostal (T12)
iliohypogastric, &
ilioinguinal nerves (L1)


conjoint tendon

Rectus abdominis
**Linea alba splits the
muscle and 3
tendinous bands
horizontally (6 pack)
External abdominal

2 tendons
Lateral attaches to the
pubic crest
Medial interlaces with
the tendon of the
opposite side to arise
from the pubic
Fleshy digitations fro
the external surface and
inferior borders of
lower 8 ribs

Attaches to the 5th, 6th,

and 7th ribs and the
xiphoid process

**Nerves of the anterior

abdominal wall lie
immediately deep to this
Flexes vertebral column,
tenses abdomninal wall, and
depresses the ribs

Lower intercostal nerves

(T7-T11), and the subcostal
nerve (T12)

Attaches to the anterior Compresses abdomen; lateral

Lower intercostal nerves
half of the iliac crest,
rotation, acting alone it bends
anterior superior iliac
the vertebral column laterally
spine, and into a broad
and rotates it to bring the
aponeurosis along a line shoulder of the same side
from the 9th costal
cartilage to the anterior
superior iliac spine.
The aponeurosis inserts
into the midline linea
*TIRE going in to out; Ill miss the point if they ask about attachments; actions are straight forward, Innervated by lower intercostals


Cremaster muscle
o Arises from the middle of the inguinal ligament and is a continuation of the internal abdominal oblique muscle
o Draws testes upward
o Innervated by the genital branch of the genitofemoral nerve (L1 and L2)
o After passing through the inguinal ring, the muscle fibers of the cremaster form a series of loops making up the cremaster fascia
which surrounds the spermatic cord
Posterior abdominal muscles:
o Psoas major & minor innervated by lumbar plexus
o Quadratus lumborum
From the transverse process of L3-5, the iliolumbar ligament, and the iliac crest to the lower border of the last rib and the
transverse processes of L1-3 vertebrae
Flexes the lumbar vertebral column, fixes the 12th rib during inspiration
Innervated by lumbar plexus (Subcostal nerve T12 and L1-3)
Above the muscle, the diaphragm forms the lateral arcuate ligament
o Iliacus innervated by femoral nerve
o Dorsal rami innervate erector spinae muscles Dorsal Rami innervate ALL deep back muscles:
Splenus Capitus
SPlenus cervicis
Errector Spinae
Respiratory muscles:
o Diaphragm, internal & external intercostals, subcostals, & transverses thoracic
Diaphragm is innervated by phrenic nerve; the others are all innervated by intercostal nerves
o Diaphragm:
Muscle mostly responsible for quiet breathing
Flat muscle in a dome-like shape that separates chest & abdominal cavities
Arises from the xiphoid process, lower 6 costal cartilages and a lumbar portion (L1-L3)
Then the muscles converge and insert into the central tendon
o The tendon is drawn downward and forward during inspiration
Inhaling contraction of diaphragm pulls down on chest (via the central tendon), drawing in air via pressure differences
The vertical dimension of the thoracic cavity is increased chiefly by contraction of the diaphragm
Exhaling contraction of abdominal forces the relaxed diaphragm upwards
Upper surface contacts heart & lungs; Lower surface contacts liver, stomach, & spleen
Innervated by the Phrenic nerve (C3, 4, 5keep the diaphragm alive)
Travels through the thorax between pericardium & pleura (between heart and lungs)
o The phrenic nerve is the nerve lying in close relation to the surface of the pericardial sac (not the vagus nerve)
Right phrenic travels anteriorly to bronchial root and does NOT leave an impression (azygos v. does)
Sends off branches to innervate the parietal pericardium

Is in direct contact in the neck with the Infrahyoid fascia

Inability to move the diaphragm is associated with a total section of the spinal cord at C2 (or above prolly)
Phrenic nerve passes anterior to which muscle Anterior scalene!!!
Has three openings:
Caval opening (T8)
o Right phrenic nerve
Esophageal opening (T10)
o Esophagus
o R & L vagus nerves
Aortic opening (T12)
o Aorta
o Azygos vein
o Thoracic duct
o I = IVC T8; T10 EG = esophagus, G vaGus; A = Aorta, Azygos, T = Thoracic duct T12
o External intercostals: (Girls gone wild Externs lifting up their shirt!)
From rib to rib in a shoulder to belly button direction hands in pocket
Pass from rib to rib & run at right angles to fibers of the intenal & innermost muscles
Continue toward sternum as the anterior intercostal MB
Active during inspiration and elevate the ribs
Innervated by the intercostal nerve, i.e. between 4th and 5th rib is the 4th intercostal space, so innervated by the 4th intercostal
nerve meaning there are only 11 intercostal nerve
o Internal intercostals:
Right angle to External intercostals
Eleven on each side between ribs
From rib to rib in a sternum to pants pocket direction
Continue toward vertebral column as the posterior intercostal MB
The upper portions (upper 4 to 5 intercostal muscles) elevate the ribs
The lateral and posterior muscles, where fibers run more obliquely depress the ribs and are active during expiration
Innervated by intercostal nerves
o Innermost intercostals:
Run in same direction as internal intercostals but are separated from them by nerves & vessels
Thought to elevate the ribs
Innervated by the intercostal nerves
o Transversus thoracis:
From posterior surface of the lower portion of the body of the sternum and xiphoid process to the inner surface of costal
cartilages 2-6
Depress the ribs
Innervated by the intercostal nerves
Muscles of Inspiration
o SCM Accessory muscle
o Scalenes (Ant, Middle, Post) Accessory muscle
o External intercostals
o Interchondral part of internal intercostals
o Diaphragm
Muscles of Expiration
o Internal intercostals (except interchondral part)
o Abdominals (TIRE Transversus abdominis, Internal oblique, Rectus abdominis, External oblique)
NOTE : the nerves of the anterior abdominal wall lie between transversus abdominis & internal oblique muscles
Active Inspiration
o Diaphragm descends
o Rib joints are active
o Lateral diameter of thorax increases


- Quadriceps femoris group
o Rectus femoris:
Crosses the hip & knee joints
Flexes thigh at hip & extends leg at knee
o Vastus lateralis, intermedius & medialis
All extend leg at knee



Muscles of the thigh posterior group

o All three:
Flex the leg & extend the thigh
Innervated by tibial nerve
o Biceps femoris
o Semitendinousus
o Semimembranous
Muscles of the thigh anterior group
o Sartorius
Flexes leg & thigh
Abducts thigh
Femoral triangle:
o Contains the femoral V.A.N.
Unhappy triad: MCL, meniscus, & ACL
o Neural PlateNeural Tube
Prominent growth of neural tissue causes folding of the embryo during the 4th week of development
This gives it a C-shaped curvature
Neural plate forms by Day 19 in the dorsal midline of the embryo
A rostrocaudal groove appears on the midline & invaginates as the lateral borders rise to form the neural folds
The neural folds begins to move together & fuse, converting the neural plate into a neural tube
The Notochord induces ectoderm to form neuroectoderm, hence promoting formation of the neural plate
The Prochordal Plate (Buccopharngeal) and the cloacal plate only have 2 layers epi and hypoderm
o Neural Tube
The neural tube develops into the CNS
Initially the neural tube is separated from the surface ectoderm by neural crest cells
Caudal end develops into the spinal cord
Basal plates motor part of CNS bottom, becomes ventral
Alar plates sensory part of CNS top, (like an altar), becomes dorsal
Rostral end develops into the brain
3 parts: rhombencephalon, mesencephalon, prosencephalon
o Neural crest:
Band of neuroectodermal cells that lies dorsolateral to developing spinal cord
Clusters of cells (neural crest cells) develop into: DRG cells, spinal autonomic ganglion cells, chromaffin cells, neurolemma
cells (Schwann cells), integumentary pigment cells (melanocytes), & meningeal covering of brain & spinal cord
Nervous tissue has two classes of cells:
o 1) Neurons: nerve cells
Transmit nerve impulses
Basic unit of the nervous system activities of the system are carried out it at the neuron level
o 2) Neuroglial cells: nerve glue
Provide support & nourishment for neurons
1) Neurons:
o Structure
Cell body (perikaryon)
Contains nucleus & most of the cytoplasm
Located mostly in the CNS as clusters called nuclei some found in periphery as ganglia
When the cell body is destroyed all of its fibers degenerate and die
Synthesizes axoplasm that is needed for increasing axon length
Contains Nissl bodies (rough ER); not found in axon or axon hillock
Process that send the impulse toward the cell body
May be one or many dendrites some neurons lack dendrites
Axon (nerve fiber)
Process that send the impulse away from the cell body
Only one axon per neuron
o Classified according to:
1) Structure (by number of processes)
Bipolar or Unipolar or Multipolar (most common)
2) Function

Motor or Sensory or Mixed

Myelin formed by Schwann cells in PNS & oligodendrocytes in CNS
Node of Ranvier is junction between two Schwann cells
o Neurolemma
The outermost portion of a nerve fiber (Dont call the myelin sheath the outer!!!!)
The nucleated layer of Schwann cells that surrounds the myelin sheath
So, from inside out: axis cylindermyelin sheathneurolemma hmmm isnt myelin sheath just cell mb around
o Motor Neurons
Babinski Sign has to do with feet?
In adults, a positive Babinski sign means damage to upper motor neurons
In newborns, a positive sign is normal
- 2) Neuroglia:
o Non-neuronal tissue of CNS that performs supportive & other ancillary functions
o Composed of various types of cells collectively called neuroglial or glial cells
o With the exception of the microglia, which derives from mesoderm, all other neuroglia cells form from ectoderm
Cells that support neurons
Stellate w/ numerous processes
Form structural support between capillaries &
neurons w/in CNS, Blood Brain Barrier
Similar to astrocytes but w/ shorter & fewer
Form myelin in CNS, guide development of neurons
w/in CNS myelinates multiple CNS axons
Minute cells w/ few short processes
Phagocytize pathogens & cellular debris w/in CNS
Macrophage of CNS
Mesodermal origin (M for M, others are from
Columnar cells that may have ciliated free surface
Line ventricles & central canal w/in CNS where
CSF is circulated by ciliary motion
Satellite cells
Small, flattened cells
Support ganglia w/in PNS
Schwann cells
Flattened cells arranged in series around axons or
Form myelin w/in PNS only myelinates 1 axon
Promote axonal regeneration

Spinal cord:
o Cylindrical, occupies ~ upper 2/3 of vertebral canal, & is enveloped by the meninges
o Centrally located gray matter & peripherally located white matter
o Ends at ~L1 in adults & at ~L3 in young children
Dura & arachnoid continue to S2 where arachnoids fuses w/ filum terminale (after fusion it is called the coccygeal ligament)
o Main areas of spinal cord:
Gray matter
H-shaped, centrally located, consists of nerve cell bodies & unmyelinated nerve fibers
Gray commissure center of the H connects two paired posterior (dorsal) horns & anterior (ventral) horns
Anterior hornmotor
o Cell bodies of somatic motor system lie w/in the ventral horn
o Cell body of a motor neuron in a spinal reflex arc is located in anterior gray column (ventral horn) of the spinal cord
o Patellar (knee-jerk) reflex: L4
o Biceps reflex: C5
o Triceps reflex: C7
o Achilles reflesx: S1
Lateral hornautonomic
Posterior hornsensory
Central canal:
w/in gray commissure & filled w/ CSF
White matter:
Composed primarily of myelinated axons (because its fatty)
Surrounds gray matter


o Fasciculus gracilus legs (Think Graceful legs like a ballerina)

o Fasciculus cuneatus arms cunning, so closer to the brain
Spinal taps
o Lumbar puncture needle inserted in space between L3-L4 (or between L4-L5)
Needle enters subarachnoid space which is filled w/ CSF (pia is not pierced)
o CSF can be aspirated most safely by inserting the needle between L3 & L4 since the spinal cord usually does not extend below L2
Spinal nerves:
o 31 pairs; all spinal nerves are mixed made up of ventral & dorsal roots
8 cervical 12 thoracic 5 lumbar 5 sacral 1 coccygeal
The cauda equina consists of the roots of the lumbar & sacral spinal nerves
o Ventral and Dorsal roots leave the spinal cord, immediately join to form the Spinal Nerve, then 3 branches, 1 to sympathetic chain
ganglion(seen in pic), 1 to the Ventral Rami (i.e. intercostals), 1 to Dorsal Rami (i.e. intrinsic muscles of the back)
Then the anterior rami can branch to form Lateral and Anterior cutaneous branches
The intercostals nerves course between the innermost and the inner intercostal muscles
Intercostals (somatic nerves) are connected to the sympathetic chain ganglia via the rami communicantes
Like how the greater splanchnic nerve comes from rami communicantes from T5-9
o Ventral roots
Contain axons of motor neurons (also ANS stuff)
Cell bodies located in spinal cord
Upon exit, become anterior rami (mixed & long nerve in pic to right) supply body
wall & limbs
In cervical, brachial, lumbar, & sacral regions the anterior rami of the spinal
nerves unite to form plexuses
o These plexuses give rise to other nerves for distribution to muscle, skin, etc.
o Dorsal roots
Contain axons of sensory neurons
Cell bodies located outside spinal cord in dorsal root ganglia Can see in pic
Upon exit, become posterior rami (mixed) supply skin & deep back muscles
o Hey, if youre confused, look at a picture somewhere

Spinal Cord tracts

o Columns of white matter w/in spinal cord that conduct impulses to CNS (ascending) & away from CNS (descending)
Ascending tracts
Anterior spinothalamic
Conducts sensory impulses for touch & pressure
Lateral spinothalamic (side of lateral horn)
Conducts pain & temperature impulses
Fasciculus gracilis (back in the midline) & fasciculus cuneatus
Conducts sensory impulses from skin, muscle, tendons, & joins;
(back offset) (THINK GRACEFUL LEGS)
also touch localization (conscious proprioception)
Posterior spinocerebellar (back corners)
Conducts sensory impulses from one side of body to same side of
cerebellum for subconscious proprioception
Descending Tracts
Anterior corticospinal (Front Midline)
Conducts motor impulses from cerebrum to spinal nerves &
outward through anterior horn for coordinated movement
Lateral corticospinal (Just next to dorsal horn, inside Post.
Conducts motor impulses from hemisphere to spinal nerves through


Tectospinal (Front offset) (Night at the Roxbury TECHNO head
Rubrospinal (In lateral grooves, in front of lat. Corticosp.)
Vestibulospinal (Front really offset)
Anterior & medial reticulospinal & lateral reticuloalspinal

anterior horns for coordinated movments

Conducts motor impulses to cells of anterior horns & eventually to
muscles that move the head
Conduct motor impulses concerned w/ muscle tone & posture
Regulate body tone & posture (equilibrium) in response to
movements of head
Control muscle tone & sweat gland activity

o Three protective tissue layers covering CNS
o The structures involved in meningitis (inflammation of meninges) if severe can become encephalitis (inflammation of brain)
o Dura mater:
Outermost MB a fused, double layer of tough fibrous CT
Layers separate to form venous sinuses in the cranial cavity
Endosteal layer adheres tightly to inner surface of the cranium
Meningeal layer forms partitions (folds) that extend between regions of the brain
o Arachnoid:
Delicate middle MB adheres to dura mater but is separated from pia mater by subarachnoid space contains CSF
o Pia mater
Innermost MB delicate vascular MB of loose CT adheres closely to brain & spinal cord
Outside the skull: SCALP
o Skin, CT, Aponeurosis, Loose CT, Pericranium
Cerebrospinal fluid
o Clear, colorless fluid formed by the choroid plexuses w/in the lateral, 3rd & 4th ventricles
o Produced by filtration, primarily from tufts of capillaries that protrude into all four ventricles
Ependymal cells also produce CSF they line the ventricles, central canal of spinal cord, & choroid plexuses
o Fluid enters the subarachnoid space through three foramina of the 4th ventricle
o Choroid plexuses regulate intraventricular pressure by secretion & absorption of CSF
o CSF along w/ ligamentous walls of vertebral canal protect spinal cord from injury
Dura mater (continued):
o Two vertical folds
Falx cerebelli separates hemispheres of cerebellum; contains occipital sinus
Falx cerebri separates the cerebral hemispheres in a sagittal direction; contains inferior & superior sagittal sinuses
o Two horizontal folds
1) Tentorium cerebelli
Separates occipital lobes from the cerebellum


Contains straight, transverse, & superior petrosal sinuses (NOT inferior petrosal sinus) look at pic on pg 59
2) Diaphragma sellae
Forms roof of sella turcica; a small central opening allows passage of infundibular stalk of the pituitary


o Blood-brain barrier (BBB):
Protected by the CIA:
Choroid plexus epithelium
Intracerebral capillary endothelium
Glucose & amino acids cross by carrier-mediated transport mechanism
L-dopa used to treat Parkinsons, since dopamine does not cross the BBB L dopa does because its AA like
o Consists of several regions: TDMMMS
Forebrain (prosencephalon)
Telencephalon & diencephalon derive from the
Midbrain (mesencephalon)
Hindbrain (rhombencephalon)
Metencephalon and Myelencephalon derive from
the Hindbrain
o Each portion of brain consists basically of three areas:
Gray matter composed primarily of unmyelinated
nerve cell bodies
White matter composed basically of myelinated nerve
Ventricles spaces filled w/ CSF
o Cerebrum:
Located w/in telencephalon & is the higher forebrain
Consists of five paired lobes w/in two convoluted
cerebral hemispheres (connected by corpus callosum)
Accounts for 80% of brains mass
Deals w/ higher functions perception of sensory impulses, instigation of voluntary movement, memory, thought, reasoning
Two layers of cerebrum:
Cerebral medulla thickened core of white matter
Cerebral cortex thin, wrinkled gray matter covering each hemisphere
o Diencephalon:
Major autonomic region of forebrain almost completely surrounded by cerebral hemispheres of the telencephalon
Chief components thalamus, hypothalamus, epithalamus, & pituitary gland (just posterior pituitary)
The 3rd ventricle forms a midplane cavity w/in the diencephalon
o Hypothalamus:
Is the inferior portion of the diencephalon & forms roof & ventrolateral walls of the 3 rd ventricle
Endocrine control
Regulates hormone synthesis in anterior pituitary
Synthesizes & releases oxytocin & ADH water/salt balance\
ADH supraoptic nucleus; Oxytocin paraventricular nucleus -- (Think LOW oxygen when you PARAshute)
Regulation of ANS
Temperature control (anterior hypothalamus think A/C: Anterior = Cooling)
Eating behaviors
Lesions of ventromedial HThobesity
Lesions of lateral HThsevere aphagia
Lesions of supraoptic nucleidiabetes insipidus (polydipsia & polyuria result from deficient ADH)
Sexual maturation & childbirth
o Thalamus:
Thalamic nuclei:
DOESNT regulate Breathing Medulla Ob does
Lateral Geniculate nucleus visual
Medial Geniculate nucleus auditory (PUT your fingers in your ears POINT MEDIALLY)
Ventral posterior nucleus sensory posterior just like dorsal area is sensory in SC
o Medial part body senses
o Lateral part facial sensation
Ventral anterior/lateral nuclei motor Again, normal, ventral anterior = motor


A Lateral Ventricle
B Corpus callosum
Identify the thalamus in the sketch above: C
D Internal Capsule
E Basal Ganglia (Caudate, Putamen, Pallidum, Substantia Nigra, Nucleus accumbens, Subthalamic Nucleus)

Most of the fibers ascending or descending to the cerebral cortex transverse the internal capsule
The fiber tracts passing from the thalamus to the cortex are found in the internal capsule
= thalamus to cortex
Four ventricles:
NOTE: formation of the brain begins w/ differentiation of the cephalic
end of the hollow neural tube
Hollow spaces persist as ventricles w/in the brain
1&2) Two lateral ventricles
Hollow C-shaped spaces w/in right & left cerebral hemispheres
Large mass of gray matter that bulges into the floor and lateral
aspect of the ventricle is the caudate nucleus
3) Third ventricle
Forms a median cavity w/in the diencephalon (forebrain)
4) Fourth ventricle:
Located in the metencephalon (hindbrain).
Contains two openings in its walls called Lateral apertures
(foramina of Luschka)
Contains a single opening in its roof called Medial aperture
(foramen of Magendie)
The apertures connect the ventricular system w/ the subarachnoid space
After circulating throughout the subarachnoid space, CSF is returned to the circulatory system by filtration
through arachnoid villi (villi protrude mainly into the venous drainage sinuses of the cranial cavity) into the
Superior Sagittal sinus
Two interventricular foramina of Monro oval openings which provide communication between the third & lateral
The cerebral aqueduct in the midbrain connects the third & fourth ventricles
Obstruction of the cerebral aqueduct causes enlargement of the two lateral & third ventricles (not the fourth)
Referred to as a non-communicating hydrocephalus which means lateral ventricles are not in communication w/
subarachnoid space
o Excessive CSF in the ventricles
Flow through ventricles:
First and Second ventricles Foramen of monro 3rd Ventricle cerebral Aqueduct out via Lateral foramen of
Luschka (2) or Medial formanen of Magendie (1)
Substantia Nigra (Black people are DOPE)
Uses dopamine as predominant neurotransmitter for S.N. (not for olivary nucleus or lateral reticular nucleus)
Consists of the vermis (medial) & two cerebellar hemispheres
External anatomy:
Each hemisphere has an anterior lobe, posterior lobe, & flocculonodular lobe
Internal anatomy:
Cerebellar cortex
o 3 layers (think MPG): Medullary, Purkinje, Granular
Arbor vitae
o Subcortical white matter
Cerebellar nuclei



Mossy fibers = excitatory fibers from the spinal cord, pons, & vestibular nuclei
Climbing fibers = excitatory fibers from the inferior olive nucleus
Golgi cells = fibers receiving input from mossy fibers & parallel fibers of the granule cells
Purkinje fibers = fibers receiving input from the climbing & parallel fibers AND inhibitory input from basket cells
Each granule cell sends its axon into the molecular layer, giving off collaterals at 90 angles = parallel fibers
o The granule cell axons stimulate the distal dentrites for the Purkinje cells & Golgi cells
o Purkinje fibers are the final common pathway for cortical output
They can stimulate OR can send a single axon through the granular layer & arbor vitae to inhibit the deep nuclei
Common symptoms of cerebellar dysfunction
Ataxia, Dysmetria, Nystagmus, Hypotonia, Intention tremor
Cerebral cortex:
o Extensive outer layer of gray matter of cerebral hemispheres
o Cerebral lobes function primarily in voluntary movement, higher intellectual processes & personality (w/ the limbic system)
o NOTE: basal nuclei gray matter structures deep w/in each cerebral hemisphere help control muscle activity

Area of Cerebral Cortex

Precentral gyrus of frontal lobe
Postcentral gyrus of parietal lobe
(Think Dorsal meaning Sensory just like
Spinal Cord)
Medial surface of the occipital lobe
Parietal lobe (near base of postcentral gyrus)
Temporal lobe (transverse temporal gyri)
Frontal lobe

Parietal lobe
Temporal lobe (Medial surface)

Motor area (initiates voluntary contractions of skeletal muscle
EX Highly skilled, discrete hand movements depend on activity of the precentral
Sensory area (receives sensory info regarding temperature, touch, pain, proprioception)
Concerned with recognition of painful stimulus from the teeth
**Sensations from Left face and Teeth are interpreted in the Right Parietal Lobe
Visual area visual center of the cerebral cortex is found here
Taste area
Hearing area the primary auditory complex is found here
(Higher intellectual functions)
(Unable to Plan or Organize Behaviors)
(Lacks Self-Discipline)
(Anti-social Behavior) PHINEAS GAGE
Somatic associated area (Integration & interpretation center)

Limbic system:
o Includes brain structures involved in emotion, motivation, & emotional association w/ memory
o Responsible for 5 Fs:
Feeding, Fighting, Feeling, Flight, & Sex (Ha, Ha) (as quoted from USMLE)
Gate Theory of Pain (outdated???)
o A controller system modulates sensory input so that there is a selective and integrative action occurring before impulses reach the
first synapse for onward transmission.
The gate controller in this system is the substantia gelatinosa
Jello would fit through the gate
o Picture: ID cross section of : pons, midbrain, medulla oblongata, spinal cord
o Corticobulbar tract bulb is old word for Medulla so this is the tract from cortex to medulla!
The fibers which separate from the corticospinal tract as it descends through the pons & medulla oblongata
Fibers of this tract innervate the motor nuclei CN V, CN VII, CN XII (perhaps also the nucleus ambiguus)
1) Which CN contralateral innvervation? CN 12 (also the upper part of 7 to the forehead, and most texts also say 2)
o I think it could be 5, 7 upper, 12 (& even nulceus ambiguus)
2) What CN crosses corticobulbar? 12
o Same answer
3) Which tract of the corticobulbar only innervates to the contralateral side of the face?
o I say its 7 lower
o Hypoglossal n. (not sure)
o From Neuroanatomy lecture: All cranial nerves have bilateral innervation with two exceptions:
1) Lower Face of VII is contralateral
upper face is bilateral
2) CN XII is contralateral - for explanations

Also see lab on desktop for explanation
CN XII receives bilateral innervation
CN V does, too


CN VII lower is only contralateral

N. ambiguus receives bilateral

o Lower extension of brain where it connect to spinal cord
o Neurological functions located in the brainstem include those necessary for survival
Breathing, digestion, HR, BP
o Most cranial nerves come from brainstem
o Motor nuclei are medial to sensory nuclei
o Pathway for all fiber tracts passing up & down between peripheral nerves & spinal cord to higher brain
o Midbrain:
Nerve pathway of cerebral hemispheres
Contains auditory & visual reflex centers
General anesthesia affects what system? The Reticular system which is located between medulla & midbrain, and is
responsible for state of consciousness
o Pons:
Bridge-like structure which links different parts of brain
Serves as a relay staion from medulla to higher cortical structures of brain
o Medulla oblongata:
Relay station for the crossing of motor tracts between spinal cord & brain
If the spinal tract of CN V were sectioned at the level of the caudal medulla, PAIN from the ipsilateral side of the
face would be most affected
Contains respiratory, vasomotor, & cardiac centers
Has many mechanisms for controlling reflex activities (e.g., coughing, gagging, swallowing & vomiting)
Medial lemniscus (from gracile and cuneate nuclei (of medulla) to the thalamus.
Large ascending bundle of fibers, composed of 2nd order neurons, carrying proprioception & discriminatory
touch sensations to the conscious
o No where else to put this. the 3rd order
neuron in pain pathway comes from thalamus
o I
o II
o III Oculomotor
o IV Only CN from Dorsal
Brainstem Trochlear
PONS (4)
o V (remember Spinal N. of V is
from Medulla) Tg motor
o VI Abducens
o VII Facial
o VIII Vestib/Cochlear
MEDULLA (4 5* if you count Spinal
of V)
o IX
o X
o XI
GSE fibers to all extraocular muscles except the superior oblique (trochlear nerve) and the lateral rectus (Abducens
Edinger-Westphal Nucleus pg. 549 Netters H&N anatomy
PARA-PRE, which give rise to GVE fibers with terminate on cells in the ciliary gaglion
Innervates the papillary sphincter muscle, sends parasympathetic
Ptosis, droopin of an eyelid, Mydriasis, and loss of accommodation



Trochlear nuclei
located near central gray matter of the lower midbrain at the level of the inferior colliculi
Located on the Dorsal side of the brain
Double vision on looking downward and away from the affected side
CN V: pg 86 Netters H&N anatomy
Sensations from the Left face and teeth are interpreted in the Right Parietal lobe
Touch receptors are most numerous per unit area in the tip of the tongue
Motor nucleus of V:
*Sends SVE fibers to muscles of mastication
Lower motor neuron control of the muscles of mastication is by way of the Motor nucleus of V
Monosynaptic jaw closing reflexes might be disrupted in Motor nucleus of V
Just medial to the Main Sensory Nucleus
Fibers are SVE and supply the 8 muscles of V3
Joins sensory nuclear complex fibers to become Trigeminal Nerve
Trigeminal sensory nuclear complex:
Axons enter the pons through sensory root & terminate in 1 of 3 nuclei of trigeminal sensory nuclear complex:
1) Mesencephalic nucleus: (MeS for Muscle Spindle and Phalic for P-DaLic)
o Mediates proprioception (ex. Musclespindle) from the face
o Primary sensory neurons of mechanoreceptors in the PDL
o Cell bodies of the proprioceptive 1st order neurons are found in mesencephalic nucleus (not trigeminal ganglion)
o Mediates Jaw jerk reflex Only nucleus in the CNS that receives proprioceptive inputs from muscle
o Only example in which the primary sensory cell bodies
reside within the CNS instead of in ganglia
2) Main sensory nucleus: (The Main role of V is sensation)
o Discriminative touch of face
o Mediates general sensation (ex. Touch)
o **All sensory information from the face
fibers cross and
ascend in the ventral TTT (Trigeminalthalamic Tract) to the
From the rest of the body it goes to the VPL
3) Spinal trigeminal nucleus of V: (SPAINAL Spine pain/temp
in lateral cord)
o Mediates pain & temperature from head & neck (Oral Cavity)
o Mx bone fracture next to central incisornociception
terminates centrally in spinal subnucleus caudalis of V
o If the spinal tract of the fifth cranial nerve were sectioned at the level of the caudal medulla, PAIN from the face
would be most affected
o The primary sensory neurons' nucleus of termination for pain from a Mx M2 is the spinal nucleus of V
o The descending tract (down to the spinal nucleus) of V contains axons of primary sensory neurons
o Fibers then cross and ascend in the ventral TTT (trigeminothalamic) tract to the VPM as well
Sensory deficits
Loss of tactile, Proprioceptive, pain sensation, temperature, etc.
Motor deficits
From lower motor neuron involvement involving the muscles of mastication
Temporalis and masseter causes weak jaw closure
Pterygoid weak jaw opening
Abducens nucleus
Located in the lower pons, ventral to the floor of the fourth ventricle near the midline
Provides GSE to the lateral rectus muscle
Paralysis causes lateral rectus palsy, leading to medial deviation of the affected eye and diplopia
CN VII pg 97 H&N anatomy
Main Motor Nucleus
To all the muscles of facial expression
NOTE the upper face receives bilateral innervation BUT the lower face receives contralateral innervation
Superior Salivatory nucleus

Located posterolateral to the motor nucleus of VII

One group of fibers enters the superficial (greater) petrosal nerve and terminates in the ptergopalatine ganglion
Lacrimal glands
Another group of fibers travels in the chorda tympani nerve to reach the submandibular gangion
and Sublingual glands
Gustatory nucleus (Nucleus Solitarius) actually VII, IX, and X
Solitary tract gives rise to the geniculate ganglion
geniculate ganglion = sensory ganglion of 7 (?)
The rostral portion of the nucleus of the solitary tract receives all the SVA fibers for taste, which pass in the seventh,
ninth, and tenth CNs
The facial receives all the anterior 2/3rds of the tongue
The taste afferents in the facial nerve arise from cells in the geniculate gangion
Flaccid paralysis of muscle of facial expression (upper and lower face)
Loss of corneal reflex (efferent limb)
Hyperacusis (due to stapedius muscle) paralysis
Loss of taste from anterior 2/3rds means lesion is proximal to the sytlomastoid foramen since the chorda tympani
joins the facial nerve in the middle ear
Bells Palsy
o Lower motor neuron damage = ipsilateral problems
o *Facial nerve:
Lower Motor Neuron lesion:
Affects BOTH upper & lower face
Causes an IPSILATERAL flaccid paralysis of facial musculature
A pt has a lower facial paralysis, where is the damage facial nerve in the facial canal!!!
o NOT after it leaves the stylomastoid foramen
Hyperactive Spastic Paralysis
Hypoactive Fasciculations, Atrophy, Flaccid Paralysis (Like in ALS)
Upper Motor Neuron lesion:
Affects ONLY lower face (upper face has backup innervation)
Most commonly affects CONTRALATERAL face below the eyeball Can still wrinkle forehead
Rt sided lower face paralysis caused by Contralateral (left side) Cerebrocortical damage
Vestibular Nuclei
Sensory from the Crista ampullaris of the semicircular canals and the maculae of the utricle and saccule
Cochlear Nuclei:
Input from the Organ of Corti, Spiral Ganglion
Glossopharyngeal nuclei
SVE fibers from the rostral nucleus amibiguus and supply the stylopharyngeus muscle
GVA fibers to the nucleus solitarius and supply the baroreceptors of the carotid sinus you guessed it: Sinus Ninus!!!
SVA fibers carrying taste sensation from the posterior 1/3rd of the tongue and terminate in the nucleus Solitarius (aka
gustatory nucleus)
GSA Fibers supplying the posterior tongue and pharynx carry the sensory limb of the Gag reflex
o The motor limb of this reflex is carried by fibers from the nucleus ambiguous, which exits via the vagus nerve
o Lesion
Up CN IX results in unilateral ipsilateral loss of gag reflex
Down CN X results in bilateral loss of gag reflex
Inferior Salivatory
PARA-PRE nerve fibers to the Otic ganglion via Lesser petrosal nerve hitchhikes on V3 (auriculotemporal) to the
Parotid Gland
Main Motor Nucleus
(aka the vagal part of the nucleus ambiguous)
Located in the anterior portion of the reticular formation and extends throughout the medulla
Sends motor fibers through the
Dorsal Motor Nucleus
Located in the floor of the 4th ventricle and ventral to sulcus limitans
PARA=PRE fibers distributed to the PostG neurons supplying the viscera of the thorax and abdomen
Nucleus Solitarius (aka Gustatory nucleus) VII, IX, and X
GVA fibers from the larynx, esophagus, and baroreceptors in the aortic arch and visceral abdominal/thoracic viscera
SVA fibers from epiglottis taste buds (present in newborns)



Nucleus Ambiguus
Sends SVE fibers to larynx, pharynx all the XI via X crap
Weakness of the palate, loss of gag, and nasal speech occurs and possibly nasal regurgitation of food
Bilateral lesions of the vagus leads to paralysis of the pharynx and larynx death from asphyxiation
Paralysis of an ipsilateal vocal cord may occur, because the recurrent laryngeal nerve supplies all of the laryngeal
muscles, except the cricothyroid, which is supplied by the superior laryngeal nerve
In a nut shell
Nucleus solitarius = sensory (taste, gut distension, etc) VII, IX, X
Nucleus ambiguus = motor (pharynx, larynx, upper esophagus) IX, X, XI
o Dorsal motor nucleus (parasympathetic) (to heart, lungs, upper GI) X only
o From IX Carotid Sinus
o From X Aortic Arch
Each CN has a nucleus of its own name, EXCEPT:
o I/II/VIII special sense only
o IX/X these share nucleus ambiguous
o VII/IX/X share nucleus solitarius (aka gustatory nucleus)
o XI arises from cervical spinal cord only called a CN because it sneaks up & exits skull w/ IX & X
Spinal accessory nerve (not nucleus):
*Sends SVE fibers to SCM & trapezoid
XI via X explanation
o Cranial root fibers originate from the caudal nucleus ambiguous to supply the intrinsic muscles of the the larynx
o The fibers join CN X and finally reach the intrinsic laryngeal muscles through recurrent laryngeal nerve
Paralysis of the SCM (difficulty in turning head) and Trapezius (shoulder droop)
Hypoglossal Nucleus
Located near the midline below the floor of the 4th ventricle in the caudal medulla
GSE fibers to intrinsic muscles of the tongue, genioglossus, hyoglossus, and Styloglossus
Ipsilateral paralysis deviateion TOWARD
o UMN Unilateral Tongue weakness W/O atrophy
Bilaterally innervated upper, so NO atrophy
o LMN Unilateral Tongue weakness W/ atrophy
Anatomic Divisions of Nervous System
Brain & spinal cord
Control center of nervous system
Receives sensory input from PNS & formulates responses
12 pairs of cranial nerves
31 pairs of spinal nerves 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, & 1 coccygeal
Afferent division:
Somatic sensory neurons carry impulses from skin, fascia & joints
Visceral sensory neurons carry impulses from viscera of body (hunger pangs, BP)
Efferent division:
Somatic (voluntary) somatic motor neurons carry impulses to skeletal muscles
Autonomic (involuntary) visceral motor neurons transmit impulses to smooth & cardiac muscles & glands
o Sympathetic & Parasympathetic
o See next section
Autonomic Nervous System
o Innervation to organs not usually under voluntary control
o Cardiac muscle, smooth muscle, visceral organs/glands
o Preganglionic neurons
Cell bodies are in CNS
Synapse in autonomic ganglia
Parasymp originate in cranial nerves & craniosacral region
PreG PS fibers have their cell bodies in association w/ the nuclei of certain cranial nerves & in the anterolateral cell
column of the grey substance of S2-4, A for AL, as



Preganglionic PS nerve fibers to the urinary bladder have their cell bodies in the spinal cord at the S2,3,4 level
Symp originate in thoracolumbar (T1-L3) region
PreG S fibers to the head/neck have their cell bodies in the intermediolateral horns of the thoracic spinal cord
PostG S fibers to the head have their cell bodies in the cervical ganglia
Postganglionic neurons
Cell bodies in autonomic ganglia
Synapse on effector organs
Prepares body for intense physical activity in emergencies (fight or flight) through adrenergic effects
HR increases & blood glucose rises
Blood is diverted to skeletal muscles
Pupils & bronchioles dilate
Adrenal medulla releases Epi & NE
Preganglionic fibers
Release ACh
Carried by white rami
Postganglionic fibers
Release NE (except for BVs in skeletal muscles & sweat glands)
Carried by gray rami
***Synapse in paravertebral or prevertebral ganglia
Conserves energy (rest & digest)
Decrease HR
Papillary & bronchiolar constriction
No effect on adrenal medulla
Maintains normality of body functions
Preganglionic & postganglionic fibers release ACh
Synapses between neurons are made in autonomic ganglia
PS NS ganglia located in or near effector organs
Symp NS ganglia located in the paravertebral chain
NOTE: Most organs are innervated by both PS & Symp NS

Cranial Sutures
o Coronal Suture
Separates Frontal bone from BOTH Parietal Bones
o Sagittal Suture
Separates BOTH Parietal Bones
o Lambdoid Suture
Separates BOTH Parietal Bones from Occipital Bone
o Squamous Suture
Separates A Parietal Bone from the Temporal Bone


Anterior Cranial Fossa: I pg 54 Netters H&N anatomy

Cribriform plate (ethmoid) perforations
Located in ethmoid bone



Contains olfactory nerves (CN I)

Middle Cranial Fossa: II-VI
Optic Canal CN II, ophthalamic artery, central retinal vein
Superior Orbital Fissure CN III, IV, V1, VI, superior ophthalamic vein NOT ophthalamic artery
Between the slit light openings between lesser & greater wings of sphenoid bone
Foramen rotundum in sphenoid bone carries maxillary nerve (V2)
Inferior orbital fissure carries the maxillary nerve (V2) AFTER IT HAS EXITED THE BRAIN
Foramen ovale in sphenoid bone carries mandibular nerve (V3) & the lesser petrosal nerve and accessory meningeal
Think: for CN V, its Standing Room Only (S. R. O.)
Spinosum middle meningeal artery
Foramen spinosum in sphenoid bone carries middle meningeal artery & vein
Posterior Cranial Fossa: VII-XII
Internal Auditory Meatus CN VII, VIII
Canal running through petrous portion of the temporal bone
CN VII enters meatus & emerges from stylomastoid foramen between styloid & mastoid processes of temporal bone
o Gives off five branches in the parotid gland supplies motor innervation to muscles of facial expression
o Anesthetic in parotid (during Mn block) paralyzes muscles of facial expression
o Gives chorda tympani (VE para/pre) branch thru the petrotympanic fissure, Q reads through which opening does
parasymp fibers run through? petrotympanic
CN VIII enters meatus, then remains w/in temporal bone
o Nerve fibers to cochlear duct (hearing), semicircular ducts & maculae (balance)
Jugular Foramen CN IX, X, XI, internal jugular vein (Found in the Posterior Cranial Fossa)
Passage between the petrous potion of the temporal bone and the jugular process of the occipital
2007 Q Jugular foramen is NOT found in middle cranial fossa
Hypoglossal Canal CN XII
Foramen magnum in occipital bone contains medulla oblongata, vertebral arteries, & spinal accessory nerve,
Mandibular foramen:
Above the occlusal plane & posterior to the Mn molars
On medial surface of ramus just below the lingula, midway between the anterior & posterior borders of the ramus
Lateral to the medial pterygoid muscle
Leads into Mn canal which opens into mental foramen below PM2
NOTE: incisive canal a continuation of the Mn canal beyond the mental foramen & below incisor teeth
NOTE: lingula bony projection that serves as the attachment for the sphenomandibular ligament pg 259
Contains inferior alverolar nerve, artery & vein
IA nerve ends at mental foramen by dividing into:
o 1) mental nerve supplies skin & mucous MB of mental region
o 2) incisive branch supplies pulp chambers of anterior teeth & adacent mucous MB
Other foramina:
Carotid canal
Located in temporal bone
Contains internal carotid artery & sympathetic nerves (carotid plexus)
Nasolacrimal canal
Located in lacrimal bone/maxilla
Contains nasolacrimal duct
Foramen cecum in frontal & ethmoid bones contains emissary vein in fetal life
Sphenopalatine foramen sphenopalatine artery/vein & nasopalatine nerve 270 netters h&n
Pterygoid canal deep & greater petrosal nerves (these form the nerve of the pterygoid canal) 270 netters h&n
Carries parasymp and sympathetic fibers
Pterygomaxillary fissure PSA artery/vein/nerve & maxillary artery
Pterygopalatine canal greater & lesser palatine artery/vein/nerve
Pharyngeal canal pharyngeal branch of V2
Greater palatine foramen in the palatine carries greater palatine nerve, artery & vein
Lesser palatine foramen carries lesser palatine nerve artery & vein
Stylomastoid foramen in temporal bone carries facial nerve
Mental foramen in mandible carries mental nerve, artery & vein
Petrotympanic fissure in temporal bone carries chorda tympani & anterior tympanic artery
Q asked: Which of the following contain ParaSymp nerves (not spinosum, rotundum, ovale)
Fracture involving petrotympanic fissure would affect the chorda tympani
Foramen lacerum in temporal & sphenoid bones carries artery of the pterygoid canal, greater & deep petrosal
nerves (through the occluded cartilage)

Supraorbital foramen in frontal bone carries supraorbital nerve artery & vein
Infraorbital foramen in sphenoid & maxilla carries infraorbital nerve (V2), artery, & vein
Incisive foramen in maxilla carries nasopalatine nerve
CN Name
Site of exit from skull
Anterior Olfactory
Cribiform plate (ethmoid
Lateral Geniculate
Optic foramen
Superior orbital fissure


Mesencephalic, Main
Sensory, Spinal, and
Trigeminal Motor

Superior orbital fissure

V1 Ophthalmic
V2 Maxillary

Superior orbital fissure

Foramen rotundum

V3 Mandibular

Foramen ovale

Functions (M= motor; S = sensory)

S = smell
S = vision
M = levator palpebrae superioris, medial,
superior, inferior, inferior oblique, ciliary m. (lens),
sphincter m. (pupil)
M = superior oblique m.

Facial, Solitarius
(Gustatory), Salivatory
Vestibular, Cochlear
Ambiguus, Inferior
Salivatory, Solitarius

Superior orbital fissure

Internal auditory meatus


Ambiguus, Solitarius,
Dorsal Motor

Jugular foramen



Jugular foramen



Ambiguus, Spinal

S = cornea, skin of nose, forehead, scalp

S = nasal cavity, palate, Mx teeth, skin of cheek,
upper lip
S = tongue, Mn teeth, Mn, skin of chin, floor of
mouth, TMJ
M = mastication mm., tensors, anterior digastric, &
M = lateral rectus m.
S = taste (anterior 2/3)
M = facial expression mm., lacrimation, salivation
S = hearing, balance
M = stylopharyngeus muscle
S = taste (posterior 1/3), pharynx, middle ear,
carotid sinuses
M = muscles of pharynx & larynx
M = smooth m. of thoracic & abdominal organs
S = taste (epiglottis)
S = thoracic & abdominal organs (viscera)
M = trapezius m. & SCM m.

Hypoglossal canal

M = intrinsic & extrinsic tongue mm.





Internal auditory meatus

Jugular foramen


Parasympathetic Nuclei & Ganglia by Cranial Nerve

Pg 542 H&N anatomy
Edinger-Westphal N.
Ciliary G.
Pupillary sphincter m. meiosis
Ciliary m. accomodation
Superior Salivatory N.
Pterygopalatine G.
Lacrimal gland & nasal cavity/nose secretion
Submandibular G.
Submandibular & sublingual glands secretion
Inferior Salivatory N.
Otic G.
Parotid gland secretion
Dorsal Motor N. of Vagus
Viscera of thorax & abdomen


Lateral to optic n.


Pterygopalatine fossa

Cranial Nerve

Autonomic Ganglia PS & Symp fibers

PS Fibers
Symp Fibers
PreG: CN III (inferior division)
Internal carotid plexus
PostG: Short ciliary nn.
PreG: CN VII greater petrosal n.,
nerve of pterygoid canal
PostG: Branches of V2,then V1

Internal carotid plexus

Deep petrosal n.

Chief Distribution
Para Ciliary m. &
sphincter pupillae
Symp Dilator pupillae
& tarsal mm.
Lacrimal gland & glands
in palate & nose



On hyoglossus m.


Below foramen ovale

PreG: CN VII (Chorda tympani)

PostG: Lingual n.
PreG: CN IX & lesser petrosal n.
PostG: Auriculotemporal n.

Plexus on facial artery

Plexus on middle
meningeal artery

Submandibular &
sublingual glands
Parotid gland

- CN V, VII, IX, X are branchiomeric (nonsomitic) in origin because they originate from the branchial arches
- Olfactory (CN I)
o Exits Cribiform plate of ethmoid bone
o Enters nasal canal for smell
o Fracture of the cribiform plate typically results in loss of sense of smell
- Optic nerves (CN II) pg 82 netters h&n anatomy
o Arise from axons of the ganglion cells of the retina which converge at the optic disk
o Optic foramen (optic canal):
Area where nerve enters the cranial cavity through the sphenoid bone
o Optic disc (aka optic papilla):
Area where optic nerve exits eye
Made up of nerve cells
Small blind spot on surface of the retina no rods or cones
Located ~3mm to nasal side of the macula
Only part of retina which contains no photoreceptors
Optic tracts consists of axons from ganglion cells
Consists of axons of ganglion cells exiting the retina to form the optic nerve
The axons are accompanied by the central artery & vein of the retina
o After exiting eyes, optic nerves meet at the optic chiasm (in the floor of the
o From optic chiasm, axons that perceive the left visual field form the right optic tract &
Fibers that arise from the nasal hemiretinas decussate & contribute to the
contralateral optic tract
o Optic nerve fibers from the nasal side cross the midline and enter the optic tract of the
other side by way of the optic chiasma (SEE PIC)
Optic tract fibers synapse in the lateral geniculate nuclei w/ geniculocalcarine
fibers (optic radiations) that terminate on the banks of the calcarine sulcus in the
primary visual cortex (Brodmanns area 17) of the occipital lobe
So, the right visual field is interpreted in the left hemisphere of the brain & vice versa
o Central artery of the retina (branch of ophthalmic artery), pierces the optic nerve & gains access to the retina by
emerging from the center of the optic disc
o If the retina were to detach this would decrease the length of the optic center and therefore the patient would be?
- Oculomotor nerve (CN III)
o Supplies: medial, superior, & inferior recti; inferior oblique; & levator palpebrae superiori
A deficit in the inferior oblique muscles can be revealed by asking the patient to elevate the adducted eye
This is the only muscle the elevates the eye from an adducted position. Sup rectus elevates it from an abducted position
o Post gang fibers leave the ganglion in the short ciliary nerves to supply the sphincter pupillae & the ciliary muscle
- Oculomotor nerve (CN III), trochlear nerve (CN IV) & abducens nerve (CN VI) and ophthalmic (V div 1) all exit the cranium through
the superior orbital fissure. They innervate the extrinsic ocular muscles, resulting in movement of the eyeball
- Trochlear nerve (CN IV):
o Supplies the superior oblique muscle Smallest nerve, supplies weirdest eye muscle, only one to exit from the back
o Smallest cranial nerve
o Only cranial nerve that emerges from dorsal aspect of the brainstem
- Trigeminal nerve (CN V):
o Exits inferolateral PONS as a sensory & motor root
o Largest of 12 cranial nerves
o Larger sensory root enters the trigeminal (semilunar, gasserian) ganglion in the middle cranial foss, Embeds in Meckels CAVE
o Three sensory divisions of the nerve arise from the ganglion & leave the cranial cavity through foramina in the sphenoid bone
o Smaller motor root passes under the ganglion & joins the mandibular division as it exists through the foramen ovale
- Semilunar ganglion (aka trigeminal or gasserian ganglion)
o Large, flattened, sensory ganglion of the trigeminal nerve
o Lies close to cavernous sinus in the middle cranial fossa
o Ophthalmic division (V1):
Enters orbit through superior orbital fissure


Sensory innervation to eyeball, tip of nose, skin on face above eyes

Three branches: lacrimal, frontal, & nasociliary
o Maxillary division (V2): pg 87
Passes through foramen rotundum
Sensory innervation to midface (below eyes & above upper lip), palate, paranasal sinuses, & maxillary teeth
o Mandibular division (V3): pg 90
Exits cranial cavity through foramen ovale
Motor innervation to tensor veli palatine, tensor tympani, muscles of mastication, and anterior belly of digastric &
Has no ParaSymp component at its origin:
Sensory innervation to:
Skin on Lower face, skin of mandible, lower lip & side of the head
TMJ (Auriculotemporal (main one), and Masseteric (V3) and Posterior Deep Temporal), mandibular teeth, mucous
MBs of cheek, floor of mouth, & anterior part of the tongue
Lingual nerve branch of V3:
Descends deep to lateral pterygoid muscle, where it is joined by chorda tympani (branch of CN VII) which conveys
pregang PS fibers to submandibular ganglion & taste fibers from anterior 2/3 of tongue
Supplies general sensation for anterior 2/3 of tongue, floor of mouth, & mandibular lingual gingiva
Submandibular duct has an intimate relation to the lingual nerve, which crosses it twice
Is directly on the lateral surface of the medial pterygoid muscle
If you cut lingual nerve after its junction w/ chorda tympani, pt loses taste & tactile sense to anterior 2/3 of tongue
In the pterygomandibular space where is lingual nerve in relation to inf alveolar n.?
Anterior and Medial
Nerve to Masseter:
Passes through mandibular notch to enter muscle on medial surface
Also a branch of V3
Carries a few sensory fibers to the anterior portion of the TMJ
Anterior portion of TMJ also supplied by branches of the posterior deep temporal nerve (branch of V3)
Auriculotemporal nerve:
Arises from posterior division of V3
Provides posterior sensory innervation to TMJ
o Pain (TMJ pt) is transmitted in the capsule & periphery of the disk by the auriculotemporal nerve
Pain from a fractured mandible
The joint only sends sensory information it does not receive motor innervation (the muscles do, duh!)
Carries some secretory fibers from the otic ganglion to the parotid gland (from CN IX)
Referred pain from the TMJ to skin over the parotid region & side of head is based on the distribution of the
auriculotemporal n.
o Innervated by: (Think PAM pic (From the office she has strong Jaw/TMJ))
Posterior deep temporal nerve (anterior portion) V3
Auriculotemporal (Primary) V3
Nerve to the masseter (anterior portion) V3
CN III, VII, IX use branches of CN V to distribute their preganglionic PS to the PS head ganglia
Abducens (CN VI):
o Supplies the lateral rectus of the eye
o NOT found within the walls of the cavernous sinus (III, IV, V1, and V2 are)
3,4,5 in the cave.
o Injury to abducens means what? Cant abduct eye
Facial nerve (CN VII): pg 97
o Contains sensory neurons that originate from taste buds on anterior 2/3 of tongue
The cell bodies are located in the geniculate ganglion, which lie in the facial canal, in the inner ear
o Associated with the second pharyngeal arch
o Innervates the facial muscles w/ motor fibers
o Supplies the Mimetic muscles (LIKE a MIME, facial expression)
o Lacrimal gland & salivary glands w/ PS fibers
o Anterior tongue w/ sensory fibers
o Originates in the pons
o Traverses the facial canal of the temporal bone & exits the stylomastoid foramen
o Also contains PS fibers to sublingual & submandibular glands (via submandibular ganglion)
o Facial nerve function:
Motor innervation:
Muscles of facial expression



Posterior belly of digastric muscle & stylohyoid muscle after CN VII emerges from stylomastoid foramen
Stapedius muscle w/in the middle ear
Damage just after it left stylomastoid foramen would cause loss of innervation to facial muscles (orbicularis oculi m.)
Which structure innervates the orbicularis oculi? Temporal and zygomatic branches of CN VII
Sensory: proprioceptive innervation: from the same muscles listed for motor innervation
Secretomotor: PS innervation. Secretion of tears from the lacrimal gland & salivation from the sublingual & submandibular
Special sensory: taste impulses (sweet sensation) from the taste
buds on the anterior 2/3 of tongue, floor of mouth, & palate
o Bells Palsy
Damage to the facial nerve or its branches may cause weakness
or paralysis of facial muscles
Peripheral ipsilateral facial paralysis
Inability to close eye on affected side
Complete destruction of the facial nucleus itself OR its
branchial efferent fibers (facial nerve proper) paralyzes all
ipsilateral facial muscles
Upper motor neuron
Can wrinkle forehead (Inability to
smile he can still wrinkle forehead because upper face gets
innervation from the BOTH sides of the brain (See Pic)
Lower motor neuron lesion (i.e. Facial Nucleus Destruction)
Complete facial paralysis (Inability to smile OR wrinkle
PS innervation controlling salivation originate in facial
& glossopharyngeal nerves
o Emerges from a small canal in posterior wall of
tympanic cavity & crosses medial surface of
tympanic MB
o Joins lingual nerve in the infratemporal fossa
Geniculate ganglion:
o Located w/in the facial canal (petrous portion of
temporal bones)
o Contains sensory neurons via chorda tympani of CN
VII (innervates taste buds on anterior 2/3 of tongue)
o Greater petrosal nerve:
Parasymp secretomotor branch of CN VII and
general visceral afferent fibers
No sympathetic fibers or general somatic
Also described as the parasympathetic root of
the pterygopalatine ganglion
Arises from the geniculate ganglion
Carries PS preG fibers to pterygopalatine ganglion
Exits cranial cavity through foramen lacerum
Enters pterygoid canal after joining w/ deep petrosal nerve to form the nerve of the pterygoid canal
o Deep petrosal nerve is carrying postG S from the superior cervical ganglion
o Both form the nerve of the pterygoid canal (Vidians)
In pterygopalatine fossa, the nerve of the pterygoid canal terminates in the pterygopalatine ganglion
PS pre-ganglionics from greater petrosal nerve synapse w/ post-ganglionics here
S (already post-ganglionics) just pass on through the ganglion w/out synapsing
Post-ganglionic autonomics distributed to lacrimal gland & glands of mucous MB of nasal cavity, pharynx, & palate
Also transmits taste centrally from palate through palatine nerves
These taste fibers also necessarily pass through the pterygopalatine ganglion & nerve of the pterygoid canal to
reach the greater petrosal nerve on their way to the tractus & nucleus solitarius in the pons
o Lesser petrosal nerve:
Pregang PS to the otic ganglion
parotid gland (via auriculotemporal nerve V3)
NOTE: the postG PS cell bodies to the parotid gland are found in the otic ganglion
Stimulation of lesser petrosal nerve causes secretion by parotid gland
Tympanic & lesser petrosal branches of CN IX supply preganglionic PS secretomotor fibers to the otic ganglion
o Preganglionic fibers leave CN IX as the tympanic nerve (SEE MIDDLE PIC)

Tympanic nerve enters middle ear cavity & participates in formation of the tympanic plexus (on the medial
Wall), where chorda tympani runs from posterior wall across lateral wall (aka medial surface of Tympanic MB)
o It reforms as the lesser petrosal nerve, leaves cranial cavity through foramen ovale, & enters otic ganglion
Diminshed salivary gland production from the parotid due to MIDDLE EAR damage has most likely affected the Lesser
Petrosal Nerve (NOT the auriculotemporal)
Glossopharyngeal nerve (CN IX):
o Originates from anterior surface of the medulla oblongata along w/ CN X & CN XI
o Passes laterally in posterior cranial fossa & leaves skull through the jugular foramen
o Splits the Superior and Middle Constrictors to enter the oral cavity
o Supplies sensation (including pain) to pharynx & posterior 1/3 of tongue
o Innervates derivatives of the 3rd branchial arch
o Innervates stylopharyngeus muscle (the only muscle supplied by CN IX)
Landmark for locating CN IX as CN IX enters pharyngeal wall, it curves posterior around the lateral margin of the
o Cell bodies of these sensory neurons are located in Superior & Inferior ganglia of this nerve pg 102
Cell bodies of pain fibers in CN IX are found in the superior ganglion of CN IX Pain no good, but its SUPERIOR in 9
o Descends through upper part of neck along w/ internal jugular vein & internal carotid artery
Reaches posterior border of the stylopharyngeus muscle supplies it w/ somatic motor fibers
o Caries 1 afferent neurons that cause the gag reflex (innervates mucous MBs of the fauces)
o ***NOTE: CN III, VII, IX, & X all carry pre-gang PS fibers
o Visceral sensory branches of CN IX:
Lingual branch of CN IX
Terminal branch of CN IX to posterior 1/3 of tongue conveying general sensation & taste to circumvallate
Also carries some secretomotor fibers to the glands
Distributed to mucous MB of the pharynx sensory limb of the gag reflex
Carotid sinus nerve
To carotid sinus (baroreceptor) & carotid body (chemoreceptor)
o Remember Sinus gets it from IX, but the whole BODY gets it from IX and X, aortic arch only from X
Otic ganglion:
o Pregang PS cell bodies originate in the Inferior Salivatory nucleus
o Small PS ganglion, functionally associated w/ CN IX
o Situated below foramen ovale; medial to V3
o Tympanic & lesser petrosal branches of CN IX supply preganglionic PS secretomotor fibers to the otic ganglion
Preganglionic fibers leave CN IX as the tympanic nerve
Tympanic nerve enters middle ear cavity & participates in formation of the tympanic plexus
It reforms as the lesser petrosal nerve, leaves cranial cavity through foramen ovale, & enters otic ganglion
o Postgang PS fibers leave the ganglion & join the auriculotemporal nervejump off at the parotid gland
Vagus Nerve (CN X):
o Leaves brain from medulla & exits cranial cavity through jugular foramen
o Contains PS pre-ganglionic fibers to thoracic & abdominal viscera
o Descends in neck in the carotid sheath behind the internal & common carotid arteries & internal jugular vein
o Both R & L Vay-Goose trunks pass through posterior mediastinum on the esophagus & enter abdominal cavity w/ the esophagus
o In the lower thorax, the esophageal branches of the right vagus branches are found mainly on the posterior esophagus
Just make the right hand turn on the wheel the left vagus goes to the anterior
o Supplies viscera of neck, thorax, & abdomen to the left colic (splenic) flexure of large intestine
Abdominal viscera below left colic flexure, & pelvis & genitalia supplied w/ pregang
PS fibers from pelvic splanchinc nerves
o Vasomotor sympathetic fibers are thought to end on BVs
o Possesses Two Sensory Ganglia:
Superior ganglion (lies on nerve w/in jugular foramen)
Meningeal supplies dura mater
Auricular supplies auricle, external auditory meatus
Inferior ganglion (lies on nerve just below the jugular foramen) pg 104
o Forms pharyngeal plexus
o Supplies:
Pharyngeal muscles, except stylopharyngeus (CN IX)
Soft palate muscles, except tensor veli palati (V3)
Superior laryngeal, divides into:


1) Internal laryngeal travels w/ superior laryngeal artery & pierces thyrohyoid MB Can see both artery and nere
piercing the MB in the pic to the right
Supplies mucous MB of larynx above vocal folds
o 2) External laryngeal travels w/ superior thyroid artery & supplies cricothyroid muscle In pic going to
cricothryoid muscle
Sensory Portion of CN X:
Somatic sensory fibers to skin of the ear
Cell bodies in the superior ganglion of CN X (somatic sensory nucleus)
Axons enter spinal tract & nucleus of CN V
Visceral sensory fibers to pharynx, larynx, & thoracic & abdominal viscera to the left colic flexure (hunger pangs)
Cell bodies in inferior ganglion of CN X (visceral sensory nucleus)
Axons enter tractus & nucleus solitarius
Visceral sensory fibers to epiglottis (taste)
Cell bodies in inferior ganglion
Axons enter tractus & nucleus solitarius
Motor Portion of CN X:
Branchiomeric motor fibers to skeletal muscle derived from visceral arch muscle in larynx, upper esophagus & pharynx
Cell bodies of these motor neurons are in nucleus ambiguus Think that its ambiguous whether or not they are from
Visceral motor fibers to smooth muscles & glands of the organs of the neck, thorax, & abdomen
These are the PS preganglionic fibers w/ cell bodies in dorsal motor nucleus of vagus
o One Q asked about the preG PS fibers of the duodenum these are found in the dorsal motor nucleus of
Left vagus nerve:
Enters thorax in front of the left subclavain artery & behind the left brachiocephalic vein So between L. SCA and BCV!
Then crosses left side of the aortic arch (pic) & is itself crossed by the left phrenic nerve (R and L phrenic nerves in pic)
Then passes behind the left lung (bottom pic to right), forms the pulmonary plexus
(pic), & continues to form the esophageal plexus
Enters abdomen in front of the esophagus through the esophageal hiatus of the diaphragm
as the anterior vagal trunk
Right vagus nerve:
Crosses anterior surface of the right subclavian artery & enters thorax
posterolateral to the brachiocephalic trunk, lateral to the trachea, & medial (& just
posterior) to the azygos vein
Passes posterior to root of the lung (pic), contributing to the pulmonary plexus
Contributes to the esophageal plexus
Enters abdomen behind the esophagus through the esophageal hiatus of the diaphragm as
the posterior vagal trunk (At T10)
R&L vagus nerves lose their identity in the esophageal plexus
At lower end of the esophagus, branches of the plexus reunite to form the anterior vagal
trunk (anterior gastric nerve)
Anterior vagal trunk can be cut (vagotomy) to reduce gastric secretion
Right recurrent laryngeal nerve pg 123
Arises from right vagus nerve in neck
Hooks around subclavian artery (pics) & passes up/backwards behind artery & ascends in groove
between trachea & esophagus (tracheoesophageal groove)
All muscles of the larynx (except cricothyroid supplied by external laryngeal branch of superior
laryngeal nerve)
o The external laryngeal brach runs with superior thyroid artery to the cricothyroid
Mucous MB of larynx below the vocal folds
Mucous MB of upper part of the trachea
Comes in contact w/ thyroid gland & comes into close relationship w/ inferior
thyroid artery
Left recurrent laryngeal nerve
Crosses arch of the aorta, hooks around ligamentum arteriosum (PIC), &
ascends in groove between trachea & esophagus
Arises from left vagus
Same muscles as right recurrent, but on left side
A few cardiac branches arise from CN X & enter cardiac plexus


When BP goes up, then these branches increase firing

These are pre-gang PS nerves
Innervate heart mucle & conducting system (SA node, etc.)
Accessory Nerve (CN X1):
o Innervation to the SCM and Trapezius
Hypoglossal Nerve (CN XII):
o Motor nerve supplying all intrinsic & extrinsic muscles of the tongue (except palatoglossus CN X and Genioglossus C1 via XII)
o Leaves skull through hypoglossal canal medial to carotid canal & jugular foramen
o Passes above hyoid bone on the lateral surface of hyoglossus muscle deep to the mylohyoid muscle (Between Hyoglossus and
o Landmark Loops around occipital artery & passes between the external carotid artery & internal jugular vein
o Soon after it leaves the skull through the hypoglossal canal. it is joined by C1 fibers from cervical plexus
TO then supply Genioglossus, Geniohyoid, Thyrohyoid
o Unilateral lesions result in deviation of protruded tongue toward the affected side due to lack of function on diseased side
o Injury of CN XII eventually produces paralysis & atrophy of tongue on affected side w/ tongue deviated to the affected side
Dysarthria (inability to articulate) may also be found
IF tongue protrudes to left when you stick it out then Left Genioglossus is not
o NOTE: if genioglossus muscle is paralyzed, tongue has tendency to fall back & obstruct
oropharyngeal airway suffocation risk

PICTURE TO RIGHT: CNXII descending from inbetween external carotid and internal
jugular vein (and looping around occipital artery). Travels from carotid to
submandibular triangle of neck. Located in classical position just at inferior border of
posterior digastric. Gives off C1 to innervate thyrohyoid. Then dives into oral cavity
between hyoglossus and mylohyoid muscles.
- Cranial Nerve lesions:
o CN V (motor) jaw deviates TOWARD side of lesion
o CN X uvula deviates AWAY from side of lesion ODDBALL ALERT.
o CN XI head turns TOWARD side of lesion
o CN XII tongue deviates TOWARD side of lesion
- Sympathetic ganglia:
o Sympathetic trunks two long chains of symp ganglia on either side of vertebral column that extend from base of skull to coccyx
Damage to the sympathetic trunk causes Horners Syndrome
Horners = (drooping eyelid- loss of tarsal muscle innervation, flushing skin on affected side loss of constriction,
loss of sweating on affected side, no dilation of pupil on affected side)
Lie close to vertebral column & end below by joining to form a single ganglion the ganglion impar (unpaired)
Sympathetic ganglia are located at intervals on each sympathetic trunk alongside vertebral column
Generally there are 3 cervical, 12 thoracic, 4 lumbar, & 4 sacral
Gray rami connect sympathetic trunk to every spinal nerve
White rami are limited to the spinal cord segments between T1 & L2
Cell bodies of visceral efferent fibers (in visceral branches of the sympathetic trunk) located in lateral horn of spinal cord
Cell bodies of visceral afferent fibers located in dorsal root ganglia
o Sympathetic nerves arise from thoracic sympathetic ganglia (T5-T12) they all pass through diaphragm
o PreG Symp fibers may pass through ganglia on thoracic part of sympathetic trunk w/out synapsing
These myelinated fibers form the splanchnic nerves:
Greater symp fibers from T5-T9 pierce diaphragm & synapse w/ excitor cells in the ganglia of celiac plexus
o Nerves consist primarily of preganglionic visceral efferent fibers
o The thoracic splanchnic nerves to the celiac ganglion consist predominantly of preG visceral efferents
o PostG fibers arise from excitor cells in celiac plexus & are distributed to smooth muscle & glands of viscera
o Travels just posterior to the azygos vein
Lesser symp fibers from T10-T11 pierce diaphragm & synapse w/ excitor cells in aorticorenal ganglion
Least symp fibers from T12 pierce diaphragm & synapse w/ excitor cells in ganglia of the aorticorenal plexus
The fibers from the thoracic splanchnics (T5-12) and the lumbar splanchnics synapse largely in 3 ganglia:
1) Celiac ganglion
2) Superior Mesenteric ganglion
3) Inferior Mesenteric ganglion
o Some nerve fibers go even more inferior to the superior hypogastric plexus to provide sympathetic innervation to the
pelvic viscera
o NOTE: PS innervation of the upper 2/3 of the abdominal viscera comes via the vagus nerve which goes through the celiac plexus
w/o synapsing like the sympathetics do


The remaining inferior portions come by way of the parasympathetics from S2, S3, S4 via pelvic splanchnics
Cervical Ganglia:
Sympathetic innervation to head & neck structures is distributed via the blood vessels (NOT CN III, VII, IX, X)
Superior cervical ganglion
Uppermost & largest lies between internal carotid artery & internal jugular vein
Most of postG sympathetic fibers that go to head region have their cell bodies located here
o EX: The postG sympathetic fibers to the vessels of the SbMn gland arise from cells in the superior cervical ganglion
o This is where the preG and postG sympathetic fibers of the cervical region synapse
o Cell bodies of sympathetic fibers in the nerve of the pterygoid canal come from the superior cervical ganglion
o Postganglionic symp cell bodies that provide innervation to the submandibular gland is located in superior cervical
Some fibers go to the upper 3 to 4 cervical nerves
Middle cervical ganglion
Fibers to the cervical nerves C5 & C6
Small, located at level of cricoid cartilage
Related to the loop of the inferior thyroid artery
Inferior cervical ganglion
Fibers to spinal nerves C7, C8, & T1
Most commonly fused to first thoracic sympathetic ganglion to form a stellate ganglion
Cervical plexus:
o Cervical nerves C1-C4 contribute motor fibers to plexus
o Motor nerves are branches of ansa cervicalis (loop formed by C1-C3)
o Positioned deep on side of the neck, lateral to the 1st four cervical vertebrae
o An important branch of each cervical plexus is the phrenic nerve (C3-C5) supplies diaphragm
o Provides cutaneous innervation to skin of the neck, shoulder & upper anterior chest
Supraclavicular nerves innervate skin over the shoulder
Transverse cervical nerve provides sensory innervation to anterior/lateral parts of the neck
o Provides motor innervation to infrahyoid (strap) muscles (except for the thyrohyoidC1 via XII & to the geniohyoid muscle)

Gives rise to the first 2 of 3 roots contributing to the phrenic nerve that innervates the diaphragm (C3, 4, 5)

The Brachial
Plexus: Structure


5 roots
3 trunks
6 divisions
3 cords
5 terminal branches



Brachial plexus (C5-T1)

o Formed in posterior triangle of the neck
o Extends into axilla, supplying nerves to the upper limb
o Axillary sheath contains the Cords of the brachial plexus and the axillary artery and vein2 (NOT subclavian artery???)
Sheet music contains Cords
o Think Robert Taylor Drinks Cold Beer
o Roots Trunks Divisions Cords Branches
(Question: What is terminal portion of brachial plexus called?)
o 5 Roots
o 3 Trunks:


Superior C 5,6
Middle C 7
Inferior C8, T1
Each splits into anterior and posterior division
3 Cords:
Lateral C5,6,7 From Superior and Middle Roots
Lateral pectoral nerve C5,6,7
Musculocutaneous nerve C 5,6,7
**Median nerve (forms from the medial & lateral cords) C5-T1
Posterior C5,6,7,8,T1 From All 3 Roots
Gives off Axillary nerve C5,6
Radial nerves C5-T1


Medial (C8, T1) From Inferior

Medial pectoral nerve C8,T1
Ulnar nerve C8,T1 ulnar nerve is a terminal brach of the medial cord
o Ulnar nerve is most sensitive at the elbow (not wrist, hands) think funny bone
**Median nerve (forms from the medial & lateral cords) C5-T1
o Brachial artery runs adjacent to and parallel with the median nerve in the arm
Think from Back to front to Medial ARMMU
**Arm & Forearm Flexors
Musculocutaneous biceps, brachialis,
coracobrachialis mm.
Median forearm flexors, thenar mm., radial
Ulnar Ulnar flexors, adductor pollicis,
hypothenar mm., interossei, lumbricals 4-5
**Arm & Forearm Extensors (posterior of the
Radial both arm & forearm extensors
o (triceps, brachioradialis, supinator, extensors
of wrist/fingers)
Thenar muscles:
Opponens pollicis, Abductor pollicis brevis,
Flexor pollicis brevis
Innervated by the median nerve (dont get
clowned by the radial nerve)
Numbness of Forefinger and thumb caused by
damage to the Median nerve
Hypothenar muscles: (all are ____ digiti minimi)
One Half LOAF
One and half Lumbricals,
Opponens d.m., Abductor d.m., Flexor d.m.
Innervated by Ulnar nerve
The lateral two lumbricals are also innervated by the
median nerve
The rest of the intrinsic muscles of the hand are
innervated by the ulnar nerve (i.e. interosseoi)

Lumbar plexus: L1-L4

o Formed in psoas muscle
o Supplies lower abdomen & parts of the lower limb
o Main branches are the femoral & obturator nerves
Sacral plexus: L4-L5 & S1-S4
o Lies in posterior pelvic wall in front of piriformis muscle
o Supplies lower back, pelvic, & parts of thigh, leg, & foot
o Main branches are the sciatic (largest nerve in body),
gluteal, & pelvic splanchnic nerves


o Area of skin supplied by a single spinal nerve
o *Supplied by either cranial or spinal nerves
o Cranial nerves
All 3 divisions of CN V supply the skin of face, anterior scalp (V1) & ear (V3)
The ear receives additional innervation from CN VII, IX, & X
All but one of the spinal nerves anterior & posterior primary divisions innervate the remaining dermatomes of the body
The greater occipital nerve (C2) supplies posterior scalp because C1 usually does not supply a dermatome
No overlapping innervation of cranial dermatomes
o Spinal (peripheral) nerve innervation of the skin (cutaneous innervation):
Usually differs from cranial nerve skin innervation because ventral primary divisions of spinal nerves form plexuses
Allows multiple spinal nerves to constitute a peripheral nerve
o EX: C5-C7 form the musculocutaenous nerve
Spinal nerve dermatomes overlap 50%
Must anesthetize T4-T6 to block feeling in T5 dermatome
Functional Components of Nerves
Spinal Nerves
***Only contain 4 of 7 functional components (just the General, not Special components)
GVE smooth muscle, cardiac muscle, glands
PreG S: C8L2 w/ cell bodies located in the intermediolateral nucleus
PreG PS: S2S4 w/ cell bodies located lamina VII (analagous to the intermediolateral nucleus)
GSE skeletal muscle arise from alpha & gamma motor neurons of lamina IX (anterior horn)
Afferent (all arise from DRGs)
GVA sensory info from the viscers (although technically not a part of the ANS)
GSA exteroceptive & proprioceptive sensation
Exteroceptive touch, pain, temp
Proprioceptive joints, muscle, tendons, fascia
Cranial Nerves
GSA see above
*SSA Vision, Hearing & Equilibrium
GVA see above
*SVA Olfaction & Taste (Southern Virginia is OuT there!!!)
Special visceral afferent fibers for taste are conveyed in VII, IX, & X
GSE skeletal muscle from myotomes
GVE PreG PS (no Symp): CN III, VII, IX, X
*SVE (Brachial Arches)
CN V mastication from motor nucleus of V
CN VII facial expression from facial nucleus
CN IX & X larynx, pharynx from nucleus ambiguus
CN XI trapezoid (lift shoulders), SCM
(turn head)
The ENTIRE Cranial Nerve MAP
CN I (Olfactory Nerve)
Special Visceral Afferent
Enter/exit cribriform plate
Conveys information from olfactory epithelium
CN II (Optic Nerve)
Special Somatic Afferent (Special Visceral Afferent
according to Moore pg. 644)
Enter/exit optic canal
Conveys information from retina
CN III (Occulomotor Nerve)
Part 1 - General Somatic Efferent


Enter/exit superior orbital fissure within annulus tendinus

Superior Division
Innervates superior rectus muscle
Innervates levator palpebrae superioris muscle
Inferior Division
Innervates inferior rectus muscle
Innervates medial rectus muscle
Innervates inferior oblique muscle
Part 2 General Visceral Efferent (PARASYMPATHETIC PART)
Carries preganglionic parasympathetic fibers along inferior division to ciliary ganglion
Fibers synapse in ciliary ganglion
Short ciliary nerves carry postganglionic parasympathetic fibers from ciliary ganglion to innervate sphincter of pupil and
ciliaris muscle
Ciliary ganglion also carries 1) postganglionic sympathetic fibers along short ciliary nerves to blood vessels of eyeball and
the tarsals, 2) Afferent fibers from nasociliary nerve (CN5 V1)
CN IV (Trochlear Nerve)
General Somatic Efferent
Enter/exit superior orbital fissure
Innervates superior oblique muscle
CN V (Trigeminal Nerve)
Exits the PONS
V1 (Opthalmic Nerve)
General Somatic Afferent
Enter/exit superior orbital fissure
Sensory nerve with 3 main branches
Frontal Nerve (Branch 1)
Enter/exit superior orbital fissure above annulus

Nerves of the Orbit:

V1 Branches

orbital n.

trochlear n.

nasociliary n.

Summary of CN V1 branches:
Lacrimal Nerve
Frontal Nerve
Supraorbital N.
Supratrochlear N.
Nasociliary Nerve
Long Ciliary Ns.
Posterior Ethmoidal N.
Anterior Ethmoidal N.
Infratrochlear N.

ciliary ns.

Main Menu

trochlear n.
ethmoid n.
ethmoid n.

lacrimal n.
frontal n.

Supraorbital Nerve
Exit supraorbital foramen
Innervates frontal sinus, conjunctiva
upper eyelid, skin of forehead
Supratrochlear Nerve
Exit on medial side of supraorbital nerve
Innervates skin in middle of forehead to hairline


Frontal Nerve cut here

Nasociliary Nerve (Branch 2) Seen beautifully in bottom of two pics

Enter/exit superior orbital fissure within annulus tendinus

pg 89 H&N

Infratrochlear Nerve
Exits of medial wall of orbit above upper eyelid
Innervates skin and conjunctiva of upper eyelid
Anterior Ethmoid Nerve
Courses w/ anterior ethmoid artery (ophthalmic artery) through anterior
ethmoid foramen
Innervates anterior ethmoid sinuses and anterosuperior part of nasal mucosa on both septum and lateral wall of
nasal cavity
Terminal branch is External Nasal Nerve, innervates skin on dorsum and tip of nose
Posterior Ethmoid Nerve
Courses w/ posterior ethmoid artery (ophthalmic artery) through posterior ethmoid foramen
Innervates posterior ethmoid sinuses and sphenoid sinuses


Long Ciliary Nerves (2)

Innervates (sensory to) iris, cornea, and ciliary body
Carry postganglionic sympathetic fibers to the dilator of the pupil
Sensory Root to Ciliary Ganglion
Sensory fibers to eyeball from nasociliary nerve pass through ciliary ganglion and course w/ short ciliary nerves
(CN 3)
Lacrimal Nerve (Branch 3) Seen great in both pics
Enter/exit superior orbital fissure above annulus tendinus
Gland is in the outer lateral side
Courses forward in lateral part of orbit to the lacrimal gland
Carries postganglionic parasympathetic fibers (secretomotor) from pterygopalatine ganglion via zygomaticotemporal
nerve (CN5 V2) from greater petrosal nerve (CN7)
[CN V1 via CN V2 via CN7]
Carries postganglionic sympathetic fibers (vasoconstrictive) from pterygopalatine ganglion via zygomaticotemproal
nerve (CN5 V2) from deep petrosal nerve (Superior Cervical Ganglion)
[CN V1 via CN V2 via Superior Cervical Ganglion]
V2 (Maxillary Nerve)
General Somatic Afferent
Enter/exit foramen rotundum then runs anterolaterally through pterygopalatine fossa
If anesthesia was injected into the pterygopalatine fossa, then V2 would be anesthetized
Within fossa gives rise to 3 branches:
Zygomatic Nerve (Branch 1) (below and on left) pg 92 Netters H&N anatomy
Arises in floor of orbit through inferior orbital fissure
Innervates skin over zygomatic arch and anterior temporal region
Best described as sensory branches of maxillary division of V
Gives rise to 2 terminal braches:
Zygomaticofacial Nerve
Exit zygomaticofacial foramen
Zygomaticotemporal Nerve
Exit zygomaticotemporal foramen
Carries postganglionic parasympathetic fibers (secretomotor) to lacrimal nerve (CN5 V1) from pterygopalatine
ganglion via zygomaticotemporal nerve (CN5 V2) from greater petrosal nerve (CN7)
[CN5 V1 via CN5 V2 via CN7]
Carries postganglionic sympathetic fibers (vasoconstrictive) to lacrimal nerve (CN5 V1) from pterygopalatine
ganglion via zygomaticotemporal nerve (CN5 V2) from deep petrosal nerve (Superior Cervical Ganglion)
[CN5 V1 via CN5 V2 via Superior Cervical Ganglion]
Other V2 Branches: Zygomatic Nerve


zygomatotemporal n.
The zygomatic nerve arises
from V2 in the pterygopalatine
fossa. It divides into 2
branches: the zygomaticofacial
nerve and zygomatical
temporal nerve.

zygomatofacial n.

Main Menu

Pterygopalatine Ganglion:
Branches & Related Ns.

superior nasal ns.


nasopalatine n.
( not depicted )

petrosal n.

zygomatic n.

petrosal n.
palatine n.
palatine n.


Ganglionic Branches (2) Supporting Pterygopalatine Ganglion (Branch 2 and 3) (above and right)
Convey general sensory fibers from maxillary nerve that pass through ganglion
(Note: all the braches of the pterygopalatine ganglion are mixed nerves with General Somatic Afferent fibers from the
maxillary nerve, and General Visceral Efferent fibers from the nerve of the pterygoid canal [see below])
Pterygopalatine ganglion gives off numerous braches:
Greater Palatine Nerve
Innervates gingivae, mucous membranes, glands of hard palate
Lesser Palatine Nerve
Innervates gingivae, mucous membranes, glands of soft palate
Nasopalatine Nerve (not depicted)
Courses through sphenopalatine foramen along posterior half nasal septum (along with the Sphenopalatine artery)
NOTE: The spenopalatine foramen is the hole on the MEDIAL wall of the pterygopalatine fossa
In other words it is the direct connection with the nasal region and the Ganglion region of V2
Innervates mucosa in this region then dives down through incisive canal
Innervates mucous membranes and gland of anterior part of hard palate
Nerve of the Pterygoid Canal (aka Vidians Nerve)
General Visceral Efferent
Carries preganglionic parasympathetic fibers from CN7 via greater petrosal nerve, these are secretomotor to mucosa
and glands and synapse in ganglion
Carries postganglionic sympathetic fibers from Superior Cervical Ganglion via deep petrosal nerve, these are
vasoconstrictive to mucosa and glands, do not synapse
Posterior Superior Lateral Nasal Nerve
Innervates mucosa on superior half of lateral wall of nasal septum
Posterior Inferior Lateral Nasal Nerve
Innervates mucosa on inferior half of lateral wall of nasal septum
Maxillary nerve then leaves pterygopalatine fossa through inferior orbital fissure
Henceforth it is known as the Infraorbital nerve (CAREFUL, youre still in bones)
Infraorbital nerve (continuation of V2 once zygomatic and branches to ganglion given off.)
It then gives rise to 3 large sensory branches:
Innervates the upper lip
Posterior Superior Alveolar Nerve
Sensory innervation to maxillary molars
Doesnt get MB of M1
Middle Superior Alveolar Nerve
Sensory innervation to maxillary molars and premolars
Anterior Superior Alveolar Nerve
Sensory innervation to premolars, a branch dives through the incisive canal and emerges as the Incisive Nerve to supply
the maxillary canines and incisors
(Note: nasopalatine nerve also courses through incisive canal)
Maxillary Nerve then continues along floor or orbit through infraorbital sulcus
It dives down through the infraorbital canal and emerges through the infraorbital foramen and serves to innervate
(sensory to) the skin of the cheek, lower lip, lateral side of nose and upper lip
Superior labial branches (skin over cheek and upper lip)
V3 (Mandibular Nerve)
Mixed nerve w/ General Somatic Afferent (sensory) and Special Visceral Efferent fibers (motor)
Enter/exit foramen ovale and enters infratemporal fossa
Divides into anterior and posterior trunks


Anterior trunk gives rise to:

Long Buccal Nerve
Innervates skin and mucosa of the cheek, vestibule, and buccal gingiva adjacent to 2nd and 3rd molars
Pain from Swelling of the gingiva would be transmitted via the Buccal nerve
Branches to Four of the Muscles of Mastication
Motor nerve to Masseter, Temporalis, Medial Pterygoid, Lateral Pterygoid muscles
Branches to Additional Muscles (not sure if these branches from anterior trunk)
Motor nerve to anterior belly of the digastric (accessory muscle of mastication), tensor veli palatini, tensor tympani, and the
(Note: muscles of mastication and innervation derived from 1st pharyngeal gill arch)
Posterior trunk gives rise to:
Auriculotemporal Nerve
Passes between neck of mandible and external acoustic
Innervates skin anterior to ear and posterior temporal
Pain from fractured mandible
Carries postganglionic PS fibers (secretomotor) from
otic ganglion to the parotid salivary gland, these general
visceral efferent fibers come to the otic ganglion via the
lesser petrosal nerve (preganglionic parasympathethic)
from CN 9 (see below)
Marker: middle meningeal artery passes between
branches that make up auriculotemporal nerve
Inferior Alveolar Nerve
Enters mandibular foramen
Sensory innervation to mandibular teeth

V3 (Mandibular) Division:

deep temporal ns.

auriculotemporal n.


inferior alveolar n.
The V3 Branches are the
Trunk Branches:
1. meningeal br. (not depicted)
2. m. pterygoid n.
Anterior Division Branches:
3. masseteric n.
4. deep temporal ns.
mylohyoid n.
5. lateral pterygoid n.
6. long buccal n.
Posterior Division Branches:
lingual n.
7. auriculotemporal n.
8. lingual n.
9. inferior alveolar n.
submandibular gland
a. mylohyoid n.

Mental Nerve
Terminal branch of mandibular nerve
Exits through mental foramen
Innervates skin of chin, lower lip, mucosa of lower lip
Pt with dentures has caused pain in the inner vestibule or something



long buccal n.

which nerve was irritated


Nerve of the Mylohyoid

Runs along the mylohyoid groove
Motor nerve to Mylohyoid muscle (accessory muscle of mastication)
Lingual Nerve
Enters mouth between medial pterygoid and ramus of mandible inferior to 3 rd molar
Sensory innervation to anterior 2/3 of the tongue, floor of the mouth, lingual gingiva
Carries Special Visceral Afferent fibers via Chorda Tympani:
Chorda Tympani
Special Visceral Afferen(taste), General Visceral Efferent (salivary gland)
Branch of CN VII, passes through middle ear over tympanic membrane
Joins lingual nerve in infratemporal fossa
Carries taste fibers to anterior 2/3 of the tongue
Carries preganglionic parasympathetic fibers (secretomotor) to submandibular ganglion for the submandibular and
sublingual salivary glands
CN VI (Abducens Nerve)
General Somatic Efferent
Enter/exit superior orbital fissure
Innervates lateral rectus muscle


What muscles Abducts the eye? Abducens Lateral rectus

Paralysis of lateral rectus muscle causes interference with?

Abduction of the eye

CN VII (Facial Nerve)

Motor and sensory nerve, see Moore pgs. 658-660
Supplies the Mimetic muscles (muscles of facial expression) Remember, the MIME.
Consists of two roots
Smaller root has taste (Special Visceral Afferent), parasympathetic (General Visceral Efferent) and sensory (General Somatic
Afferent) fibers
Larger root carries motor fibers to muscles from 2nd pharyngeal arch (Special Visceral Efferent)
Nerve enters internal acoustic meatus
Within facial canal it gives rise to:
Greater Petrosal Nerve
(General Visceral Efferent)
Carries preganglionic parasympathetic fibers to pterygopalatine ganglion
Joins the deep petrosal nerve as it passes through cartilage of foramen lacerum
(Note: These two nerves form the nerve of the pterygoid canal)
After synapse, postganglionic parasympathetic fibers
innervate lacrimal gland (See Above), and mucous
CN VII: Nervus
Intermedius VE Fibers
glands of nasal cavity, palate, upper pharynx
Nerve to Stapedius (not pictured)
(Special Visceral Efferent)
Innervates stapedius muscle in middle ear
Prevents excess movement of the stapes
Chorda Tympani Nerve
Passes through middle ear over tympanic membrane
Joins lingual nerve in infratemporal fossa
Carries taste fibers to anterior 2/3 of the tongue
(Special Visceral Afferent)
Carries preganglionic parasympathetic fibers
(secretomotor) to submandibular ganglion for the
submandibular and sublingual salivary glands
(General Visceral Efferent)
(Note: Sensory fibers (General Somatic Afferent) to
concha of auricle of external ear arise here)



Main Menu

greater petrosal n.


tympani n.
motor root
The nervus intermedius:
VE-para/pre fibers to the
pterygopalatine ganglion (via
the greater petrosal n.) and
submandibular ganglion (via
the chorda tympani). Also
Motor root: SVE to
stapedius, muscles of facial
expression, stylohyoid


muscles of facial

Larger motor root (Special Visceral Efferent) exits stylomastoid foramen

Gives off motor braches to occipitalis and auricular muscles (via Posterior Auricular Branch)
Gives off motor branches to posterior belly of the digastric and stylohyoid muscles
Pierces parotid gland
Gives off five terminal motor branches to muscles of facial expression: (TZBMC)
Two Zebras Broke My Coccyx
Temporal Branch
Zygomatic Branch
Buccal Branch
Mandibular Branch
Cervical Branch
CN VIII (Vestibulocochlear Nerve)
Special Somatic Afferent
Enter/exit internal acoustic meatus
Conveys equilibrium, balance (Vestibular fibers) and hearing (Cochlear fibers) information from inner ear
CN IX (Glossopharyngeal Nerve)
Motor (General Visceral Efferent and Special Visceral Efferent) and sensory (General Somatic Afferent and Special Visceral
Afferent) nerve,
From Inferior Salivatory Nucleus
Goes to tympanic plexus as tympanic nerve, then turns into lesser petrosal nerve (carrying Pregang PS to the otic ganglion,
which then sends Postgang PS to the parotid via the auriculotemporal (V3)


Enter/exit jugular foramen

Gives off two small branches:
Tympanic Nerve
Courses through middle ear
Forms tympanic plexus on promontory of middle ear
Provides sensory innervation (General Somatic Afferent) to the internal surface of the tympanic membrane
Clogged ears from pressure on the auditory tubes is sensed via CN IX (dont get clowned by vestibulocochlear)
Reforms as the lesser petrosal nerve
Carries preganglionic parasympathetic fibers (General Visceral Efferent) to the otic ganglion to supply the parotid gland via
the auriculotemporal nerve (CN5V3) (See Above)
Carotid Branch
Special Visceral Afferent
Provides baroreceptor innervation to the carotid sinus One more time SINUS NINUS!!!
Follows and gives motor innervation (Special Visceral Efferent) to Stylopharyngeus muscle (derived from 3rd pharyngeal arch)
Gives of Pharyngeal Branch to Pharyngeal Plexus of nerves (CN9 and CN10), this gives sensory innervation (General Somatic
Afferent) to the oropharynx
Passes b/w superior and middle constrictor muscles to reach oropharynx
Gives of two branches in oral cavity:
Tonsilar Branch
General Somatic Afferent
Provides sensory innervation to the palatine tonsil
Lingual Branch
Provides general sensory innervation (General Somatic Afferent) to posterior third of tongue
Provides taste fibers (Special Visceral Afferent) to posterior third of tongue
CN10 (Vagus Nerve)
Motor and sensory nerve,
Enter/exit jugular foramen
Joins with cranial root of CN11
Enters carotid sheath and continues to root of the neck
Gives off multiple branches:
Pharyngeal Branch
Innervation to pharyngeal constrictor muscles (Special Visceral Efferent), except cricopharyngeus, and pharyngeal
longitudinal muscles, except stylopharyngeus (Note: pharyngeal muscles derived form 4th through 6th pharyngeal arches)
Provides general sensory innervation (General Somatic Afferent) to laryngopharynx
(Note: motor innervation is really cranial root CN11 via CN10)
Superior Laryngeal Nerve
Divides into two terminal nerves:
Internal Laryngeal Nerve
Sensory (General Somatic Afferent) to root of tongue to vocal folds
Carries preganglionic parasympathetic (General Visceral Efferent) to mucous membrane in same area
External Laryngeal Nerve
Motor innervation (Special Visceral Efferent) to the cricothyroid muscle (ONLY laryngeal m. not done by
Recurrent Laryngeal Nerves
Sensory (General Somatic Afferent) and parasympathetic (General Visceral Efferent) to laryngeal mucous membrane from
vocal folds down
Motor innervation (Special Visceral Efferent) to muscles of larynx and cricopharyngeus muscle, Except Cricothyroid
Cardiac Branches
Provides sensory (General Visceral Afferent) and preganglionic parasympathetic fibers to heart
Passes through superior thoracic aperture into thorax


Provides sensory (General Visceral Afferent) and preganglionic parasympathetic (General Visceral Efferent) innervation to
organs of thorax
Passes through esophageal hiatus as anterior and posterior vagal trunks
Provides sensory (General Visceral Afferent) and preganglionic parasympathetic (General Visceral Efferent) innervation or
organs of abdomen as far as left colic flexure
CN11 (Accessory Nerve)
Enter/exit jugular foramen
Motor nerve with many branches, see Moore pgs. 666-667
CN12 (Hypoglossal Nerve)
Enter/exit hypoglossal canal
Motor nerve with many branches, see Moore pgs. 667-669
CNs involved in swallowing:
V3, IX, X, XI, XII
A review of the principle body cavities:
Posterior (dorsal) cavity
Cranial cavity contains brain
Spinal cavity contains spinal cord
The two cavities communicate through foramen magnum
The cavities are lined by meninges
Anterior (ventral) cavity
Thoracic cavity:
Pericardial cavity surrounds heart
Pleural cavity (R & L) each surrounds a lung
The portion between the two pleural cavities is called the mediastinum (the heart & pericardial cavity are located
Abdominal cavity:
Abdominal cavity contains the stomach, spleen, liver, gallbladder, pancreas, and small/large intestines
Pelvic cavity contains the rectum and urinary bladder
In the male, also the paried ductus deferens & seminal vesicle and prostate gland
In the female, also the paired ovaries & the uterus
Superior mediastinum:
Aortic arch w/ its branches, R & L brachiocephalic veins, upper of SVC, trachea, esophagus, thoracic duct, thymus,
phrenic nerve, vagus nerve, cardiac nerve, & left recurrent laryngeal nerve
Inferior mediastinum: (T4 to T12)
1) Anterior mediastinum
Part of the thymus gland
Some lymph nodes
Branches of the internal thoracic artery
2) Middle mediastinum
Pericardium & Heart
Phrenic nerves & its accompanying vessels
Parietal Pericardium forms a boundary
3) Posterior mediastinum
Think of the 4 birds in the back of the thoracic cage:
Va-goose, Esopha-goose, Azy-goose, & Thoracic duck
Descending (thoracic) aorta
Thoracic duct
Azygos system of veins (including hemiazygos vein)
Vagus nerves on the esophagus
Splanchnic nerves
Many lymph nodes
Sympathetic chain ganglia (sympathetic trunks)
NOT phrenic nerves
Cross Section at T8 of the Posterior Mediastinum


From Back to Front

Azygos vein
Thoracic duct (off-center to right)
Thoracic duct anterior to vertebrae. As it ascends, it has azygous vein to right, and aorta to left.
Descending aorta (off-center to left)
Vagus Nerve around esophagus
Trachea (but here its already bisected into bronchi)
HEART general info:
Size of a closed fist
Located in the middle mediastinum
Two thirds of hearts mass is to the left of body midline
The developing Heart is anterior to the notochord (It delineates the posterior part of the heart..
Surrounded by the Pericardium
Inner is the Visceral Pericardium (epicardium)
Outer is the Parietal Pericardium
Visceral and parietal pericardia are continuous at the veins & arteries entering & leaving the heart
Serous fluid fills in between to minimized friction went the heart beats
Close relation laterally to the phrenic nerves (which innervate the parietal pericardium)
The apex fits into a depression in the diaphragm
Chambers of the Heart
2 Atria
Separated by thin, muscular interatrial septum
Fossa Ovalis
Shallow depression
Site of foramen ovale in the fetus, which permitted blood flow from atrium to atrium, bypassing pulm circ.
The foramen eventually becomes closed with fibrous CT and becomes fossa
Valve of foramen ovale lies in the medial wall of the left atrium
Anulis ovalis forms the upper margin of the fossa
2 Ventricles
Separated by thick, muscular interventricular septum
Apex of the heart located at level of the 5th intercostal space (left)
Enlarge due to coarctation (constriction) from the aorta
Left ventricle is thicker
Layers of the heart:
Internal endocardium:
Homologous with the tunica intima of the blood vessles
Lines the surface with simple squamous endothelium and underlying loose CT with small blood vessels
Homologous to the tunica media
Bulk of heart mass with cardiac muscle cells arranged in the spiral configuration
Allows heart to wring blood from the ventricles toward aortic and semilunar valves
Right and left coronary arteries supply myocardium, come from ascending aorta
Epicardium or pericardium:
Serous membrane
Externally, it is covered by simple squamous epithelium supported by thin layer of CT
The adipose tissue that surrounds the heart accumulates in this layer
Cardiac muscle:
Makes up myocardium
Intercalated discs to form a functional network
DOES NOT contract voluntarily
Fibers are separate cellular units, which dont contain many nuclei
Respond to increase demands by increasing fiber size (compensatory hypertrophy)
Pectinate muscles: The woven muscles on flapped R. Atrial wall
Located on the inner surface of the right atrium
They are prominent ridges of atrial myocardium in right atrium and both auricles
(which are small conical pouches projecting from the upper anterior portion of
each atrium)
Crista terminalis: The Ridge that the pectinate muscles are coming from


Vertical muscular ridge that runs along the right atrial wall from the opening of the SVC to the IVC.
Provides origin of the pectinate muscle.
Represents junction btw the sinus venosus and the heart in the developing embryo
The line of junction between the primitive sinus venosus and the auricle
Also represented on the external surface of heart by the vertical groove called the sulcus terminalis
NOTE: There is also a Sulcus Terminalis in the tongue!
SA node is located in the crista terminalis near opening of SVC
Papillary muscles:
Cone-shaped muscles that terminate in tendinous cords (chordae tendineae that attach to the cusps of the AV valves)
Papillary muscles do not help the valves to close
Help prevent the cusps from being everted or blown out into the atrium during ventricular contraction
Chordae tendinae do the same thing
Sinus Venarum (Can see in pic)
Smooth portion of the right atrium
Develops from embryonic sinus venosus
Receives blood from sup. and inf. vena cavae, coronary sinus, and anterior cardiac veins
Separated from muscular portion by the Crista terminalis
Septomarginal Trabecula
Band of trabeculae carneae connect the interventricular septum to the base of the anterior papillary muscle
Contraction of this muscle prevents over distention of the ventricle
Interventricular Septum
Largely muscular, except for superior aspect, which is a small membranous portion that is common site for
ventricular septal defects
Ligamentum Arteriosum
Remanants of Ductus Arteriosum (fetal bypass of pulm. circ)
Connects Aortic arch to Pulmonary Veins
Left Recurrent Laryngeal hooks around it
Valves: (TPMA Tee Pee My Ass)
best heard over the right half of the lower end of the body of the sternum
Anterior, Septal, Posterior cusps
valve best heard over the second left intercostal space, just lateral to sternum
NO chordae tendinae or papillary muscles
Anterior, Right, and Left Semilunar cusps
More Anterior than Aortic Valve (Remember that because it has an Anterior Cusp, where Aortic has Posterior)
Mitral valve (bicuspid)
best heard over apex of heart, (Left 5th intercostal space at the mid clavicular line)
Only valve of the 4 that has 2 cusps
Posterior and Anterior Cusps
Aortic valve
best heard over the second right intercostal space, just lateral to the sternum
NO chordae tendinae or papillary muscles
Left, Right, and Posterior Semilunar cusps
Blood Flow
The cardiac veins lie superficial to the arteries
These all empty into the right atrium:
Coronary sinus
Largest venous pathway
Opens into the right atrium
Most of the cardiac veins empty here, except for anterior cardiac veins, which empty directly into the right
Superior Vena Cava
Opens into the upper part of the right atrium
Returns blood from upper half of the body
Inferior Vena Cava
Larger than Superior VC
Opens into the lower part of the right atrium
Blood from lower half
Anterior Cardiac Veins THINK ARTRIA Cardiac VEIN
Empty direct into R atrium


Then blood goes through the Tricuspid valve into the R ventricle then through Pulmonary valve and goes to pulmonary
Blood gas exchange occurs and is return to heart via pulmonary veins
Increased resistance to pulmonary blood flow in
the lungs would cause a strain on the right
Enters left atrium, passes through Mitral valve to left
ventricle, and out the aortic valve to the rest of the
After entering the aorta, immediately the blood can
leave the aorta through the right and left coronary
arteries, sending blood right back to the heart
This does NOT happen during contraction of
left ventricle
Coronary arteries fill during diastole
Obstruction of either artery can lead to anoxia to
the heart, resulting in MI, spasms, or death
The small and middle cardiac veins return blood
from the myocardial capillaries to the Coronary
Small comes from right
Middle from back
The anterior interventricular (AKA the L.A.D.)
artery accompanies the great cardiac vein
The posterior interventricular artery accompanies the
middle cardiac vein
**Thrombosis in coronary sinus might cause
dilation in small, great, oblique, and middle
cardiac veins, but NOT THE ANTERIOR cardiac
Anterior cardiac vein drains directly into the right atrium whereas all others drain into the coronary sinus.
Impulse-conducting system of heart:
Consists of specialized cardiac muscle (which contain modified cardiac muscle fibers) present in the SA node, the AV node, and
the Bundle of His (including the Purkinje fibers)
Fibers capable of depolarizing more rapidly than regular fibers, but are weakly contracting
The Sinoatrial node (SA node):
Located in the crista terminalis at the junction of the superior vena cava and the right auricle. Its the most rapidly
depolarizing (Pacemaker)
Depolarizes spontaneously at 70 to 80 per minute
The conduction system of heart is all modified cardiac muscle fibers and NOT NERVES
Innervation to the heart is by what???
the Vagus nerve and sympathetic nerves
SA Node Atria AV Node AV Bundle Purkinje fibers
Parasympathetic fibers from the vagus slow the heart where the sympathetic fibers from the sympathetic trunk speed up the
heart beat
Usually (60% of the time) the SA Node receives blood supply from the right coronary artery (AV node supplied by RCA, too)
Pericardial sac
With heart removed, look for the Transverse pericardial sinus (under the pulmonary trunk)
Also oblique pericardial sinus, is a col-de-sac behind the heart
The Respiratory System:
Has two major partsa branching, tree-like set of hollow tubes (the conducting airways) and very thin-walled pouches (the
alveoli) at the ends of these tubes
Cartilaginous rings found in the main bronchi
Left lung has a smaller capacity than the right
BC that is where the heart is, less lung space
Alveoli form the functional unit of the lung
Assists in vocalization and olfaction
Consists of the nasal cavity , pharynx, larynx, trachea, and the bronchi, bronchioles, and alveoli within the lungs
Developed from an outpocketing of the gut tube (so did liver, pancreas, & gallbladder not spleen)
Pair of resp organs that lie within the thoracic cavity and are separated by the mediastinum


Each lung is shaped like a cone

It has a blunt apex, a concave base (that sits on the diaphragm), a convex costal surface, and a concave mediastinal surface
At the middle of the mediastinal surface, the hilum is located
Which is a depression in which the bronchi, vessels, and nerves that form the root enter and leave the lung.
The small bronchial arteries also enter the hilum of each lung and deliver oxygen rich blood to the tissues
They tend to follow the bronchial tree to the respiratory bronchioles where they anastomose with the pulmonary vessels
Branches of the vagus nerve also pass the hilum of each lung
Innervation is by what???
the Vagus nerve and sympathetic chain ganglia nerves
Right lung:
Has 3 lobes (superior, middle, and inferior) and three secondary (lobar) bronchi
Contains ten bronchial segments (tertiary bronchi)
Usually receives one bronchial artery
Slightly larger capacity than the left lung
More common to aspirate foreign bodies into the Right lung (less acute angle)
Left Lung:
Has 2 lobes (superior and inferior) and two secondary (lobar) bronchi separated by an oblique fissure
Two lobes because the heart takes up too much space for a third lobe
Contains eight bronchial segments (tertiary bronchi)
Contains a cardiac notch on its superior lobe
VERY ODD Usually receives two bronchial arteries (Where Right only gets 1, eventhough 3 lobes)
Contains a lingulaa tongue-shaped portion of its superior lobe that corresponds to the middle lobe of the right lung.
A stab wound creating a pneumothorax on the left side would result in the collapse of the left lung only(Not pericardial sac)
Pulmonary Veins usually anterior and inferior
Pulmonary Arteries are then Anterosuperior
Brochus usually most posterior
Structure of the Lung:
Each lung is enclosed in a double-layers sac called the pleura
One layer is called the visceral pleura, the other is called the parietal pleura
Between the two layers is the pleural cavity, which is filled with serous fluid
Root of the lung major structures found therein:
1) Primary bronchusarise from trachea and carry air to the hilum
Part of the conducting division of the respiratory system = pulmonary conduction system
2) Pulmonary arteryenters the hilum of each lung carrying oxygen poor blood
3) Pulmonary veinssuperior and inferior pair for each lung leave the hilum carrying oxygen rich blood
Top to Bottom:
Tube that begins below the cricoid cartilage (C6) of larynx and splits at the level of the sternal angle (T5) [about the same
level where the trachea passes behind the aortic arch] where it divides at the carina into primary bronchi (right and left
primary or mainstem bronchus, which lead to each lung and are part of the pulmonary conduction system
Two main bronchi branches divide into five lobar bronchi (secondary bronchi):
Right main bronchus divides into three lobar bronchi
Straighter, shorter, and larger than the left primary bronchus
It is also in a more direct line with the trachea (important in dental chair because if patient swallows an object it
tends to lodge in the right bronchus)
Left main bronchus divides into two lobar bronchi
Each secondary or lobar bronchus serves one of the five lobes of the two lungs
Secondary bronchi branch into tertiary bronchi (segmental bronchi) which continue to divide deeper in the lungs
into tiny bronchioles, which subdivide many times, forming terminal bronchioles
Each of these terminal bronchioles gives rise to several respiratory bronchioles
Each respiratory bronchiole subdivides into several alveolar ducts, which end in clusters of small, thinwalled air sacs called alveoli
These alveoli open into a common chamber called alveolar sac, which forms the lungs functional unit
Differs from a bronchiole by possessing cartilage plates & pseudostratified columnar epi
Main support provided by Hyaline Cartilage
Characterized by:
Diameter < 1mm
Epithelium that progresses from ciliated pseudostratified columnar to simple cuboidal (respiratory bronchioles)
Small bronchioles have non-ciliated bronchiolar epithelial cells (Clara cells) that secrete GAGs that protect the lining
No glands, no hyalinecartilage, no lymphatic nodules


Smaller diameter prevents them from collapsing at end of expiration

Scattered goblet cells
Abundant smooth muscle to regulate the bronchiolar diameter
Variation of the size of the lumen of the bronchiole during inspiration and expiration is caused primarily by smooth
muscle and elastic fibers
Contraction is from parasymp stimulation
*Conduction bronchioles
Smaller extensions of bronchi (little bronchi)
Those devoid of alveoli in their walls are nearer the hilum of the lung
*Terminal bronchioles
Lined by low columnar epithelium
*Respiratory bronchioles
Continues to progress to low simple cuboidal
Continuing from terminal bronchioles, branch nearer the alveolar ducts and sacs and have occasionally alveoli in their walls
These bronchioles capable of respiring are the first generation of passageways of the respiratory portion of the bronchial tree
As air passes from the trachea into the lungs, the respiratory bronchiole is the 1st structure in which gaseous exchange through
the wall of an alveolus may occur
In proceeding from the bronchus to the respiratory bronchiole, there is a decrease in cartilage and an increase in
elastic fibers
In proceeding from the trachea to a respiratory bronchiole, the following structural changes occur:
Decrease in goblet cells, decrease in ciliated cells, total loss of cartilage from the walls
Not a progressive change from stratified squamous to cuboidal epithelial lining (from Columnar to cuboidal)
As you go down respiratory tract what is the last thing to go
Smooth muscle??? See physio book
Type I Pneumocyte
Account for 97% of alveolar lining
Extremely thin (as thin as 25 nm)
Provide minimal barrier to facilitate diffusion of gas
Type II Pneumocyte (GREAT cells)
Account for 3% of alveolar surface
Produce/secrete surfactant (a lecithin)
Phosphlipid-containing substance that reduces surface tension
Pharynx (throat) tube
Serves as passageway for respiratory and digestive tracts. Extends from mouth and nasal cavities to the larynx and esophagus.
Has three regions:
The Nasopharynx: Internal Structures
Main menu
Contains the eustachian canal (connects the nasopharynx to
The nasopharynx is posterior to
the apertures of the nasal cavities
middle ear), salpingopharygeal fold, pharyngeal recess, &
and above the soft palate. Most
pharyngeal tonsils (called adenoids when inflamed), (not
superiorly it contains the
pharyngeal tonsil: a large
piriform recess) Which is on either side of epiglottis
collection of lymphoid tissue.
tube opening
Lies above the soft palate and is continuous with the nasal
On each lateral wall we see:
Opening of the auditory tube
Torus tubarius: bulge on the
Lies directly behind the nasal cavities or choanae
pharyngeal wall formed by the
The pharyngeal tonsils may become inflamed & block
rim of the auditory tube opening
Salpingopharyngeal fold:
salpingothe choanae, causing pt to becoe a mouth breather
mucosal elevations and folds
post. to the opening of the tube.
The tensor veli palatine and the levator veli palatine
Pharyngeal recess: a deep area
muscles prevent food from entering the nasopharynx
posterior to the torus tubarius
and the salpingopharyngeal fold.
The uvular muscle does, too, but it wasnt an answer
The Oropharynx: Internal Structures
Main menu
soft palate
The oropharynx is posterior to
the oral cavity, inferior to the soft
soft palate
palate and above the epiglottis.
Extends from the plane passing through the anterior pillars
The anterior wall is the posterior
to the beginnings of the laryngopharynx
third of the tongue, containing
the lingual tonsil: a large
It communicates with the oral cavity through the isthmus
collection of lymphoid tissue.
of the fauces
On each lateral wall we see:
Oral part of the Pharynx communicates directly with the
Palatoglossal arch: boundary
between the oral cavity and the
Nasopharynx and the Laryngopharynx
fossa (with
the palatine
Receives food from mouth and air from nasopharynx
Palatopharyngeal arch:
posterior and medial to the
Contains palatine and lingual tonsils
palatoglossal arch;
pharyngeal anterior 2/3
Between the soft palate and the epiglottis
Palatine tonsil: a large
collection of lymphoid tissue
Laryngopharynx (also hypopharynx):


in the tonsillar fossa or bed.

Visible through the oral cavity.

posterior 1/3



Extends from the oropharynx (tip of the epiglottis and inferior)

The SUBGLOTTIS receives sensory innervation from the Superior Laryngeal Nerve
Serves as a passageway for food and air
Air entering the laryngopharynx goes to the larynx while food goes to the esophagus
Food entering the larynx would be expelled by violent coughing
Food moves from oropharynx , prompting soft palate to rise and seal off the nasopharynx.
Epiglottis bends downward while the laryngeal apparatus moves upward, closing off the laryngeal inlet (Aditus)
Bolus of food cascades around the epiglottis and passes through the piriform fossae (recesses) on either side to enter the
We swallow 2000 times a day
Mostly done during the daytime, NOT eating
What makes up the nose? Medial and lateral nasal processes
Air enters through nostrils (external nares) lead to the vestibules of the nose
The bony roof of the nasal cavity is formed by the cribiform plate of the ethmoid bone
The lateral walls have bony projections called conchae that form shelves which have spaces beneath them called meatuses
The paranasal sinuses
(maxillary, frontal, ethmoidal, and sphenoidal) drain into the nasal cavity by way of these meatuses
The nasal bone does NOT contain paranasal sinuses
Maxillary is the Largest Paranasal sinus
NOTE: Sphenoidal sinus doesnt drain into any of the meatuses
The nasolacrimal ductdrains tears from surface of eyes, also empties into the nasal cavity by way of the inferior meatus
The floor is formed by the hard palate
Nasal cavity & oral cavity are connected by the incisive foramen??? (other options: gr. pal. & less. pal)
The nasal cavity opens posteriorly into the nasopharynx via a funnel-like opening called the choanae (posterior nares)
Vestibules are lined with nonkeratinized stratified squamous epithelium
Conchae of the nasal fossae and the sinuses are lined with pseudostratified ciliated columnar epithelium
The cell of the maxillary sinus is pseudostratified ciliated columnar epithelium
The specialized columnar epithelium is very prominent in the upper medial portion of the nasal cavity
The nasal cavity receives sensory innervation from the olfactory nerve for smell and from the trigeminal nerve for other
Nasal cavities lined with specialized columnar epithelium (called olfactory epithelium)
Blood supply is from the branches of the ophthalmic and maxillary arteries
Emergency tracheotomy:
Tracheotomy allows for air to pass between the lungs and the outside air
Done in the cricothyroid space (between thyroid and cricoid cartilages) or through the median cricothyroid ligament
Most easily made by an incision through the median cricoid cartilage to the thyroid cartilage and is inferior to the space between
the vocal cords (rima glottides) where aspirated objects usually get lodged
If you cut below the cricoid cartilage you will damage the trachea
What type of epithelium is covering the vocal folds???
Upper vocal folds (FALSE folds)
Lower vocal folds (TRUE folds)
Nonkeratinized stratified squamous
Organs of the Female Reproductive System
Are almond-shaped organs located on either side of the uterus, but vary with age.
Round, smooth, and pink at birth
Grow larger, flatten and turn grayish by puberty
During childbearing years take on almond shape and rough, pitted surface
After menopause, they shrink and turn white
Produce ova and steroid hormones:
Estrogenstimulates the development of the female sex organs, the breast, and various secondary sexual characteristics
Progesteronestimulates secretion of uterine milk by the uterine endometrial glands; also promote development of the
secretory apparatus of the breasts
Purpose of ovaries is to produce mature ova
Oogoniaserve as source of oocytes
1 oocytes begin meiosis I during fetal life & complete meiosis I just prior to ovulation
During the in between year, meiosis I is arrested in prophase
Meiosis II is arrested in METaphase until fertilization (until the egg has MET a sperm)


Just prior to ovulation the preovulatory follicle produces and secretes large amounts of Estrogen
Primordal folliclescontaining oocytes in their sexually mature ovary are stimulated to develop by secretion of FSH from the
anterior lobe of the pituitary
Primary follicles (in first meiotic division) become secondary follicles with the formation of the antrum (cavity)
Fully mature Graafian follicles containing secondary oocytes (in second meiotic division) release the egg into the abdominal
cavity under the influence of LH to be swept into the ostium of the Fallopian tube (uterine tube, oviduct) to be fertilized and
subsequently implanted in the uterus or discarded if not fertilized
During maturation of the egg, four daughter cells are produced, one of which is the large fertilizable ovum, while the others
are small, rudimentary ova known as polar bodies or polocytes.
Zona pellucida is associated with a oocyte in a mature follicle
Atretric Follicles
A follicle that degenerates before coming to maturity; great numbers of such atretic follicles occur in the ovary before
puberty; in the sexually mature woman, several are formed each month
Corpus luteum
Endocrine body that secretes progesterone and is formed in the ovary at the site of a ruptured ovarian (Graafian) follicle
immediately after ovulation.
If pregnancy does not occur, the corpus luteum regresses to a mass of scar tissue (corpus albicans) which eventually disappears.
If pregnancy does occurcorpus luteum persists for several months until the placenta matures enough to produce the hormones
Develops directly from the cells remaining in the remnants of the preovulatory follicle after ovulation
In the ovary:
Progesterone production is primarily by the corpora lutea
Uterine/Fallopian Tubes
Convey secondary oocyte toward the uterus
Site of fertilization
Convey developing embryo to uterus
The uterine cavity is roughly triangular in shape and compressed in an anteroposteriorly
Site of implantation
Blastocyst usually occurs in the upper portion of the uterine cavity
Protects and sustains life of embryo and fetus during pregnancy
Active role in parturition
What initiates menstruation? decreased estrogen and progesterone
Round ligament of the uterus normally found in the inguinal canal of the female.
It is a fibromusuclar band attached to the uterus on either side in front of and below the openings of the fallopian tube. It
passes through the inguinal canal to the labia majora
Convoys uterine secretions to outside of the body
Receives erect penis and semen during coitus and ejaculation
Passage for fetus during parturition
Path of menstrual flow to outside
Mammary Glands
Produces and secretes milk for nourishment of an infant
Lie in the superficial fascia
Are actually a modified sweat gland
Contain myoepithelial cells (aka basket cells) (star-shaped)have processes that spiral around some of the secretory cells
of these glands
Contraction forces the secretion of the glands toward the ducts
Located in the spaces between the basement membrane and secretory cell!!!!!
The breast receives arterial blood through branches of the lateral thoracic (branch of the axillary artery) and internal thoracic
Coopers ligaments support breastsare strong, fibrous processes that run from the dermis of the skin to the deep layer of
superficial fascia through the breast
Nipple usually lies at the level of the fourth intercostal space
Breast cancer causes dimpling of the overlying skin and nipple retraction
Most of the lymph from the mammary glands goes to the axillary lymph nodes
Organs of the Male Reproductive System
Testis produce spermatozoa and secret sex hormones
They are firm, mobile organ lying within the scrotum
Each develops retroperitoneally and descends into the scrotum about time of birth
Seminiferous tubules
Sperm are produced in the seminiferous tubules and stored outside the testis in the epididymis until ejaculated
Meiosis occurs here (it does NOT occur in the ductus epididymis, stratum germanitivum, or ovarian germinal epi)


Lining consists of a complex stratified epithelium

Contain two cell types:
Sertoli cells
Produce spermatozoa
Form the blood-testes barrier with tight junctions connecting each cell
Spermatogenic cells germ cells found between Sertoli cells
The development of germ cells depends on pituitary FSH & testicular testosterone
Interstitial cells
Produce and secrete male sex hormones
Androgens, the most important one being testosterone, are synthesized and secreted into the blood stream by interstitial
cells (of Leydig) found in the interstitium of the testis between the seminiferous tubules
Testosterone is required for development of the testes and secondary sex characteristics and initiation and maintenance of
sperm production and secondary sex characteristics.
One found on each testis
Epididymis displays stereocilia
It is a tortuous, C-shaped, cordlike tube located in the scrotum
Tube emerges from the tail as the vas deferens, which enters the spermatic cord
Provides storage space for the spermatozoa and allows them to mature
Carries sperm from the seminiferous tubules of the testis to the vas deferens
Ductus Deferens (Vas)
Store spermatozoa
Conveys sperm from the epididymis to the ejaculatory duct
Cordlike structure
Contains Stereocilia also
Ejaculatory Duct
Receive spermatozoa and additives to produce seminal fluid
Passageway formed by the union of the deferent duct (vas deferens) and the excretory duct of the seminal vesicle
The ejaculatory duct opens into the prostatic urethra
Speaking of ejaculation: just think, Point & Shoot = Parasympathetic for erection, Sympathetic for emission
Seminal Vesicles
Secrete alkaline fluid containing nutrients and prostaglandins
Prostate Gland
Secretes alkaline fluid that helps neutralize acidic seminal fluid and enhance motility of spermatozoa
Encloses and protects testes
Conveys urine and seminal fluid to outside of the body
Sperm development:
Spermatogenesis occurs in Seminiferous tubules
Spermatogonium1 spermatocyte2 spermatocyteSpermatid
Diploid, 2NDiploid, 4NHaploid, 2NHaploid, N
What cell out of all the above is against the basement membrane?
Organs that produce semen:
Seminal vesiclespaired sacs at the base of the bladder
Bulbourethral gland (Cowpers gland)paired located inferior to the prostate
Prostate glandunder the bladder and surrounds the urethra. Continually secretes prostatic fluid, a thin, milky, alkaline fluid.
Copora amylacea are present in the alveoli of this gland
Inguinal canal:
It transmits the spermatic cord in males and the round ligament of the uterus in females; as well as the ilioinguinal nerve in both
It begins at the deep inguinal ring and extends to the superficial inguinal ring
It is much larger in males than in females:
The anterior wall is formed by aponeuroses of the external oblique and partially by the internal oblique muscle
Cremaster muscle
Testicular artery
Internal spermatic fascia
Pampiniform plexus of vein
NOT the epidiymis
Spermatic Cord
Covered by 3 concentric layers of fascia derived from the layers of the anterior abdominal wall


Internal and external spermatic fascia

Cremasteric fascia (cremaster muscle and fascia)
Spermatic cord contents:
Testicular artery: branch of the abdominal aorta; supplies mainly the testis and cremaster muscle
Testicular veins: pampiniform plexus forms testicular veins; drains into the left renal vein on the left side and into the inferior
vena cava on the right side
Passageway for urine between the urinary bladder and the outside of the body
Female urethra
4 cm
Females have more frequent bladder infections
Opens into the vestibule between the clitoris and the vagina
Male urethra
20 cm because it travels in the penis
Paired passageway which transports the urine from the kidney to the urinary bladder for concentration and storage until voided
Reproductive Anatomy
See Kaplan pp. 515-521 for all the details
Hyoglossus and Mylohyoid Relationships
Lingual Nerve, Hypoglossal nerve, Submandibular Duct
SubMan duct and lingual nerve cross 2 x
ALL superficial (Lateral) to the Hyoglossus
ALL deep (medial) to the Mylohyoid
Lingual Artery
Deep to BOTH (Medial)
Which nerve does NOT follow its artery???
Lingual nerve
External Carotid
What nerve follows the external carotid??
Great Auricular Nerve???

Random Questions from 2007

Boundaries of the Axilla: Pectoralis major, subscapularis, serratus anterior, bicipital groove of the humerus
Which of the following is a feature of the Y Chromosome?

it is submetacentric

Sensory Nucleus for 5,6,7,9,10?

principal, abducent, geniculate, inferior petrosal, superior of X


Circulatory System
Stretch receptors in carotid sinus
Most important for short term BP reg
High BP activates the Carotid Sinus nerve
Activation of parasympathetic nervous system and inhibition of sympathetic to drop BP
Stimulation leads to decreased heart rate, decreased arterial blood pressure and decreased venous return
Increased pressure in the carotid sinus increases the discharge of efferent fibers that travel in the 9 th CN
Then through local medullary circuitry, descending fibers are activated that inhibit sympathetic neurons
associated with the heart
Respond to actual stretching, not chemicals
Stretch receptors in the atria
Elicit Bainbridge reflex --- Think Bridging the gap from the heart to the Lungs
Initiated by excess blood volume in R atrium
Sensitive to both Pressure and stretch
Goal is to get heart to pump harder to transfer excess blood from pulm circ to systemic circ
A sudden increased inflow into the R atrium will cause an increased blood flow to the lungs in 2-3 heart beats
Afferent to the medulla via the vagus nerve
Stimulation of the heart by the vagus nerve keeps the HR down
The effect on basal HR of cutting successively the vagus & the sympathetic nerves in an animal reveals
predominance of vagal over sympathetic innervation in determining HR
Increased vagal activity also results in decreased cardiac oxygen consumption
Increased vagal activity does not result in decreased transit time through the AV node
Then efferent sympathetic increases the HR and strength of contractions
Central (Think C for Central and CO2)
MAJOR regulators of ventilation
Kaplan states central receptors are sensitive to low pH
Detect H+ changes in CSF (cerebrospinal fluid)
NO detection of PO2
Detect increase in PCO2
When PCO2 goes up, also increases H+ because CO2 + H2O forms carbonic acid, which then disassociates
to H+ and bicarbonate
Breathing a gas mixture with 5% CO2 ultimately leads to a stimulation of central chemoreceptors
Normally, air is 78% N2, 21% O2, and traces of other gases like CO2
CO2 affects central chemoreceptor the most
Located in carotid and aortic bodies
Detect change in blood PO2 (if <60mmHg), PCO2, and H+ (or pH) ion concentrations
Transmit to resp. center in brain to reg.
A marked fall in the oxygen tension in arterial blood would stimulate the receptors in the aortic & carotid bodies
Normal Hemoglobin concentration is about 15gm/dl blood and normal arterial oxygen content is about 20ml/dl
An anemic individual breathing room air with a hemoglobin concentration of 10 gm/dl blood is expected to have
Normal arterial oxygen tension and reduced arterial oxygen content
Breathing a gas mixture containing 10% O2 and 90% N2 will stimulate respiration because low oxygen tension has
an Excitatory effect on the peripheral chemoreceptors receptors
Different Q, but it reads administration of 90:10 N20 to O2 will DEPRESS RESPIRATION??? And it will
result in Respiratory Acidosis
NOTE Subanesthetic doses of nitrous (20-40% N2O) cause increased respiration
Blood Volume
64% in systemic veins
By far the most
13% in systemic arteries
7% in arterioles and capillaries
7% in heart
9% in pulmonary vessels

Largest share of systemic CO
Highest blood flow per gram of tissue especially the adrenals
Large arteriovenous O2 difference
Increased O2 demand is met by increased coronary blood flow, NOT by increased extraction of O2
Total Peripheral Resistance (TPR)
Regulates the flow of blood from the sys. arterial to venus circulation
Resistance to blood flow from the entire circulatory system
Caused by accumulation of vasodilator local metabolites (lactate, K+ ions, & adenosine)
Factors determining Autoregulation of blood flow
O2, adenosine, NO (Unique in that when hypoxic causes vasoconstriction)
CO2, pH
Myogenic and tubuloglomerular feedback
Hypoxia causes vasoconstriction (* Unique like the heart)
Skeletal Muscle
Local metabolites, Lactate, Adenosine, K+ (vasodilators)
Adenosine causes vascular smooth muscle to relax
Accumulate due to increasing metabolism of exercising muscle
Posseults Law
= Viscosity (of blood) x length (of vessel) / (Radius)4
Factors affecting blood resistance
Vessel Radius
Most Powerful relationship (Vasoconstriction is King)
Resistance is inversely proportional to the 4th power of vessel radius (= 1/r 4)
If you Half the vessel, then resistance goes up 16 times
Larger the vessel, the less resistance
Directly proportional to resistance
The vena cava contains the highest viscosity blood in the body (95% sure from the other answer options of
aorta, vasa recta, pulmonary vein, pulmonary artery)
Viscosity increases with polycythemia, Hyperproteinemic states (Multiple Myeloma), and Hereditary
May vary with hematocrit
Vessel Length
Directly proportional to resistance
Increasing the radius produces the greatest decrease in resistance in a single artery (versus changing the length or
reducing viscosity) due to the 4th power relationship
Cardiac Output (CO)
Regulates flow of blood from veins back into arterial side
CO = HR x SV
During exercise, CO increases initially as a result of an increase in SV
After prolonged exercise, CO increases as a result of an increase in HR
If HR is too high, diastolic filling is incomplete and CO drops (i.e. ventricular tachycardia, pulse >200)
Most important factor in relation to circulation
Average resting is 5.6 L /min for men
10-20% less for women
Heart Rate (HR)
The parasympathetic NS regulates HR
Stroke Volume (SV)
= End Diastolic Volume End Systolic Volume
Average is 70-80ml
Contractility (increases SV)
Increased with
Catecholamines (increased activity of Ca2+ pump in sarcoplasmic reticulum)
Sympathetic action of increasing HR, conduction velocity, and contractiility
Increased intracellular Ca2+
Decreased Extracellular Ca2+
Digitalis (increased intracellular Na+, resulting in increased Ca2+)

Resulting in bigger contractility, and slows down (more efficient)

Decreased with
B1 Blockers
Heart Failure
Afterload (decreases SV)
Diastolic arterial pressure (proportional to peripheral resistance)
Vasodilators decrease afterload (i.e. hydralazine)
Preload (increases SV)
Ventricular EDV
Venous Dilators decrease preload (i.e. nitroglycerin)
Venous Return
Most important determinant of CO
A drop in BP results from decreased venous return
Assisted by:
Contraction of skeletal muscles (especially in legs)
Pressure changes in thorax and abdomen during breathing
Increase of thoracic/abdominal pressure will decrease VR
Valsalva Maneuver
VR would be reduced by a forced expiration with the glottis closed
Pressure of venous valves
Decrease venous compliance
Sympathetic action decreases compliance, and increases VR
NOTE: Peripheral vasodilation reduces venous return to the heart
Initial length of cardiac muscle fibers affects the strength of contraction
Matches CO with venous return
Greater the filler, the harder the contraction because of more linking of actin and myosin
Increased filling of the ventricle during diastole causes a more forceful heartbeat
This is due to the increase in end-diastolic fiber length
NOTE: in a denervated heart, adjustments to increased workload are mediated by mechanisms
associated with increased end diastolic volume
Another Q:In the completely isolated, blood perfused mammalian heart, adjustments to increase
workload appear to be mediated primarily by mechanisms associated w/ increased diastolic volume
Mean Arterial Pressure (MAP) = CO x TPR (Total Peripheral Resistance)
Similar to Ohms law = Voltage = Current x Resistance
ALSO MAP = Diastolic + 1/3 pulse pressure
Pulse Pressure = Systolic Diastolic
Pulse Pressure Stroke Volume
Example 120/80 MAP = 80 + (120-80)/3 93.33
This is why doctors say the Diastolic BP is more important to monitor
Ejection Fraction
= (EDV ESV/ EDV) = SV/ EDV (Whats leaves/ what you started)
An idex of of ventricular contractility
Is normally 60-70%
Ventricular Filling
Rapid Filling Phase
Rapid flow of blood into the ventricle actually produces a decrease in atrial and ventricular pressures, but a sharp
increase in ventricular volume
Diastasis (Slow Filling Phase)
Gradual rise in atrial, ventricular, venous pressures and ventricular volume
The volume of the ventricle is greatest at end diastolic volume
Compliance (Larger compliance, larger the dilation)
A measure of how much a vein reacts to an change in pressure
Highly compliant veins dilate a lot
Determines the amount of blood flow in the veins
Sympathetic decreases venous compliance and returns more blood back to the heart
Vascular compliance = Increase in volume/increase in pressure
Blood Flow
= Pressure difference/Resistance


The greater the pressure gradient, the greater the flow

The flow rate decreases with increased resistance
CO = BP/TPR V = IR = (BP) Pressure = Flow (CO) x Resistance (TPR)

Measuring BP What indicates systole when using a sphygmomanometer? First sound

A fall in BP causes increased activity of the vasoconstrictor center and decreased activity of the cardioinhibitory center
The characteristic of the aorta most responsible for the maintenance of diastolic BP is elastic distensibility
Systemic Arteries
High pressure
Systolic BP may be abnormally high when arterial compliance is decreased (think arteriosclerosis)
Another Q: Prior to surgery, an anxious patient has a higher systolic BP than previously noted the
most likely reason is decreased arterial compliance (From the NE, sympathetics??)
Strong muscular walls
Always carry blood A for Away from the Heart
The main factors directly involved in the maintenance of systemic arterial blood pressure are
cardiac output, blood volume, blood viscosity and peripheral resistance (not heart rate)
Another Q: A drop in BP results from decreased CO
Now think of things that could cause a decrease in CO, like venous return for example
The arterial blood pressure might be abnormally high in a cerebrovascular accident (not cardiac shock, heart
failure, anaphylactic shock, or ventricular fibrillation)
Greatest drop occurs in the arterioles
In the presence of a constant HR, changes in BP may be attributed mainly to alterations in resistance in
Another Q: Postural hypotension is compensated by constriction of systemic arterioles
Another Q: The most likely cause of hypertension is generalized constriction of arterioles
Small vessels with diameter of 0.5 mm
Small lumen, but thick tunica media (almost all smooth muscle)
Primary resistance vessels, hence determine distribution of CO
Control valves for the capillaries
Local blood supply is regulated by tissue metabolism
Humoral factors affect diameter as well as sympathetic activation
Where exchange occurs
Walls are very thin
Only a single layer of endothelial cells
Surrounded by a thin basal lamina of the tunica intima
The amt of blood passing through the capillaries of the systemic circulation/min = amt of blood passing through
the aorta/min
More capillaries arranged in parallel
BP decreases as it flows through circulation
If two vessels are connected in parallel, their total resistance to blood flow is less than the resistance
of either vessel alone
Capillary diameter is directly influenced by byproducts of metabolism
Small veins which collect blood from capillaries
Gradually coalesce into larger veins
Systemic Veins
Conduits for blood to get back to the heart
The blood pressure of the circulatory system is the lowest in the veins
Greater osmolarity is in the IVC
Larger lumens and thinner walls than arteries
Higher compliance, act as reservoirs
Valves, especially in limbs to prevent backflow
The primary effect of substituting a rigid arterial system for a compliant arterial system would be that continuous flow in the
capillaries would change into pulsatile flow
Another Q: The continuous flow of blood in arteries during diastole is made possible by energy stored in arteries during

From capillary fluid pressure and increased colloid osmotic pressure of interstitium
These two act in the same direction when it comes to movement of water between interstitium & plasma
Capillary pressure
Force out fluid by filtration
Determined by venous pressure and arterial pressure
Interstitial fluid pressure
Opposes cap pressure
Oncotic pressure (or colloid osmotic pressure of the plasma)
Pulls fluid back into the plasma (same axn as the interstitial fluid pressure)
Colloid osmotic pressure of the blood is important because it prevents excess loss of fluid from capillaries
Another Q: Plasma colloid osmotic pressure acts in the same direction as tissue pressure
Main protein contributing to oncotic pressue is albumin
Is produced in the liver
Aldosterone and Vasopressin are NOT
Smallest, most abundant protein in the blood plasma
Type: a simple protein
Important buffer in the blood and is partly responsible for blood viscosity
The role of the liver in edema may be the result of diminished albumin synthesis
Forms a complex with free FAs to be transported in the blood
Kidney is main organ responsible for reg of osmotic pressure with reg of water resorption via ADH
When balance is off, edema occurs and lymphatics pick up the extra fluid left in the interstitium
Pulmonary Circuit
BP is much lower than systemic circuit
Pulmonary arteries are usually dilated and have little resistance are a lot of compliance
Compared with systemic circulation under normal conditions, pulmonary circulation is characterized by low
pressure, equal flow and low resistance (Great example of paralleling capillaries)
Think V = IR, aka pressure = current*resistance
From right side of the heart to the lungs and back to the left side of the heart
Only supplies the alveoli
Systemic Circuit
To all tissues except the alveoli
***Volume flow for BOTH circuits is 5 L/min (vol. flow/min is the same for both the systemic & pulmonary
BY Total Body Weight
92% Body Fluids and Tissues
8% Blood
55% Plasma
45% Formed Elements
= Plasma Clotting Factors (i.e. fibrinogen)
Clear, thin, sticky fluid portion after removal of fibrin clot and blood cells
No platelets, RBCs, or Fibrinogen
= Serum + Fibrinogen
= Blood Formed elements
Liquid portion of the blood
55% of the blood
No cells
Proteins (7%) albumins 55%, globulins 38%, and fibrinogen 7%
Water (91%)
Other Solutes (2%) Metabolic end-products, food materials, respiratory gases, hormones, and ions
Fibrinogen, prothrombin, calcium ion, and ascorbic acid are all found in plasma (thrombin is not)
Formed elements
The other 45%

PMNs 40-70%, Lymphocytes 20-40%, Monocytes 2-10%, Eosinophils 1-6%, Basophils <1%
Biconcave discs
7.5 microns in diameter
Function to transport O2 and CO2
No nuclei or mito
The membrane of the RBC
Composed of hemoglobin & other soluble proteins necessary for gaseous respiratory exchange
Has lipid membrane of A, B, or O antibodies
Blood Type
Blood groups
Antigens on RBC
Antibodies in Plasma
O (Universal dOnOr)
Anti-A and Anti-B
AB (Universal Recipients)
A and B
Proportion of RBCs in a sample of blood
46.2% -- Males
Hematocrit of 45% is a typical finding for a normal 23-year-old man
Abnormal: venous pH = 7.2, WBCs = 10,000/mm3, RBCs = 7 million/mm3, pulse pressure = 80
Normal Venous pH
Venous = 7.36
Arterial = 7.41
40.6% -- Females
Bile excretion is a good indicator of RBC destruction per day
Hemoglobin (Hb)
Constitutes 33% of the cell weight in RBCs
1 RBC contains up to 300 million Hb molecules
Hb synthesis involves iron & copper
Heme synthesis occurs in the liver and bone marrow
The committed step is Glycine + Succinyl CoA
gamma-aminolevulinate (ALA)
This is done by the NZ aminolevulinate synthase (inhibited by product heme)
Another Q: Some parts of a hemoglobin molecule iron, protein, histidine, pyrrole ring (not magnesium)
Globin portion
Consists of 2 alpha and 2 beta chains
Exists in 2 Forms:
Taut (T) has low affinity for Oxygen
Increased Cl-, H+, Temp, CO2, and DPG favor the T form (Unloading O2)
CO2 binding favors the T form
CO2 transport binds to the amino acids in the globin chain (at the N-terminus) and not at the Heme site
Relaxed (R) has high affinity for Oxygen (300x)
Heme Portion
Consists of 4 ring-shaped heme molecules
N-containing organic pigment molecule that has single atom of Fe2+ (ferrous) in its center, which can combine
one molecule of O2
Hb is important due to its ability to combine reversibly with O2 at the ferrous heme prosthetic group (not
ferric heme group)
Attached to Globin polypeptide chains
Each Fe can bind reversibly with 1 molecule of O2, so Hb molecule can associate with 4 O2 molecules
Remember that O2 binds with positive cooperativity and negative allostery, meaning that the binding
of the first O2 helps with the binding of the other 3
This accounts for the sigmoid shape dissociation curve (unlike myoglobin)
Hb can bind CO2 and that decreases amount that can bind to O2
Carbon monoxide has a 200x greater affinity for hemoglobin than does O2
Carbon monoxide (CO) decreases the amount of O2 that can be transported by hemoglobin

CO competes w/ O2 for hemoglobin for hemoglobin binding sites this makes CO toxic
Has its iron in Fe3+ (ferric) state and cannot function (NOT reduced hemoglobin)
Remember ferrOus (O for oxygen carrying)
So, the consequence of appreciable conversion of hemoglobin to methemoglobin is a noticeable decrease in
the ability of blood to transport oxygen

2/3rds of the bodys Iron is in Hb

Other 1/3rd is in liver, spleen, bone marrow, etc. in the form of ferritin or hemosiderin
Body normally has about 4 gms
Absorbed in the upper part of small intestine, primarily in duodenum
Combines in blood plasma with beta globulin apotrasferrin to form transferrin, which is then transported in
The major storage form of iron is ferritin So ferritin to store it, transferring to transport it in blood
Dominant factor controlling GI absorption of iron is saturation of mucosal cells
Hb Types
Hb A Normal type
Hb C Abnormal in which Lysine has replace glutamic acid causing reduced plastiCity of the RBCs
Hb H Abnormal composed of 4 beta chains (resulting in alpha-thalassemia)
Hb M Abnormal Hbs in which single amino acid substitution favors the formation of methemoglobin
Hb A1C Hemoglobin of a diabetic pt
Hb S (Sickle Cell anemia)
Abnormal Hb in which valine replaced glutamic acid in the beta chain
This causes Hb to become less soluble under low O2 tension & to polymerize into crystals that distort the
RBCs into a sickle shape (sickle-cell anemia)
Major effect of sickle cell anemia is from decreased solubility of the deoxy form of hemoglobin
This would cause an increase of the isoelectric pH
The pH at which number of positive charges equals the number of negative charges
Another Q: Sickle-cell anemia is caused by the presence of a valine substitution for glutamate in the sixth amino
acid from the N-terminal end of the hemoglobin B-chain. This amino acid substitution is the result of a base
change in the DNA of the B-chain gene
Involves a missense mutation
Another Q: The substitution of valine for glutamic acid is a result of a change in DNA coding (due to a genetic
Hb test
Measures the grams of Hb contained in 1dl of whole blood and provides an estimate of carrying capacity of RBCs
Normal Concentrations
Women 12 to 16 gm/dl
Men 14 to 18 gm/dl
Infants 14 to 20 gm/dl
Value depends on # of RBCs and amount of Hb in each
Low value indicates anemia
An anemic patient breathing room air is expected to have normal arterial O2 tension & reduced arterial O2
Remember that arterial O2 tension has nothing to do with Hb & accounts for only 2% of total O2 content
It has to do with arterial saturation w/ O2, which occurs quickly in the blood
Oxygen transport
O2 picked up in the lungs forms oxyhemoglobin (HbO2)
Then in tissues, O2 splits away from Hb and creates reduced hemoglobin (HHb) or deoxyhemoglobin
A dental patient presents with a bluish discoloration of the mucous MBs indicative of cyanosis most likely the
result of increased levels of reduced hemoglobin
NOTE: Cyanosis, by definition, is a bluish discoloration of the skin due to the presence of deoxygenated Hb in
BVs near the skin surface
Axn is reversible
Depends of PO2
When PO2 is high, (in pulmonary caps), Hb has higher affinity for O2
Among the larger blood vessels, O2 tension is highest in the pulmonary veins
When PO2 is low, (in tissue caps), Hb has lower affinity and unloads O2

Conversion of HbO2 to Hb is the most important process in preventing a decrease of >0.2 units in
blood pH when CO2 enters
Causes of O2 unloading (Decreased affinity for O2) Curve shift to the Right
Low PO2
Bohr effect
The equilibrium expression for oxygen association to hemoglobin includes participation of H+ ions
Decreased pH = increased arterial [H+] = decreased affinity for O2
Increase in arterial pCO2 Causes oxyhemoglobin to shift to deoxyhemoglobin
Has the most effect in stimulating respiration
Increase in Diphosphoglycerate (DPG)
Hypoxia increases the formation of DPG
Increase in tissue temperature (exercise)
So basically, when CO2 enters the blood, pH drops, causing unloading of O2, which then keeps the
blood pH from dropping too much
In question form: The hemoglobin dissociation curve is shifted to the right by an increase in arterial
pCO2 & an increase in arterial H+ concentration
Curve shift to the left
This would be area representing times of Hypoxemia or cyanosis

Oxygen dissociation equation:

y = (pO2)n/[ (pO2)n + (P50)n]
y is the fractional occupancy of O2-binding sites
P50 is the pO2 at which 50% of sites are filled
n = 2.8 for hemoglobin (I have no idea where the 2.8 comes in)
At 100mm Hg , Hb is essentially fully saturated (98%)
The PO2 must drop below 70 mmHg before there is a significant lowering of the total bound O2
At 40 mmHg, (venous blood), approximately 75% of heme sites are occupied (or 3 bound
P50 (pressure where half the sites, or 2 molecules, are bound) is 27 mmHg
EX: Given P50 = 26 torr & pO2 = 30 torr, the average # of O2 molecules bound per Hb is greater than 2, since
the equation yields y = 0.6 or 60%
Blood leaving lungs is 98% saturated in O2
Blood returning is 75% saturated in O2
Carbonic anhydrase
CO2 is carried from tissue to the lungs in 3 ways
90% Bicarbonate
5% Bound to Hemoglobin as carbaminoglobin
5% Dissolved CO2
[CO2 + H2O H2CO3 H+ + HCO3-]
Present within tubular cells, and it catalyzes the formation of carbonic acid from carbon dioxide and water
Carbonic acid dissociates into hydrogen ion and bicarbonate
One of the fastest known enzymes and is found in great concentration in erythrocytes
Zinc is an essential component
The steps:

Waste CO2, released from respiring tissues into the blood plasma enters the erythrocyte
Within the erythrocyte, carbonic anhydrase facilitates the combination of CO 2 and water to form carbonic acid
[CO2 + H2OH2CO3]
Carbonic acid dissociates into hydrogen ions and bicarbonate ions [H2CO3H+ + HCO3-]
Carbonic anhydrase in erythrocytes increases the rate of dissociation of H2CO3
HCO3- reenters the blood plasma for transport to the lungs
Because the RBC membrane is not very permeable to cations, the HCO3- efflux is balanced with
a Cl- influx, which is known as the Cl- shift
Chloride passes from the plasma into the cell as HCO3- passes from cell into plasma
Because HCO3- is much more soluble in blood plasma than CO2, this roundabout route increases the
bloods capacity to carry carbon dioxide from the tissues to the lungs
In the lungs, HCO3- reenters the erythrocyte and combines with hydrogen ions to form carbonic acid,
which is split by carbonic anhydrase into CO2 and water
This CO2 diffuses into the alveoli and is exhaled
So, carbonic anhydrase in erythrocytes increases the rate of dissociation of H2CO3
Haldane Effect
In the lungs, oxygenation of Hb promotes dissociation of CO2 from Hb
Carbonic anhydrase in the kidney tubular cells is associated with reabsorption of bicarbonate ion
Although not required for CO2 and water to form carbonic acid, it greatly increase the reaction in both respects
Absence of carbonic anhydrase drastically reduces blood CO2 carrying capacity
Most of the CO2 is transported in the blood as bicarbonate ion (HCO3-)
It is converted to carbonic acid more rapidly in whole blood than in plasma
The reason: whole blood contains erythrocytes w/ carbonic anhydrase, while plasma does not contain RBCs
The greatest concentration of carbonic anhydrase is found in erythrocytes
The bicarbonate buffer system of blood is very efficient because CO2 is rapidly eliminated through the lungs
Oxygen Tension vs. Oxygen Content
A marked fall in the oxygen tension in arterial blood would stimulate the receptors in the aortic & carotid bodies
Normal Hemoglobin concentration is about 15gm/dl blood and normal arterial oxygen content is about 20ml/dl
blood. An anemic individual breathing room air with a hemoglobin concentration of 10 gm/dl blood is expected to
Normal arterial oxygen tension and reduced arterial oxygen content
NOTE: Hb concentration is about 15 g/dl, and each gram can combine with 1.36 ml O2, so blood can carry 20
ml/dl of O2, compared with only 0.3 ml of physically dissolved O2
Breathing a gas mixture containing 10% O2 and 90% N2 will stimulate respiration because low oxygen tension has
an excitatory effect on the peripheral receptors
Hb that is carrying CO2
Hb carries 97% of O2 transported
Hemostasis preventing or minimizing blood loss
Platelet aggregation
The important role that platelets play in hemostasis is that they agglutinate and plug small, ruptured vessels
Thromboxane A2 is released by platelets & causes platelets to stick together
Increased bleeding (in a patient w/ leukemia) is most likely due to thrombocytopenia (when anemia, leukopenia,
Ca2+ deficiency, and Factor VIII deficiency are your other options
Basically all the blood progenitor cells are too busy making WBCs and so no energy to make platelets
Coagulation Cascade (picture)

Extrinsic pathway
Remember something else started it
Upon injury to endothelial cells tissure factor (factor III) rlsd
Which combines w/ factor VII & Ca+2 to form activating complex for factor X
Then activates factor IX to activated complex which becomes common pathway
3- 7- 10
Then activate factor X then factor II activated (prothrombin thrombin)
10- ProT(2)- Throm- Fibrinogen- Fibrin- x-linked fibrin
Also 10- ProT(2)- Throm- 13- Fibrin Monomer- x-linked fibrin
Intrinsic pathway:
When platelets adhere to injured subendothel region factor XII rlsd which becomes activated by
kallikrein and HMWK (high MW kininogen)
Which activates factor XI which activates IX then common pathway
12- 11- 9- 10
Factor X upon activation is first slow once thrombin made factor V is activated (back door from
Thrombin) speeds up Factor Xs rsn (prothromb thromb)
Speeds up HUGE (800,000 FOLD when V and Ca2+ added)
Also speeds up back door via activation of factor VIII from thrombin which joins IX making it stronger
Catalyzes: fibrinogen fibrin monomer rxn
In other words, fibrinogen represents the normal substrate of thrombin
Research has shown that thrombin acts upon the arginyl-glycine linkages in fibrinogen to produce
a fibrin monomer
Factor XIIIa catalyzes: fibrin monomer cross-linked fibrin reaction
When BVs are ruptured, usually both intrinsic and extrinsic pathways are activated
In severe degenerative disease of the liver (such as advanced alcoholic cirrhosis), prothrombin and
fibrinogen levels will be markedly deficient
Thromboxane A2
Release by platelets and causes them to stick together or aggregate
First thing to happen in formation of platelet plug? Adherence of platelet to subendothelium. This
happens before TbA2 is released
Things required for normal blood clotting:
Ca2+, thrombin, vitamin K, phospholipid, proteolysis
Vitamin K is cofactor 2 (prothrombin), 7,9,10
(Plasmin breaks down clots)
Another Q: Fe2+ is not involved in coagulation of blood


Heparin, dicumarol, sodium citrate, any antithrombin substance
Mediates dissolution of the fibrin clot during vessel repair
Bleeding disorders
Hemophilia A represents a bleeding disorder due to lack of factor VIII
Stimulates RBC production in bone marrow
Glycoprotein hormone produced in the kidneys
Negative feeback mech sensitive to the amount of O2 in blood
Site of action
Hemcytoblast (a pluripotent stem cell)
Can have hypo (anemia) or hyper (polycythemia) secretions of erythropoietin
Plasma Calcium Levels
8.5 to 10.5 mg/dl
Regulated by PTH
Vit D3 regulates uptake in GI
Low Plasma Ca results in hyperirritability of nerves and muscles
High Plasma Ca results in CNS and Cardiovascular depression
Plasma Phosporus levels
3.0 to 4.5 mg/dl
Regulated by PTH
Causes kidneys to increase the rate of phosphate excretion
Blood glucose levels
80-100 mg/dl
Reg. by insulin and glucagons
Glucose normally does not appear in urine although it is filtered because it is reabsorbed in the proximal convoluted
TPMA (Toilet Paper, My A**)(Tricuspid/Pulmonary/Mitral/Aortic)
Between Right A and V
Tough, fibrous tissue flaps of endocardium
Secured to papillary muscle via chordae tendineae
Damage to the tricuspid valve results in blood leakage from the right V to the right A
Entrance of pulmonary artery
3 cusps
Mitral (bicuspid)
Between Left A and V
Tough, fibrous tissue flaps of endocardium
Secured to papillary muscle via chordae tendineae
Entrance of ascending aorta
3 cusps
First Heart Sound
Closure of the AV valves at beginning of ventricular contraction
Immediately following the closure of the AV valves is the period of isometric contraction, (not isotonic)
Louder and stronger
Systole starts with 1st sound
Diastole ends with 1st sound
Second Heart sound
Closure of semilunar valves (pulmonary and aortic)
Aortic closes before pulmonary, so sound can be split
The second heart sound is related to closure of aortic valve


Systole ends with 2nd sound

Diastole starts with 2nd sound
Sounds heard in the antecubital space during systole are produced by turbulent blood flow through the artery
All 4 valves are NEVER open at the same time
Cardiac Cycle
1 Atrial Systole
2 Isovolumetric Contraction
Period between mitral valve closure and aortic
valve opening, so all valves are closed
Period of highest oxygen consumption
3 Rapid Ejection
4 Reduced Ejection
5 Isovolumetric relaxation
Period between aortic valve closing and mitral
valve opening
6 Rapid Ventricular Filling
7 Reduced Ventricular Filling
1 Mitral and Tricuspid Valve Closure (Lub)
2 Aortic and Pulmon. Valve Closure (Dub)
3 Start of Ventricular filling
4 High atrial pressure/stiff ventricle
Isovolumetric ventricular relaxation
Pulmonary and aortic valves close
Ventricular pressure decreases
During this period, blood flow to the coronary arteries is the greatest in a resting individual
Another Q: During early diastole, blood flow to the left coronary artery is greatest
Opening of tricuspid and mitral (bicuspid) valves [Passive Filling]
Atrial Systole
Following SA node depol, atria depol and contract [Active Filling]
The wave of depol slows in the AV node, allowing time for blood filling of ventricles
Ventricular volume is greatest at end of atrial systole = at the end of ventricular diastole
Isovolumetric ventricular contraction
Mitral and tricuspid valves close (All valves are closed during isovolumetric ventricular contraction)
Another Q: Ventricular pressure rises rapidly
Ventricular ejection
Opening the aortic and pulmonary valves
Empty rapid at first, then rate slows and ventricular pressure drops
Ventricular pressure is greatest at beginning of ventricular ejection
The largest volume flow of blood through the left coronary artery occurs during diastole
An immediate effect of diminished oxygen tension in the myocardium is vasodilatation of coronary vessels
Chronotropic State (Heart Rate)
Positive = Increase in Rate
Epinephrine administration causes both Positive Chronotropy and Inotropy
Inotropic States (Myocardial Contractility)
Term used to describe the degree to which the fibers are activated at a given preload and afterload
Positive Inotropy
Most commonly related to increased availability of intracellular Ca2+
Agents include:
Epi, NE, other Beta-1 agonsists
Increase the probability that a Ca channel is open
An injection into the left ventricular wall increases cardiac output and is a positive inotropy
Increased Extracellular [Ca2+]
Causes an increased influx of Ca during phase 2 of the action potential
Cardiac glycosides (Digitalis)
Inhibit the Na+/K+ ATPase, causing an increased intracellular [Ca2+]
Digitalis is given to increase strength of contractions & decrease HR


I think this makes it a positive inotrope & a negative chronotrope

Negative Inotropy
Related to decreased availability of intracellular Ca2+
Ca channel blockers
Which blocks Ca2+ channels
Beta-1 receptor antagonists
Which decrease the probability that a given Ca2+ channel is open
Myocardial ischemia
Decreases Ca2+ influx in the atria, but not in the ventricles
3 major effects are essential for proper circulation during exercise:
Mass discharge of sympathetic NS
Constricts vegetative muscles
Vasodilates skeletal muscles
Increase heart stuff, etc.
Moderate exercise increases HR & coronary blood flow
Increase in CO
Skeletal muscle contraction facilitates more venous return, so stroke volume goes up, CO goes up
Increase in arterial BP
From symp action, increasing CO
Heart Muscle Refractory Periods
Ventricular Muscle 0.25 - 0.30 seconds
Atrial Muscle 0.15 seconds
Types of refractory periods
Another AP is not even possible (H gate stuck)
Interval in which no stimulus is effective in creating an AP
Another Q: Absolute refractory period is determined by duration of Na gate inactivation
Limits the maximum frequency of effective nerve stimulation (maximum # of impulses a nerve can carry)
Begins at end of absolute and continues until membrane potential returns to resting level
Another AP is possible if stimulus is larger than usual
Excitation time for total heart 0.22 seconds
Skeletal muscle cells have short refractory periods
Also can undergo tetanus, which increases strength of contraction
Cardiac muscle does not tetany because of its long refractory period
Autonomic NS and the heart
Controlled in medulla oblongata of brain stem
Increase in HR
Fibers are from T1-T4 (accessory nerves)
Decrease in HR
Parasympathetic nervous system regulates heart rate
Fibers in the vagus nerves
Right vagus nerve SA node (pacemaker)
Left vagus nerve AV node (slowest conductor in the heart)
***NOTE: Vagal stimulation in the mammalian heart has
primarily a rate effect because there are few vagal endings
distributed to the mammalian ventricles
Myocardial Action Potential (RIGHT)
Phase 0
Rapid upstroke
Voltage-gated Na+ channels open


Phase 1
Initial Repolarization
Inactivation of voltage-gated Na+ channels
Voltage-gated K+ channels begin to open
Phase 2
Plateau Ca2+ influx through voltage-gated channels balances K+ efflux
Ca2+ influx triggers myocyte contraction
Phase 3
Rapid repolarization
Massive K+ efflux due to opening of voltage-gated slow K+ channels and closure of voltage-gated Ca2+ channels
Phase 4
Resting Potential
High K+ permeability through K+ channels
Cardiac Conduction
SA Node
The following changes in the electrical properties of a pacemaker cell can slow down the rate at which the cell
initiates impulses:
The threshold potential becoming more positive
The rate of spontaneous depolarization decreasing
The maximum diastolic potential becoming more negative
In posterior wall of R atrium by the opening of superior vena cava
The rate of the heart beat in a human is determined by the SA node
Internodal pathways
0.04 Seconds
Transmit depol to L atrium and AV node
AV Node
In the lower R interatrial septum
Delays impulse 0.13 seconds so atria can contract first
The slowest rate of conduction velocity
AV Bundle (of His)
Orginates in AV node
Divides into 2 bundle branches to 2 sides of interventricular septum
Purkinje fibers
Originate in right and left bundle branches and extend to papillary muscles and lateral walls of the ventricles
Very fast depol through bundle branches and purkinje fibers 0.03 seconds
ECG or EKG Know the P, QRS, & T waves

P wave
activation of the atria
PR segment
the duration of the AV conduction
QRS complex
activation of both ventricles
ST-T wave
ventricular recovery
Each 1 mm square represents 0.04 sec (40 ms)
Rate: 300 # of large boxes between 2 consecutive R waves
P wave
Atrial depolarization
P waves occurring in ST segment indicating ectopic beats originating in the atria
AV Blocks
1st Degree
Prolonged PR interval (>200msec)
2nd Degree
Type I (Wenckebach) shows a progressive prolongation of PR interval until a P wave is blocked and
not followed by a QRS complex
Type II (Mobitz) shows sporadic/episodic dropped QRS complex
Extra P waves before each QRS complex on an EKG are indicative of partial heart block (second
degree block)


Another Q: An EKG showing a consistent rhythmical ratio of three P waves to each QRST complex
indicates an AV node partial block
3rd Degree
Complete AV block with P waves completely dissociated from QRS complexes
Another Q: When the P wave and QRS complex are dissociated, it is indicative of complete (3rd
degree) heart block
QRS Complex
Ventricular depol
T wave
Ventricular repol
S-T segment
Ventricles are completely depolarized??? (Only point where this happens in ECG)
P-R interval
What is the PR interval
Length of time between depol of atria and depol of ventricles
The P-R interval is related to propagation of the cardiac impulse between the SA node and the AV node
Index of the conduction time between the atria and the ventricles
Index of the atrial depolarization and conduction through the AV node
Another Q: When an increased PR interval is observed, this represents slow conduction of impulses through the
AV node
Approx 0.16 seconds (0.13 + 0.03, see above)
Q-T interval
Period between ventricular depol and repol
Approx 0.35 seconds
T-P section
Isoelectric (aka ventricle is at resting membrane potential) no electric signal to the heart during this section
Ventricle is filling with blood
Shortens a lot at high HRs
Standard Bipolar Limb Leads
Right Arm (-)
Left Arm (+)
Right Arm (-)
Left Leg (+)
Left Arm (-)
Left Leg (+)
Standard Unipolar Limb Leads
Right Arm (+)
Left Arm (+)
Left Leg (+)
Doesnt matter which one you used for cardiac arrythmias, BUT it does w/ voltage abnormalities & axis deviations
Chest Leads
V1, V2, V3, V4, V5, V6
Represent 6 places on the anterior chest wall
Heart NZs:
Creatine kinase (CK) also called creatine phosphokinase (CPK)
The first heart enzyme to appear in blood after a heart attack
Glutamate oxaloacetate transmaminase (GOT)the second to appear
Glutamate pyruvate transmaminase (GPT)
Lactate dehydrogenase (LDH) different isozyme characteristic of heart muscle
The plasma levels of these enzymes are commonly determined in the diagnosis of myocardial infarctions
They are particularly useful when the ECG is difficult to interpret
NEW GOLD STANDARD for Dx of a MI Troponin C
Congestive heart failure
Causes bulging veins in the neck
A person with left heart failure might show signs of dyspnea when placed in the supine position because of edema caused by
excessive pulmonary capillary hydrostatic pressure
Respiratory System
Gas exchange
Oxygen passes from alveolar air into blood by diffusion
Depends on:


Thickness of the membrane

Thin is better
Rate of diffusion is inversely proportional to the diffusion distance
Surface area of the respiratory membrane
Rate of diffusion is directly proportional to the surface area
Increasing the cross-sectional area can increase the rate of oxygen diffusion at the alveolar membrane
Solubility of gas
Gas dissolved in liquid exerts partial pressure
So partial pressure includes both gas particles and liquid gas particles
CO2 is 20x more soluble than O2
Partial pressure difference between two sides of a membrane
Net diffusion from high to low pressure
In addition to the respiratory system, the exchange of gases between plasma & tissue fluid is a function of
partial pressures (NOT due to osmotic pressure differentials or differences in volume % of the gases)
Another Q: The actual diffusion of gases is 1 controlled by differentials in partial pressures of the gases
Alveolar PO2 is greater than pulmonary arterial pressure
Alveolar PCO2 is lower than pulmonary arterial pressure
The diffusion coefficient for the transfer of each gas through the respiratory membrane depends upon BOTH
solubility and molecular weight
Partially pressures of respiratory gases found in arterial blood most closely correspond to partial pressures found in
the alveoli
So, O2 removal from the alveoli is facilitated by low PO2 of alveolar blood, increased total alveolar surface area, and
increased blood flow through alveolar capillaries
Another Q: As blood passes through alveolar capillaries, blood PO 2 rises, hemoglobin releases CO 2 & H+ (blood
PCO2 does not rise)
NOTE Hb does release H+, but NOT into the blood, only to be available in the RBC to make Carbonic acid
with the influxed bicarb
Pulmonary Circulation
Normally a low-resistance, high compliance system
PO2 and PCO2 exert opposite effects on pulmonary and systemic circulation
A decrease in PAO2 causes a hypoxic vasonconstriction that shifts blood away from poorly ventilated regions of the
lung to well-ventilated ones
A consequence of pulmonary hypertension is cor pulmonale and subsequent right ventricular failure (Jugular venous
distention, edema, hepatomegaly)
Pulmonary Ventilation
Total volume of gas per minute inspired or expired
Coordinated in the brain stem (medulla)
V/Q Mismatch
Ideally Ventilation is matched to perfusion such that V/Q = 1
Actual is 0.8
Lung zones
Apex of the lung = V/Q = 3 (wasted ventilation)
Just think blood is flowing through the base of the lungs, so base of the lungs, and air rises so V is greater
in the apex
Base of the lung = V/Q = 0.6 (wasted perfusion)
BOTH ventilation and perfusion are Greater at the base of the lung than at the apex
V/Q = 0 (means airway obstruction)
V/Q = infinity (means blood flow obstruction)
Minute ventilation
Volume of air moved in to the respiratory passageways in one minute
= Tidal volume x Breaths/min
Alveolar ventilation
Is the actual air that reaches the alveoli and can participate in gas exchange
Expressed in per minute OR per breath
= Respiratory Rate x (Tidal volume Dead air space volume)
Dead air space
Air that is filled in the non-gas exchange areas of the lung (all but alveoli)
Is the best criterion for effectiveness of breathing
Lung Volumes and Capacities



FVC = Forced Vital Capacity

Tidal volume (VT)

Amount of air entering the lungs with each breath
Normal is 12/min
Inspiratory capacity (IC)
Amount of air entering lungs with maximal inhalation
Vital capacity (VC)
Maximum volume a person can exhale slowly
= Vt + IRV + ERV
Functional residual capacity (FRC)
This is the volume left in lungs at the end of a normal quiet expiration
At FRC the tendency of the lungs to collapse is exactly balanced by the tendency of the chest wall to expand
= ERV + RV
One should expect Nitrous sedation to take longer than normal in a person with functional residual capacity
larger than normal
Residual volume (RV)
Volume left in lungs at the end of a forced maximal expiration
ANATOMIC Deadspace
Inspiratory Reserve Volume (IRV)
Extra volume of air that can be inspired in addition to Vt
Approx 3000ml
Expiratory Reserve Volume (ERV)
Extra volume of air that can be exhaled after normal expiration of Vt
Approx 1100ml
Total lung capacity (TLC)
Vital capacity + residual volume
Forced vital capacity (FVC)
Maximum volume a person can exhale with maximal force
Forced expiratory volume in one second (FEV1)
Volume of air forcefully exhaled in one second
Note, this is a measure of flow whereas FVC is a measure of volume
This ratio is useful in differentiating obstructive and restrictive lung conditions
A patient with emphysema exhibits increased FRC & increased compliance
is the measure of distensibility of a chamber expressed as a change in volume per unit change in pressure
You cant measure RV, FRC, and Total lung capacity
Lung Receptors
Lung stretch receptors


Located in smooth muscle of airways

During inspiration (when distended):
Stimulate Hering-Breuer reflex, which prevents overinflation
The adequate stimulus for the Hering-Breuer reflex is the stretching of alveoli
Think Bruer Hockey Gear to keep your lungs tight
Send stimuli over afferent vagus nerve to resp center in medulla
LungVagusMedullaSpinal cordRespiratory muscles
Not used much in normal breathing, only protective
Expansion of the lungs stimulates vagal nerve endings in the lung parenchyma & inhibits inspiration
J Receptors
Located in the alveolar walls
When stimulated, cause rapid, shallow breathing
Jake is a shallow person
Irritant Receptors
Located between airway epi cells
Stimulated by noxious substances
Joint and muscle receptors
Are activated during exercise to stimulate breathing
NOTE: PCO2 is the most important stimulus for the respiratory center in medulla
An increase in arterial CO2 has the greatest effect in stimulating respiration
Another Q: After a period of voluntary hyperventilation, respiration becomes depressed mainly due to reduced blood
Another Q: Apnea occurring after hyperventilation of an anesthetized patient results from decreased CO 2 tension
Respiratory Products
Dipalmitoyl Phosphatidylcholine (Lecithin)
Collapsing Pressure = 2 (tension)/Radius
Decreases alveolar surface tension and increases compliance
Difficulty breathing in neonates due to deficient surfactant resulting in increased surface tension
Angiotensin Converting Enzyme (ACE): cleaves AI AII, inactivates bradykinin and causes cough, angioedema)
Kallikrein: Activates Bradykinin
Respiratory Terms
Apnea cessation of breathing
Hypercapnea Excess CO2 in arterial blood
Hypocapnea Duh
Hyperpnea Abnormally deep and rapid breathing
Resp Arrest Permanent cessation of breathing
Hyperventilation Increased ventilation in excess of metabolic requirements
Results in loss of CO2 from blood, causing a decrease in BP and may result in fainting (Brown Bag it)
Results in decreased CO2 and increased pH (decrease in H+)
Another Q: Voluntary overventilation of the lungs results in decreased [H+]
decreased ventilation
The most important test for hypoventilation is the determination of arterial CO2 tension
Caused by:
Drugs that depress respiratory center in the medulla (barbiturates)
Obstruction paraylysis of the respiratory muscles
Lung Disease
Pressures in the respiratory system:
Atmospheric Pressure
= 760mmHg = same pressure in alveoli when lungs are at rest (aka after a normal expiration)
Collapsing force of lungs
By the elastic CT of the lungs and surface tension from surfactant
NOTE: Pulmonary surfactant acts to increase both lung compliance & vital capacity
So obviously w/o it you have decreased both compliance and vital capacity
Expanding force of the lungs
***Both forces are equilavent at FRC or the end of expiration, or the point of rest
Here, both inspiration or expiration would require muscle involvement


Partial Pressures (in mmHg)

Venous Blood

Arterial Blood



In the resting state, the average difference between O2 content of arterial & venous blood is 5 volume percent
Jake: how does this correlate with the 40 vs. 100mmHg thing above? Does it have to do with total content, and
not PO2, which changes drastically
Another Q: When the partial pressure of oxygen in arterial blood is lower than that in alveoli, this suggests
thickening of the alveolar membrane??? (Sounds normal to me)
Another Q: The partial pressures of respiratory gases found in arterial blood correspond most closely to those partial
pressures found in the alveoli
Another Q: In a pulmonary AV shunt, the O2 partial pressure in arterial blood is low
Another Q: Under physiological conditions the lowest partial pressure of oxygen is in Venous Blood NOT expired
Intrapleural Pressure
Pressure w/in the pleural cavity
In resting position, approx 4 mm Hg less than the atm pressure (so 756mm Hg)
Intrapleural pressure is always less than the intrapulmonary pressure
Another Q: Intrapleural pressure during normal respiration is subatmospheric
Simultaneous contraction of the external intercostal muscles & the diaphragm results in a decrease in
intrapleural pressure
(the pressure becomes more negative thats a decrease)
Physiologic Dead Space
= Anatomic dead space + any part of the lung that should be ventilated and perfused but is not
= the volume of the conducting pathways (trachea and Bronchiosomething)
Establishing a tracheostomy results in decreased respiratory work
Non perfusing alveoli, PHYSIOLOGIC dead space
Work, which is defined as P x V is reduced because volume is reduced
You would decrease anatomic dead space with a tracheostomy
Another Q: The RQ for a man who uses 4 liters of oxygen and produces 3 liters of CO is 0.75
Respiratory Quotient
= The rate of Vco2/ Rate of vO2 How much CO2 you make/ How much O2 you use
RQ = CO2/O2 remember the 0.8
RQ quotient for a person taking pure glucose as food source is higher than normal (normal is 0.8, with pure
glucose is 1.0)
NOTE the RQ may be used to calculate the basal metabolic rate via the technique of indirect calorimetry
RQ: for fat = 0.7; for carb = 1.0
If the respiratory quotient is 0.7, the primary energy source is: fat, ketone bodies, glucose, etc.
Signs/Symptoms of asthma attack
Airway Edema
Increased Mucous secretion
Increased airway resistance
NOT Decreased Surfactant
Adrenergic Beta-2
Consequences of pts respiratory difficulty
Causes, Hypoxia, Hypercapnia, Tachycardia, Acute Respiratory Acidosis
NOT Increased Renal Bicarbonate Production
(Because Increased CO2 already shifts the equation back to having lots of Bicarb, so no need for
Motor Unit
Alpha motor neuron and all of the muscle fibers it innervates
Each muscle has several muscle fibers
Each muscle fiber is innervated by a single alpha neuron


Each alpha neuron innervates many muscle fibers

All of the fibers innervated by a motor neuron contract when that motor neuron fires an AP
In other words, when a nerve arrives at a motor unit, it will cause all of the motor unit to contract
Size Principle
Motor neurons are recruited in order of size
If small force is needed, only small fibers activated, etc.
You do NOT need to activate all motor units in a muscle at once
Recruitment with respect to motor neurons refers to progressive increase in the number of motor units involved

SEE for a sweet Animation

Muscle Contraction (ABOVE PICS)
Controlled by nervous system
The sarcomere represents the basic contractile unit of muscle myofibril
APs traveling down somatic alpha motor neurons cause depolarization of the skeletal fibers at which they terminate
Neuromuscular junction = junction between the terminal of the motor neuron and a muscle fiber
When an AP arrives at a neuromuscular junction, calcium ions enter the nerve terminal causing the release of Ach
from synaptic vesicles within the motor neuron
Ach then binds to the nicotinic cholinergic receptors in the muscle fiber plasma membrane. This causes
depolarization which triggers an AP (the action potential travels along the membrane t-tubules)
Acetylcholine esterase is the NZ that is involved in the termination of the neuromuscular transmission
The depolarization of the skeletal muscle cell membrane by motor nerves is directly produced by the
change in end plate potential level to a critical value
Transmission of impulses from the motor nerve to the muscle cell regularly produces an action potential in
the muscle cell
This AP triggers the release of calcium ions from the sarcoplasmic reticulum
The calcium release form the S.R. into the cytoplasm is the 1st measurable event in the myofiber
following generation of an AP in the sarcolemma
Calcium is sequestered/stored in Sarcoplamic Reticulum
This leads to crossbridge formation between actin and myosin. These interactions are responsible for
the development of tension and the shortening of the fibers
The length-tension diagram shows that the maximum active tension of a muscle occurs when there
is maximum overlap of crossbridges
The excitation-contraction coupling is measured by the release of calcium from the sarcoplasmic
Calcium binds to troponin C on the thin filaments Think C for calcium
Calcium ions trigger contraction of muscles when they bind to troponin
The stimulation of muscle contraction (via calcium) is mediated via troponin C (not mediated by
actin, tropomyosin, troponin I, or the sarcoplasmic reticulum)
Cardiac muscle only needs 1 Ca to activate, other muscles need 2 Ca2+
2 sites are always filled by Mg
Causes a conformational change in troponin that permits Troponin I to release from tropomyosin
and then tropomyosin changes allowing myosin and actin to bind
After calcium binds with troponin, tropomyosin moves from its blocking position permitting actin
and myosin to interact


High energy myosin binds weakly to actin subunits, however, when inorganic phosphate is
released from the myosin, the myosins bind tightly to the actin subunits
High energy myosin has ATP bound to it; upon release of Pi, myosin can bind tightly to actin
Energy stored in the high-energy myosin is discharged, and the myosin head swivel, pulling on the
thin filaments
Mg2+ comes in to Activate the ATPase, which then gives the energy to stroke
This repeated pulling of the thin filaments past the thick filaments toward the centers of the
sarcomeres draws the Z lines closer together, and the muscle fiber shortens (contracts)
During an isotonic contraction, the A band does not change in width or length
HIZ contracts!!!
H band, I band, and consecutive Z lines, sarcomeres, & series elastic elements do change
This process is repeated as long as calcium ions are bound to troponin and ATP is available
Once calcium ions are returned to the sarcoplasin reticulum, tropomyosin moves back into its
blocking position and prevents further interaction between high-energy myosins and actin subunits
Then contraction ceases and the muscle fibers relax
The dissociation of the actomyosin complex results from ATP replacing ADP on the myosin head
NOT rephosphorylation of ADP
Submaximal direct stimulus to skeletal muscle will cause some fibers to contract, but not the whole
Another Q: Ratio between the amount of work done & total energy expended determines the mechanical
efficiency of muscular contraction
A muscle devoid of tonus is atonic

Muscle Energy Sources

Another Q: ATPADP + Pi is the reaction providing the immediate source of energy for muscular contraction (1-2
Then, creatine phosphate is used to rephosphorylate the now unbound ADP to ATP (next 2-5 seconds)
Glycogen is then the 3rd participant and is used to reconstitute both ATP and creatine phosphate
At moderate levels of muscle activity (>20 minutes), the predominant source of ATP is from FAs
Another Q: FAs is the predominant source of ATP at MODERATE levels (>60 min) of activity
During prolonged period of starvation, the primary fuel is NOT glycogen
Another Q: ATP is essential to the transformation of G-actin to F-actin
Types of muscle fibers:
Extrafusal fibers:
Fibers that make up the bulk of the muscle
Innervated by alpha-motor neurons (efferent neurons)
Provide the force for muscle contraction
Intrafusal fibers AKA muscle spindles
Are encapsulated in sheaths to form muscle spindles
Innervated by gamma-efferent (motor) neurons, slow conducting
Two types of fibers:
Nuclear bag fibers:
Detect fast, dynamic changes in muscle length and tension
Innervated by group 1a afferents fastest in body
Nuclear chain fibers:


Detect static changes in muscle length and tension

Innervated by the slower group II afferents
Chain gangs are slow
Discharge of impulse in small motor (fusiform) neurons innervating muscle spindle serves to sustain
extrafusal muscle contractions
Another Q: the gamma efferent system controls the excitability of the muscle spindle
Spinal Reflex
*The spinal cord is the only structure in the CNS necessary for a simple reflex
Two important spinal reflexes influence the contraction of skeletal muscles
Stretch reflex:
It is initiated at receptors called muscle spindles that are sensitive to muscle length and tension
This reflex stimulates the stretched muscle to contract
Stretch reflex is monosynaptic (not withdrawal)
Another Q: The sensory endings serving the stretch reflex are classified as propriocecptors
An example is the patellar reflex (knee jerk reflex) in which the striking of the patellar tendon at the knee causes
the quadriceps muscle to contract and swing the leg forward
Another example of a spinal reflex is reflex shivering upon application of a local, cold stimulus applied to
an extremity but not leading to lowering of body temperature
Another Q: The tone of masseter muscle is maintained by stretch reflex (via muscle spindles)
Another Q: Strong stimulation of spindles in the masseter muscle results in contraction
Another Q: Tapping on the side of the face elicits a contraction of the masseter muscle; this is an example of a
stretch reflex
Maintain muscle tone for
Increase efficiency for
Postural reflexes are
maintain by muscle
Smooth out movements
Act as site of
coordination for higherorder inputs
Muscle spindles: (muscle
length and tension)
Are found within the
belly of muscles
Connective tissue sheath
that encloses 2-12
intrafusal muscle fibers
Consists of two afferent
fibers, group Ia and
group 2 fibers
Encapsulated intrafusal fibers that run in parallel with the main muscle fibers so that the spindle will stretch
when the muscle relaxes or stretches
Detect both static and dynamic changes in muscle length
The stretrching gives rise to a generator potential and ultimately to an action potential in the group Ia and 2
fibers that arise from the spindle
The intrafusal fibers in addition to being innervated by sensory fibers also receive motor innervation
from gamma efferents
The activation of these gamma fibers stretches the intrafusal muscle fibers and gives rise to an action
potential in the group Ia fibers
Relaxation of intrafusal muscle fibers decreases impulse activity in the group Ia fibers
Finer movements require greater number of muscle spindles in a muscle
3 components:
Specialized muscle fibers (intrafusal) see below
Separate from the exrafusal fibers, that make up the bulk of the muscle fiber
Sensory terminals: group Ia and II afferents
Wrapped around specialized muscle fibers (intrafusal fibers)


Motor terminalis: gamma motor neurons

Activation maintains the spindle sensitivity
Muscle spindles are the sensory organs concerned with maintenance of skeletal muscle tone
Another Q: The annulospiral (primary) ending of the skeletal muscle spindle is stimulated when the
muscle is stretched
Another Q: Frequency of impulse activity in the afferent nerve from a muscle spindle (Group Ia
afferent fibers) is increased by an increased activity in gamma efferent fibers AND a passive stretch
of the muscle
Spasticity is best characterized by exaggerated stretch reflexes
Constant stimulation of muscle spindle, leads to spastic paralysis
Golgi Tendon reflex:
Initiated at receptors called neurotendinous organs (golgi tendon organs)
Sensitive to tension which occurs as a result of muscular contraction or muscle stretch
Stimulates the contracted muscle to relax
Reverse of stretch reflex
Also depolarize in response to stretch, but this reflex inhibits alpha neuron causing the muscle to relax
Golgi tendon organs (tension):
Innervated by a single group Ib sensory fiber
Reciprocal inhibition
When the stretch reflex stimulates the stretched muscle to contract, antagonistic muscles that oppose the
contraction are inhibited
The neuronal mechanism that causes this reciprocal relationship is called reciprocal innervation
Reciprocal innervation is the process by which motor neurons to extensor muscles acting at a particular
joint are inhibited by stretch of the flexor muscles acting at the same joint
Jaw opening reflex
When a person bites down rapidly on an unexpectedly hard surface while chewing, the result is cessation of motor unit
recruitment in jaw closing muscles by causing a stimulation of periodontal mechanoreceptors
Jaw Jerk reflex
Is an example of a dynamic stretch reflex
Is seen when you tap on the chin, causes the masseter to jerk close
Reflex after-discharge????
Can be explained in terms of internuncial pool circuits
Internunial A neuron functionally interposed between two or
more other neurons
Types of muscle:
Smooth muscle
First a hormone combines with a hormone receptor and activates a
G protein
Then the alpha subunit goes and opens the Calcium channel
Calcium comes in and binds to Calmodulin
Then the CaCM complex binds to Myosin kinase and
activates it
MK attaches phosphate from ATP to myosin
heads to activate the contractile process
A cycle of cross-bridge formation, movement,
detachment, and cross-bridge formation
Relaxation occurs when myosin phosphatase
removes phosphate from myosin
Characterized by:
Slow Ca2+ channels
NO transverse T tubules
NO Troponin
Ach Stimulates Think glands and rest and digest muscles
from Parasympathetic
Spontaneous activity in the absence of nervous stimulation
(Hormones arent nervous!)
They have intrinsic nerves that are contained within
plexuses (GI myenteric plexus)


Sensitivity to the chemical agents either released locally from nerves, or carried in the circulation
They could cause the release of more Ca2+
Another Q: Slow wave potentials are commonly observed in smooth muscle
Another Q: The contractile process in smooth muscle involves actin & myosin
Another Q: Smooth muscle contraction can be maintained for a longer time than skeletal muscle contraction
Another Q: Smooth muscle contains each of the following muscle proteins:
Actin, myosin, tropomyosin (but not troponin)
Another Q: In smooth muscle contraction, myosin kinase is responsible for initiating cross-bridge cycling
Skeletal muscle
Has the greatest membrane potential difference across the membrane
NO slow Ca2+ channels
Has Transverse T tubules
NOT inhibited by Ach
Cardiac muscle
(Calcium-induced Calcium release)
Contraction is dependent on Extracellular Ca2+, which enters the cells during plateau of action potential and
stimulates Ca2+ release from the cardiac muscle Sarcoplasmic reticulum
Cardiac is different than skeletal because:
Action potential has a plateau, which is due to the Ca2+ influx
Cardiac nodal cells spontaneously depolarize, resulting in automaticity
Cardiac myocytes are electrically coupled to each other by gap jxns
A type of striated muscle containing transverse tubules, a slow rate of calcium sequestration, & is inhibited
by Ach
The strength of cardiac muscle contraction is increased when extracellular Ca 2+ is increased
Muscle Cells/Energy
Use the Phosphorylated form of creatine to store energy
Normal metabolism cannot supply energy as quickly as a muscle cell can use it, so an extra storage source is needed
The phosphate group can be quickly transferred to ADP to regenerate ATP necessary for muscle contraction
Autoregulation of bloodflow in muscle determined by muscle metabolites (PAL: K+, lactate, adenosine)
Adenosine causes vascular smooth muscle to relax
Your muscles relax because ATP has been broken down to adenosine
Phosphate compounds found in living organisms can be divided arbitrarily into two groups based on their standard free
energy hydrolysis:
Higher phosphate group-transfer potential than ATP:
Acetyl phosphate
1,3-diphosphoglyceric acid
Carbamoyl phosphate
Creatine phosphate
***1,3-diphosphoglyceric acid & creatine phosphate are energy-rich phosphate carriers
Lower phosphate group-transfer potential than ATP: (Sugars and De-Pi Creatine)
ATP and muscle contration
Hydrolysis of ATP (ATPADP + Pi) provides immediate source of energy for muscle contraction
Although muscle fibers contain only enough ATP to power a few twitches, its ATP pool is replenished as needed
Sources of high-energy Pi:
Creatine Pi
Glycolysis of glucose from stored glycogen
Cellular respiration in the mitochondria of muscle fibers
Slow vs. Fast Twitch
Fast twitch are twice as large
Twice for Type II
Slow Twitch (type I) Think Fast twitch (type II)
Myosin-ATPase activity
Speed/intensity of contraction


Resistance to fatigue
Oxidative capacity
Enzymes for anaerobic Glycolysis
Sarcoplasmic reticulum
Glycogen content

Many (Youve got time for
Less extensive

Low (Burn out quickly)
More extensive
Few (white muscles)

Spinal Cord
Gray Matter
Dorsal Horn (DRGanglia)
Sensory impulses
Anterior Horn (Ventral)
Motor impulses
White Matter
Consists of myelinated nerve fibers, which form the ascending and descending tracts
A tract represents a group of axons within the CNS having the same origin, termination, and function, and is
often named for its origin and termination (i.e., spinothalamic tract)
Sensory impulses
Travel via the afferent of ascending neural pathways to the sensory cortex in the parietal lobe of the brain
where they are interpreted
Sensory information is processed on the contralateral side
Spinothalamic tract (anterior and lateral)
Travel in the anterolateral quadrant of the spinal cord and are also called the anterolateral system
Sensations originate in the dorsal horns of the spinal gray mater, cross to the opposite side of the
cord and ascend via the spinothalamic tracts through the anterior and lateral white columns of the
cord to terminate at the levels of the brain stem and in the thalamus
Lateral spinothalamic tracts
Impulses concerned with pain and temperature
Anterior (ventral) spinothalamic tracts
Impulses from receptors sensitive to light touch
Dorsal Column-Medial Lemniscal System:
Carries sensations mainly in the posterior (dorsal) columns of the cord and them, after synapsing and
crossing to the opposite side in the medulla, upward through the brain stem to the thalamus by way
of the medial lemniscus
Conveys well-localized sensations of touch, pressure and vibration
Fasciculus gracilus
In the medulla, nerve fibers from the fasciculus gracilis synapse in the nucleus gracilis
Fasciculus cuneatus
Fibers from the fasciculus cuneatus synapse in the nucleus cuneatus also in the medulla
**Processes from the two nuclei cross to the other side of the medulla and give rise to a tract
called the medial lemniscus
Nerve fibers from the lemniscus synapse in the thalamus
**Spinocerebellar tract
Destruction of the left spinocerebellar tract at T2 would eliminate positional sense on the LEFT side of
the body below T2
Motor impulses
Travel from brain to muscles via motor (efferent or descending) pathways
Originate in the motor cortex of the frontal lobe
These impulses reach the lower motor neurons of the PNS via the upper motor neurons
Two systems:
Pyramidal system (corticospinal)
Composed of lateral (70 90%) and anterior or ventral (10 30%) corticospinal tracts
Impulses in this system travel from the primary motor cortex through the internal capsule to
the medulla, where they cross to the opposite side and continue down the spinal cord
This system is responsible for fine, skilled, movements of skeletal muscle


Section of the pyramidal tracts produces loss of fine voluntary movements

Think it took fine, skilled movements to build the pyramids
Extrapyramidal system:
Impulses originate in the premotor area of the front lobe (and other areas) and travel to the
pons, where they cross to the opposite side
Then the impulses travel down the spinal cord to the anterior horn, where they are relayed to the
lower motor neurons. These neurons, in turn, carry impulses to the muscles
This system controls gross motor movements for posture and balance
Tracts in this system include
Rubrospinal, reticulospinal, olivospinal, vestibulospional, and tectospinal (neck muscles)
Flaccid Paralysis
Damage to the spinal nerves or to the cell bodies of lower motor neurons resulting in reduced
muscle tone, depressed stretch reflexes, and atrophy

Situated below and posterior to the cerebrum and above the pons and medulla
Divided into two lateral hemispheres and a middle portion
Maintain equilibrium
Muscle coordination (voluntary movement)
Another Q: The cerebellum modifies the pattern of muscular response in reflex and voluntary contractions
Divided into right and left hemispheres, which are connected by nerve fibers called the corpus collosum
Majority of the cortex is involved in associative and higher order functioning such as ideation, language, and thought
Frontal lobes: control skilled motor behavior (think pyramidal tract)
Parietal lobes: interpret somatosensory input
Occipital lobes: interpret visual input
Temporal lobes: interpret auditory input
Controls many homeostatic processes, which are often associated with the ANS
The major center in the brain for ANS regulation is the hypothalamus
Body temperature
A patients internal temperature is monitored by central thermoreceptors located in the hypothalamus
Stimulation of the anterior hypothalamus by a reduction in core temperature will produce shivering
Water balance
Gastrointestinal activity
Carbohydrate metabolism (Gets out epi, which triggers glycogenolysis, etc.)
Sexual activity
Emotions such as fear and rage
Does not control respiration (medulla does)
Does not control pupillary diameter
Does not control PTH
Also regulates release of hormones of the pituitary gland thus, it greatly affects the endocrine system
The hypothalamus-pituitary complex controls hormonal secretions of the corpora lutea, ovarian follicles, and interstitial
cells of the testes (NOT the parathyroids)
Large ovoid mass of gray matter that relays all sensory stimuli (except olfactory) as they ascend to the cerebral cortex
Output from the cortex also can synapse in the thalamus
Located in the lower region of the brain
Contributes to the subconscioius activities of the body, like controlling BP and respiration
Basal Ganglia
Caudate nucleus
Globus pallidus
Substantia nigra


Subthalamic nucleus
Function is control complex patterns of voluntary motor behavior
Basal ganglia & Cerebellum are large collections of nuclei that modify movements on the minute-to-minute basis
Cerebral cortex sends information to both, & both structures send information back to the cortex via the
Output of the cerebellum is excitatory, while the basal ganglia are inhibitory
Balance between these two systems allows for smooth, coordinated movement, and a disturbance in either system
allows for smooth, coordinated movement, (i.e., Parkinsons, Huntingtons, Dysmetria and Ataxia)
Functions in the consolidation of memories and in learning
Sea Horse Shape
Brain stem
Lies immediately inferior to the cerebrum, just anterior to the cerebellum
Consists of:
Connects dorsally with the cerebellum
Contains large voluntary motor nerve tracts
Connects cerebellum with the cerebrum and links the midbrain to the medulla oblongata
Serves as the exit point for cranial nerves V, VI, and VII
Medulla oblongata:
Lowermost portion of the vertebrae brain, continuous with the spinal cord
Joins the spinal cord at the level of the foramen magnum
Contains the cardiac, vasomotor, and the respiratory centers of the brain
Responsible for blinking, coughing, vomiting, and swallowing (not patellar reflex)
Breathing ceases upon destruction of the medulla oblongata
The activity of the respiratory center is decreased directly by increased pH (increased pH means there is
not excess CO2 causing increased H+ [ pH])
Things that can alter the function of the medullary centers for respiration:
1)The central & peripheral chemoreceptors
Nucleus tractus solitarius and nucleus retro ambiguus are the nuclei in the medulla responsible for
generating the respiratory rhythm
Peripheral chemorectors from the aortic and carotid bodies synapse onto the NTS in the medulla to
increase respiration
2)The apneustic & pneumotaxic centers in the pons
Apneustic center
Initiates respiration by activating the inspiratory center in the medulla
Inhibited by lung stretch receptors (Hering-Bruer Reflex)
Remember Hockey, and the Ducks play on the PONd (Pons)
Pneumotaxic center
Inhibitory center in the upper pons
Stimulated by medullary inspiration neurons during inspiration to inhibit the apneustic
center until inspiration stops and expiration begins
3)The CNS at the conscious level
A note on swallowing (no where else to put it):
In swallowing, the larynx is elevated, respiration is inhibited, the epiglottis covers the trachea, & the
eustachian tubes open
Before swallowing can be initiated, afferent information must be received from mucosal mechanoreceptors,
indicating the consistency of soft bolus of food
Trouble swallowing pills
Limbic system
Primitive brain area deep within the temporal lobe
Located in the mid-basal region of the brain
Initiates basic drives (hunger, aggression, emotional feelings and sexual arousal)
Emotional feelings are most closely linked to the limbic system in the brain
Screens all sensory messages traveling to the cerebral cortex
Lets put this one 1st, in case it shows up: Tetrodoxin blocks sodium channels in nerve-axon MBs (its the puffer fish


Action potential is initiated by a depolarizing stimulus:

If it reaches threshold (about 20 mV positive to resting membrane potential) an excitable cell will fire an AP
If neuron does not reach this critical threshold level, then no AP will occur (all or none)
So long as they can reach the threshold, suprathreshold stimuli produce the same AP that threshold stimuli do
Excitable cells include neurons and muscle cells

Makes membrane potential less negative (interior of cell becomes less negative)
Following a depol, a membrane is then more permeable to Na+, which causes a further depol and the opening of
Na+ channels
Membrane potential actually reverses (becomes positive inside the overshoot) as the Na+ influx drives membrane
potential towards Na+ equilibrium potential
If an axonal MB transiently becomes very permeable to Na + ions, the cell MB potential approaches +60mV
Another Q: A depolarized membrane is more permeable to ion flow
Another Q: The generation of an action potential is attributed to a rapid but brief increase in Na+ conductance
Another Q: an AP is related to the entry of Na+ followed by the exit of K+
Another Q: Under normal conditions, the resting potential across a muscle cell membrane is lower than the
equilibrium potential for potassium because the membrane has a low permeability to the sodium ion
Another Q: Sodium permeability of an axon membrane is maximal during the ascending limb of the action potential
Another Q: The primary ionic movement during the depolarization phase of a nerve AP is best described as sodium
ions moving from outside the MB to inside the MB
Another Q: The generation of the spike or action potential is attributed to a rapid but brief increase in Na+
If a nerve cant produce ATP, then the intracellular level of Na+ will slowly rise cant use Na+/K+ ATPase!!
Occurs due to:
Rapid decrease in membrane perm to Na+ (stop flowing in)
Slower increase in membrane perm to K+ (start leaking out)
Membrane potential becomes more negative
Happens because K+ conductance is greater than at rest (relative refractory period)
if you have high extracellular potassium, what occurs?
SAME AS Failed Pump
SAME as Digoxin which prolonges contraction and wrings out the heart longer and more efficiently
SAME as HyperKalemia
Gradual hyperpolarization this is what I put Because K+ cant rush out and make cell more neg
Case in point Hypokalemia can produce a hyperpolarized cell membrane potential
Many K+ channels remain open for several milliseconds after repolarization of the membrane is complete
Increased K+ conductance allows for additional K+ efflux, leaving the interior of the cell more negative (the
This opening of K+ channels, although delayed, is due to the initial depolarizing stimulus


Relative refractory period

The phase at which Sodium activation is ending
In order to trigger a second AP, the depolarizing stimulus must be of a greater magnitude to achieve
Increased K+ permeability (not change in Na+ perm) has primary control over the relative refractory period
The relative refractory period of a nerve corresponds to increased potassium permeability
Absolute refractory period
Determined by the duration of Na+ inactivation gate closure
No matter how strong the second stimulus, the AP cannot be propagated, as H ball is stuck, inactivating the
Sodium channel
The length of the absolute refractory period limits the maximum frequency of effective nerve stimulation
Resting membrane potential (RMP):
Difference in electrical charge between the inside and the outside of the cell membrane of an unstimulated
(nonconducting) neuron
Due to an imbalance of charged particles (ions and proteins) between the extracellular and intracellular fluids
More positive ions (cations) outside the membrane and more negative ion (anions) on the inside
The membrane is said to be polarized (a voltage exists [called the RMP] across the membrane)
RMP varies, but in excitable cells runs between (-) 40 and (-) 85 millivolts
If one could extract the cytoplasm from a resting neuron and measure it, the electrical charge would be negative
Comes from 2 activities:
There is a resting K+ membrane potential which allows (+) charges to leave cell down their electrochem. gradient
In most excitable cells this is the most important determinant of RMP
The Na+/K+ pump establishes the Na+ and K+ gradients across the membrane using ATP
This pump is electrogenic, i.e., it exchanges two K+ ions into the cell for every three Na+ ions it pumps out of
the cell for each ATP that binds to the cytoplasmic-side ATP binding site, resulting in a a net loss of positive
charges within the cell
Cardiac Glycosides (digitoxin) block this pump and keep the inside of the cell more positive and closer to
its threshold, thus increasing cardiac contractility
Ouabain inhibits by binding to the K+ site
The resting potential of a nerve membrane is maintained by active transport of Na + & K+ ions
Another Q: an example of primary active transport is the movement of potassium into a nerve cell
Another Q: Visceral smooth muscle & cardiac pacemaker cells both lack a stable RMP
Another Q: The gradual (phase 4) depolarization in a pacemaker cell is generated by progressively
decreasing K+ conductance, meaning leaky K channels are becoming less leaky
Another Q: At rest, the potential difference across the membrane of skeletal muscle is the greatest (more than the
sinoatrial node & visceral smooth muscle)
Which changes can slow down the rate of the pacemaker cell?
Threshold becomes more positive
The rate of spontaneous depolarization decreases
The maximum diastolic potential (resting potential) becomes more negative
Nernst Equation

n is the number of electrons transferred in the half-reaction.

E0' is the formal electrode potential
E is the electrode potential
Allows you to compute the electric potential difference required to produce an electrical force that is equal to and
opposite to the force of the equilibrium
At the peak of the action potential, the rapid increase in sodium conductance causes the membrane to move toward the
equilibrium potential for sodium
Another Q: The limit of the peak of the AP is solely determined by the Nernst equilibrium potential for Na+ between the
inside of the axon and the surrounding tissue fluid
Think K+ controls the Baseline (RMP)
Think Na+ controls the Changes
Local anesthetics and the membrane
Reversibly block impulse conduction and produce reversible loss of sensation at their administration site
Small, myelinated nerve fibers which conduct pain and temperature sensations are affected first, followed by touch,
proprioception, and skeletal tone


Bind to the inactivation gates of fast voltage gated Na+ channels, stabilizing them in a closed position, effectively
prolonging the absolute refractory period
This decreases Na+ membrane permeability, and therefore reduces membrane excitability
Local chemical anesthetics block nerve conduction by preventing the increase in membrane permeability to Na+
When the excitability has been reduced below a critical level, a nerve impulse fails to pass through the anesthetized
K+, Ca2+, and Cl- conductances remain unchanged
When anesthetics are applied to a neural membrane:
K+ flux remains unchanged
Pores of the membrane become "frozen"
There is a Ca2+ flux through the membrane?????
Resting potential does not drop to a more negative value
An impulse can travel from one nerve to another in only one direction because the synapse limits the direction of travel
Another Q: An AP initiated at the midpoint along the length of an axon will propagate towards BOTH the soma & the
nerve ending
NOTE: The impulse from the 2nd Q will terminate at the soma, because of the reasoning in the 1st Q
Unmyelinated neurons
Impulse travels along the entire membrane surface and is known as continuous conduction
It is relatively slow (1.0 m/sec)
Myelinated neurons
Myelin sheath decreases membrane capacitance and increases membrane resistance Makes you jump,
preventing movement of Na+ and K+ through the membrane
Conserve energy since the Na+ and K+ pumps have to re-establish concentration differences only at the nodes of
Ranvier (spread .2m and 2mm apart)
Travels up to 100 m/sec
Saltatory conduction:
Increase the velocity of nerve transmission along myelinated fibers
Allow repolarization to occur with little transfer of ions
Depends on the presence of nodes of Ranvier
Conduction velocity depends on:
Diameter of nerve fiber an increase in diameter reduces resistance to current flow down the axon
Presence of myelin sheath
Neurilemma (aka sheath of Schwann or Schwanns membrane)
Thin membrane spirally enwrapping the myelin layers of certain fibers, especially those of peripheral nerves, or the
axons of certain unmyelinated nerve fibers
All axons of PNS have a neurilemma (made up of the outer layer of Schwann cells) around them
When a Schwann cell is wrapped successively around an axon it becomes a myelin sheath
Peripheral fibers can sometimes regenerate if the soma (cell body) is not damaged and some of the neurilemma
remains intact
The neurilemma forms a regeneration tube through which the growing axon reestablishes its original connection
If the nerve originally led to a skeletal muscle, the muscle atrophies in the absence of innervation but re-grows when
the connection is re-established
Regeneration of severed axons does not take place in the CNS because of the absence of a neurilemma
Right-sided lesions of the spinal cord result in loss of motor activity on the same side, and pain &
temperature sensation on the opposite side
Remember Motor crosses above in the medulla, where pain crosses right away at the spinal cord
Anatomical junction between 2 neurons depolarization of presynaptic cell initiates a response in postsynaptic cell
An axon terminal of a presynaptic neuron closely approaches a dendrite or cell body of a postsynaptic neuron
But, the two cells are separated by a small synaptic cleft
Neurotransmitters are stored within the axon terminal of a presynaptic neuron in synaptic vesicles
When an AP depolarizes the presynaptic MB, voltage-gated calcium channels are opened causing an increase in
intracellular calcium
Calcium causes the synaptic vesicles to empty the neurotransmitters into the synaptic cleft
Neurotransmitters diffuse across the synaptic cleft and bind to specific receptors on the postsynaptic cell
This process is called synaptic transmission and the time required is called synaptic delay
Synaptic delay explains the following phenomenon:


When an impulse is carried by a chain of two or more neurons, the total transmission time is greater than
the sum of the transmission times for each neuron
Electrotonic or Subthreshold potentials examples:
Inhibitory post-synaptic potentials
Excitatory post-synaptic potentials
Generator potentials in Pacinian corpuscles
Endplate potentials at the neuromuscular jxn
End Plate Potentials
Depolarization of the skeletal muscle cell membrane by motor nerves is directly produced by the change in the endplate potential level to a critical value
Another Q: If AChE is inhibited, there will be prolongation of the endplate potential
Miniature End-Plate Potentials (MEPP)
Due to the release of subthreshold amounts of Ach
Spatial Summation
Occurs when two excitatory inputs arrive at a postsynaptic neuron simultaneously converging circuits
This increases probability of causing an AP in the postsynaptic neuron (excitatory postsynaptic potential = EPSP)
Results from the convergence of several afferent impulses on the same postsynaptic nerve soma
Another Q: Spatial summation in spinal reflexes is dependent upon simultaneous arrival of impulses from a large
number of receptors
Temporal Summation
Occurs when two excitatory inputs arrive at a postsynaptic neuron in rapid succession
There is an increase in the frequency of nerve impulses in a single presynaptic fiber
The amplitude of the AP may be increased by increasing the extracellular concentration of Na+
Point at which nerve signals are arriving fast enough to cause a big steady contraction, not just individual twitches
A tetanic contraction results from a high frequency stimulation

**When are nerve fibers hypoexcitable

During Positive after-potential:
Spontaneous or inducible increase in transmembrane potential following the completion of repolarization
In the heart, this usually corresponds to the U wave on the EKG
Excitatory neurotransmitters in the CNS
Depolarize the postsynaptic membrane bringing it closer to threshold and closer to firing an AP
The altered membrane potential is known as an excitatory postsynaptic potential (EPSP)
Includes: Ach, NE, Epi., Dopamine, Glutamate, Serotonin
Inhibitory neurotransmitters (including glycine and GABA) in the CNS
Hyperpolarize the postsynaptic membrane moving it away from threshold and farther from firing an AP
An inhibitory postsynaptic potential (IPSP)
could result from either an increase in membrane permeability to Cl-, which must run into the cell, or an
increase in membrane permeability to K+ out of the cell
GABA increases the permeability of postsynaptic membranes to chloride ions ClGlutamate decarboxylase, which catalyzes formation of GABA by decarboxylation of glutamate, is unique to
nervous tissue
Cl- then hyperpolarizes the cell, making it harder to feel pain
Secreted by nerve terminals in the spinal cord, cerebrum, basal ganglia, and in the cortex
binds to specific receptors (mainly in the spinal cord) opening chloride channels
Glycine is the immediate precursor for creatine, purines & porphyrins
CNS (= spinal cord + brain)
Peripheral Nervous System (afferents from sensory receptors to CNS + efferents from CNS to muscles, organs, glands)
Somatic nervous system
Consists of:
12 pairs of cranial nerves and 31 pairs of spinal nerves
Autonomic nervous system: has two subdivisions:


Actions of the ANS are largely involuntary (in contrast to those of the somatic system)
Also differs from the somatic system in using two efferent neurons from the CNS to the effector
Preganglionic neurons arise in the CNS and run to autonomic ganglia in the body
Here they synapse with postganglionic neurons, which run to the effector organ (cardiac muscle, smooth
muscle, visceral organs, or glands)
Preganglionic autonomic nerve fibers are exclusively cholinergic
Postganglionic neurons have their cell bodies in the autonomic ganglia and synapse on effector organs
Sympathetic nervous system
Ganglia located in the paraverterbral chain or prevertebral ganglia
Preganglionic neurons originate in the spinal cord segments T1L3 (thoracolumbar)
Pregang symp cell bodies are found in thoracic & lumbar segments of the spinal cord
Uses Ach (cholinergic)
Majority of sympathetic post G are noradrenergic (NE)
Exception: BVs in skeletal muscle, terminal fibers to the adrenal medulla (Ach) & sweat glands
use Ach at muscarinic cholinergic receptors
When the sympathetic nervous system is activated, arterial pressure, mental activity, blood glucose
concentration and blood flow to skeletal muscles all increase (blood flow to the skin does not increase)
NE is NOT used at the terminal sympathetic fibers to the heart epinephrine is
High ratio of postganglionic sympathetic to preganglionic is indicative that stimulation of the sympathetic
NS leads to widespread effects
Sympathetic Stimulation most likely produces Bronchial Dilation
Parasympathetic nervous system
Ganglia located in or near effector organs
Preganglionic neurons originate in the nuclei of cranial nerves in spinal cord segments S2S4 (craniosacral)
Uses Ach (cholinergic)
Postganglionic fibers are all cholinergic
Innervation of salivary gland cells in humans is predominantly parasympathetic postganglionic
Main nerves of the PNS are the vagus nerves
They originate in the medulla oblongata
Each preganglionic PS neuron synapses with just a few postganglionic
The synapses in the CNS are the most susceptible sites in the nervous system to acute anoxia
Absence or almost complete absence of oxygen from inspired gases, arterial blood, or tissues; to be
differentiated from hypoxia.
Cholinergic receptors
Use Ach as neurotransmitter
Membrane receptor proteins located on autonomic postganglionic neurons or on effector organs regulated by Ach
They are always excitatory in preganglionic
Effects of postganglionic PS can be either excitatory or inhibitory (PS fibers innervating heart cause a slowing)
Preganglionic autonomic neurons (both Symp and PS) and all postganglionic PS
Ach is released at sympathetic ganglia, parasympathetic ganglia, somatic efferents to skeletal muscles, & terminal
sympathetic fibers to the adrenal medulla (but not at terminal sympathetic fibers to the heart) Nor is NorEpi
Located on all effector organs innervated by postG neurons of the PS division
Located on those effector organs innervated by postG cholinergic neurons of the Symp division (e.g., sweat
Located at the ganglia of both the Symp and PS divisions
Neuromuscular junction:
Ach is the neurotransmitter released from the presynaptic terminal and the postsynaptic membrane
contains a nicotinic receptor
Ach opens Na+ channels in the motor endplate resulting in depolarization and the opening of voltage
gated Na+ channels in the sarcolemma
Leads to an AP in the skeletal muscle fiber which travels down the transverse tubules resulting in
a release of calcium from the sarcoplasmic reticulum and muscle contraction
Ach Synthesis
Synthesized in the neurons from which it is released
Choline acetyltransferase catalyzes formation of Ach from acetyl CoA & Choline in the
presynaptic terminal
Stored in the synaptic vesicles


Following its release form the presynaptic terminal, Ach is rapidly broken down into acetate and
choline by the enzyme Actylcholinesterase (AChE)
AChE is responsible for the termination of neuromuscular transmission
Another Q: If AChE is inhibited, there will be prolongation of the endplate potential
Receptors: structures that are generally activated by changes (stimuli) in either the internal or external
environment of the body. As a result of the activity of these receptors, nerve impulses are initiated within
the sensory nerve cells
Adrenergic receptors:
Membrane receptor proteins located on autonomic effector organs that are regulated by catecholamines (Epi & NE)
Two main types:
Think 1s are Cons, and the 2s are both Relaxers
Alpha 1: located on smooth muscle, produces excitation (contraction or constriction)
Alpha 2: located in presynaptic nerve terminals, platelets, fat cells, and the walls of the GI tract; produce
inhibition (relaxation or dilation)
Beta 1: located in the heart; produces excitation (increased HR, and contractility)
Beta 2: located on smooth muscle; produce relaxation (dilation)
Treatment of asthma symptoms requires activation of the adrenergic beta-2 pathway
NE stimulates mainly alpha receptors (remember NE doesnt go to the Heart)
Epi stimulates both alpha & beta receptors
Epi at high concentrations B 1 predominates, like Anesthesia, but at low, its B 2 and does vasodilation
Monoamine oxidase (MAO)
Enzyme that catalyzes the oxidative deamination of monoamines such as NE, serotonin, and Epi
Normally NE is uptaken into the nerve endings via active transport or diffused away into body fluids and then
into the blood, but if there is some left over, MAO takes care of it
This deamination process aids in metabolizing excess neurotransmitters that may build up at post-synaptic terminals
MAO is present in the nerve endings themselves
MAOIs increase the available stores of serotonin, NE and epi
Two classes of receptors:
Respond to stimuli from the body surface, including touch, pressure, pain, temperature, light, and sound
Two-point discrimination requires that two sensory receptors are innervated by two different axons
Sensitive to pressure, pain, and chemical changes in the internal environment of the body
Aortic Arch
Transmits via vagus nerve to medulla
Carotid Sinus
Transmits via glossopharyngeal nerve to medulla
Specialized types of receptors:
Specialized receptors that are sensitive to light energy
Located only in the retina of the eye (specifically the rods and cones)
Sensitive to pressure or stretch
Pacinian corpuscles, muscle spindles, golgi tendon organs, Meissners corpuscles, and hair cells which transduce the
senses of hearing and balance
Tactile Sensation
Meissners corpuscles, found in demal papillae
Meissners corpuscles are rapidly adapting touch receptors for 2 point discrimination
Merkels and Pacinian are slowly adapting
Free nerve endings sensitive to changes in temperature
Stimulated by various chemicals (in food, the air, or blood)
Receptors for:
Taste (taste receptors)
Sensations of taste are generated in the taste buds and conveyed to the CNS through CN VII & IX and X
Low threshold of taste for BITTER
Smell (olfactory receptors)


Monitoring pH & gas levels in the blood (osmoreceptors and carotid body O2 receptors)
Carotid and Aortic bodies
respond to decrease in PO2, increased PCO2, and decreased pH
Peripheral carotid body receptors are stimulated most effectively by low arterial O2 tension
Another Q: Increased pulmonary ventilation at high altitudes results directly from the effect of
hypoxia on the carotid body
Respond to changes in PCO2 and pH of CSF, which are influenced by systemic PCO2
DO NOT directly respond to PO2
NOTE on taste/smell: The following are similar characteristics of taste & smell: ??? from 2001 pilot
Receptors are replaced regularly
There are primary classes of taste & odor
Receptors are located on cilia or microvilli at the apical ends of cells
Molecules must be dissolved in saliva or mucus to interact with receptor membrane proteins
Not correct: Receptors initiate APs directly to respective cranial nerve sensory fibers
Smell does have directly firing AP cells with ciliary sensors
BUT TASTE uses G Protein mechanism, Do NOT have axons, and do NOT generate own APs
Free nerve endings sensitive to painful stimuli
Type of interoceptor that provides information concerning the position of body parts, without the necessity of
visually observing the parts
Located in muscles, tendons, joints, and the vestibular apparatus
These sensory receptors serve the stretch reflex
Intracellular Receptors
Remember, steroid hormones can go directly into the cell w/o using an Extracellular receptor and cAMP, etc.
Primary recognition of B-estradiol by its target cell, depends upon the binding of its hormone to a specific
cytoplasmic receptor
The principal mechanism by which glucocorticoids stimulate their target cells is by activating specific genes
Adaptation (to constants They both have 2 Ts)
is a property of certain receptors through which they become less responsive or cease to respond to stimuli of constant
Accomodation (to change)
the property of a nerve by which it adjusts to a slowly increasing strength of stimulus, so that its threshold of excitation
is greater than it would be were the stimulus strength to have risen more rapidly
The enhancement or reinforcement of a nervous activity by the arrivals of signals from other neurons
Another Q: The generator potential of a receptor is characterized by being graded according to strength of the stimulus
Special Sensory Organs
Innermost layer of the eye
Receives visual stimuli and sends the info to the brain
Photoreceptors called rods and cones compose the visual receptors of the retina and contain photopigments
Four different types of photopigments, each consisting of a protein called opsin to which a chromophore molecule
called retinal is attached
Opsins differ from pigment to pigment and confer specific light-sensitive properties on each photopigment
Retinal (retinaldehyde) is produced by vitamin A
Rods and Cones:
Contain a photopigment called rhodopsin
Their response indicates different degrees of brightness characterized by relative lack of color discrimination
They are numerous in the periphery of the retina
Visual purple is seen with rhodopsin in the retina
Usually formed in the retina
During dark adaptation (night vision) rhodopsin is synthesized in the rods of the retina
NOT part of accommodation for near vision
Rods are more abundant, have higher sensitivity, and lower acuity compared to cones


Primarily responsible for color vision

Three different types of cones (red, green, blue)
Each one contains a different photopigment and is selectively sensitive to a particular wavelength of light
Concentrated in the center of the retina especially in the fovea
Principal photoreceptor during daylight or in brightly lit areas
Intraocular structure:
Tough white outer layer; maintains size and form of the eyeball
Transparent dome on surface of the eye
Serves as a protective covering & helps focus light on the retina at the back of the eye
Circular colored area of the eye
Amount of pigment in the iris determines the color of the eye
The ciliary body is made up of three muscles and the iris
It controls the lens thickness
Circular opening (black area) in the middle of the iris, through which light enters the eye
Pupil size is controlled by the papillary sphincter muscle, which opens and closes the iris
Situated directly behind the iris at the papillary opening, by changing its shape, the lens focuses light onto the retina
Lines the inner aspect of the eyeball beneath the retina; very vascular
The eyeball itself is divided into two segments, each filled with fluid
Anterior segment
Has two chambers (anterior and posterior)
Filled with aqueous humor (watery fluid)
Posterior segment
Filled with vitreous humor (thick, gelatinous material)
Made with Type II Cartilage
Changes during accomodation for near vision:
Constriction of pupils
Convergence of eyeballs
Contraction of ciliary muscle
Problems with eyesight:
Myopia (nearsightedness) (My opia, its what I have)
The primary effect of myopia is related to eyeball length relative to refractive power of the lens
The eye is too long for the refractive power of the lens, and far objects are focused at a point in front of the
The eye can focus on very near objects
Tx with concave lenses
Hyperopia (farsightedness)
The eyeball is too short for the lens, and near objects are focused behind the retina
A slight detachment of the retina results in a decrease of length from the optical center, and the subject
therefore exhibits farsightedness (99% sure that farsightedness is the answer)
So in a detached retina, you cant read!
Distant objects are focused correctly
Tx with convex lenses
Occurs when the curvature of the lens is not uniform
Tx with cylindric lenses
Inability of the eye to focus sharply on nearby objects
Results from the loss of elasticity of the lens with advancing age
Tx with bifocals
The constriction of the pupil of the eye
Can be caused by a normal response to an increase in light, certain drugs or pathological conditions


Prolonged abnormal dilation of the pupil of the eye induced by a drug or caused by a disease
Parts of the ear: Pg. 474 Netters h&n anatomy
External ear:
Auricle (pinna)
Directs sound waves
External auditory canal (meatus)
Contains hair and cerumen (brown earwax) serves as a resonator
Middle ear:
Air-filled cavity in the temporal bone
Auditory (eustachian) tube:
Equalizes pressure
Ear aches may develop as a result of blockage of the eustachian tube because pressure in the middle ear is not
equalized with atmospheric pressure
Ossicles (malleus, incus, stapes)
Link together to transmit sounds to the oval window
Inner ear:
Formed by a bony labyrinth and a membranous labyrinth
Vestibule (saccule and utricle):
Associated with sense of balance
Responsible for static positioning (affected by gravity)
Responds to LINEAR acceleration or deceleration
Semicircular canals:
Concerned with equilibrium, angular acceleration and deceleration
Each one contains an enlarged region called the ampulla containing the receptor organ, the Crista ampullaris
The receptor contains hair cells whose processes are embedded in a gelatinous matrix
Rotary acceleration in any plane will cause a sense of rotation opposite to the direction of the endolymph
An angular (NOT LINEAR) acceleration or deceleration represents an adequate stimulus for semicircular canals
Cochlea (contains two membranes, vestibular and basilar):
Portion of inner ear responsible for hearing
The spiral organ (organ of Corti)
Responsible for perception of sound
Contains receptors (called hair cells) for hearing
Basic functional unit of hearing it transforms fluid vibration from sound waves (mechanical energy) into
a nerve impulse (electrical energy)
Impulses for hearing are transmitted to the brain from receptors in the cochlea
Low pitch, low frequency (Bass) at the apex or middle of the snail
High pitch, High frequency at the big base of the snail
The Elderly lose which type first? High pitched or at the base

GI System
Ptyalin AKA amylase
NZ in the saliva for digesting starches
The regulation of Gastric Secretion
Cephalic stage:
Eating, tasting, smelling, and thinking about food increases the rate of gastric secretion via activation of the PS
nervous system, specifically the vagus


The cephalic phase of gastric secretion is a reflex mediated by the vagus nerve
What allows your stomach to become bigger?
Receptive relaxation is an increase in the stomach volume before the arrival of food
Vagotomies are sometimes used to control gastric ulcers
Vagus nerve also causes contraction of the gallbladder (not part of the cephalic stage)
Gastric stage:
Stretch associated with a volume of food filling the stomach also increases the rate of gastric secretions
This phase accounts for about 70% of the total gastric secretion
Involves both neural reflex pathways and the release of gastrin
Enteroendocrine cells (gastrin or G cells) of the pyloric glands of the stomach mucosa secrete it
Absorbed in the blood and carried to the oxyntic glands (gastric glands) in the body of the stomach
There it stimulates the parietal cells to secrete HCL
Relaxes the pyloric sphincter, activates the pyloric pump, and contracts the esophageal sphincter
THINK opposite to the enterogastric reflex
Intestinal stage:
The delivery of acidic, high osmolarity food/stuff into the small intestine
Inhibits gastric secretion via the enterogastric reflex and hormonal mechanisms (secretin)
Nitrous Oxide
Causes smooth muscle relaxation (lower esophageal sphincter)
Gastric glands of stomach mucosa:
Stomach glands produce as much as 23 liters of secretions per day
The pH of gastric secretion is 1.03.5
Gastric juice usually has a [H+] > 1x10-3 M (among answer choices of bile, urine, saliva, & pancreatic juice)
The mucus produced by mucus-secreting cells is very alkaline and protects the stomach wall from being exposed to the
highly acidic gastric secretion
G cell
Secretes Gastrin
Stimulates secretions of Acid, IF, and Pepsinogen
Stimulates Gastric motility
Inhibited by secretin or stomach pH <1.5
Stomach emptying is enhanced by gastrin & the presence of food in the stomach
Mucous neck cells (pyloric glands):
Secretes Mucus and some pepsinogen
Adheres to the stomach walls, lubricates the walls and protects the gastric mucosa from acidic secretions
Chief (peptic or zymogenic) cells:
Secretes Pepsinogen
Formed inside chief cells in the inactive form (pepsinogen)
In the upper part (Fundus) of the stomach
Once pepsinogen is secreted & comes in contact with previously formed pepsin in the presence of HCl, it is
converted to form active pepsin
Begins protein digestion
The most important function of HCl is activation of pepsinogen
Then that active pepsin, activates its other pepsinogen buddies
Does NOT secrete Bicarbonate
Parietal (oxyntic) cells:
K+ and Cl- go out of the cell via a cotransporter
Then K+ goes back down the gradient formed by that cotransporter via the H+/K+ ATPase and H+
goes out causing gastric acid
Secretes HCl
Kills bacteria, breaks down food, activates pepsinogen to pepsin
Sterilizes chyme
Stimulated by histamine, Ach, and gastrin
Inhibited by Prostaglandin (PGI2 and PGE2) and GIP
NOT essential for digestion
Secretes Intrinsic factor
Vitamin B12 absorption in terminal ileum
So no parietal cells, you get pernicious anemia
Secretion is increased by Ach, gastrin and histamine


Peptic ulcers can result either from the oversecretion of acid and pepsin or a diminished ability of the mucosal
barrier to protect against these secretions
Intestinal secretions
Mainly mucus, are secreted by goblet cells and enterocytes
The pH of the secretions in the small and large intestines is 7.5-8.0
Surface cells (duodenum)
Neutralizes acid
Stimulated by secretin (potentiated by vagal input) CCK
I cells (duodenum and jejunum)
Cholecystokinin (CCK)
Stimulates gallbladder, and pancreatic enzyme secretion
Inhibits Gastric emptying
Stimulated by FAs and AAs
Augmented flow from the gallbladder during feeding results in part from the release of CCK
Stimulates gall bladder contraction, releasing bile
pH ~7.8
Produced by the liver and stored in the gallbladder
Composed of bile salts, phospholipids, cholesterol, bilirubin, and water (97%)
Aids in the emulsification, digestion, and absorption of fats
S cells (duodenum)
Natures antacid
Stimulates pancreatic Bicarb secretion
Inhibits gastric acid secretion
Stimulated by FAs and AAs
D cells (pancreatic islets and GI mucosa)
Inhibits Gastric acid and pepsinogen secretion, Pancreatic and intestine fluid secretion, Gallbladder contraction,
and Release of both insulin and glucagons
Stimulated by acid and inhibited by the vagus
Vasoactive Intestinal Peptide (VIP)
Secreted by smooth muscle and nerves of the intestines
Relaxes intestinal smooth muscle
Causes pancreatic bicarb secretion
Inhibits gastric H+ secretion
Pancreatic secretions
From pancreatic acinar cells include enzymes involved in protein breakdown including:
Alpha-amylase starch digestion, secreted in active form
Proteases protein digestion, secreted as proenzymes
Trypsin Converted from trypsinogen by enterokinase, then trypsin activates the other proenzymes
Lipase Fat digestion
Bile salts aid in the action of pancreatic lipase
Activated by?
Acid, Trypsin, Enterokinase , bile salts
Cholesterol esterase
Phospholipase A Fat digestion
Pancreatic enzymes are secreted in an inactive form and are then activated in the small intestine
Pancreatic duct cells (I cells?) secrete a fluid that is high in bicarbonate ion concentration (pH of 8.0 8.3)
Pancreatic secretions stimulated by:
Ach Major stimulus for zymogen release, poor stimulus of bicarb
CCK Major stimulus for enzyme-rich fluid by pancreatic acinar cells
Secretin Stimulates ductal cells to secrete bicarb-rich fluid
Somatostatin Inhibits the release of gastrin and secretin
Gastric empyting:
Foodstuff entering the duodenum, especially fats and acidic chyme, stimulates hormone release
Hormones released in duodenum:


Gastric inhibitory peptide (GIP)

Inhibits the pyloric pump
So, fat ingestion most markedly affects (inhibits) the rate of gastric emptying
ParaSympathetic activation
Usually excitatory in the GI tract
Increases production of saliva
Increases H+ secretion
Increases pancreatic enzyme and Bicarb secretion
Stimulates enteric nervous system to create peristalsis and relax sphincters
Sympathetic activation can have either excitatory or inhibitory effects
Increases the production of saliva (serous watery, parotid)
Decreases splanchnic blood flow in flight or fight response
Decreases motility
Constricts sphincters
Stimulation of the sympathetic nervous supply to the gastrointestinal tract generally causes inhibition of motility
Semifluid contents of the stomach, consisting of partially digested food and gastric secretions
The volume and composition of chyme that enters the duodenum (beginning of the small intestine) exerts a major
influence on gastric motility and the rate of gastric emptying
When a portion of the small intestine becomes distended with chyme, the stretch of the intestinal wall elicits localized
rhythmic contractions, called segmentation
Segmentation (aka rhythmic segmentation)
Occurs at a rate of 11 to 12 cycles/min in the terminal ileum
The contractions chop the chyme many times a minute
In this way they promote progressive mixing of the food with digestive secretions of the small intestine
Intensity can be influenced by mechanical, neural, and hormonal inputs
For example, distension of the intestine by chyme and
PS neural activity both increase the contractile force,
while Symp neural activity decreases it.
Two major types of contractions in the GI tract:
Contraction generates propulsive movements
Starts when food enters the stomach
Mixing contraction:
Serve to spread out the food and increase the surface area
available for digestion and absorption
***Smooth muscle control in the GI tract is under the
control of the myenteric plexus of the enteric NS
Entering the intestinal mucosa:
Fatty acid:
In the lumen of the small intestine, dietary TGs are
emulsified by bile salts into smaller fat droplets (micelles)
where they are enzymatically digested into free FAs and 2
The free FAs and monoglycerides readily diffuse across
the brush border by simple diffusion
Then are reconstituted in the ER into TGs and finally
transported by lymphatics
Dipeptides and amino acids
The end-products of protein digestion
The final digestive stage occurs by brush border peptidases
and absorption immediately follows
Absorption across the brush border occurs by multiple
secondary active transports utilizing either the Na+ or
H+ gradients
Disaccharides and small glucose polymers
Occurs at duodenum and proximal jejunum
Hydrolyzed at the brush border by lactase, sucrase,
maltase and alpha-dextrinase


The resultant monosacchariades, glucose and galactose are then absorbed by secondary active transporters
driven by the Na+ gradient this is an example of a co-transporter
The immediate energy source for glucose transport into
intestinal endothelial cells is a Na+ gradient across the
luminal MB
The Odd-ball Fructose absorption is mediated by
Facilitated diffusion (F for F)
The following secrete HCO3- into the GI tract:
Colon mucosa
Salivary glands
Stomach mucosa
(NOTE: Chief cells do not)
Functions of liver:
Bile formation
Protein metabolism (deamination of aa, , formation [not
elimination], plasma protein formation, synthesis of aa)
Another Q: Death from advanced liver disease caused by
Hepatitis C is PRIMARILY due to inhibition of urea
Steroid conjugation
Carbohydrate storage
Prothrombin synthesis and fibrinogen production
Another Q: Thrombin itself is not found in blood plasma, only its precursor prothrombin
Liver disease results in missing prothrombin and fibrinogen (not thrombin)
Formation of plasma proteins
Regulation of blood sugar level
NOT Secretion of digestive NZs
Bile is NOT an NZ, it is an emulsifying agent
NOT elimination of urea
Occurs mainly in the liver (90%), but the kidney is a minor contributor (10%)
During prolonged starving the kidney becomes the major glucose-producing organ
Is the synthesis of glucose from compounds that are not carbohydrates
Glucose can be made from lactate, glycerol, pyruvate, and fructose (but not acetyl CoA, which comes from
Found only in the liver and functions at a significant rate only after a meal
This enzyme uses ATP to catalyze the phosphorylation of glucose to glucose-6-phosphate during glycogen synthesis
Then the G-6-phosphate cannot diffuse back out of the cell membrane and can be used to make glycogen
**Other tissues use hexokinase to do the same thing as glucokinase
ONLY hexokinase is feedback inhibited by Glucose-6-Phosphate
**Liver does not participate in the regulation of immediate blood glucose
Functions of liver in protein metabolism:
1. Deamination of amino acids:
Required before they can be used for energy or before they can be converted into CHO or fat
2. Formation of urea for removal of ammonia from the body fluids:
The liver is the organ pimarily responsible for the formation of urea
Removes ammonia from body fluids if the liver fails to do this, the result is a hepatic coma and death
Urea cycle
Ordinarily, Careless Crappers Are Always Freaks About Urination
Ornithine + Carbamoyl phosphate
Citrulline + Aspartate Argininosuccinate (Fumarate),
Arginine Urea


Occurs almost exclusively in the liver

It represents the fate of most of the ammonia that is channeled there
Ammonia is converted to urea in the liver for eventual excretion
The level of non-protein nitrogen in the blood is due primarily to the level of urea
Another Q: The major component of non-protein nitrogen in the blood is urea
Another Q: The main product of protein nitrogen metabolism in urine is urea
The two nitrogen atoms that are incorporated into urea enter the cycle as ammonia and aspartate
1 from GLUTAMATE (ammonia), 1 from an AA (aspartate)
Urea is produced by the hydrolysis of arginine, which is ureas direct precursor
Another Q: Arginase directly catalyzes urea formation in a cell
Carbomyl Pi is formed from carbon dioxide and ammonia
The first two reactions (ammonia to carbamoyl Pi then added to Ornithine to form Citrulline) occur in the
mitochondria, whereas the remaining cycle enzymes are located in the cytosol****
Ordinarily Careless Crappers
Nitrogen can also come from Carbomyl Pi : Glutamic acid goes to NH3 + CO2 = carbamyl phosphate
Urea that is formed in the urea cycle is passed via the blood stream to the kidneys & is excreted into urine
Carbamoyl Pi is added to ornithine to become citrulline
Aspartate is added to citrulline to make argininosuccinate
Fumarate is released resulting in arginine
Arginine is hydrolyzed and yields urea and ornithine
3. Formation of plasma proteins:
Accounts for 90% of all plasma proteins
4. Ability to synthesize certain amino acids and other important chemical compounds from amino acids
The nonessential amino acids can all be synthesized in the liver
To do this for most aa, a keto acid having the same chemical composition (except at the keto oxygen) as that of
the aa is first synthesized
Then the amino radical is transferred through transamination from an available aa to the keto acid to take the
place of the keto oxygen
Most abundant non-phospholipid component of the cell membrane
Least Polar
1) Primarily used by mammalian cells as a component of the cell membrane
2) Secondarily used as the immediate precursor of bile acid
3) Thirdly, used as precursor to various steroid hormones
Mainly synthesized in the liver from acetyl CoA
NADPH is necessary for the de novo synthesis of cholesterol AND FA SYNTHESIS
NADPH is used in the reduction of cholesterol
Key intermediates in biosynthesis of cholesterol are:
HMG CoA, mevaolonic acid, isopentyl pyrophosphate, and squalene


NOT Cholic acids

The major regulatory enzyme is HMG CoA reductase
Rate Limiting Enzyme of Cholesterol Synthesis HMG CoA Reductase
Statins inhibit HMG-CoA reductase
Bile salts are formed from cholesterol (via cholic acid)
Most endogenous cholesterol in the liver is converted into cholic acid
Another Q: In certain endocrine tissues cholesterol is converted to steroid hormones:
The most potent naturally occurring human estrogen
Estrogens a class of steroids that contains 18 carbon and an aromatic ring
Vitamin D is also formed from cholesterol by a series of reactions requiring the skin, liver and kidney
UV activation of precursors in the skin are required for vitamin D3 synthesis
Cholesterol absorption depends upon the presence of bile salts in the intestinal lumen
Cholesterol is mostly esterified with FAs when circulating in blood plasma
Circulating cholesterol is taken up into liver cells
Here it inhibits synthesis of additional cholesterol from acetyl CoA via allosteric inhibition of HMG CoA reductase
This provides intrinsic feedback control system to reduce excess cholesterol synthesis
Liver releases glucose back into the circulating blood during exercise
The skeletal muscle and the brain take up this extra glucose
Liver has the major responsibility for maintaining blood glucose levels
Releases glucose into the blood during muscular activity and in the interval between meals
The released glucose is derived from two sources:
1) Breakdown of stored glycogen
2) Formation of new glucose by gluconeogenesis
Fasting State vs. Fed State
Fed State
Digestive System
Glucose (liver)
Glu-6-P Glycogen OR Glycolysis OR HMP Shunt
Amino Acids (liver)
Proteins OR Glycolysis
Chylomicrons (liver) Fatty Acids Glycolysis OR Fats VLDLs
Fasting State
Fatty Acids (liver)
Acetyl CoA Ketone Bodies
Amino Acids/Glycerol/Lactate (liver)
TCA Cycle Acetyl CoA Ketone Bodies
(liver) Glycogen
G6P Pyruvate Acetyl CoA Ketone Bodies
OR (liver) Glycogen
Glucose (out of the liver) Glucose
So, fasting for several hours leads to decreased liver glycogen
NOTE: Heres a question that uses info from all over the place:
Each of the following occurs during prolonged starvation:
Circulating T4 is converted to rT3 (reverse T3)
Ketoacidosis develops progressively
Insulin levels are depressed
(Primary fuel is not glycogen)
Glucose is required particularly by tissues such as the brain and RBCs
RBCs oxidize glucose to pyruvate and lactate
Glucose is the major fuel for the brain
It oxidizes approximately 140 g/day to CO2 and water, producing ATP
The brain contains no significant stores of glycogen, and is therefore completely dependent on the availability
of blood glucose
In skeletal muscle
Glucose is phosphorylated, then degraded by glycolysis to pyruvate, which is converted to acetyl-CoA and oxidized
via the citric acid cycle
Glucose is the major end-product of CHO ingestion
Liver enzymes:
Glutamate-pyruvate transmaminase (GPT): also called alanine animotransferase (ALT)
Glutamate-oxaloacetate transmaminase (GOT): also called asparatate aminotransferase (AST)


Countercurrent mechanism: (picture)
The countercurrent theory is used to explain the functioning of the kidney
Essential for the concentration of urine
This is the mechanical system employed by a kidney dialysis machine (Counter current)
System in the renal medulla that facilitates concentration of the urine as it passes through the renal tubules
Responsible for secretion of hyperosmotic urine in response to elevated plasma osmolarity and requires that the
penetration of the loop of Henle into the renal medulla for the development of the medullary osmotic gradient
The loops of Henle are responsible for the establishment of an osmotic gradient within the medulla of the kidney
Depends on the special anatomical arrangement and transport properties of the loops of Henle
Countercurrent multiplier in the loops of Henle is dependent upon:
Active reabsorption of sodium ions by the thick ascending limb of the loop of Henle
Osmotic equilibrium between interstitial fluid and tubular fluid in the descending limb of the loop of Henle
Continued inflow of new sodium chloride from the proximal tubule into the loop of Henle
The sodium chloride reabsorbed from the ascending loop of Henle keeps adding to the newly arrived sodium chloride,
thus multiplying its concentration in the medullary interstitium
Countercurrent exchange in the medullary BVs, called the vasa recta
The vasa recta do not create the medullary hyperosmolarity but do prevent it from being dissipated and can carry
away the water which has been reabsorbed
The kidneys basic structural and functional unit
Parts: pg 384 in First Aid
Proximal convoluted tubule:
Workhorse of the nephrons
Requires the greatest amount of ATP
80% of ATP is used for Na+ reabsorption
67% occurs in the PCT
Water Permeable!!!, as solutes get pumped actively, water follows
Reabsorption of ALL glucose and AAs, most of the bicarbonate, water, and Na+, chloride, phosphate, calcium
Secretes Ammonia which acts as buffer for secreted H+
Approximately 2/3 of the glomerular filtrate is reabsorbed in the proximal convoluted tubule
This includes 100% of the filtered glucose and amino acids
Another Q: The osmotic pressure of the filtrate at the end of the proximal convoluted tubule is about the same
as that of plasma
Another Q: Most fluid reabsorption by the kidney occurs here
Thin Descending limb of loop of Henle:
Reabsorption of solutes and water
Impermeable to Na+
Thick Ascending limb of loop of Henle (Thick and Thin)
Has a thick wet suit on
Impermeable to Water
Reabsorbtion Actively of Na+, Cl-, and K+
Indirectly induces the reabsorption of Mg2+ and Ca2+
This, in the thick portion, is the basis for the countercurrent multiplier activity
Henles loop is the segment of the nephron wherein the tubular fuid has the highest osmolarity &
Osmolarity of 1400 at the bottom
Dont get clowned the Collecting duct is not part of the nephron
Distal convoluted tubule:
(controlled by aldosterone)
Secretion of H+ and K+
Proximal Secreted Ammonia
Reabsorption Actively of Na+ and ClReabsorption of Ca2+ is under control of PTH
Collecting duct
Where the distal ends of each distal convoluted tubule join
Reabsorbs Na+ in exchange for secreting K+ and H+ (controlled by aldosterone)
Secretes H+ and reabsorbs water (controlled by ADH = vasopressin)
Osmolarity of medulla can reach 1200-1400mOsm
Juxtaglomerular vs. Cortical Nephrons


Have their renal corpuscles close to the base of the medullary pyramid
Have Long loops of Henle and long thin segments that extend into the inner region of the pyramid
Have their renal corpuscles in the outer part of the cortex
Have Short Loops of Henle and the hairpin turn occurs in the distal thick segment
Inbetween the other two, duh!
Juxtamedular & cortical nephrons differ primarily in length of the thin segment of the loop of Henle
Glomerular filtration
Filtration process as blood flows through the kidney
Some of the plasma (16-20%) is filtered out of the glomerular capillaries and into the glomerular capsules of the renal
tubules as the glomerular filtrate
Formation of glomerular filtrate does not rely on diffusion
Another Q: Energy for filtrate formation is derived from the hydrostatic pressure of the blood
Glomerular filtrate contains everything contained in plasma (urea, glucose, NaCl) except plasma protein
Glomerular filtrate contains the same concentration as plasma does of urea, glucose, amino acids, and plasma
NOT Steroid hormones
Glucose & sodium chloride are filtered and subsequently reabsorbed
The fact that increased concentration of colloids in plasma diminishes the formation of filtrate supports that the
glomerulus acts like a simple physical microfilter
Glomerular Filtration Barrier
Composed of:
1. Fenestrated capillary endothelium (size barrier)
2. Fused basement membrane with heparan sulfate (negative charge barrier)
The charge barrier is lost in nephritic syndrome, resulting in albuminuria, hypoproteinemia,
generalized edema, and hyperlipidemia
3. Epithelial layer consisting of podocyte foot processes
A starch that is given by mouth
NOT natural, thats the creatinine one
Is freely filtered from the glomerular capillaries into Bowmans capsule, but does not undergo tubular secretion or
If the clearance of a substance which is freely filtered is < inulin, then there is a net reabsorption of the substance
If the clearance of a substance which is freely filtered is > inulin, then there is a net secretion of the substance
Measures Clearance Rate
Glomerular filtration rate (GFR)
Can be calculated by the clearance of inulin from plasma
GFR may be measured by a substance that is filtered but not reabsorbed or secreted (not creatinine)
A substance that is actively secreted by the kidney is not useful in measuring GFR; it is useful is measuring:
Renal blood flow
Renal plasma flow
Filtration fraction
Tubular Maximum
The rate at which a substance is cleared from plasma
Renal clearance equation
Cx = UxV/Px
Cx Volume of plasma cleared
Ux Urinary [ ] of x
V Urine Volume
Px Plasma [ ] of x
= (plasma volume completely cleared)/(unit time) = (urinary concentration of the substance * urine volume) /
(plasma concentration of the substrate)
Assessment of blood urea nitrogen (BUN) and serum creatinine can also be used to estimate the GFR
Creatinine is freely filtered, is not reasorbed, slightly secreted, and produced endogenously at a constant rate
Q: Creatine is not slightly reabsorbed
Another Q: Creatinine is the natural metabolite measured clinically as a predictor of GFR
(Dont mix this Q up with inulin)
Clearance rate for a substrate that is completely removed in one pass through the kidney = renal plasma flow


Simply put, the amount of the substance removed correlates to the amount of plasma that flows through the kidney
Decrease in GFR is caused by:
Constriction of afferent arteriole:
Decreases the glomerular capillary hydrostatic pressure and decreases the renal blood flow (RBF)
Relaxation of efferent arterioles:
Decreases the glomerular capillary hydrostatic pressure
Increased plasma protein concentration of glomerular capillary blood:
Increases plasma oncotic pressure
Ureteral blockage (increased hydrostatic pressure in Bowmans capsule):
Blockage of urine transport through the ureters will increase hydrostatic pressure in Bowmans capsule
Capsule hydrostatic pressure is the major force causing glomerular filtration
Excessive constriction of the efferent arteriole will decrease RBF and GFR
Another Q: A proportionate increase in resistance of afferent and efferent arterioles of the kidney would
result in a decrease in RBF with no change in GFR
Increase in GFR is caused by:
Decreased plasma oncotic pressure (synonym with osmotic)
Vasodilation of afferent arterioles
Decreased pressure in Bowman's capsule
Moderate vasoconstriction of efferent arterioles
The most likely cause of an increase in filtration fraction is efferent arteriolar constriction
PAH used to measure eefective renal plasma flow
Both filtered and secreted and is used to estimate renal plasma flow
(Filtration of PAH is also know as Effective Renal plasma flow (RPF))
Secreted in proximal tubule
Secondary active transport system
Mediated by a carrier system for organic acids
Competitively inhibited by probenecid
Filtration Fraction
= GFR/RPF or Cinulin/CPAH
The most likely cause of an increase in filtration fraction is efferent arteriolar constriction
Prostaglandins dilate afferent arterioles ( RPF and GFR, so FF stays the same)
So NSAIDs can cause renal failure because they inhibit the renal production of prostaglandins, which
normally keep the afferents dilated to maintain GFR
ACE Inhibitors
Angiotensin II constricts efferent afterioles ( RPF and GFR, so FF would increase)
End in PRIL
So if you inhibit ACE, no Angiotensin II and FF would be less)
Free Water Clearance
CH2O = V - Cosm
V = Urine flow rate
Cosm = Uosm V/Posm
Glucose Clearance
At a normal level, all glucose is reabsorbed in proximal tubule
At plasma glucose level of 200mg/dL, glucosuria begins (Threshold)
At plasma glucose level of 300mg/dL, transport mechanism is completed saturated (Tm)
Glucosuria can be caused by low insulin level, high blood sugar level, impaired tubular reabsorption, & high
The best explanation why glucose does not appear in the urine is that glucose is freely filtered, but is removed
by reabsorption in the proximal convoluted tubule
The normal clearance of glucose is 0 mg/min
Glucose transport from the lumen of the nephron depends on Na + transport (via a cotransporter)
The presence of glucose in the urine proves a person has exceeded his/her renal threshold for glucose
So a High renal threshold usually wont result in glucosuria
Amino Acid Clearance
Resorption by at least 3 different carrier systems, with competitive inhibition within each group
Secondary active transport occurs in proximal tubule and is saturable
Kidney normally excretes 1-2 L urine/day


When tubular secretion and reabsorption processes are completed, the fluid remaining within the tubules is transported to
other components of the urinary system to be excreted as urine
Urine consists of water and other materials that were filtered or secreted into the tubules but not reabsorbed
Although about 180 L per day of glomerular filtrate are produced, the kidneys only excrete 1-2 L
Approximately 99% of filtrate is returned to the vascular system, while 1% is excreted as urine
Water and substances the body needs are returned to the blood, whereas waste products and excess fluid and solutes
remain in the tubules and are excreted form the body as urine
In response to elevated plasma osmolarity, a small volume of concentrated urine will be produced
If plasma osmolarity is lower than normal, a large volume of dilute urine will be excreted
Excretion rate = filtration rate reabsorption + secretion
Movement of solutes from the tubular fluid into the interstitial fluid
Occurs in the following:
Proximal tubule
Loop of Henle
Distal convoluted tubule
Collecting duct
Processes include: 1 active transport, 2 active transport, facilitated diffusion, simple diffusion, and solvent drag
Transport can be either transcellular or paracellular
***The osmolarity of the renal fluid at the end of the proximal tubules equals that of plasma
Movement of solutes from the interstitial fluid into the tubular fluid
Normal urine
Consists of Na+, Cl-, K+, calcium, magnesium, sulfates, phosphates, bicarbonate, uric acid, ammonium ions,
creatine, and urobilinogen
The main route of calcium excretion from a normal human adult is FECES
Is clear, straw-colored, slightly acidic, and has the characteristic odor of urea
Normal specific gravity of urine is between 1.005 and 1.030
Formation is important in the regulation of acid-base balance, maintenance of ECF volume and BP, and in
maintaining the normal osmolarity of ECF
Results from a decrease in the tubular reabsorption of water (often after ingesting a large quantitiy of water)
Another Q: An osmotic diuresis is observed during diabetes mellitus
Causes of dilute urine:
Absence of ADH, diabetes insipidus
Causes of concentrated urine:
Decreased plasma volume, cellular dehydration, diabetes mellitus, excess ADH
Think in DM, all of the glucose in the urine, so it still is concentrated even though you get osmotic diuresis
to go with it
In cellular dehydration water moves from interstitial and Extracellular to inside the cells, now you have a
decrease in plasma volume
This decrease produces action potentials to the supraoptic hypophyseal tract and into the neural lobe of
the posterior pituitary resulting in the release of ADH
ADH of course gets water reabsorbed and leaves the urine more concentrated
***Na+ has the greatest influence on water retention, even more than Cl- & K+
The ability to concentrate urine is most closely related to the length of the loop of Henle
Produced from the metabolism of a variety of compounds
Amino acids is the most important because most Western diets are high in protein and provide excess aa, which are
deaminated to produce ammonia
Sources of ammonia:
From amino acids:
Many tissues, but particularly the liver, form ammonia from amino acids by the aminotransferase and glutamate
dehydrogenase reactions
From glutamine:
The kidney (specifically, the tubular cells) form ammonia from glutamine by the action of renal glutaminase
Most of this ammonia is excreted into the urine as NH4, which is an important mechanism for maintaining the
bodys acid-base balance
From amines:


Amines obtained from the diet and monoamines that serve as hormones or neurotransmitters give rise to
ammonia by the action of amine oxidase
From purines and pyrimidines:
The catabolism of purines and pyrimidines, amino groups attached to the rings are released as ammonia
Amino acids are the source of most of the nitrogen in purines
Ammonia & the alpha amino acids:
Ammonia NH+ is formed from glutamine in the kidney
Cellular levels of ammonia must be maintained at low concentrations due to its toxicity
Glutamate dehydrogenase can catalyze the formation of glutamate from ammonia and a-ketoglutarate using NADPH
as a cofactor (SEE UREA CYCLE CHART)
Formation or urea in the liver is qualitatively the most important disposal route for ammonia
Urea travels in the blood from liver to kidneys, where it passes into the glomerular filtrate
Ammonia is excreted in high amounts after prolonged acidosis
Endocrine Fxns of the Kidney
Conversion of 25-OH vitamin D to 1,25-(OH)2 vitamin D via 1alpha-hydroxylase, which is activated by PTH
JG cells secrete erythropoietin to stimulate bone marrow and also secretes renin in response to decreased renal arterial
pressure and increased renal nerve discharge (Beta 1 effect)
Secretion of prostaglandins that vasodilate the afferent arterioles to increase GFR
Hormones that act on the Kidney
Vasopressin (ADH)
Induced by increased plasma osmolarity and decreased blood volume
Actions: H2O permeability, urea absorption in collecting duct, and Na+/K+/2Cl- transporter in thick
ascending limb
Induced by decreased blood volume (via Angiotensin II), and by plasma [K+]
Actions: Na+ resorption, K+ secretion, H+ secretion in distal tubule
Angiotensin II
Induced by Decreased blood volume (via Renin)
Actions: Contraction of efferent arteriole ( GFR), Na+ and HCO3- reabsorption in proximal tubule
Atrial Natriuretic peptide (ANP)
Induced by Increased atrial pressure
Actions: Decreased Na+ reabsorption, GFR
Induced by Decreased plasma [Ca2+]
Actions: Ca2+ reabsorption, 1,25 (OH)2 vitamin D production, Decreased PO 43- reabsorption
Acid/Base Regulation
Kidneys regulate acid-base balance by the secretion of hydrogen ions (H+) into the renal tubules and the reabsorption of
bicarbonate ions (HCO3-).
Measured by urine pH, ammonium excretion and phosphate excretion
Secretion of ammonia is aid to the kidney in the elimination of H+ ions
Another Q: The kidney is the organ chiefly responsible for resistance to change in the blood pH
Hydrogen ions are secreted into the tubules by tubular cells
Secretion mechanism derives hydrogen ions from carbonic acid
Carbonic anhydrase
[CO2 + H2O H2CO3 H+ + HCO3-]
Present within tubular cells, and it catalyzes the formation of carbonic acid from carbon dioxide and water
Carbonic acid dissociates into hydrogen ion and bicarbonate
One of the fastest known enzymes and is found in great concentration in erythrocytes
Carbonic anhydrase in the kidney tubular cells is associated with reabsorption of bicarbonate ion
Although not required for CO2 and water to form carbonic acid, it greatly increase the reaction in both respects
Absence of carbonic anhydrase drastically reduces blood CO2 carrying capacity
Phosphate compounds (HPO) and ammonia (NH3)
The kidney can eliminate cations due to the high ratio of HPO42- to H2PO4Eliminating Cations, i.e. H+, just like HCO3- to H2CO3
Mechanism for recovering from metabolic acidosis
Act as buffers to tie up hydrogen ions in the tubular fluid
Ammonia is formed in the tubular cells by the deamination of certain aa, particularly glutamic acid
Ammonia interacts with the H+ and forms the ammonium ion to be removed from the body
It acts in the elimination of H+ in the kidney and allowing for the reabsorption of Na+ into blood
Secretion of ammonia aids in the elimination of hydrogen ion from the kidney


Ammonia helps to reduce the Hydrogen Ion concentration in body fluids. This mechanism involves the
reabsorption of Sodium into the blood
Phosphate and ammonium excretion measurements provide good information on how much acid is being
eliminated by the kidneys because phosphate and ammonium buffer the acid
Phosphate compounds are excreted in combination with a cations such as Na+
Ammonium ions are excreted in combination with anions such as ClNormal blood bicarbonate:carbonic acid ratio is 20:1. A patient with 10:1 ratio is in uncompensated acidosis
SO basically you have a 20:2 ratio, more carbonic acid, so H+ needs to go out!!!!
The most important secretory mechanism for conservation of Na+ by kidney is H+ secretion for the reabsorption of
Na+ & HCO3- (1st Na+ is reabsorbed into epi cell from lumen via countertransport against H+, then the Na+
gets into the blood vessel via a cotransport with Bicarb)
Reproductive System
Male puberty:
During early childhood, a boy does not secrete gonadotropins, and thus has little circulating testosterone
During puberty, the penis and testis enlarge and the male reaches full adult sexual and reproductive capability
In males, growth and development of secondary sex organs are under direct control of testosterone
Puberty also marks the development of male secondary sexual characteristics
Secretion of gonadotropins from the pituitary gland, which usually occurs between the ages of 10 and 15, marks the
onset of puberty
The normal delay in sexual development until puberty is attributed to lack of hypothalamic stimulation of
gonadotropin release
Pituitary gonadotropins stimulate testes functioning as well as testosterone secretion
At puberty, an alteration in brain function leads to an increased production of gonadotropin-releasing hormone (Gn-RH)
by the hypothalamus
GnRH stimulates the secretion of FSH and LH (gonadotropins) by the anterior pituitary gland
The birth control pill inhibits the release of GnRH which thereby stops ovulation
It also alters endometrial lining so no implantation, and alter the cervical mucus making sperm less penetrable
These gonadotropins stimulate the growth and function of the testes
(FSH & LH act on both ovaries & testes)
promotes the maturation of sustentacular cells (Sertoli cells)
in females it does ovarian follicle development and secretion of estrogen from ovaries
(FSH, S for Sertoli & Sperm)
which are involved in sperm development and maturation
produce ABP (Androgen Binding Protein) which ensures that testosterone (testes?) is high in seminiferous
produce Inhibin, which inhibits FSH (negative feedback)
stimulates the interstitial (Leydig cells) of the testes
(Leydig for LH)
to produce testosterone secondary sex characteristics
Anabolic Steroid Use
A person who used anabolic steroids, but who has recently stopped will experience
Low FSH, and LH levels
Low Testosterone levels
Decreased number of spermatids
NOT Sterility (Looked it up, it may take a few months, but gonads will get back to full production)
DHT> Testosterone> Androstenedione
Testosterone is converted to DHT by 5alpha-reductase
Testosterone and androstenedione are converted to estrogen in adipose tissue by the NZ Aromatase
Differenetiation of wolffian duct system into internal Gonadal structures
Secondary sexual characteristics and growth spurt during puberty
Required for normal spermatogenesis
Anabolic effects: increased muscle size, increased RBC production
Inhibits GnRH (negative feedback)
Fuses epiphyseal plates in bone
Increased Libido (Whoo-whee!)


Female Puberty
Female reaches puberty 1 or 2 years earlier than males
Puberty is marked by the first episode of menstrual bleeding, which is called the menarch
An alteration in brain function leads to increased gonadotropins-releasing hormone (GnRH) secretion by the
GnRH stimulates the secretion of FSH and LH by the anterior pituitary gland, which ultimately leads to an increased
production of estrogens (androgen hormone) by the ovaries
The events of puberty in the female (such as enlargement of the vagina, uterus, and uterine tubes; deposition of fat in the
breasts and hips) are largely a result of increased production of estrogens by the ovaries
Estradiol> Estrone> Estriol
Estradiol from the Ovary
Estriol from the Placenta
Causes the development of female 2 sex characteristics (genitalia)
Causes the development of the breast
Maintains pregnancy
Growth of the follicle
Endometrial proliferation, myometrial excitability
Female Fat distribution
Hepatic synthesis of transport proteins
Feedback inhibition of FSH
LH Surge (Estrogen feedback on LH secretion switches to positive from negative just before LH surge)
Is effective at very low concentrations & generates a slowly developing long-term response in target tissues by binding
to an intracellular receptor
Contains 18 Carbons and an aromatic ring
Androgens do NOT (19 carbons, no ring)
Progesterones, Glucocorticoids, Mineralcorticoids (NO ring 21 Cs)
Estrogen Hormone Replacement Tx
Decreases risk of heart disease
Decreases hot flashes and postmenopausal bone loss
Unopposed Estrogen Tx
Increases risk of endometrial cancer
Decreased risk when used with Progesterone
Stimulation of endometrial glandular secretions and spiral artery development
Maintenance of Pregnancy
Elevation of progesterone levels is indicative of pregnancy
Decreased myocardial excitability
Production of thick cervical mucous which inhibits sperm entry
Increased body temp
Inhibition of Gonadotropins (LH, FSH)
Uterine smooth muscle contraction
Promotes secretory changes in the endometrium during the latter half of monthly period, thus preparing
endometrium for implantation of fertilized egg
Synctiotrophoblast of placenta
Maintains the corpus luteum for the 1st trimester by acting like LH
In 2nd and 3rd trimesters, the placenta synthesizes its own estrogen and progesterone and the corpus luteum
Used to detect pregnancy because it appears in the urine 8 days after successful fertilization (blood and urine Testing)
Elevated hCG in women with hydatidiform moles or choriocarcinoma
Precocious puberty
A condition in which the changes associated with puberty begin at an unexpectedly early age
Results from hyperactive adrenal cortex
Is due to an excess of androgenic (in boys) & estrogenic (in girls) substance produced by the adrenal cortex
NOTE: Androgens are produced in the testis & the adrenal cortex
These substances resemble the male and female sex hormones


Cessation of estrogen production with age-linked decline in number of ovarian follicles

Average age of onset is 51 (earlier in smokers)
Therapy - Estrogen replacement
HAVOC Hot flashes, Atrophy of Vagina, Osteoporosis, Coronary heart disease
Menstrual cycle:
Ovulation occurs 14 days before menses, regardless of cycle length
Average menstrual cycle usually occurs over 28 days, although the normal cycle may range from 22 to 34 days
Menstrual phase:
Aunt Flow begins the cycle
Cycle starts with menstruation (cycle day 1), which usually lasts 5 days
Proliferative (follicular) phase:
Lasts from cycle day 6 to day 14
LH and FSH act on the ovarian follicle (mature ovarian cyst containing the ovum)
This leads to estrogen secretion from the follicle, which in turn stimulates buildup of the
Development of ovarian follicles to the point of ovulation is stimulated primarily by FSH Follicle
stimulating hormone
Late in this phase, estrogen levels peak, FSH secretion declines, and LH secretion increases, surging at midcycle (around day 14)
LH Surge (Estrogen feedback on LH secretion switches to positive from negative just before LH surge)
The LH surge leads to final maturation of follicle, rupture of follicle and ovulation
Another Q: ovulation is believed to be caused by a shift in anterior pituitary gonadotropin secretion with LH
predominating in the mixture
Without the LH, even though large quantities of FSH are available, the follicle will not progress to the
stage of ovulation
FSH and LH are both glycoproteins and act in both the ovaries (in females) and the testis (in males)
FSH is a polypeptide
FSH exerts its action on germinal epithelium
Then, estrogen production decreases, the follicle matures, and ovulation occurs
Day 15 14 days after Day 1 of menstruation, BUT does VARY
Occurs as a result of the estrogen-induced LH surge
The discharge of an mature ovum (oocyte) from the follicle (Graafian follicle) of the ovary
The ovum generally disintegrates or becomes nonviable if it is not fertilized within 4 days
Being used as oral contraceptive substance due to their ability to suppress ovulation
Remember Progesterone is usually the maintainer of pregnancy, so body is fooled into thinking its prego
Luteal (secretory) phase:
Lasts about 14 days
FSH and LH levels drop
The corpus luteum begins to develop, and it synthesizes estrogen and progesterone
hCG is promoting this in the 1st trimester
The blood concentration of estradiol does NOT increase as corpus luteum develops
This is why prego women are not horny in the 1st trimester, the corpus luteum is taking care of
itself and there is no circulating estradiol to stimulate them to go find their man!!
But the 2nd Trimester is Great The Madonna period
Ruptured mature follicle forms the corpus luteum, which secretes progesterone and estrogen
If fertilization does not occur, the corpus luteum degenerates (become nonviable)
As a result, estrogen and progesterone levels decrease until their levels are too low to keep the
endometrium in a fully developed secretory state
The endometrial lining is shed as menstrual fluid during menstruation or menses
Decreasing estrogen and progesterone levels stimulates the hypothalamus to produce GnRH, and the cycle beings
Two significant results of the female sexual cycle:
Only a single mature ovum is normally released from the ovaries each month so that only a single fetus can begin to
grow at a time
Organic compounds that do not dissolve in water but do dissolve in alcohol and other organic solvents


Are not able to move in body fluids due to their hydrophobic nature so they are packaged in micellar structures called
Various lipoproteins are classified in terms of density
Since lipids are much less dense than proteins there is an inverse relationship between lipid content and density
(i.e., high lipid content means low density particle) HDL good because little lipid content
The major components of lipoproteins being transported are phospholipids and proteins which make up the micellar
membrane (the protein component alone is called apolipoprotein)
The major lipids include triacyglycerols or TGs (the most common lipids) phospholipids, and steroids
Lipid is required in the average diet because it provides essential fatty acids
Another Q: Among cellular components, lipids are most characteristic of membranes
Another Q: Which of the following is least descriptive of lipids:
Hydrophilic (among answer choices of nonpolar, carbon-containing, and amphipathic)
Lipids that are relatively polar, contain more Oxygen
Triglyceride: (TGs)
Provide more than half the energy requirements of some organs, particularly the liver, heart, and skeletal muscle
When hormones signal the need for metabolic energy, TGs stored in adipose tissue are brought out of storage and
transported to those tissues (skeletal muscle, heart, renal cortex) in which FAs can be oxidized for energy production
TGs are not membrane constituents
TG is the principal lipid stored in adipose tissue
Type of lipid that contains a phosphate group
Major lipid that makes up cell membrane
Would likely form a micelle when mixed with water & agitated
Like a phospholipid bilayer, but its only one layer, small circular
Another Q: Lipid micelles have spherical structures that are stabilized by hydrophobic interactions of lipid groups
The major driving force for formation of a liquid micelle is hydrophobic interaction between hydrocarbon tails
Three major types of Body Phospholipids:
Lecithins: (aka phosphatidylcholine)
Major component of cell membrane of RBCs, of myelin, of bile, and of surfactant (DPPC)
Phospholipid present in liver bile
They are water soluble emulsifiers
Are a group of phospholipids that upon hydrolysis yields:
1) Two fatty acid molecules
2) One molecule each of glycerol, phosphoric acid, and CHOLINE
Lipotropic effect of lecithin upon fatty liveralso produced by choline
Another Q: Choline is an important lipotropic substance
Lipotropic substance one that promotes taking fat out of the liver
Another Q: Outer lamella of cell MB contains sphingomyelin & phosphatidylcholine (not
Both choline and lecithin are lipotropic substances
A compound synthesized by the body and is found in most animal tissues
Is essential for the metabolism of TGs, particularly lipoprotein secretion, in the liver
A deficiency of choline in the diet can cause abnormalities in fat/lipid metabolism
Is a natural amine that is often classified with the B vitamins, although it is not a vitamin, and is a
constituent of many biologically important molecules such as Ach and lecithin
It prevents the deposition of fats in the liver and facilitates the movement of fats into the cells
When converted to betaine, is also a source of transferable methyl groups in metabolism
A deficiency of choline in animals leads to fatty liver disease and eventually hepatic cirrhosis
W/o choline you cant put fat in the other cells, because no choline no lecithin so no
lipotropic effect
Choline, choline phosphate and cytidine diphosphocholine are involved in the synthesis of
phosphatidylcholine, a major phospholipids constituent of membranes and lipoproteins. It is
synthesized de novo in liver cells
The cephalins:
A group of phospholipids having hemostatic properties and found especially in the nervous tissue of the brain
and spinal cord
They resemble lecithin, except they contain either 2-ethanolamine or L-serine in the place of choline
The sphingomyelins:
Phospholipids that are found especially in nerve tissue and yield:
Sphingosine, choline, a fatty acid, and phosphoric acid upon hydrolysis


They are membrane constituents

Basic structure of phospholipids: glycerol + fatty acids + phosphate group + R group
Types of Lipoproteins:
Lipid-binding proteins, responsible for the transport in the blood
Least dense lipoprotein
Most triglyceride and the least protein content
Transport primarily dietary triacylglycerols around the body and dietary cholesterol to the liver
Secreted by intestinal epithelial cells
Remember micelles emulsify in water to give phospholipids, (NOT TGs SEE PICTURE ABOVE)
Another Q: triglyceride absorbed into the lymphatic system is transported to the liver as chylomicrons
They are the largest of the lipoproteins
Are plasma lipoprotein
Carry FAs obtained in the diet to the tissues in which they are consumed or stored as fuel
Remnants of chylomicrons, depleted of their tracylglycerols but still containing cholesterol, move through the
bloodstream to the liver, where they are taken up, degraded in lysosomes, and their constituents recycled
VLDLs (very low-density lipoproteins):
More dense than chylomicrons
High content of triacylglycerides
Secreted by the liver
Transport endogenous (hepatic) triacylglycerols to various tissues (primarily muscle and adipose tissue)
LDLs (low-density lipoproteins):
Large spherical particles made of a core of esterified cholesterol surrounded by a lipid bilayer containing protein
Denser than VLDLs
Less TG and more protein content
High phospholipids content
Highest cholesterol content
Delivers hepatic cholesterol to peripheral tissues
They are the primary plasma carriers of cholesterol for delivery to all tissues carrying cholesterol, cholesterol esters,
and phospholipids from liver to body
Another Q: LDLs are transported into the cells by way of receptor-mediated endocytosis
When cholesterol is needed, a cell will make a receptor for LDL and insert the receptor in the plasma membrane
Then LDL binds to the receptor and is engulfed (via endocytosis)
When the cell has enough cholesterol, gene regulation for the LDL receptor is down regulated
Which one adjusts the Cholesterol level in blood?
HDLs (high-density lipoproteins):
Most dense lipoproteins
Has the lowest triglyceride and highest protein content
Transfers cholesterol as an acyl ester derivative from other tissues back to the liver
Mediates reverse cholesterol transport (from periphery to liver)
Secreted from both liver and intestine
Familial Hypocholesterolemia
The key problem is a decrease in LDL receptors
Comes with Xanthomas (Achilles heel)
Contains three molecules of fatty acid combined with one molecule of glycerol
Neutral fats contain mixtures of one or more fatty acids esterified with glycerol
Is a long chain compound with an even number of carbon atoms and a terminal COOH group
Can be saturated, monounsaturated, or polyunsaturated
Classified by the number of double bonds between carbon atoms in their fatty acids molecules:
Ending in -ic
Saturated fat:
No double bonds between carbon atoms
Arachidic(spelled right) acid, behenic acid, butyric, capric, caproic, caprylic, lauric, myristic, palmitic, stearic
Upon complete hydrogenation, oleic, linoleic and linolenic acids yield stearic acid (20 cs)
Monounsaturated fat:
One double bond between carbon atoms
Erucic, oleic, palmitoleic
Polyunsaturated fat:


Multiple double bonds between carbon atoms

Arachidonic, linoleic, linolenic
Prostaglandins are made within cells from polyunsatured fats
***Stearic oleic linoleic linolenic (arachidonic): a sequence that shows increasing number of double bonds
Arachidonic acid has the most double bonds, among oleic, stearic, and palmitic
Fatty acids:
Essential FAs cannot be synthesized because we lack the lack the enzymes to place double bonds at certain
positions (omega 3 and omega 6) and must therefore obtain them from the diet
Essential FAs:
Arachidonic, linoleic, and linolenic Polyunsaturated fats
Linoleic is a polyunsaturated fatty acid commonly found in animal cell MBs (thats why we eat those
All fatty acids are building blocks of phospholipids and glycolipids and are therefore needed for the synthesis of MBs
Cells derive energy from them through beta oxidation
The predominant source of ATP at moderate levels of activity (>20 min) are fatty acids
Freeing stored fat/Free fatty acids:
Epinephrine and glucagons
Increase glycogen and lipid breakdown
Activate adenylate cyclase
Lies in the adipocyte plasma membrane
Raises the intracellular concentration of cAMP
Activated by Epi, Glucagon, and PTH, NOT Insulin
A cAMP-dependent protein kinase, in turn, phosphorylates & thereby activates hormone-sensitive
triacylglycerol lipase
Mobilization of fat stored in adipocytes involves activation of triglyceride lipase by a cAMP dependent
protein kinase
cAMP is broken down by cAMP phosphodiesterase
Methyl xanthines such as caffeine & theophylline enhance lipolysis in adipose tissue by
inhibiting cAMP phosphodiesterase
Triglyceride Lipase
This NZ initializes the hydrolysis of the ester linkages of TGs forming 3 free FAs and glycerol
SIDE BAR Fat, monoglycerides, and Proteins are broken down by Hydrolysis
The 3 FAs that are released bind to serum albumin and travel to the tissues where they dissociate from
albumin and diffuse into the cells in which they will serve as fuel
Glycerol released by lipase action
Is phosphorylated by glycerol kinase, and the resulting glycerol-3-phosphate is oxidized to
dihydroxyacetone phosphate
This compound is then converted to glyceraldehyde-3-phosphate by the enzyme triose phosphate
G3P is then oxidized via glycolysis to go on to make Pyruvate
Acetyl CoA Krebs
Insulin causes activation of a phosphorylase which dephosphorylates the hormone-sensitive lipase and thereby
diminishes lipolysis
Fatty acid degeneration occurs in the mitochondria and uses FADH+/NAD+ --- Think FAD Fatty Acid Degeneration
Degeneration occurs where its product (Acetyl CoA) will be used in Krebs!!
Fatty acid synthesis occurs in the cytosol and uses NADPH, other different enzymes, and Malonyl CoA
Both require phosphopantothenic acid (the Q discussed the 2 previous lines)
Fatty Acid Catabolism
Involves beta oxidation
Transported to the liver by employing carnitine as a carrier substance, which is inhibited by cytoplasmic MalonylCoA
Once inside the mitochondria, the fatty acid is transferred from the carnitine to a CoA and is oxidized (via beta
oxidation) to acetyl CoA
Acetyl CoA molecules enter into the citric acid cycle (Krebs cycle) to form carbon dioxide and reducing equivalents
The reducing equivalents are then reoxidized by electron transport system and the energy released by that process is used
by the oxidative phosphorylation system to form ATP
18 carbon FA 9 molecules of acetyl CoA when broken down
Ketone bodies:
Synthesized by cleavage of B-hydroxy-B-methyglutaryl CoA


Which of the following is a ketone body? Acetoacetate (not glycerol, glucagon, acetyl CoA, and
Sometimes referred to as D-Beta-hydroxybutyrate or 3-hydroxybutyrate
Not utilized by the body as fuel
May normally leave the body via the lungs
Fruity smell of the breath
During conditions of low glucose availability (starvation or fasting, or a case of diabetes mellitus), adipose
tissue breaks down its triacylglycerol stores into FAs and glycerol, which are released into the blood
Glycerol is converted into glucose, by first getting converted to Glyceraldehye 3 Phosphate, which is an
intermediate in glycolysis, it makes Pyruvate, then because the brain needs energy, you get
gluconeogenesis happening to send glucose out of the liver to the brain
When there is inadequate insulin, utilization of fat for energy in increased
Through the process of -oxidation, the LIVER converts the FAs to acetyl CoA
Acetyl CoA is used by the liver mitochondria for the synthesis of the ketone bodies
The liver is the site for production of ketone bodies
Another Q: In relative insufiicient insulin, acetyl CoA is usually channeled into ketone-body formation
They are transported in the blood to peripheral tissues, where they can be reconverted to acetyl CoA and
oxidized by the citric acid cycle (Krebs cycle)
They are important sources of energy for the peripheral tissues
They are soluble in aqueous solution and therefore do not require carriers in blood
Unlike fatty acids, ketone bodies can be oxidized by the brain
Metabolized to 2 molecules of Acetyl-CoA by the brain
Under circumstances that cause acetyl-CoA accumulation (starvation or untreated diabetes, for example),
thiolase catalyzes the condensation of two acetyl-CoA molecules to acetoacetyl-CoA, the parent of the
three ketone bodies
High concentrations in the blood result in keto acidosis
Condition characterized by an abnormally elevated concentration of ketone bodies in the body tissues and fluids
Occurs when fatty acids are incompletely metabolized, a complication of untreated diabetes mellitus, starvation,
fasting and alcoholism
In severe diabetic acidosis, one would expect an increase in plasma keto acids
Another Q: Excessive ketone bodies in blood & urine are possible indications of diabetes mellitus
Another Q: Ketosis may be produced experimentally by fasting
Characterized by ketones in the urine (ketonuria), K+ loss in urine, and a fruity odor of acetone on the breath
Acetone is a compound that may leave the body by way of the lungs
A diabetic coma can be caused by the buildup of ketone bodies
It is commonly fatal, unless appropriate therapy is instituted promptly
Glucose is the only effective substance in reversing ketosis in a non-diabetic patient
Another Q: Excessive use of fat as energy source can lead to ketosis, acidosis and ketonuria (but not alkalosis)
Fatty Acid Biosynthesis
WRITE OUT THE PROCESS: A good reference is pg. 66 in the blue Kaplan book called Biochemistry notes
Summary of fatty acid synthesis: Acetyl CoA malonyl CoA malonyl-ACP acetyl ACP acetoacetyl
ACP butyryl ACP fatty acid
Occurs in the cytosol, and gets there via a citrate shuttle
Active processes during FA biosynthesis: TCA cycle, pyruvate dehydrogenase, amino acid catabolism, glycolysis (not oxidation) these arent necessarily a part of FA biosynthesis; the Q is going for us knowing about -oxidation
Is not a simple reversal of -oxidation used for the catabolism of fatty acids
Involves two carbon additions from acetyl CoA and an acyl carrier protein (ACP)
Acetyl CoA is the immediate precursor for fatty acid synthesis
The important step
The first one in which acetyl CoA, ATP, and bicarbonate form malonyl-CoA
A key intermediate in the synthesis of FAs is malonyl-CoA, a 3-carbon intermediate, which is formed from acetylCoA, bicarbonate, and ATP
This is the committed step, the essential control point
Acetyl CoA is carboxylated by Acetyl CoA carboxylase to Malonyl-CoA
Similar to the carboxylation of Pyruvate to start gluconeogenesis
The pathway for synthesis of even-numbered fatty acids differs from that of the catabolism of fatty acids in that
malonyl CoA is an intermediate in synthesis
Another Q: CO2 is incorporated into acetyl coenzyme A, forming malonyl coenzyme A (2 Carbon 3 carbon)


This irreversible reaction is the committing step in fatty acid synthesis and is the principal regulator Acetyl
Co A carboxylase
The diet is the primary source of FAs
The next source is from the biosynthesis
In many instances, the saturated straight chain 16 carbon acid palmitic acid is first synthesized and all other
FAs are made by modification of palmitic acid
Important points:
Glucose is first degraded to pyruvate by aerobic glycolysis in the cytoplasm
Pyruvate is then transported into the mitochondria, where pyruvate forms acetyl CoA (by pyruvate dehydrogenase)
and oxaloacetate (by pyruvate carboxylase)
Acetyl CoA and oxaloacetate condense to form citrate
Then Oxaloacetate can either go up the Gluconeogenesis tract to PEP via PEPCKinase (the committed Step)
OR Oxaloacetate plays an important role in the body by reacting with acetyl CoA to form citrate in the first step
of Krebs
Citrate, in turn, can be transported out of the mitochondria to the cytoplasm (where fatty acid synthesis occurs), and
there it splits to generate cytoplasmic acetyl CoA for fatty acid synthesis
Citrate is a positive modulator that allosterically regulates the enzyme catalyzing the rate-controlling step in the
de novo synthesis of fatty acids
Another Q: The enzyme that catalyzes the 1st step in the fatty acid synthesis pathway is acetyl CoA carboxylase
It is an allosteric enzyme & is the principal regulator of the pathway
So, for a little clarity, the 1st step of FA biosynthesis is the conversion of acetyl CoA to malonyl CoA
Citrate is a positive modulator of acetyl CoA carboxylase in this step
Acetyl CoA Carboxylase is the principal regulator of FA synthesis
Coenzyme A (CoA)
A pantothenic acid containing coenzyme that is involved in both fatty acid synthesis and catabolism
*Coenzyme A participates in activation of carboxyl groups
*Acetyl CoA is a common intermediate of the metabolism of fatty acids, amino acids and CHOs
Transporting FAs in the blood
The body uses 3 mechs for transporting FAs in the blood
1) FAs to albumin
2) Chylomicrons (Cholesterol binds to fat and phospholipids to form chylomicrons)
3) Ketone bodies (aceto-acetate and beta hydroxyl butyrate
Bile Salts:
Are sodium salts composed of cholic acid (cholate & deoxycholate most abundant) conjugated with glycine or taurine
to form glycocholate and taurocholate respectively
Sodium taurocholate/glycocholate are necessary for absorption of fatty acids. These are conjugated bile components
Bile salts are amphipathic (hydrophilic and hydrophobic)
Bile salts are synthesized in the liver and pass, via the bile duct, into the duodenum and then into the jejunum
They aid in intestinal digestion and absorption of lipids by emulsifying and solubilizing them in micelles
Reabsorption of the bile salt micelles occurs in the ileum, from which a large proportion return via the blood to
the liver
The bile ducts carry bile salts from the liver to the gallbladder, where they are stored; excreted (excess) cholesterol is
dissolved in the bile salt micelles
Overall 90% of bile salts involved in absorption of lipid from w/in the jejunum are recycled in a process called
enterohepatic circulation they are reabsorbed into the portal circulation and reused
Actions of bile salts:
Help in absorption of FAs, monoglycerides, cholesterol, and other lipids from the intestinal tract (form water-soluble
complexes [micelles] with FAs and glycerides)
Aid in the absorption of ADEK Vitamins
NOTE on micelles:
The major driving force for forming a lipid micelle is hydrophobic interaction between hydrocarbon tails
Have a detergent action on the fat particles in the food, which decreases the surface tension of the particles and
allows agitation in the intestinal tract to break the fat globules into minute sizes
Cytoplasmic membrane = cell membrane:
Function is to regulate the flow of material into and out of the cell
A selectively permeable barrier, meaning that the movement of molecules across the MB is selectively restricted
Some small (<75), uncharged, nonpolar molecules move across the membrane quite readily
Molecules and ions that are large, highly charged &/or polar move across the membrane via transport systems


Mammalian cell membranes do NOT have endotoxin (but they do have LPS)
Passive Diffusion
Simple diffusion
Simple diffusion is movement down its concentration gradient
No transport or carrier system is needed
Facilitated diffusion (aka Mediated Diffusion)
A form of passive diffusion that uses the assistance of transport or carrier proteins
Requires no energy & moves molecules down the concentration gradient
Mediated diffusion of substances across cell membranes differs from simple diffusion in that mediated
diffusion exhibits saturation kinetics
Because the carrier can become saturated by the presence of large solute concentrations
Another Q: Facilitated diffusion differs from active transport in that facilitated diffusion requires a concentration
Another Q: What characterizes both active transport & facilitated diffusion? Competitive inhibition
Another Q: The process involving nonpenetrating solutes (e.g., proteins) best describes facilitated diffusion
(The other answer options were osmosis, diffusion, & epithelial transport)
Active transport
Primary active transport uses energy derived from ATP
EX: sodium-potassium pump
Secondary active transport uses the gradient of one molecule to move another no direct ATP coupling is used
EXs: sodium-calcium exchanger (counter-transport), glucose symporter (co-transport)
The rapid movement of a substance across a biologic membrane against a concentration gradient requires the
participation of an energy-requiring active transport system
***Another Q: the movement of Ca2+ across many cell MBs involves a Ca2+/Na+ countertransport system
Active transport systems generally involve specific binding molecules that are protein (not lipid, lipoprotein, CHO)
Another Q: Active transport is distinguished from facilitated diffusion by its requirement of metabolic energy
Which of the following occur when active transport is involved in the movement of a solute across a biologic
Expenditure of metabolic energy
A gain in free energy by the system (Because basically you are creating a potential energy state)
A unidirectional movement of the solute
Movement of the solute against a concentration gradient
Polar & hydrophilic
Molecules or groups that are soluble in water (e.g., ions, glucose, and urea)
Hydrophilic molecules require a carrier protein to cross the cell membrane
Nonpolar, hydrophobic
Molecules or groups that are poorly soluble in water (e.g., O2, CO2, and alcohol)
The cell MB is more permeable to O2, CO2, H2O, ethanol & palmitic acid than to Na+
Hydrophobic molecules are transported across cell membranes by simple diffusion
Most abundant non-phospholipid component of the cell membrane
The least polar molecule when listed with ethanol, palmitic acid, & glycocholic acid
Another Q: Lipids that are relatively polar contain more oxygen
Amphipathic = amphiphilic
Both polar and nonpolar functional groups are essential for a substance to act an amphipathic molecule
An example of an amphiphilic molecule is phospholipid
Is a fluid mosaic model of lipids and proteins
The plasma membrane is described best as a fluid mosaic composed primarily of phospholipids, cholesterol and
Another Q: The chief constituents of biologic membranes are lipids & proteins
Another Q: The most abundant nonphospholipid component of the cell membrane is cholesterol
The phospholipid forms the bilayer component
The hydrophilic head groups interact with water on both the extracellular & intracellular surfaces
The hydrophobic fatty acyl chains in the central portion of the membrane
Globular Proteins
Peripheral proteins are embedded at the periphery
Integral proteins
span from one side of the membrane to the other side & are associated with the hydrophobic phase of the
May move freely within the plane of the membrane


Integral proteins are the reason for the selective permeability of biological membranes
Leucine & valine are found on the interior of globular proteins (LV is the center of the Globe)
CHOs are attached to proteins and lipids on the exterior side of the cell membrane
The membrane mosaic is fluid because the interactions among lipids and between lipids & proteins are noncovalent,
leaving individual lipid and protein molecules free to move laterally in the plane of the membrane
The primary force stabilizing the lipid-protein complex in cell membranes is the hydrophobic interaction
Bilayers arise through the operation of two opposing forces:
1) attractive forces between hydrocarbon chains (van der Waals forces) caused by the hydrophobic effect forcing
such chains together
2) repulsive forces between the polar head groups
Lipid classes commonly incorporated into the cell membrane:
Glycolipids found on various cell surfaces; have N-acetylneuraminic acid residues in addition to sphingosine
Named so because many cells in CNS ganglia have them
Cholesterolprimarily used as component in cell membrane
Six common features of biological membranes:
1. Sheetlike structure: only a few molecules thick (60-100 angstrom)
2. Consists mainly of lipids and proteins (CHOs are attached to exterior)
3. MB lipids small molecules with hydrophobic and hydrophilic groups that form lipid bilayers in aqueous media
The hydrophobic center of the bilayer forms a barrier to the flow of polar molecules across the membrane
4. The proteins function as transporters, enzymes, receptors, etc.
5. Are noncovalent assemblies: the proteins and lipid molecules are held together by many noncovaelnt interactions
6. Are asymmetric: inside and outside faces are usually different
The plasma membrane has most of the CHOs (as glycoproteins and glycolipids) on the outer face while
The lipids phosphatidylethanolamine and phosphatidylserine are more concentrated on the cytoplasmic face
Two examples describing an asymmetric model of membrane assembly:
Some membrane proteins may have their N-terminal residues predominately on one side of the membrane
The polar head groups of the phospholipids may be primarily oriented toward one side of the membrane
Proteins in cell membrane function as:
Transporters transport substances across the membrane
Enzymes catalyze biochemical reactions
Receptors bind hormones or growth factors
Mediators aid in triggering a sequence of events

Buffer systems:
Most commonly consist of a weak acid (the proton donor) and a salt or conjugate base of that acid (the proton acceptor)
These systems minimize the pH changes brought about by a change in the acid or base content of the solution
These buffer systems reduce the effect of an abrupt change in H+ ion concentration by:
1) releasing H+ ions when pH rises
2) accepting H+ ions when pH drops
Major buffer systems include:
Sodium bicarbonate carbonic acid buffer system:
The major buffer in extracellular fulid
Is very important in the oral cavity for acid neutralization in foods & those produced by oral bacteria
Phosphate buffer system:
The minor buffer in the extracellular fluid
Protein buffer system:
Intracellular proteins absorb hydrogen ions generated by the bodys metabolic processes
Proteins contain many functional groups with diferring pKs, making them able to buffer over a wide pH range
An increase in pK means a stronger ability to bind hydrogen ions (better base or proton acceptor)
pK High pK means very low [H+] (1.0 x 10-14), so it will accept H+ faster
Hemoglobin is a major intracellular buffer
*** H2CO3, NaHCO3, Na2HPO4, NaH2PO4 all function in buffer systems in blood
Is slightly basic, between pH 7.35-7.44


Acid-base balance is controlled precisely because even a minor deviation from the normal range can severely affect
many organs
The body uses three mechanisms to control the acid base balance:
1. Excess acid is excreted by the kidneys as H+, NH4+ or combined with phosphate
2. The body uses pH buffers in the blood to guard against sudden changes in acidity
The major blood buffers are bicarbonate, hemoglobin, and albumin
The most important buffer system in maintaining physiological pH of plasma is carbonic
3. The excretion of CO2: the blood carries carbon dioxide to the lungs where it is exhaled
Respiratory control centers in the brain regulate the amount of carbon dioxide that is exhaled by controlling the
speed and depth of breathing
An abnormality in one or more of these pH control mechanisms can cause one of two major disturbances in acid
base balance: acidosis or alkalosis
From the Henderson-Hasselbach relationship we can see how plasma pH is determined by the plasma levels of carbon
dioxide and bicarbonate. 6.1 is the pKa of the bicarbonate-carbon dioxide buffer system
pH = 6.1 + log [bicarbonate]/ (0.03 x partial pressure of carbon dioxide)
Henderson-Hasselbach equation:
pH = pKa + log[A-]/[HA]
ph = pkA WHEN [HA] = [A-]
Or when the acid is Half Neutralized
Describes the relationship between the pH, pK (the negative log of the dissociation constant) and the concentration of an
acid and its conjugate base (aka, the salt of the acid)
EX: If adrug has a pK of 6.4, at pH = 7.4, the ratio of A- to HA is 10
7.4 = 6.4 + log[A-]/[HA] 1.0 = log[A-]/[HA] 101.0 = [A-]/[HA] = 10:1 ratio
A useful way of restating the expression for the dissociation constant of an acid (K a)
Ka = [H+][A-]/[HA]
The larger the Ka, the stronger the acid, because most of the HA has been converted into H+ and A-.
Conversely, the smaller the Ka, the less acid has dissociated, and therefore the weaker the acid
Shows that pH = pK when an acid is half neutralized
Because from our equation pH = pK then 0 = log[A-]/[HA] 100 = ratio 1 = ratio
The pH of a buffer system depends on the pK of the weak acid & the ratio of molar concentrations of salt and
weak acid
At pH = pKa, there is maxiumum buffer capacity i.e. half neutralized, and could then go either way
Another Q: The optimum pH for an enzyme is the pH of the most rapid reaction rate
This type of problem is solved by using the following equation: Kw = [H+][OH-]
Kw is the ion product of water and always equal 10-14
[H+] is the hydrogen ion concentration (pH = -log[H+])
[OH-] is the hydroxide ion concentration (pOH = -log[OH-]
14 = pH + pOH
Use the pH scale
14 = pH + 4
pH = 10
EX: The pH of a solution having a 10-5 M concentration of OH- ion is 9 (from 14 5 = 9)
EX: The pH of a solution of 0.01 M HCl = 2
pH = -log[0.01] -pH = log[0.01] 10(-pH) = 0.01 10-2 = 0.01 pH = 2
EX: If the pH = 5.7, the [H+] = 1x10-6
EX: Solution A has a pH = 7.0; Solution B has a pH = 6.0; volumes are equal; A has 1/10 as many H + ions than B
This just recapitulates that pH is a fxn of log, or powers of 10!!!
Isoelectric point
The pH at which number of positive charges equals the number of negative charges
The amino acid composition of a protein having an isoelectric pH of 10 has more basic than acidic amino acids
The pH at which a solute has no net electric charge & thus does not move in an electric field (i.e., during electrophoresis)
It is designated pl for that solute
For example, at its isoelectric pH of 6.06, glycine will not move in an electric field
Another Q: Electrophoresis is a procedure that depends primarily on electrostatic net charge
A protein in an electrophoretic system, has the pH lowered below its isoelectric point
then protein would
migrate to negative pole
This means you have more H+ and will move Negative
This information has practical importance for a solution containing a mixture of amino acids, the different amino acids
can be separated on the basis of the direction and relative rate of their migration when placed in an electric field at a
known pH. The same applies to protein molecules and is frequenly used to separate proteins


Example: Glycine has a net negative charge at any pH above its pl, so it will move toward the positive electrode
At any pH below its pl it has a net positive charge and moves towards the negative electrode
The farther the pH of a glycine solution is from its isoelectric point (pl), the greater the net electric charge of the
population of glycine molecules
At physiologic pH, all amino acids have both a negatively charged carboxyl group (COO-) and a positively charged
amino group (NH3+) They are therefore dipolar ions (zwitterions)
In aqueous solution at pH 7, a peptide containing 1 amino group side chain & 2 carboxyl group side chains, the net
charge would be (-1)
pH Problems
Metabolic acidosis:
Excessive blood acidity characterized by an inappropriately low level of bicarbonate in the blood
Major causes chronic renal failure, diabetic ketoacidosis, lactic acidosis, poisons and diarrhea
Ketoacidosis can result from a sustained, severe CHO deficiency in the diet
Ammonia is the nitrogenous product that is excreted in high amounts after prolonged acidosis
The kidney responds to metabolic acidosis by synthesizing NH3 to then pull out H+ and make NH4+ and
excrete it
Respiratory acidosis:
Excessive blood acidity caused by a buildup of CO2 in the blood as a result of poor lung function or slow breathing
Major causes hypoventilation, emphysema, chronic bronchitis, severe pneumonia, pulmonary edema, & asthma
In respiratory acidosis, CO2 content increases and pH decreases
Signs/symptoms of elevated PCO2:
Acute pain, anxiety, hyperventilation (to attempt to compensate), dizziness, signs of loss of consciousness
Administration of a 90:10 nitrous oxide:oxygen mixture causes respiratory depression. Respiratory acidosis is likely
to result (from the respiratory depression or hypoventilation). Dont misunderstand this one.
In respiratory acidosis, there would not be increased production of renal bicarbonate
Having all that CO2 would shift the equation back to HCO3- + H+
There would be hypoxia, hypercapnia, and a response of tachycardia
Metabolic alkalosis:
A condition in which the blood is alkaline because of an inappropriately high level of bicarbonate
Major causes vomiting acidic gastric contents or as a result of ingestions of alkaline drugs
Renal compensation for chronic metabolic alkalosis involves a partial reabsorption of the filtered HCO3Normally, over 99% of bicarb is reabsorbed to continue as a buffer, but in alkalosis, there would be an excess
of bicarb, so the kidney secretes more than usual into the urine to get the alkaline serum back down to
Respiratory alkalosis:
A condition in which the blood is alkaline due to rapid or prolonged deep breathing
Results in a low blood CO2 level, which causes H+ and HCO3 to shift to make CO1, hence reducing the
H+ Low HCO3
Alkalosis can cause hypocalcemia and tetany by promoting the binding of calcium to albumin, hence reducing
the ionized Calcium in blood
Major causes hyperventilation (most common cause), pain, cirrhosis of liver, & low levels of oxygen in the blood
(high altitude)
Hyperventilation causes some degree of temporary alkalosis
Another Q: Hyperventilation often produces muscle spasms because the loss of CO 2 has caused alkalosis
Chronic respiratory alkalosis
Low CO2, Low HCO3, normal venous pH
High Altitude Respiratory Resopnse
Acute increase in ventilation
Increased pulmonary ventilation at high altitudes results directly from the effect of hypoxia on the carotid body
Chronic increase in ventilation
Increased erythropoietin increased hematocrit and hemoglobin
Increased 2,3-DPG (binds to Hb so that Hb releases more O2)
Cellular changes (increased mitochondria)
Increased renal excretion of bicarbonate (to compensate for respiratory alkalosis)
Chronic hypoxic pulmonary vasoconstriction results in right ventricular hypertrophy
In water intoxication, most of the excess water will be found in the intracellular compartment (as opposed to extracellular,
intravasacular, or interstitial compartments)
Types of Hormones
Steroid hormones:


Derivatives of cholesterol
Pet for heavy Petting (Sex Hormones) and Cat for Catabolism Hormones
**Progesterone, Estradiol, Testosterone, and Cortisol, Aldosterone, Thyroxine
NOT relaxin
Not water soluble and bind to intracellular receptors, forming complexes that activate or inactivate genes
Best characterized by binding to intracellular receptors
Adrenal Steroids
This is the Main chain, first NZ is Desmolase, which is controlled by ACTH and inhibited by ketoconazole
Mineralocorticoids Aldosterone ( 21 Cs)
Glucocorticoids Cortisol (21 Cs)
Androgens Testosterone (19 Cs)
Estrogens Estrone/Estradiol (18 Cs)
Amine hormones:
Derived from tyrosine, an essential amino acid found in most proteins
They include thyroid hormone (T3 and T4) and the catecholamines (epi and NE and dopamine)
Polypeptide hormones:
Proteins with a defined, genetically coded structutre
Synthesized in precursor form (a pre-prohormone)
Usually transported unbound in plasma
Stored in secretory vesicles
Act by binding to a plasma MB receptor & generating second messengers
Another Q: Polypeptide hormones usually exert their effect by binding to receptors on the cell MB & altering the
specific activity of certain enzymes
Another Q: Hormones that exert there effects through the activation of second messengers are usually water soluble
peptide/protein hormones thats like a definition!!!
They include:
Anterior pituitary hormones (GH, TSH, FSH, LH, & prolactin)(FLAT PEG)
Thyroid hormones, glucocorticoids & gonadal steroids are similar in that each is released in response to
signals from the hypothalamic-anterior pituitary complex
Posterior pituitary hormones (ADH & oxytocin)
Pancreatic hormones (insulin and glucagon)
Inhibitory of GH, TSH, Insulin, Glucagon, and Gastrin
Elaborated primarily by the median eminence of the hypothalamus and by the D for delta cells of
pancreatic islets
There is a positive N2 balance following administration of GH (somatotropin)
A particular hormone does not necessarily affect all cells; only its target cells
Target cells of a hormone possess receptors to which molecules of a hormone can attach
These receptors can be located either on the plasma membrane or within the cell itself
Second messenger:
A molecule found inside a cell which responds to the presence of a hormone outside the cell
cGMP and cAMP are second messengers that carry signals from the cell surface to proteins within the cell
cAMP is the intracellular, "second" messenger for many peptide and polypeptide hormones
Another Q: cAMP (adenosine-3, 5-monophosphate) is directly invovled in the action of hormones on target cells
Another Q: cAMP increases the rate of glycogenolysis by promoting the phosphorylated form of glycogen
Frequently they act to stimulate protein kinase
They are rapidly broken down in cells (to terminate response) by enzymes called phosphodiesterases
Some hormones that use cAMP as a second messenger are:
Parathyroid hormone


Glucagon, epinephrine, & PTH induce activation of cAMP (insulin does not)
This increases the rate of glycolysis & gluconeogenesis
cAMP is formed from ATP in a reaction catalyzed by adenylate cyclase
Adenylate cyclase is an integral protein of the plasma membrane
Many hormones act by way of stimulation of the MB-bound adenylate cyclase
Signal Molecule Precursors
ATP cAMP via adenylate cyclase
GTP cGMP via guanylate cyclase
Glutamate GABA via glutamate decarboxylase (requires Vitamin B6)
Choline Ach via choline acetyltransferase (ChAT)
Arachidonate Prostaglandins, thromboxanes, Leukotrienes via cyclooxygenase/lipoxygenase
Fructose-6-Phosphate Fructose 1,6-bisphosphate via phosphofructokinase (PFK), the rate limiting NZ of glycolysis
1,3-BPG 2,3-BPG via bisphosphoglycerate mutase
Located on the floor of the forebrain
ADH and oxytocin are synthesized in certain hypothalamic nuclei (supraoptic --ADH and paraventricular -- Oxytocin) of
the brain, which contain the cell bodies of neurosecretory cells
Hormones are then transported along the axons of the neurosecretory cells to the pars nervosa (posterior pituitary)
Neural inputs to the brain influence their release
Secretions of the anterior pituitary are controlled by hormones called hypothalamic releasing and inhibitory factors,
which are secreted within the hypothalamus itself
These tropic hormone releasing factors conduct to the anterior pituitary through minute BVs called the
hypothalamic-hypophyseal portal system
The function of hypophyseal portal vessels is to carry hypothalamic releasing factors to the adenohypophysis
Center of the brain regulating body temperature Anterior Hypothalamus (A/C)
Center of the brain for ANS regulation
Factors include:
Gonadotropin releasing hormone (GnRH) stimulates release of both FSH and LH
Thyrotropin releasing hormone (TRH) stimulates release of TSH
Corticotrophin releasing hormone (CRH) stimulates release of ACTH
Stimulated by: low plasma cortisol, hypoglycemia, pyrogen, and stress
Suppressed by: high plasma glucocorticoids
Growth hormone releasing hormone (GH RH) stimulates release of GH
Dopamine (DA) inhibits release of prolactin
Somatostatin inhibits release of GH
Pituitary (Hypophysis)
Has direct hormonal control over the mammary glands (among many things)
Posterior Pituitary = pars nervosa = neurohypophysis
The neurohypophysis produces vasopressin & oxytocin, which both affect contraction of smooth muscle
Antidiuretic hormone (ADH) = vasopressin
Produced in the Hypothalamus (specifically in the supraoptic nuclei)
Vasopressin is a peptide that is stored and released into the bloodstream by the posterior pituitatry
End organ resistance to ADH is called nephrogenic diabetes insipidus
Kidneys fault for not absorbing the water
This results in the inability to concentrate urine, polyuria, and increased serum osmolarity (resulting from
the loss of free water in the urine)
Urine Osmolarity of less than 200 mOsm/L
Decreases the urine volume by increasing the reabsorption of water by the renal tubules (increases the
permeability of the collecting ducts and distal convoluted tubules to water)
ADH receptors are located on the membranes of these collecting ducts and distal tubules
Released in response to:
Increased plasma concentration of Na+
Most important variable regulating ADH is plasma osmolarity
Most sensitive hormone to plasma osmolarity
Decreased blood volume
Ethanol and caffeine decrease ADH release, while nicotine increases its release
Sweating causes an increase in ADH, while drinking large amounts of water causes a decrease in blood ADH


Hyposecretion of ADH results in diabetes insipidus (polyuria, polydipsia and polyphagia)

Diabetes insipidus would also result from the hypoactivity of the posterior pituitary
Infusion of vasopressin results in a decrease in osmolality
Causes muscle of the uterus and milk ducts in the breast to contract
What causes contraction of the uterus oxytocin
Released from the posterior pituitary in response to dilation of the cervix and to suckling
Stimulates smooth muscle cells of myoepithelium of mammary gland alveoli
Oxytocin is responsible for causing contractions of the uterine smooth muscle during labor
ADH and oxytocin are stored and released form the pars nervosa, but neither hormone is produced there
Produced by the paraventricular nuclei in the hypothalamus
Anterior Pituitary (FLAT PEG) = pars distalis = adenohyposphysis
Complete destruction of anterior pituitary would result in Addisons disease, myxedema, & hypogonadism
FSH (Follicle Stimulating Hormone)
Stimulates graafian follicle development and induces secretion of estrogens
Exerts its action on the germinal epithelium
LH (Luteinizing Hormone)
Stimulates ovulation and the development of the corpus luteum
FSH and LH work together to cause ovulation & the formation of the corpus luteum
GnRH (produced by the hypothalamus) stimulates release of both FSH and LH
Adrenocorticotropic hormone (ACTH)
Called the stress hormone
Controlled by the hypothalamus
When body is stressed, corticotropin-releasing hormone (CRH) produced by the hypothalamus travels
through a portal system to the anterior lobe of the pituitary, where it induces the production and secretion of
ACTH by the basophils of the pars distalis
ACTH stimulates the adrenal cortex to synthesize cortisol
Cortisol influences CHO, lipid, & protein metabolism
The mineralcorticoid aldosterone and the glucocorticoids are collectively called corticosteroids
Aldosterone secretion from the adrenal cortex is induced by elevated plasma K+ & angiotensin II, not by
IV injections of KCl would increase the secretion of aldosterone
Aldosterone primary effect is on the kidney tubules, where it stimulates Na+ retention and K+ excretion
Results in high Na & low K in plasma
Another Q: Aldosterone causes increased renal tubular reabsorption of sodium
Another Q: Reabsorption of sodium chloride is controlled in the kidney tubules by an adrenal cortical
hormone (aldosterone)
Another Q: Aldosterone is normally associated with partial regulation of sodium balance
Another Q: Aldosterone increases K+ secretion into the urine
The following statements describe aldosterone:
It is a mineralocorticoid
It increases Na+ uptake from the kidneys
Its production is stimulated by angiotensin II
NOTE: it is not produced in the zona fasciculata of the adrenal cortex (its made in the zona glomerulosa)
Thyroid Stimulating hormone (TSH)
Aka thyrotropin
Secreted by basophils of the pars distalis of the anterior pituitary gland
Controls the rate of secretion of thyroid hormones (thyroxine and triiodothyronine)
Thyroxine in turn controls the rates of many metabolic processes and the metabolic rate
Exposure to cold increases the rate of TSH secretion
Thyroid secretion is stimulated by prolonged exposure to a cold environment
Stress can inhibit TSH secretion, most likely by way of neural influences that inhibit the secretion of TRH
from the hypothalamus
TSH is stimulated by TRH. There are several negative feedback loops which regulate:
High levels of circulating thyroid hormone decreases the secretion of both TRH and TSH
Elevated levels of TSH decreases secretion of TRH
Hypersecretion of TSH results in Graves disease (and Plummers)
Hyposecretion of TSH results in Cretinism (in young people) and Myxedema (in adults)


**NOTE ACTH and TSH are pituitary tropic hormones

Prolactin (aka lactogenic or luteotropic hormone)
Produced by eosinophils (remember PeG e is for Eosins) of the pars distalis of the anterior pituitary gland
Stimulates milk production by the mammary glands (during pregnancy for breast development and after
delivery of the child for lactation)
Basically, Prolactin increases dopamine synthesis, then Dopamine inhibits Prolactin secretion
Hypothalamus synthesizes a prolactin inhibitory factor (dopamine)
Under normal conditions, large amounts of dopamine are continually transmitted to the anterior pituitary
gland so that the normal rate of prolactin secretion is slight
This is why prolactin is said to be under predominant inhibitory control by the hypothalamus
This is also why blocking the hypothalamic-hypophyseal venous portal system increases the release of
During pregnancy and lactation, the formation of dopamine itself is suppressed, thereby allowing the
anterior pituitary gland to secrete an elevated amount of prolactin
Most anterior pituitary hormones are enhanced by the neurosecretory releasing factors transmitted from the
hypothalamus, but not prolactin
Blocking the hypothalamic-hypophyseal venous portal system increases the secretion of prolactin
But, it does not increase the secretion of ACTH, TSH, and oxytocin
Not oxytocin, because it is a hormone of the posterior pituitary
Not ACTH & TSH, since release is stimulated by CRH & TRH, respectively from the hypothalamus
Prolactin secretion increases, because release is inhibited by dopamine from the hypothalamus
In females, Prolactin inhibits GnRH synthesis and release, which inhibits ovulation (Breast feeding CAN be
birth control)
Growth Hormone (aka Somatotropin)
From the anterior pituitary alpha cells:
Does not function through a target gland but instead exerts effect on all or almost all tissues
GH causes the liver (and to a much lesser extent other tissues) to form several small proteins called
somatomedins (also called insulin-like growth factors) that in turn have the potent effect of increasing all
aspects of bone growth Somatomedin is increased by somatotropin
Insulin-like growth factor 1 (IGF-1) is secreted by the liver; IGF-1 secretion is stimulated by GH in
Basic metabolic effects:
Increased rate of protein synthesis in all cells of the body
Decreased rate of carbohydrate utilization throughout the body
Increased mobilization of fats and the use of fat for energy
Causes cells to shift from using carbohydrates to using fat for energy Think you lose your baby Fat
Secretion is increased by: sleep, stress, starvation, exercise, hypoglycemia, hormones related to puberty
Secretion is decreased by: somatostatin, somatomedins, obesity, hyperglycemia, and pregnancy
The rate of GH secretion increases and decreases within minutes
Most of the time it is in relation to the persons state of nutrition or stress
GH is released in a pulsatile fashion
Acidophile Hormone of Hypophysis??
GH is also released in response to a decline in plasma glucose concentration and an elevated plasma level of
certain amino acids, particularly arginine
Growth hormone undersecretion produces pituitary dwarfism in children
Oversecretion of GH causes gigantism in children or in adults, acromegaly
Hypersecretion of GH causes hyperglycemia
This is because GH stops usage of CHOs and makes you use FAs for energy
Nitrogen Balance
Positive Nitrogen Balance
Means that nitrogen intake exceeds nitrogen output
Patients taking GH are likely to exhibit a positive nitrogen balance
A positive nitrogen balance is likely to take place following administration of GH
Growth, Protein Synthesis because the ammonia is incorporated into the alpha amino groups of amino
acids and therefore less nitrogen will be secreted
Negative Nitrogen Balance (BAD for wasting or NOT growing)
Means the nitrogen output exceeds nitgrogen intake
A negative nitrogen balance is most likely to occur during old age
Negative nitrogen balance may be caused by a dietary lack of essential amino acids
Not during fetal growth or adolescence for obvious reasons
Not during convalescence, which is a period of recovery from injury, surgery, etc


Nitrogen can be used as a measurement of protein level in meat

An example of synergism is GH & thyroxine on skeletal growth
Ovaries (From F for FSH and L for LH)
Produce ova, the female sex hormones (progesterone and estrogen) and follicles
The corpus luteum
Is a yellowish mass of cells that forms from an ovarian follicle after the release of a mature egge
If the mature egg is not fertilized and pregnancy does not occur, the corpus luteum retrogresses to a mass of scar
tissue (corpus albicans) which eventually disappears
If the mature egg is fertilized and pregnancy does occur, the corpus luteum does not degenerate but persists for
several months. Human chorionic gonadotropins HCG which is produced by the placenta stimulates the corpus
luteum to produce estradial and progesterone
Granulosa cells in the corpus luteum produce progesterone and estrogen
It produces more progesterone than estrogen
Oral contraceptives prevent ovulation:
Most contraceptives are combined pills which contain synthetic estrogen-like (ethynl estradiol, mestranol) and
progesterone-like (norethindrone, norgestrel) substances
Being used as oral contraceptive substance due to their ability to suppress ovulation
It stops LH, but does NOT decrease FSH secretion
Preventing the rise in LH prevents ovulation
Primary recognition of B-estradiol by its target cell depends upon the binding of the hormone to a specific
cytoplasmic receptor
Exact mechanism is thought to be as follows:
In presence of either estrogen or progesterone, the hypothalamus fails to secrete the normal surge of LH
releasing factor
This inhibits the release of LH from basophils of the anterior pituitary gland
Subsequent ovulation does not occur
Ovulation occurs as a result of the estrogen-induced LH surge
Unlike other steroid hormones, all estrogens have an aromatic A ring
Adrenal Medulla (From A for ACTH)
Specialized ganglion of Symp NS
Preganglionic fibers synapse directly on chromaffin cells in the adrenal medulla
These cells secrete epi (80%) and NE (20%) into the circulation
Both of these hormones are direct-acting adrenergic agonists and are biosynthesized from tyrosine
Tyrosine is a metabolic precursor for epinephrine
Epinephrine is most closely related structurally to Tyrosine
NE and its methylated derivative epi act as regulators of CHO and lipid metabolism
NE & epi increase degradation of triacylglycerol & glycogen, AND increase heart output (specifically, epi) & BP
These effects are part of a coordinated response to prepare the individual for emergencies fight or fright reactions
Increase in response to fright, exercise, cold, low levels of blood glucose
The adrenal medulla is supplied by cholinergic preG Symp neurons that release Ach
In terms of origin & function, the adrenal medulla is comparable to a postganglionic sympathetic nerve
In response to this, the adrenal medulla releases mainly epi (and some NE) into the bloodstream, which carries the
secretions to the effector organs
The pathway of Origin (NE and Epi)
Tyrosine L-Dopa Dopamine NE Epi
Dopamine is synthesized in 2 steps from which of the following compounds (Tyrosine)
Epinephrine (adrenalin):
The release of epinephrine is controlled mainly by nerve impulses
Stimulates glycogenolysis and gluconeogenesis (except in the liver), which tend to raise blood glucose levels
When injected, epinephrine causes an increase in blood sugar
Another Q: Sympathetic stimulation affects CHO metabolism because epinephrine increases liver
Also stimulates lipolysis in adipose tissue (breakdown of TGs into glycerol and fatty acids)
Increases rate, force, and amplitude of heart beat
Administration of local anesthetic w/ epinephrine will most likely produce an increased heart rate
Constricts BVs in skin, mucous membranes, and kidneys
Sympathetic stimulation dilates bronchioles in the lungs & relaxes bronchiolar smooth muscle
Another Q: Increased parasympathetic activity causes bronchiolar smooth muscle contraction


Another Q: Epi activates muscles glycogen phosphorylase

Tags glycogen to be degraded
Norepinephrine (noradrenalin):
Increases heart rate and the force of contraction of heart muscle
Promotes lipolysis in adipose tissue
Constricts blood vessels in almost all areas of the body, thus increasing total peripheral resistance
Has the LEAST effect on Calicum Metabolism
NE can be released in two ways:
1. By the adrenal medulla into the bloodstream
The effects are more widespread when NE is released into the bloodstream by the adrenal medulla as
opposed to directly onto an organ by the postganglionic sympathetic neuron
2. Directly onto an organ by a postganglionic sympathetic (adrenergic) neuron which stores NE
Cortisol (hydrocortisone)
Has direct inhibitory effect on hypothalamus and anterior pituitary gland
Is a glucocorticoid
The principal mechanism by which glucocorticoids stimulate their target cells is by activating specific genes
Release of cortisol is controlled primarily by ACTH, which is secreted by basophils in the pars distalis of the
anterior pituitary
Release of ACTH is influenced by corticotrophin-releasing hormone (CRH) from the hypothalamus
Cortisol exerts an inhibitory influence on both ACTH and CRH by way of negative feedback
Main glucocorticoid produced and secreted by the cells of the zona fasciculata in the adrenal cortex
Allows glucagon and epi to work more effectively at their target tissues, but antagonizes the action of
Increases hepatic glycogen content, gluconeogenesis, protein breakdown, & adipose tissue breakdown
Anti-inflamatory properties
Impairs cell-mediated immunity
Influences behavior (decreasing stress)
Stimulates leukocytosis
Inhibits synthesis of nucleic acids (except liver)
Affects immune system, bone, calcium absorption from the GI tract, and the CNS
blood glucose (by stimulating gluconeogenesis and inhibiting glucose uptake)
Cortisol stimulates synthesis in the liver of pyruvate carboxylase (NZ of gluconeogenesis)
amino acids (by stimulating protein breakdown)
fatty acids (by stimulating lipolysis)
Decreases glucose utilization from the cells
A patient taking cortisol for a long period of time may experience atrophy of the adrenal cortex due to inhibition of
ACTH production
15-30 mg released daily in diurnal rhythm, mostly in morning, same is true for ACTH
90% is bound to transcortin (corticosteroid binding globulin = CBG)
Cushings syndrome
Metabolic disorder resulting from the chronic and excessive production of cortisol
The most common cause of this syndrome is a pituitary tumor that causes an increased secretion of ACTH
Characterized by hypertension, hyperglycemia, hypokalemia, increased androgen levels, and increased
protein catabolism (All the things a pheochromoctyoma does)
NOT increased protein anabolism
Thyroid (From T for TSH)
TSH from the pituitary gland stimulates synthesis and the release of thyroid hormones
Thyrotropin releasing hormone (TRH) from the hypothalamus promotes TSH secretion
Glycoprotein prohormone (10% carbohydrate)
Contains iodine which is attached to tyrosine molecule
The follicle cells of the thyroid gland synthesize thyroglobulin and secrete it into the colloid-containing regions of
the follicle
Here the thyroglobulin undergoes iodination and coupling processes that produce the thyroid hormones
Thyroglobulin molecules containing these hormones are then stored in colloid-containing regions of the follicle
So if your body needs iodine, then it breaks down thyroglobulin and releases iodinated T3 and T4


When the thyroid is actively secreting, these thyroglobulin molecules are then taken back into the follicle cells
and broken down into the two hormones (T4/T3)
An iodine deficiency will increase the secretion of thyroglobulin (not T3, T4, or TSH)
Thyroid hormones:
Thyroglobulin (stored)
Hydrolysis of thyroglobulin liberates a number of iodinated compounds, only 2 are considered thyroid
T3 (Triiodothyronine)
T4 (Thyroxin)
T3 (triiodothyronine) has several times the biologic activity of T4 (thyroxine)
T4:T3 = 20:1
T4 could be said to act primarily as a pro-hormone for T3; T4 is converted to T3 primarily in the kidney
and liver, also can be converted to rT3, which is produced during illness, malnutrition or induced by
some drugs
0.03% of T4 is free and 0.3% of T3 is free, the rest are bound to thyroxine binding globulin (TBG)
4 Bs of T3
Brain Maturation
Bone Growth
Beta-adrenergic effects
BMR increased (Basal Metabolism Rate)
Thyroid secretes two iodine containing amine hormones that have a structural differences of one iodine atom
The majority of T4 is converted peripherally by target cells to T3 which is a more potent hormone
This is done by the enzymatic removal of one iodine atom
Iodine is important in the biochemical synthesis of thyroxin (T4)
Thyroid hormones are lipophilic hormones which exert their effects via transcriptional processes
Thyroid hormones are synthesized from Tyrosine
Important for normal growth and development (especially for brain)
Affect many metabolic processes and the metabolic rate
Basal Metabolism Rate is an increase in H2O, related to surface area???
Increased BMR is done via increasing Na+/K+ ATPase activity = increased O2 consumption,
increased body temp
Increase glycogenolysis, gluconeogenesis, and lipolysis, protein degradation (SAME AS CORTISOL)
This is why removal of the anterior pituitary (TSH) would result in a drop of blood glucose level
Regulate metabolism by speeding up cellular respiration
Beta-adrenergic effects
CV: increased CO, HR, SV, contractility, and RR
Stimulate bone maturation as a result of ossification and fusion of the growth plates
Synthesized and secreted by the parafollicular cells (C cells) of they thyroid gland that are located in the interstitium
Its secretion is stimulated by a increase in serum calcium
The immediate effects of calcitonin secretion are decreased serum levels of both calcium and phosphate
Most significant immediate result of lowered serum calcium is hyperirritability of nerves and muscles
It acts on bone cells to suppress bone resorption and enhance bone formation
Along with parathyroid hormone 1,25 DHC, it is a regulator of calcium metabolism
Is a linear polypeptide consisting of 32 amino acids
Is not required in adult humans
Although it is important during bone development, the major regulator of plasma calcium level in the adult is PTH
Parathyroid hormone (PTH)
Phosphate Trashing Hormone (Decreases Serum Phosphate, but increases Urinary Phosphate)
Secreted by Chief Cells in the parathyroid glands in response to decreased plasma calcium levels
NOT in response to Hypothalamus-Pituitary Complex
Plasma calcium level is the major controller of PTH, NOT Hormonal
Another Q: Bone resorption seen in elderly patients with low dietary calcium is enhanced by PTH (not insulin,
estrogen, aldosterone, or TSH)
The principal controller of calcium and phosphate metabolism and is involved in the remodeling of bone
The most prominent function of bone is a calcium reservoir
Increases the plasma calcium concentration and decreases the plasma phosphate concentration
In a parathyroidectomized animal, plasma calcium is low and plasma phosphate is high
PTH modes of action: daddy


The major target tissues of the calcium regulating hormones are: bone, intestine, kidney
Stimulates BOTH osteoclasts and osteoblasts
Bone cells (osteoclasts) increase bone resorption, leading to release of calcium & phosphate into blood
Accelerates removal of calcium and phosphate from skeleton, but NOT from teeth
Q: Theories of the effect of PTH on bone:
PTH influences the rate of bone resorption
The action on bone is related to its action on phosphate excretion
The effect of parathyroid extract is to influence osteoclastic activity
PTH does NOT cause a decrease in new bone formation
Increases Kidney reabsorption of Calcium in DCT
Acts on the kidney to decrease calcium excretion and increase phosphate excretion in the urine
Also stimulates 1-alpha-hydroxylase in the kidneys Activates Vitamin D
Causes an increase in 1,25 hydroxycholecalciferol formation, which then causes an increase in Calcium
absorption from the intestine
Increases the absorption of calcium in the GI tract
Diseases associated with PTH
Hyperparathyroidism (von Recklinghausens disease)
Causes extensive bone decalcification
A patient w/ hyperparathyroidism is predisposed to an increased likelihood of bone fracture
Is marked by extremely high blood calcium levels and low blood phosphate levels
BOTH PTH and Calcitonin lead to Low serum phosphate levels
This leads to muscular weaknesses
The low serum phosphate level in hyperparathyroidism is caused by increased renal loss of phosphate
Renal calcium excretion is increased in hyperparathyroidism
Seems a little counterintuitive, but websites confirm it must be due to the excess of PTH, since
normal PTH levels would decrease calcium excretion
This is the stones part of moans, groans, stones, bones & psychiatric moans symptoms
(tetany) (hyperirritability of neuromuscular areas )
Causes decreased bone resorption, decreased renal calcium reabsorption, increased renal phosphate
reabsorption, and decreased production of the active form of vitamin D (1,25 dihydroxycholecalciferol)
Together these effects decrease serum calcium & increase serum phosphate
Marked reduction in serum calcium will result in increased muscular irritability
***Another Q: the movement of Ca2+ across many cell MBs involves a Ca2+/Na+ countertransport
Another Q: Complete removal of the parathyroid glands leads to tetany
Hormonal Calcium Metabolism
Androgen, Estrogen, Thyroid Hormone, and Parathyroid Hormone all have effects
Norepinephrine is the LEAST involved
Secretions are stimulated by blood levels of certain molecules
A piece of pancreas transplanted under the skin (re-established circulation) would secrete after ingestion of food
A piece of parotid gland would not secrete
Proinsulin is converted to insulin (a segment of proinsulins polypeptide chain is removed) This segment is called
Secreted by beta cells in the islets of Langerhans of the pancreas in response to a rise in the blood glucose level
Insulin is secreted more in the absorptive state than the post-absorptive state
It causes glycogenesis in the liver
Insulin lowers the blood glucose level by stimulating and facilitating the uptake of glucose and the utilization of
glucose as an energy source by many cells
A principal action of insulin is to enhance cell permeability to glucose
It also promotes the synthesis of glycogen, triglycerides, and proteins
GLUT 1 receptors are found on RBCs, Brain, Renal Cortex
GLUT 2 receptors are found in Beta cells
GLUT 4 receptors are found in muscle and fat
Has NO effect on glucose uptake by the brain
Inhibits lipolysis (it enhances triglyceride synthesis)


Stimulates protein synthesis (inhibits protein breakdown)

Increases entry of glucose into muscles & adipose tissue
Brain uptakes Glucose Independent of Insulin
Enhances cell permeability to glucose
Another Q: Insulin increases the rate of anabolic (biosynthetic) reactions
Another Q: Insulin conserves protein, carbohydrate, & fat stores in the body
Another Q: Insulin increases the activity of phosphofructokinase
Basically, tells to cell to get storing the energy and also pushes the glucose down the chain faster
Remember the Factory, and the Truck that showed up analogy
Secretion inhibited by:
Decrease in blood glucose
Secretion of somatostatin
Secretion of either epi or NE
BUT NOT by secretion of glucagons - I guess insulin is KING
Insulin released by beta cells is promoted by:
Rise in blood glucose: this is the major factor governing insulin release
Elevated level of amino acids (especially arginine, lysine, and leucine) in the blood plasma
Glucagons, GH, and cortisol because all of the following blood glucose levels
PS stimulation
Removal of the anterior pituitary gland increases the sensitivity to insulin
(To pick up what little glucose there is!!) Because w/o Anterior Pituitary, Blood glucose goes down
Another Q: The blood glucose level in diabetes mellitus is decreased by removal of the anterior pituitary
I think this might be due to the absence of T4, GH, and ACTH, which would normally elevate blood glucose,
hence activating Insulin
Insulin stimulates the tyrosine kinase receptor
Insulin vs. Glucagon
Insulin (If your house is insulated, you can take stuff off, i.e. Phosphates)
Dephosphorylates stuff
Turns Glycogen Synthase (A) ON, but Phosphorylase (B) OFF
Phosphorylates stuff
Turns Glycogen Synthase (B) OFF, but Phosphorylase (A) ON
The A Form is ON FORM
Secreted by the alpha cells in the Islets of Langerhans of the pancreas in response to blood glucose level
Most important function = ability to cause glycogenolysis in the liver (which, in turn, plasma glucose)
Cyclic AMP rate of glycogenolysis by promoting formation of phosphorylated form of Glycogen
cAMP PKA P form of glycogen phosphorylase glycogen-P glycogenolysis
The phosphorylation of phosphorylase b to phosphorylase a operates in liver cells to regulate
breakdown of glycogen
Glucagon is found in standard medical emergency kits because it promotes glycogenolysis in hypoglycemic pts
Does not stimulate glycogen degradation in muscle Because it cant leave the cell anyway (No G-6-P)
Frequently called the hyperglycemic factor
Hyperglycemic affect of glucagon is mediated primarily through the liver glycogenolysis
Glucagon released by Alpha cells is promoted by the following:
A fall in blood glucose level (hypoglycemia): this is the major regulator of glucagon
NOTE on hypoglycemia: clinical manifestations of hypoglycemia include:
Dizziness, confusion, convulsion, coma (not hyperventilation)
Same Pt has a seizure
Most likely due to Hypoglycemia
Sympathetic stimulation
Epinephrine and norepinephrine secretion
Elevated level of amino acids (especially arginine) in the blood plasma
Cholecystokinin secretion
Factors that decrease glucagon secretion
Rise in the blood glucose level


Free FAs
Exhibits main effect on the distal convoluted tubule and the collecting duct to increase Na+ permeability
Stimulates Na+ retention and K+ excretion
This restores extracellular fluid volume and blood volume to normal
Is the principle mineralcorticoid
Secreted by cells located in the zona glomerulosa of the adrenal cortex
Secretion is induced by 1) plasma K+ levels and 2) the renin-angiotensin system
Decreased [Na+] causes JG cells of the kidneys secrete renin
(Reduced renal blood flow causes hypertension by the release of renin)
Your kidney thinks BP is down, so it kicks out renin to preserve Na+, which preserves fluid, which
raises BP
Renin-Angiotensin System
Renin is released by the kidneys upon sensing decreasing BP
Renin cleaves angiotensinogen to angiotensin I (in the blood)
ACE cleaves Angiotensin I to angiotensin II primarily in the lung capillaries
Angiotensin II
Stimulates the adrenal cortrex to release aldosterone
Potent vasoconstrictor
Release of ADH from posterior pituitary
Stimulates Hypothalamus (increase thirst)
**ANP (Atrial Natriuretic Peptide) released from the atria may serve as a check
Addisons disease
Caused by the hyposecretion of aldosterone and cortisol
GI Hormones:
Stimulates gastric acid secretion (HCl) by parietal cells coupled with the release of pepsinogen by chief cells
Released caused by:
Presence of peptides and amino acids in gastric lumen
Distension of stomach
Synthesized and stored in the cells of the antrum and duodenum (Antrum is the distal end of the stomach)
Secretion of gastric acid inhibits gastrin secretion an example of feedback regulation
Also inhibited by secretin
Includes secretin, cholecystokinin, and gastric inhibitory peptide, GIP
Are released by the small intestine in response to the acidity of the duodenal chyme and the presence of amino acids
and free fatty acids
The hormones enter the blood and are carried to the stomach, where they depress the pyloric pump (pumping action
of the stomach), thus inhibiting gastric motility, which slows down gastric emptying
The enterogastric reflex
Initiated when the duodenum fills with chyme, also inhibits the pyloric pump, thereby inhibiting gastric motility
and emptying and secretions
The rate of gastric slow waves is unchanged but gastric emptying is reduced
The enterogastric reflex produces a decrease in gastric motility
Fats have the largest control over the release of the gastrones and the subsequent rate of gastric emptying
Fat in the small intestine inhibits gastric emptying through activity of enterogastrone
Produced in the small intestine in response to the presence of certain amino acids and free fatty acids
Stimulates the release of pancreatic enzymes (trypsin, chymotrypsin, and carboxypeptidase)
Stimulates the contraction & emptying of the gallbladder
Delays gastric emptying following fat ingestion
NOTE: although secretin also inhibits gastric emptying, the Q was asking about it in relation to fat
Secreted in the duodenum, and is an enteroendocrine cell


Is released when the gastric contents (especially, H+) are delivered to the duodenum
In turn secretin stimulates pancreatic duct cells to secrete a fluid high in bicarbonate (HCO3-), which neutralizes
the H+ in the duodenum
Functions of secretin:
Inhibits stomach motility and gastric acid secretion
Stimulates the pancreatic duct cells to secrete a fluid which contains a lot of bicarbonate ion but is low in
Stimulates the secretion of bile from the gallbladder
Secretin functions in digestion of proteins by increasing flow of pancreatic juice (which contains trypsin,
chymotrypsin, carboxypeptidase)
Gastric inhibitory peptide:
Like secretin, is secreted from the mucosal cells in the duodenum
Inhibits gastric acid secretion (HCl) and motility and stimulates the release of insulin from the beta cells in
response to elevated blood glucose concentrations
Release stimulated by presence of fat & glucose in small intestine
Enterokinase (enteropeptidase)
This hormone causes the release of pancreatic zymogens (e.g., trypsinogen, chymotrypsinogen, proelastase, and
procarboxypeptidase A & B) and the contraction of the gallbladder to deliver bile to the duodenum when chyme comes
into contact with the mucosa
Enterokinase is found in the succus entericus but NOT found in the pancreatic juice
Converts trypsinogen to trypsin
Pancreatic proteases are secreted in inactive forms (zymogens) that are activated in the small intestine:
Site of Synthesis
Active NZ
Procarboxypeptidase A
Carboxypeptidase A
Procarboxypeptidase B
Carboxypeptidase B
Secreted by the chief cells of the body (or Fundus -- BOTH) of the stomach (Pepsinogen)
Activated by pepsin and low stomach pH
The most important fxn of Hydrochloric acid in the stomach is activation of pepsinogen
Pepsinogen is not found in pancreatic juice (but lipase, amylase, trypsinogen, and chymotrypsinogen are)
Activated to trypsin by enterokinase
Cleaves peptide bonds in which the carboxyl group is contributed by lysine and arginine (basic amino acids)
Converts trypsinogen, chymotrysinogen, proelastase, and procarboxypeptidase A and B to their active form
Serine is an important aa in the active site of both chymotrypsin & trypsin
Hydrolyzes peptide bonds on the alpha carboxyl side of aa residues with large polar side chains, like Tyrosine,
Tryptophan, Phenylalanine, Methionine, and Leucine
Phenylalanine, Tyrosine, Tryptophan are AROMATIC
Serine is an important aa in the active site of both chymotrypsin & trypsin
Cleaves at the carboxyl end of aa residues with small, uncharged side chains such as alanine, glycine or serine
Carboxypeptidase A
Has little activity on aspartate, glutamate, arginine, lysine, or proline
Carboxypeptidase B
Cleaves basic amino acids: lysine and arginine
Eicosanoids: prostaglandins and the related compounds of thromboxanes and leukotrienes
20-carbon FAs that contain a five carbon ring
Chemical messengers present in every body tissue
Differ from true hormones in that they are formed in almost all tissues rather than in specialized glands
Act as primarily as local messengers that exert their effects in the tissues that synthesize them


Have a very short half-life

Synthesis can be inhibited by a number of unrelated compounds including aspirin, indomethacin, ibuprofen,
phenybutazone, which are all NSAIDs
Major Classes
Seem to modulate the action of hormones rather than act as hormones
They enhance inflammatory effects, whereas aspirin diminishes them
Arachidonic acid:
A polyunsaturated fatty acid
The major compound from which prostaglandins, prostacyclins, thromboxanes, and leukotrienes are derived
Prostaglandins are made within cells from polyunsaturated fatty acids
Linoleic & arachidonic acids serve as precursors to prostaglandins
Upon complete hydrogenation, oleic, linoleic, linolenic acids yield steric acid
It is part of phospholipids in the plasma membranes of cells
When a cell is stimulated by a neurotransmitter or hormone, a plasma membrane enzyme called phospholipase A is
activated, and this enzyme splits arachidonic acid from the phospholipids
Cortisol inhibits phospholipase A activity which results in the formation of arachidonic acid from MB lipids
Different metabolic pathways utilize different enzymes that convert arachidonic acid into:
Cyclooxygenase: prostaglandins, prostacyclins, and thromboxanes
Lipooxygenase: Leukotrienes
Prostacyclin (PGI2) (Platelet Gathering Inhibitor)
Acts to prevent platelet formation and clumping
Also a potent vasodilator
Physiologic Anticoagulant
Contrast to Thromboxane A2 which is secreted by platelets
Is a heteropolysaccharide that serves as a powerful anticoagulant that prevents the formation of active thrombin
Another Q: Heparin administration results in symptoms similar to vitamin K deficiency increased bleeding time due to
lack of thrombin formation
Unlike other glycosaminoglycans that are extracellular compounds, heparin is an intracellular component of mast cells
These mast cells line arteries, especially the liver, lungs, and skin
Mast cells are abundant in the tissue surrounding lung capillaries & to a lesser extent in liver capillaries
Small quantities are produced by basophils functionally almost identical with mast cells
Used in treatment of certain types of lung, blood vessel, and heart disorders, and during or after certain types of surgeries
(open heart or bypass surgeries)
Concentration in the blood is normally slight, so that only under limited physiological conditions does it have significant
anticoagulant effects
HEPARIN Think Hugh Heffarin with his PERFECT 10 girls stops 10 from doing its thing
Administration of heparin will result in an increase in bleeding time due to the activation of antithrombin, a
major protease inhibitor, which rapidly inhibits thrombin.
It is used in treating pts who have suffered a coronary thrombosis
Heparin can also enhance the removal of lipoproteins from the blood by binding apolipoprotein E (protein found on
some liposomes) and by activation lipoprotein lipase
Vasodilation (particularly the arterioles by the decarboxylation of histidine)
Decarboxylation of the aa histidine results in formation of a vasodilator (histamine)
Secretion of HCL H2
Decreased blood pressure
Increased vascular permeability (particularly in the capillaries and venules)
Found in tissues, mast cells, basophils (and is in highest concentration in the lungs)
Secreted by mast cells as a result of allergic reactions or trauma
When tissue is injured, histamine is liberated by the damaged tissue into the surrounding fluids
This increases the local blood flow as wells as capillary & venule permeability, allowing large quantities of fluid
protein to leak into the tissue characteristic wheal
Powerful pharmacologic action from two receptors:
H1 receptors:
Mediate the typical allergic and anaphylactic responses to histamine bronchoconstriction, vasodilation, and
increased capillary permeability


H2 receptors:
Mediate other responses to histamine, such as the increased secretion of gastric acid and pepsin
Serotonin: (aka 5HT)
Synthesized from the aa tryptophan (also secretes another tonin melatonin and Niacin NAD)
Released from platelets upon damage to the blood vessel walls
Acts as a potent vasoconstrictor and increases vascular peripheral resistance
In gastric mucous membranes it is secreted by the enteroendocrine cells and causes the smooth muscle to contract
In brain it acts as a neurotransmitter
Lysergic acid diethylamide interferes with the action of serotonin in the brain
Diabetes mellitus:
The most common pancreatic endocrine disorder
A metabolic disease involving mostly carbohydrates (glucose) and lipids
In uncontrolled DM,
Delayed Wound Healing
Type I DM pt scheduled for extractions, dentist should be most concerned about Increased potential for
Caused by:
(Type I)
An absolute deficiency of insulin
Defective or absent beta cells in the pancreas
(Type II)
Resistance to insulins actions in the peripheral tissue
Results from loss of the insulin receptor fxn in the target tissue
80-90% of diagnosed cases
Polygenetic etiology
Middle aged, obese
Insulin is present at elevated or near normal levels
Cardinal symptoms include: polydipsia, polyuria, polyphagia, weight loss, loss of strength
In untreated diabetes mellitus, polyuria is related to the osmotic effect of glucosuria
Another Q: Glucosuria with hyperglycemia usually occurs in diabetes mellitus
Level of insulin secretion
Typical age of onset
Percentage of diabetes cases
Basic defect
Associated with obesity
Speed of development of symptoms
Development of ketosis

Type 1
None or almost none
10 20%
Destruction of B cells
Common if untreated
Insulin injections, dietary mgmt

Type 2
May be normal or exceed normal
80 90%
Reduced sensitivity of insulins target cells
Dietary control, weight reduction,
occasionally oral hypoglycemic drugs

Diabetes insipidus:
A disorder in which insufficient levels of antidiuretic hormone (ADH) cause excessive thirst (polydipsia) and excessive
production of very dilute urine (polyuria)
Results from hypoactivity of the posterior pituitary gland or destruction of the supraoptic nuclei of the hypothalamus
ADH deficiency results in failure of tubular water reabsorption (kidney) and the consequent passage of a large amount of
dilute urine and great thirst
Body fluid volumes remain close to normal so long as the pt drinks enough water to make up for increased H2O
Nephrogenic diabetes insipidus:
Congenital and familial form of diabetes insipidus due to failure of the renal tubules to reabsorb water
Excessive production of ADH but the tubules fail to respond
Inadequate perfusion of tissue


Tiredness, sleepiness, and confusion

Skin becomes cold and sweaty and often bluish and pale
Pulse is weak and rapid
Blood pressure drops as well
Stages of shock:
Compensatory mechanisms
Activation of the sympathetic nervous system, increased cardiac output, and increased total peripheral
resistance in order to maintain perfusion to vital organs
If blood has been lost & the pt is in shock, the following are likely to occur:
Decrease in GFR
Decrease in urine formation
Decreased heart perfusion leads to cardiac depression and decreased cardiac output
Depletion of high energy phosphate reserves
Death occurs even if treatment can restore blood flow
Major categories of shock:
Produced by a reduction in blood volume
Results from severe hemorrhage, dehydration, vomiting, diarrhea, and fluid loss from burns
Results in a decrease in GFR and a decrease in urine formation
A patient is dehydrated due to severe vomiting; a symptom he/she might present with is an increased pulse rate
Circulatory collapse resulting from pump failure of the left ventricle
Most often caused by massive myocardial infarction
Due to severe infection
Causes include endotoxin from G- bacteria
From severe injury or trauma to the CNS
Occurs with severe allergic reaction
Yellow discoloration of the skin and white of eyes caused by abnormally high levels of the bile pigment, bilirubin, in the
Heme is scavenged from the RBC (after their 120 day life span) and the Fe2+ is reused
Actively taken up by hepatocytes
Heme Biliverdin Bilirubin
Sparingly water soluble, toxic to CNS, and transported by albumin
Bilirubin is the product of heme degradation
Another Q: RBC destruction is measured by the bilirubin (bile pigments) excreted from the liver each day
Another Q: The amount of bile pigment secreted by the liver is deteremined by the amount of hemoglobin
Heme portion of the hemoglobin, the part of the red blood cells that carries oxygen is broken down into bilirubin
Bilirubin is carried to the liver as unconjugated and bound to albumin
UNconjugated is INdirect and INsoluble
Free bilirubin-albumin complex
Converted to the diglucuronide derivative (conjugated bilirubin) in the liver
Conjugated is Direct
Conjugated version is water-soluble
Conjugated is then ready to be excreted via bile
excreted into intestines as a component of bile
OR excreted by the kidneys as urobilirubin
Bacterial conversion to urobilinogen in the colon (precursor for urobilirubin???)
Some excretion as stercobilin in feces
But most is recycled via enterhepatic circulation of urobilinogen
If the excretion from the liver is hindered, excess conjugated bilirubin passes into the bloodstream, resulting in jaundice


Very common the leading manifestation of liver disease

Can occur at any age and in either sex
Symptom of many disorders liver disease, gallstones, pancreatic cancer, and acute biliary obstruction
Normal plasma concentration of bilirubin averages 0.5 mg per 100 ml of plasma
In jaundice it can rise to as high as 40 mg per 100 ml
Causes of jaundice:
Increased destruction of red blood cells with rapid release of bilirubin into the blood
Obstruction of bile ducts or damage to liver cells causes inability of bilirubin to be excreted into the GI tract
Phenylketonuria (PKU):
An abnormal presence of phenylketone and other metabolites of phenylalanine in the urine
PKU is caused by the absence of or a deficiency of phenylalanine hydroxylase, the enzyme responsible for the
conversion of the amino acid phenylalanine into tyrosine
Metabolic defect in phenylketonuria results in failure to hydroxylate phenylalanine adequately
Tyrosine lessens the need for Phenylalanine
Tyrosine becomes essential
Phenylalanine is the amino acid that can be converted to Tyrosine most easily in the human body
Accumulation of phenylalanine is toxic to brain tissue
It will impair normal development of the brain causing severe retardation
Signs: mental retardation, musty smell, fair skin, excema NO melanin
Alkaptonuria (aka homogentisuria): Think AKU
Due to the failure to catabolize tyrosine beyond the intermediate, homogentisic acid, which is excreted in the urine and
makes it appear black
THINK you make melanin from tyrosine, so of course its intermediate is dark colored
Homogentisic acid accumulates in the urine
Results from a deficiency of a dioxygenase (homogenetisate)
Usually, the condition does not result in any serious ill effects
A hereditary disorder characterized by excessive urinary excretion of cystine and other amino acids
COLA Cysteine, Ornithine, Lysine, and Arginine
Caused by a defect in the renal tubules that impairs the reabsorption of these amino acids
Excess cysteine in urine can lead to kidney stones
Due to the failure to convert tyrosine to melanin, as a result of a deficiency of the enzyme, tyrosinase
Tyrosine is a precursor of the pigments of the skin, hair & nails
Albinos do not have problems with epinephrine synthesis, despite melanin and epinephrine having DOPA as a common
intermediate, because of different enzymes used in malanocyte for DOPA synthesis
Highly mineralized structure containing approximately 95% inorganic matter
Hydroxyapatite (HA) crystals
Made up of calcium & phosphate
Are the largest mineral constituent (90-95%) of enamel
Have a multi-ionic structure
Solubility is pH-dependent (as pH , solubility )
Tends to bind polar substances
Substitution of carbonate into HA increases the solubility (instead
of phosphate) around the Ring
Fluorapatite forms during hard tissue formation by a substitution
of OH ions by F ions in the center of the Ring
The distribution of carbonate within dentin and enamel follows the same
surface to DEJ pattern as NONE of the above??? (Not Lead, Calcium,
Fluoride, or Strontium) maybe the same as phosphate as it
substitutes in HA
Ameloblasts produce an enamel matrix (organic matrix) with protein
components called amelogenins and enamelins
Amelogenin forms the collagen Rods by which are then calcified by Ca,
PO4 and OH minus
AMELOGENIN disappears makes the rods, but then disappears when
collagen and water decrease


Enamelins stay behind as an interrod structure and are the MOST abundant
This organic matrix makes up about 1-2% of enamel and water makes up about 4%
Protein content of enamel from mature teeth is approximately 0.1-1%
The tooth becomes more resistant to acid-producing bacteria because fluorapatite has lower solubility product
constant than hydroxyapatite
Fluorapatite is less soluble than hydroxyapatite in solutions with low pH
What LEAST contributes to Fluorides anti-caries effectiveness??????
Substitutes for PO4, because it doesnt
Enamel is harder than bone
The main reason for this is that enamel hydroxyapatite crystals are larger and more firmly packed
These tightly packed masses of hydroxyapatite crystal are called enamel prisms and they are structural units of
These crystals in enamel are four times larger than those in bone, dentin, and cementum
Dentin is not metabolically inert it is in dynamic equilibrium with blood and metabolites
Another Q: Collagen is the major protein produced by odontoblasts & is contained in the organic matrix of dentin
Another Q: Phosphophoryn is the noncollagenous protein component that best characterizes dentin matrix
Collagen is the major protein component of cementum
Enamel Hypoplasia
A defect in the formation of enamel matrix
The enamel of primary and permanent teeth appear pitted, yellow to brown and have open contacts
Radiographically the enamel is either absent or very thin over tips of cusps and IP areas
Can be caused by nutritional deficiencies, hereditary
Vitamin A and C deficiency may cause it as well as inadequate intake of calcium, fluorosis, congenital syphilis, high
fever, rickets, injury or trauma to the mouth
Vitamins A and D are primarily responsible for enamel tooth formation
A vitamin A deficency in a developing tooth most likely affects enamel (more than dentin, pulp, & cementum)
Hypoplasia results only if the assault occurs during the time the teeth are developing
So, a prolonged vitamin A or D deficiency, Rickets, or inadequate intake of calcium can produce enamel hypoplasia
The Least important in producing enamel hypoplasia is Fluoride intake of less than 0.2ppm in the water
Another Q: Vitamins A, C, & D are all involved in tooth development & calcification; Vitamin B1 is not
Another Q: The lack of Vitamins A & D during tooth formation induces enamel hypoplasia
Enamel Hypocalcification
A defect in the mineralization of the formed enamel matrix
Proprioceptors are not found in pulp
The hemodynamics of flow in the tooth pulp are most likely analagous to those in the cranium
Caries activity is directly proportional to:
Consistency of fermentable carbohydrates ingested
Frequency of ingesting fermentable carbohydrates (most important factor)
Oral retention of fermentable carbohydrates ingested
Caries development:
The first event in the development of caries is the deposit of plaque on the teeth
Plaque arises primarily as a result of bacterial enzymatic reaction using sucrose & saliva (fermentable CHOs)
SUCROSE is the most important factor for caries
Large numbers of bacteria (mainly S. mutans and Lactobacilli) inhabit plaque and are readily available to cause caries
However, these bacteria depend to great extend on CHOs (sucrose) for their food
When carbohydrates are available, their metabolic systems are strongly activated and they also multiply
As a result of the metabolic activity they release acids, particularly lactic acid, and proteolytic enzymes
When the acidity level (pH level) of the mouth drops below 5.5, demineralization of the teeth can occur
Carbonated Beverages
Carbonic acid, H2CO3, is a weak acid, but when ingested in large quantities can slowly decalcify teeth due to
low pH (They also contain Phosphoric acid which has the same effect)
Drinking large quantities of carbonated cola type beverages could lead to enamel decalcification due to low pH
Another Q: Tooth erosion in bulimic (bulimia) patients is due to solubility of hydroxyapatite in acid
Extracellular dextrans
An extracellular polysaccharide synthesized by cariogenic streptococci (not a mucopolysacch) in the presence of
The structural component of plaque


Are formed from sucrose by bacterial enzymes (glycosyl trasferase GTF ) which are located on the cell surface of certain
lactic acid bacteria (e.g., S. mutans and Lactobacilli)
Another Q: Sucrose most directly contributes to the addition of polysaccharides to dental plaque
Dextrans are essential for the cariogenicity of these bacteria
Acquired Pellicle
Essentially absent of microorganisms
Brownish structureless film that accumulates on the surfaces of the teeth
Brownish color from tannin
Forms the interface between tooth structure and dental plaque and calculus
Calcium phosphate is NOT in the pellicle
The acquired pellicle is primarily composed of salivary glycoproteins
Most similar to organic composition of plaque????
pH of saliva is between 6.0 and 7.0
Saliva is able to neutralize acids mainly due to its bicarbonate content
Another Q: The principal buffer system in stimulated parotid saliva is carbonic acid/carbonate
Approximately 2/3 of the ~1 L/day produced by an average adult comes from the submandibular glands
~1/4 comes from the parotid glands & the remainder is produced by the sublingual & buccal glands
Occurs Most inbetween Meals
Saliva production drops at night
Composition of saliva:
97% to 99.5% water, contains electrolytes (Na+, K+, Cl-, and HCO3- ions; not F-)
Some chemicals, like Potassium, Iodine, and Mercury are excreted in part by the saliva
High K+ and HCO3- concentration (at least in the mucous portion)
Low Na+ and Cl- concentration
Hypotonic due to the fact that the salivary ductal cells reabsorb Na + and Cl- in exchange for K+ and
HCO3Also contains proline-rich proteins which have antimicrobial properties
Saliva supplies calcium and phospate for remineralization
Control of salivary secretion:
Both PS & Symp stimulations cause secretion
PS has the greatest effect
Vagal stimulation increases saliva production, so a vagotomy inhibits saliva production xerostomia
Atropine also prevents saliva secretion (normally stimulated by chorda tympani)
Sidenote: The chorda tympani nerve contains preganglionic parasympathetic secretory fibers
This isnt all it contains see Anatomy section for notes on its taste fibers, etc
It prevents the action of Ach on the secreting cells (anticholinergic competitve inhibitor of Ach)
Salivary Secretions:
Mucous secretion:
Contains mucins, which are proteins w/ polysaccharides attached to them lubricates mouth and food
Mucins are glycoproteins
Sublingual & buccal glands produce mucous secretions
Serous secretion:
Contains salivary amylase (ptyalin)
This enzyme splits starch into alpha dextrin, maltotriase, and maltose (see below)
So, -amylase ptyalin is secreted by the parotid glands
NOT produced from a zymogen
NOTE: The digestive action of salivary amylase continues for some time after swallowing, because the
amylase inside the bolus is protected from the inactivating action of gastric HCl
A number of proteins (proline-rich proteins, statherin, etc.) play important roles in maintaining the enamel
surface and preventing calculus formation
Parotid glands produce serous secretions
Parotid saliva is believed to be hyposmolar because reabsorption of water by striated duct cells is less
than reabsorption of sodium
Submandibular produce both mucous & serous secretions
Functions of Saliva:
1) Lubrication for the mastication and swallowing of food
2) Protection prevents dehydration of the oral mucosa
3) Oral hygiene antimicrobial properties and washes away food particles
Salivary lysozymes have bactericidal activity


4) Digestion starch digestion by alpha amylase (ptyalin) [not required]

Digest starches by hydrolysis
Alpha amylase:
Converts starch to oligosaccharides
Salivary amylase (ptyalin) and pancreatic amylase are this type
They both hydrolyze 1,4 glycosidic bonds in starch yielding alpha-dextrin, maltotrios, and maltose
Malatase, alpha dextrinase, and sucrose in the intestinal brush border then hydrolyze the
oligosaccharides to glucose
Salivary amylase is inactivated by acidic environment of the stomach
Beta amylase:
Converts starch to maltose and dextrin
Converts starch to glucose
Monosaccharides are absorbed in the small intestines
Glucose + Glucose
Must be digested into an absorbable form that can be ingested by the enterocytes
Glucose + Fructose
Degraded by sucrase
Glucose + Galactose
Isomaltase cleaves a glucose-linked 1,6 to another glucose as is found at branch points in starch/glycogen
The belief that the secretion of saliva is an active process is supported by the observation that secretion continues even
when the pressure within the salivary duct is higher than the blood pressure
Xylitol increases salivation
DNA double helix:
The two antiparallel polynucleotide chains of double helical DNA are not identical in base sequence or composition
Instead they are complementary to each other
Because strands are complementary, separated strands are able to reassociate
Wherever adenine appears in one chain, thymine is found in the other
Watson and Crick deduced this specificity of base pairing because of stearic and hydrogen bonding factors
In their structure the two chains or strands of the helix are antiparallel one strand runs 5 3 & the other runs 3 5
The DNA double helix is held together by two sets of forces:
1) hydrogen bonding between complementary base pairs
2) base stacking interactions
The two chains of dsDNA are so arranged that hydrophobic aromatic nitrogen bases are held close to each other
The helix structure results in a major and minor groove being formed along the DNA molecule
The major groove is the binding region for many proteins which control the transcriptional activity of the DNA
DNA backbone: picture


It is constant throughout the molecule

Monomeric units of nucleic acids are linked by phosphodiester bonds
The 3 hydroxyl group of one nucleotide bonds to the 5 hydroxyl group of the next nucleotide by a phosphodiester
The covalent backbones of a nucleic acid consists of alternating phosphate & pentose residues, w/ a purine or a
pyrimidine base is attached to each pentose
Phosphodiester bond connects the pentose hydroxyl groups of DNA and RNA are always 3 to 5
Bond formed from the esterification of 2 or 3 hydroxyl groups of phosphoric acid to adjoining nucleotide residues
Two free hydroxyl groups are present on the 3C and 5C
Is hydrophilic and highly polar
The hydroxyl groups of the sugar residues form hydrogen bonds with water
The ribose phosphate portion of purine & pyrimidine nucleotides comes from 5phosphoribosyl-1-pyrophosphate
PRPP is synthesized from ATP and ribose-5-phosphate, which is primarily formed by the pentose phosphate
So, ribose phosphate needed for nucleic acid synthesis can be derived from the pentose phosphate pathway
What happens when DNA is denatured? (from 2 Qs)
UV light absorption increases
Complementary strands become random coils
Base stacking becomes disrupted
Hydrogen bonds are broken
Peptide bonds are broken
Loss of native conformation, 2 & 3 structure
Loss of biological activity
*Total G-C or A-T content does not change
Nucleic acids
Store and transmit information to synthesize the polypeptides and proteins present in the bodys cells
Nucleic acids are complex molecules composed of structures known as nitrogenous bases (purines and pyrimidines), five
carbon sugars (pentoses) and phosphates groups (which contain phosphorous and oxygen)
The backbone of nucleic acids is made up of alternating phosphate and pentose units, with a purine and pyrimidine
attached to each
Nucleotide = a single base sugar phosphate unit
The nucleotide is the basic unit of DNA
NOTE: catabolism of nucleotides yields no energy production in the form of ATP (unlike lipid, protein & CHO)
Another Q: An example of a nucleotide is thymidylate (dTMP); urate, uracil, ribose, adenosine are not nucleotides
Nucleoside = a single base sugar phosphate unit w/o a phosphate group


These individual nucleotides are linked together to form a polynucleotide chain (the link or bond is between a phosphate
group of one nucleotide and the sugar of the next)
If the polynucleotide chain contains the sugar ribose, the chain is called a ribonucleic acid (RNA); if it contains the sugar
deoxyribose, the chain is called deoxyribonucleic acid (DNA)
2-deoxyribose is always found in DNA
Hydrolysis of nucleic acids yields
Ribose, adenine, deoxyribose, phosphoric acid, NOT acetic acid
Have 2 rings
Guanine has a ketone
Adenine (A) and guanine (G)
The C-G bond results from 3 H-bonds
The A-T bond results from 2 H-bonds(AT (annual training) is 2 weeks long)
Purine bases consumed in the human diet in the form of DNA or RNA are mostly excreted in the form of uric acid
Another Q: The end product of the catabolism of purine is uric acid
Another Q: Xanthine oxidase catalyzes this formation of uric acid from purine bases (NOT hydrolysis)
Xanthine oxidase is involved in the last step of purine degradation changing xanthine to uric acid
What is inhibited by allopurinol? Xanthine oxidase
Hypoxanthine and xanthine are also purine bases
Nucleoside derivatives of these bases will contain either ribose or 2 deoxyribose linked to the purine ring
through a beta N-glycosidic bond at N9
The link between Ribose (Sugar) and Purine (Base) is via a glycosidic bond
In the final rxn of the de novo synthesis of purine ribonucleotide, inosine monophosphate (IMP) is formed
IMP is converted to adenosine phosphates and guanosine phosphates
Purine ribonucleoside phosphates are all synthesized de novo from the common intermediate inosine
Have 1 ring
Thymine has a Methyl
Uracil does not
In DNA, pyrimidine bases are thymine (T) and cytosine (C)
In RNA, pyrimidine bases are uracil (U) and cytosine (C)
Uracil is the pyrimidine base that is present in RNA, but not in DNA
Three H bonds are formed between G and C, but only two form between A and T
The melting temperature of the double helix is a function of the base composition
Higher GC content having a higher melting temperature and an increased stability of the double helix
If the molar % of A in a native DNA specimen is 22%, then the molar content of G is28% (do the math)
Bacteria found in hot springs, high G-C content for high Bpoint, from 3 bonds
The weaker bonding between A and T is used in transcription to aid in the release of the newly formed RNA from the
DNA template
Remember U substitutes T in RNAthey both bind to A
The use of tetrahydrofolic acid (TFA) by several of the enzymes in purine and pyrimidine synthesis have made TFA
metabolism a prime target for a number of antimetabolites such as methotrexate, used in cancer chemotherapy
Methotrexate works in the S phase
Tetrahydrofolic acid is a coenzyme required in the general reaction for the transfer one-carbon fragments
Another Q: DNA damage by ultraviolet light is due to induction of dimerization by way of covalent bonds
between adjacent thymine groups
Just Like SAM???
The pyrimidine dimers then interfere with replication and transcription
Replication: Good review in blue book called Biochemistry pg. 123
The process of completely duplicating the DNA within a cell
The process is semi-conservative
Each new double helix will consist of one old and one newly synthesized strand
The primary enzyme in this process is DNA polymerase
The polymerase that initiates the primary synthetic reaction is polymerase 3
But first needs primer to initiate synthesis. Note: RNA replicaion does not require a primer
Reads a single strand of DNA from 3 to 5 while forming the new, complementary, continuous strand from 5 to 3
As the DNA polymerase complex moves along the DNA molecule, the original complementary stand (lagging
strand) is also duplicated


DNA polymerase moves along the lagging strand from 5 to 3 and thus cannot form a continuous copy
of the lagging strand
Instead, it forms ~1000-5000base long multiple segments (Okazaki fragments)
The fragments are joined together by DNA ligase to form a continuous strand
DNA Ligase
Involved in DNA Replication, Repair, and Recombination (The 3 Rs)
NOT transcription
Immediately following the production of Okazaki fragments, the gap between fragments becomes
connected through the action of DNA-ligase
Another Q: DNA ligase seals single stranded nicks in DNA
DNA polymerase can only add nucleotides to a pre-existing piece of nucleic acid (primer)
During replication the primer is provided by RNA polymerase (which has no primer requirement)
The short 10-base segments created by RNA polymerase are removed, once the DNA has been added to it, by an
exonuclease and the gap in the sequence is filled in by a DNA polymerase
RNA polymerase
is an enzyme that synthesizes polynucleotide sequences from nucleotides and does not require a primer chain
(opposite to DNA polymerase)
No proofreading fxn
RNA polymerase binds to TATA box on ssDNA
But can initiate chains
RNA polymerase II opens DNA at promoter sites (A/T rich upstream sites, i.e. TATA and CAAT)
DNA Repair
First a special glycosylase recognizes the error
Endonuclease cuts internal phophodiester bonds cuts DNA into pieces
Exonuclease removes jacked-up pieces
Cuts at the end of the chain
DNA polymerase fills the gaps
DNA Ligase seals

FROM PIC, read it 3- 5 and Make 5 FIRST

The Genetic Code
Degenerate nature of the genetic code:
Implies that many amino acids are designated by more than one codon
Unambigous = only one codon for that amino acid (Tryptophan, Selenocystein, and Methionine)
The other 18 amino acids are coded by 2+ codons
Codons (sometimes referred to as a triplet)
A sequence of three adjacent nucleotides (AUG, for example) in a nucleic acid that codes for a specific aa
How many nucleotides are required to code for a protein with 150 amino acids? Ans: 450
Codons that specify the same amino acid are called synonyms
Multiple codons for an amino acid usually differ in the third base (at the 3 end)
Several of the Codons Serve Special Functions:
Initiation codon (AUG or rare GUG):


Signals the beginning of polypeptide chains and codes for methionine (all proteins begin with methionine)
Starts the inAUGural Methionine (In prokaryotes its f-met)
Termination codon (UAA, UAG, and UGA):
Signals the end of polypeptide chain sythnesis
These codons are also referred to as STOP codons or Nonsense codons
Selenocysteine is the 21st genetically coded aa
The codon UGA occurring in the correct contex, leads to the incorporation of this serine derived aa
A specific sequence of three nucleotides in transfer RNA complementary to a codon for an amino acid in a
messenger RNA
The aa inserted in a polypeptide chain during protein synthesis is determined by a complementary
relationship between mRNA & tRNA
The two RNAs are paired antiparallel:
DNA Polymerase reads from 3 to 5 on the DNA, and makes 5 to 3 mRNA to match
Then, tRNA matches the 5 to 3 mRNA by its anticodon which is a 3 to 5, BUT anticodons are
ALSO read 3 to 5
The first base of the codon pairs with the third base of the anticodon (both are read in the 5 to
3 direction)
EX: If the codon on mRNA is CGU, then the corresponding anticodon on tRNA is ACG
Dont get clowned by simply lining up the codon & anticodon and giving that as your answer
Its really 5CGU3 and 5ACG3
So, you could just match up 5CGU3 and 3GCA5, then switch it up to 5ACG3 for your answer, got it?
Process in which DNA serves as a template for the assembly of molecules of RNA (all three types)
Cellular process of making RNA from DNA
This process involves the enzyme RNA polymerase
From way out in right field: Rifampin is effective in treating active TB because it targets transcription
Translation (L for last step)
Is the process by which genetic information flows from RNA to protein
Involves 4 steps
Involves joining the correct amino acid to the correct tRNA (AUG)
Small subunit of ribosome binds to the 5 end of the mRNA
Uses the help of Initition factors
The first step in the utilization of amino acids for protein synthesis requires aminoacyl-tRNA synthetase
Next AA in line will form complex with Elongation factor and GTP
In prokaryotic protein synthesis, the elongation factor G serves to translocate the growing peptide chain and to
move the ribosome along the mRNA
At the end of each elongation cycle, the growing polypeptide is found as peptidyl-tRNA bound to the P site
When A site faces nonsense codons (UAA, UAG, UGA), no tRNA can recognize it, but releasing factor will
recognize it and release the newly synthesized protein
Types of RNA:
Messenger RNA (mRNA or RNA polymerase II):
M for Massive
Single-stranded; made in the nucleus; made as a complement to one strand of DNA; template for protein synthesis
Molecules carrying information (genetic code) from DNA in the nucleus to ribosomes in the cytoplasm, where
polypeptides and proteins are synthesized (translationmRNA is the template for protein synthesis)
Random Q: Addition of synthetic polyuridylic acid to a cell-free system capable of protein synthesis results in
greatly enhanced incorporation of phenylalanine into peptide linkages. In this system, polyuridylic acid is
performing a function normally performed by mRNA.
A landmark experiment was formed where polyuridylic was dumped into a cell-free, but protein synthesizing
system. It resulted in the production of polyphenylalanine, and lead us to the breaking of the genetic code, so
here the polyuridylic acid served as the mRNA that brought in the instructions for translation
Small lariot shaped intermediate is formed
Then a SnRNP (small nuclear ribonucleoprotein particle splices out the intron)


Intron vs Exon
Exons stay in the mRNA to EXIT the nucleus
Another Q: During nuclear processing of hnRNA to mRNA the portion of the molecule that is removed is
the intron
Occurs in the nucleus
Capping on the 5 end (7 methyl G)
What is the reason for the GGG repetition in prokaryotes
Protects the mRNA from degradation outside the nucleus
For the ribosome movement, translation process
Polyadenylation on 3 end (300 As)
Pre-processed transcript is called hnRNA heterogenous RNA, where post is called mRNA
Transfer RNA (tRNA or RNA polymerase III):
T for Tiny
Made in the nucleolus
Molecules carry the amino acids to ribosomes, where the amino acids are linked together in the order specified by
mRNA to form particular polypeptides and proteins
Clover shaped, with the amino acid covalently bound to 3 end
Amino acyl-tRNA synthetase
is a group of ligases (enzymes) that ensures that the correct amino acid is attached to the tRNA with the correct
anticodon to be used during protein synthesis
Uses ATP for its monitoring energy
SO, ATP is used for Activation tRNA
BUT, GTP is used to bind tRNA to ribosome
tRNA activates and selects specific amino acids for protein synthesis
Individual enzymes are highly specific for one amino acid
No error checking occurs during the translation process on the ribosome
Ribosomal RNA (rRNA or RNA polymerase I):
R for Rampant
Made in the Nucleolus
Molecules are the major component of ribosomes, which are the physical and chemical structures on which protein
molecules are actually assembled
rRNA is the most abundant of the three types of RNA (rRNA > tRNA > mRNA in abundance)
mRNA is the largest (Massive mRNA, Rampant rRNA, and Tiny tRNA)
Small structures found floating free in the cytoplasm (polyribosomes) that contain rRNA and protein
Translation (aka protein synthesis)
At a ribosome, amino acids are linked together in the order specified by mRNA to form a polypeptide or protein
Have E, P, and A sites for Translation
Come in on A site, shift to P site to be added to, and then bumped out on the E site
Ribosomes have enzymatic activity
They catalyze the formation of peptide bonds, which link amino acids to one another
Rough ER
Carboxy-terminal of protein attaches to the RER????
Some are attached to the cytosolic suface of the endoplasmic reticulum membrane
Proteins formed by ribosomes attached to the RER are destined for secretion from the cell, incorporation into the
plasma membrane, or formation of lysosomes
Since all protein synthesis begins on free ribosomes, attachment of a ribosome to the ER requires the presence of a
specific sequence at the amino end of the growing protein chain to signal the attachment of the ribosome to the ER
70s ribosomes are the sites of protein synthesis (translation) in bacterial cells and chloroplasts
80s ribosomes are the sites of protein synthesis (translation) in eukaryotic cells
Most protein synthesis occurs on polyribosomes
Hydrolysis of DNA will yield:
Phosphoric acid
Deoxyribose (sugar)
Nitrogenous bases (A,G,T,C)
Hydrolysis of RNA yields the same stuff (but U instead of T and ribose instead of deoxyribose)
Ribose and uracil are the only differences between the products of RNA and DNA hydrolysis
Another Q: Hydrolysis of nucleic acids produces pentoses, phosphates, amino acids, purine bases, pyrimidine bases
Replication forks are sites at which DNA synthesis (replication) is occurring


Helicases unwind the helix

Topoisomerases act to decrease the degree of supercoiling of the helix, aiding in unwinding the DNA at the replication forks
DNA gyrase, a topoisomerse found in prokaryotes, in addition to reducing the supercoiling prior to replication induces a
negative supercoil following replication
Secures the replication fork
Reverse transcriptase:
Certain RNA viruses contain within the viral particle a unique RNA-directed DNA polymerase which is called reverse
Building DNA from RNA
On infection, the single stranded RNA viral genome and the enzyme enter the host, and the reverse transcriptase
catalyzes the synthesis of a DNA strand complementary to the viral RNA or mRNA (different question)
This enzyme is found naturally in certain viruses called retroviruses
These viruses in which the genetic information is carried on an RNA molecule
When one of these viruses infects a host cell, it uses this enzyme to make a complementary DNA (cDNA) copy of
its genetic information which is then incorporated into the host DNA
cDNA Library
A collection of DNA sequences generated from mRNA sequences
This type of library contains only protein-coding DNA (genes) and does not include any non-coding DNA
*NOTE: The distinguishing feature of a cDNA library is the presence of multiple copies of RNA transcriptase
*NOTE: Reverse transcriptase is used in vitro to make cDNA from mRNA
The human immunodeficiency virus (HIV) the causative agent in AIDS, is a retrovirus
The drug AZT (a thymidine analog) is a competitive inhibitor of the HIV reverse transcriptase
NOT Flurouracil antineoplastic drug used in carcinoma pts to interfere with DNA and RNA
NOT Methotrexate Antineoplastic drug that interferes with DNA synthesis, repair, and cellular
Inhibits dihydrofolate reductase, inhibiting formation of THF, which inhibits thymidine
synthesis, which inhibits DNA synthesis, etc.
Methotrexate works in S phase
The wild-type reverse transcriptase seems to have a higher affinity for AZT and other base analogs
Reverse transcriptase is one of the enzymes used in genetic engineering, where it can be used to obtain a copy of a
particular gene from the relevant mRNA
NOTE on viruses: Certain viruses isolated in crystalline form have been found to be nucleoproteins
This didnt fit anywhere else in the document
Results in termination of protein, usually mutation to a stop codon
Changed AA, but similar in strucure
Same AA, but codon was changed
Usually in 3rd position of codon
Frame shift
Results in entire misreading down-stream
Usually results in truncated protein
Transition vs Transconversion
Transition = purine for purine
Transconversion = purine for pyrimidine or vice versa
Genetic recombination experiments:
Depend heavily upon the action of DNA ligase and endonucleases
*NOTE: Restriction enzymes are best described as site-specific endonucleases
Purpose of Restriction Endonuclease? Fragment DNA
Used to cleave both the DNA to be clones and a plasmid DNA
The specificity of the nuclease is such that when mixed, the DNA to be cloned and the plasmid DNA will
anneal (base pair) and can then be joined together by a DNA ligase
The first organism used for DNA cloning was E. Coli and it is still the most common host cell
Bacterial cloning vectors plasmids, bacteriophages, and cosmids
Plasmid vectors suitable for cloning have 2 genes conferring resistance to different antibiotics (its true!)


Commercial products of recombinant DNA technology include:

Human insulin (for diabetes)
Anticoagulants (tissue plasminogen factor)
Erythropoietin for anemia
Human growth factor (for dwarfism)
Some other enzymes that are used in recombinant DNA technology include:
DNA polymerase I (not RNA polymerase) fills in gaps in duplexes by step-wise addition of nucleotides to 3end
Reverse transcriptase makes a DNA copy of an RNA molecule
Exonuclease removes nucleotides from 3 ends of a DNA strand
DNA ligase, DNA polymerase I, restriction nucleases, reverse transcriptase are involved in gene cloning
RNA polymerase is not Huh???
Restriction Nucleases (Site specific Endonucleases)
Find specific sites to cut open in the DNA
Usually work in dimers and create palindromic 5 to 3 segements
Used for the Introduction of recombinant DNA into a bacterial cell
*NOTE: Restriction enzymes are best described as site-specific endonucleases
Southern Blotting (S for Same)
The type of blotting used to identify DNA restriction fragments is Southern blotting
DNA-DNA Hybridization
Northern Blotting
DNA-RNA hybridization (northeRN)
Which is used for mRNA
Western Blotting (Think Western society with their protein bars/shakes, etc.)
Antibody-Protein Hybridization
Southwestern Blotting
DNA-protein interaction
ELISA (Enzyme linked immunosorbant assay)
Basically test the blood with an antigen, it it links with an antibody, it luminsces a bright color
HIV test
PCR (Polymerase chain Reaction)
Used to synthesize many copies of desired DNA
Heat DNA to denature it
Then cool it with added premade primers
Then a heat stable DNA polymerase copies
Then repeat
The polymerase chain reaction is most useful for amplifying a specific DNA sequence
Sanger Methods
You throw a bunch of dideoxynucleotides, that lack OH at the 2 and 3 position, and they are used to terminate DNA
synthesis at specific bases
Four separate reactions are carried out, when the dideoxynucleotide is incorporated, DNA synthesis stops, so each of the
4 reactions would yield a series of products extending from the primer to the DNA terminating dideoxynucleotide
Products are then separated by electrophoresis and analyzed by autoradiography to determine the DNA sequence
Basic principles for sequencing DNA in the Sanger procedure derive from Replication

Proteins/Amino Acids
A polypeptide chain of ~100 or more amino acids linked by peptide bonds


10+ amino acids linked in a chain by peptide bonds form a polypeptide

Proteins function as hormones, catalysts, structural elements, & oxygen carriers
NOT carriers of genetic information
Proteins are able to buffer physiologic solutions over a wide range of pH because they contain many functional groups
with varying pKs
Deficiency in proteins may be indicative of: lack of vigor and stamina, weakness, mental depression, poor resistance to
infection, impaired wound healing, slow recovery from disease
Primary structure
Amino acid sequence (linked together by covalent peptide bonds)
From N-amino terminal to carboxy terminal of the protein chain
Always linked from N to C
The primary structure of proteins is best described as the polymer formed by amide linkages between alphacarboxyl group and alpha-amino groups
The Amide bond links amino acid residues to form proteins
Secondary structure
Refers to the spatial arrangement of a portion of a polypeptide chain determined by the amino acids present
The most common types of secondary structures are:
Alpha helix (coiled conformation of a peptide chain)
Beta pleated sheets (an extended, zigzag arrangement of a polypeptide chain)
Beta bends (reverse turns)
Secondary protein structures are stabilized by hydrogen bonds
Tertiary structure
Stabilized by hydrophobic interactions, then hydrogen bonds
Refers to the irregular folding of a polypeptide chain
The overall 3D conformation of the polypeptide (globular, fibrous, and pleated sheet)
Proline contributes to the tertiary structure of a protein by causing a bend when it occurs in the primary
Cysteine can stabilize the tertiary structure by forming a covalent bond in its side chain
Quaternary structure
Refers to the spatial arrangement of subunits in a protein consisting of >1 polpeptide chain
Two EXs of proteins with quaternary structures are 1) hemoglobin and 2) Ab molecules found in blood
This is the level of protein structure in which 2+ individual polypeptides interact to form a noncovalent complex
Protein Bonds
Ionic, Hydrogen, and Hydrophobic
Peptide (Amide)
X-ray diffraction
Requires a protein in crystalline form
Beam of x-rays is diffracted by the electrons around each of the atomic nuclei in the crystal and with an
intensity proportional to the number of electrons around the nucleus
Another Q: The best method for determining the 3D structure of a protein is by x-ray diffraction
Used to separate various proteins based on protein size and charge
Procedure that depends primarily on electrostatic net charge
Separates and characterizes proteins based on molecular weight and size
Peptide bond:
A specific type of amide bond
Because a peptide bond is a form of an amide bond, amide bonds link amino acid residues to form
Covalently joins the alpha-carboxyl group of one aa and the alpha-amino group of another aa
Formation of peptide bond results from the removal of a molecule of water between the carboxyl group of one
amino acid and the amino group of a second amino acid
Extremely stable and cleavage generally involves the action of proteolytic enzymes
Characteristics of peptide bonds:
No freedom of rotation around the bond
Has partial double-bond character means it is shorter than a single bond and is therefore rigid & planar
Bonds involving the alpha carbon can rotate freely


Is generally a trans bond (instead of a cis bond)

Is uncharged but polar
Proline, due to formation of a tertiary amine, restricts the range of rotation of the -carbon in the peptide bond
Disulfide bond:
Another type of covalent bond that occurs in many proteins
Formed from the sulfhyrdyl group (SH) of each of two cysteine residues, to produce a cystine residue
(A residue is a single aa unit within a polypeptide chain)
It is widely thought that these strong, covalent bonds help stabilize the structure of proteins and prevent them from
becoming denatured in the extracellular environment
EXs insulin & immunoglobulins
Cysteine is the aa that can stabilize the 3 structure of some proteins via a covalent bond involving its side chain
Protein Denaturation
Denaturation usually destroys hydrogen, hydrophobic, & electrostatic bonds (but not covalent bonds)
Characterized by
Loss of native conformation, secondary and tertiary structures
Loss of biological activity
Breakage of H bonds
Amino Acids (AAs) I need pictures/diagrams
Have a central or alpha carbon to which is attached a H atom, a COOH carboxyl group, an NH2 amino group, and a 4 th
group, Rwhich determines the AAs identity
Except Glycine, which has 2 H groups (in other words, R = H for glycine)
Used for Energy
First the AA loses its amino group and is converted to alpha-keto acids that can enter Krebs cycle
An alpha-keto acid is similar to an AA, except that is has O2 rather than an amino group bonded to its
alpha carbon
When proteins are broken down for energy, most of the energy is derived from the oxidation of the alpha-keto
acids (Pyruvate, Oxaloacetate, and alpha-ketoglutarate)
Negative nitrogen balance (nitrogen output exceeds intake) may be caused by a dietary lack of essential AAs
Another Q: Total urinary nitrogen excretion is least when an individual is on a diet containing adequate fat & CHO
but no protein
Higher temperatures facilitates the increase intake of salts
Metabolism of carbohydrates serve as a principal source of carbon for nonessential AAs
All are stereoisomers (aka optical isomers or enantiomers) EXCEPT Glycine
All have a chiral center (4 different groups attached to a central carbon)
Non-superimposable mirror images of each other
The reference compound for naming all other compounds is the smallest sugar w/ an asymmetric carbon
(An asymetric carbon is characterized by having 4 different groups attached to it)
In other words, the arrangement of sugars into D- and L- configurations is based upon their resemblance
to D- and L-glyceraldehyde
Established by x-ray diffraction analysis
All AAs are L designated compared to glyceraldehydes (except for some D in ABX and bacteria cell
(aLL for L)
Grouped by their R Group (5)
Nonpolar, aliphatic R groups:
alanine, valine, leucine, isoleucine, glycine and proline (All Gay Lovers Lay w/ Vernas pussy)
Aromatic (generally nonpolar):
phenylalanine, tyrosine, and tryptophan
Forming tyrosine from phenylalanine only requires hydroxylation of the benzene ring at carbon 3
That is why it is most easily converted in the human body
Polar, uncharged R groups:
serine, threonine, cysteine, methionine, asparagines, and glutamine
(the polarity of cysteine and methionine is contributed by their sulfur atom, and that of asparagines
and glutamine by their amide group)
Negative charged:
aspartate and glutamate (Aspartic ACID and Glutamic ACID)
Positively charged: (Think HAL plays the Bass)
lysine, arginine, and histidine


Arg and Lys have an extra NH3 and are found in large amounts in Histones, which bind to negatively
charged DNA
**Arg is the most basic AA
Essential vs. Nonessential
Essential AAs (9):
Phenylalanine, Valine, Tryptophan, Threonine, Isoleucine, Methionine, Histidine, Arginine, Lysine,
**Arginine and Histidine are required during periods of growth
Methionine is a thio-ether
One question lists groups of 3 AAs & asks which group contains only essential AAs
Is an essential AA needed for optimal growth in infants and for nitrogen equilibrium in adults
Forms 5 HT (serotonin), melatonin, niacin, and the nicotinamide moiety of NAD and NADP
NOTE: proteins obtained from corn are poor in nutritional values for man because they are low in lysine
& low in tryptophan both are essential AAs, get the drift?
Nonessential AAS (11):
Glutamate, glutamine, proline, serine, glycine, aspartate, asparagines, alanine, cysteine, & tyrosine
Ten of the nonessential amino acids contain carbon skeletons that can be derived from glucose
What makes glutamine from glutamate? Glutamine synthase
They are not needed in the diet
Can be synthesized from:
The corresponding alpha keto acid
An alpha amino acid (as the NH3 donor)
A specific transaminase enzyme
And the coenzyme pyridoxal phosphate (vitamin B6)
These AAs include alanine, aspartate, and glutamate
The other nonessential AAs are synthesized by amidation (glutamine and asparagine)
Glutamate, glutamine, proline, arginine, serine, glycine, aspartate, asparagines, alanine, cysteine, &
Cysteine and tyrosine become essential when their precursors, methionine and phenylalanine, are
In a phenylketonuric person, tyrosine is an essential aa
Cysteine and methionine have sulfur containing side chains
Although its carbon skeleton can be formed from carbohydrates, requires the essential amino acid
methionine to supply the sulfhydryl group
Is synthesized by hydroxylation of the essential amino acid phenylalanine
Presence of tyrosine lessens the need for phenylalanine
Another Q: Phenylalanine can most easily be converted to tyrosine in the human body
Synthesizes dopamine, the thyroid hormones (triiodothyronine and thyroxine), melanin,
norepinephrine and epinephrine
Dopamine is synthesized in two steps from tyrosine
can be synthesized by transamination directly from pyruvic acid, using glutamic acid as an
amino group donor
Glycine is the immediate precursor for creatine, purines & porphyrins
Has a hydroxyl group that often participates in NZ reactions
Classified as ketogenic, glucogenic, or both according to the nature of their metabolic end-products:
Amino acids whose catabolism yields either acetoacetate or one of its precursors, acetyl CoA or acetoacetyl
EXs leucine and lysine
Glucogenic and ketogenic:
Amino acids whose catabolism yields both ketogenic and glucogenic end-products
EXs tyrosine, isoleucine, phenylalanine, and tryptophan


Amino acids whose catabolism yields pyruvate or one of the intermediates of the citric acid cycle (alpha
ketoglutarate, oxaloacetate, fumarate, and succinyl CoA)
EXs the remaining amino acids
Synthesis of Amino Acids:
Alpha ketoglutarate gives rise to glutamate (think a comes first ate before ine)
-ketoglutarate + alanine glutamate + pyruvate
which in turn is the precursor of glutamine, proline, and arginine
3 phosphoglycerate gives rise to serine
which, in turn, is the precursor of glycine and cysteine
Oxaloacteate gives rise to aspartate
which in turn is the precursor of asparagines, methionine, threonine and lysine
Threonine along with pyruvate is the precursor of isoleucine
Pyruvate gives rise to alanine, valine, leucine, and isoleucine
*Isoleucine can be formed by either pyruvate or threonine
Phosphoenolpyruvate and erythrose 4 phosphate produces shikimate
which is converted to Chorismate
Chorismate gives rise to tryptophan, tyrosine and phenylalanine
Tyrosine is synthesized from phenylalanine in humans
Ribose 5 phosphate gives rise to histidine
Catabolism of Amino Acids????
The first step in the catabolism of most AAs involved the removal of the alpha amino group
Once removed, this nitrogen can be incorporated into other compounds or excreted
The enzymes that catalyze these reactions are known as transaminases or aminotransferases
Involve the transfer of amino group from one AA to an alpha keto acid
Glutamate and alpha ketoglutarate are often involved in these reaction, serving as one of the amino
acid/alpha keto acid pairs
ALL transaminases require the coenzyme pyridoxal phosphate (PLP) = vitamin B6
Transamination of the alpha amino to a keto acid is the 1st step in the catabolism of many amino
Pyridoxal phosphate (PLP) derived from vitamin B6 & serves as the cofactor for these reactions (required in all
transaminase reactions)
Vitamin B6 (pyridoxal phosphate) acts as a coenzyme in transamination reactions
PLP functions as the intermediate carrier of amino groups at the active site of aminotransferases
It undergoes reversible transformations between its aldehyde form, pyridoxal phosphate (PLP) which can accept
an amino group, and its aminated form, pyridoxamine phosphate (PMP) which can donate its AA to an alpha
keto acid
Glutamate Dehydrogenase: (Top