Anatomy & Physiology II: Exam 2 Review

Circulatory System: Heart

1. Circuits
a. Pulmonary circuit: carries blood to the lungs for gas exchange and returns it to the heart
b. Systemic circuit: supplies blood to the rest of the body
c. Arteries: carry blood away from the heart (efferent); oxygen rich, carbon dioxide poor
d. Veins: carry blood to the heart (afferent); oxygen poor, carbon dioxide rich
2. Membranes
a. Epicardium (visceral pericardium): outermost serous membrane
b. Myocardium: middle layer of cardiac muscle that performs the work of the heart
c. Endocardium: innermost layer that covers valve surfaces
d. Pericardial space: area between the parietal and visceral membranes that contains fluid which
prevents friction during contractions
3. Anatomy
a. Atria: superior chambers that receive blood returning to the heart
b. Ventricles: inferior chambers that pump and eject blood from the heart
c. AV valves: regulate the openings between the atria and ventricles
d. Chordae tendinae: prevent the AV valves from opening when the ventricles contract
e. Pulmonary valve: controls the opening from the right ventricle into the pulmonary trunk
f. Aortic valve: controls the opening from the left ventricle into the aorta
4. Blood flow
a. Deoxygenated blood enters right atrium from the superior and inferior vena cava
b. Blood flows from the right atrium through the right AV valve into the right ventricle
c. Contraction of the right ventricle forces the pulmonary valve to open
d. Blood flows through the pulmonary valve into the pulmonary trunk
e. Blood is distributed to the lungs through the pulmonary arteries where it loads oxygen
f. Oxygenated blood returns from the lungs to the left atrium through the pulmonary veins
g. Blood flows from the left atrium through the left AV valve into the left ventricle
h. Contraction of the left ventricle forces the aortic valve to open
i. Blood flows through the aortic valve into the aorta
j. Blood is distributed to the body through the aorta where it unloads oxygen
5. Cardiac Muscle
a. Intrinsic rhythmicity (autohythmic): heart can self depolarize; does not rely on the nervous system
b. Muscle Fiber: one nuclei per cell, non mitotic, large mitochondrial density (aerobic respiration), uses
any substrate to make ATP (glucose, lipids, lactic acid, etc), no tetanus (twitch only), long contraction
time (~250 msec), fibers connected by intercalated discs, gap junctions, and desmosomes
i. Gap Junction: allows for flow of water and electricity through channels
ii. Desmosomes: allows for transfer of force between fibers, prevents tearing
6. Conduction System
a. The SA node (pacemaker) in the right atrium near the superior vena cava initiated each heart beat
b. Signals from the SA node travel through the atria
c. The AV node near the right AV valve acts as a gateway to the ventricles
d. The AV bundle (Bundle of His) forks into left and right towards the apex
e. The purkinje fibers distribute the electrical excitation through the ventricles
7. Activity of the Heart
a. Systole: contraction (depolarization)
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b. Diastole: relaxation
c. Pacemaker Potential at SA Node (one heartbeat)
i. Gradual depolarization from slow inflow of sodium without potassium outflow
ii. Potential reaches threshold
iii. Rapid inflow of sodium and calcium (depolarization)
iv. Sodium and potassium channels close
v. Potassium flows out of the cell (repolarization)
vi. Potassium channels close and potential starts over
d. Action Potential of Cardiocytes
i. Sodium voltage gates open
ii. Inflow of sodium depolarizes the membrane
iii. Sodium gates close
iv. Calcium slowly enters through channels prolonging the depolarization creating a plateau
v. Potassium leakage causes minor drop in plateau
vi. Calcium channels close and calcium transported out of the cell
vii. Potassium channels open and potassium flows out returning the membrane to resting
potential
8. Electrocardiogram
a. P wave: signal from SA node spreads through atria and they depolarize
b. PQ interval: atrial systole, impulse travels from SA node to AV node
c. QRS complex: signal from AV node travels through ventricles and they depolarize
d. ST interval: ventricular systole and blood ejection from ventricles
e. T wave: ventricles repolarize
9. Pressure and Volume Relationship
a. Pressure = 1 / Volume
b. Pressure gradient: fluids flow down their pressure gradient from high pressure to low pressure
c. Blood Pressure = Systole / Diastole
i. Normal = 120/80
d. Pulse Pressure = Systolic – Diastolic
i. Normal = 40mmHg
e. Flow or Cardiac Output (I) = Pressure (V) / Resistance (R)
f. Cardiac Output (L/min) = Stroke Volume (mL/beat) × Heart Rate (beats/min)
i. Cardiac Output: the amount of blood ejected by each ventricle in 1 minute
ii. Exercise increases CO; stress, anxiety, drugs, blood loss increase HR; sleep and hypothermia
decrease HR
g. Stroke Volume (amount ejected) = End Diastolic Volume – End Systolic Volume (amount remaining)
i. Stroke volume
1. Preload: Ventricles contract more forcefully  expel more blood
a. Frank-Starling Law: stroke volume is proportional to the end diastolic volume
and the more the ventricles are stretched, the harder they contract on the next
beat (more blood in = more stretch on fibers and greater sarcomere length =
more force production = more stroke volume)
2. Contractibility: how hard the myocardium contracts for a given preload i.e. calcium
increases the strength of each contraction
3. Afterload: the blood pressure in the aorta and pulmonary trunk immediately distal to
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the semilunar valves; opposes opening these valves  limits the stroke volume.
a. Anything that restricts pulmonary circulation or impedes arterial circulation
can increase the afterload
10. Cardiac Cycle
a. Ventricular filling (diastole)
i. Pressure of ventricles drops below pressure of atria and AV valves open
ii. Ventricular pressure rises as atrial pressure drops
iii. Blood flows into ventricles and atria depolarize and contract and generate P wave
b. Isovolumetric contraction (systole)
i. Atria repolarize and relax
ii. Ventricles depolarize and generate QRS complex
iii. Pressure in ventricles rises and AV valves close
iv. No blood ejection and no volume change
c. Ventricular ejection (systole)
i. Ventricular pressure exceeds arterial pressure and aortic and pulmonary valves open
ii. Blood begins to flow out and generates start of T wave
iii. Some blood will remain in the ventricles
d. Isovolumetric relaxation (early ventricular diastole)
i. Ventricles begin to expand and generate end of T wave
ii. Aortic and pulmonary valves close and AV valves remain closed
iii. No blood entering the ventricles
11. Effects of the Autonomic Nervous System: both nodes are innervated by sympathetic and parasympathetic
nervous system
a. Medulla Oblongata: Cardiac Centers
i. Can be stimulatory or inhibitory
ii. Sympathetic postganglionic fibers are adrenergic (release NE) which activates a second
messenger system and opens calcium or sodium chemical gates  accelerates
depolarization of the SA node and contraction  speeds up the heart
1. Innervates the S and AV nodes and the myocytes
b. Vagus nerve
i. Parasympathetic postganglionic fibers are cholinergic (release ACh) which binds to muscarinic
receptors and opens potassium chemical gates  cells become hyperpolarized and heart
slows down
1. Innervates the SA and AV nodes
c. Types of Receptors
i. Proprioceptors: located in muscles and joints, information on changes in physical activity and
can increase CO
ii. Baroreceptors: located in aorta and arteries, information on changes in pressure that send
signal to cardiac centers in medulla
1. Drops in pressure  increase heart rate bringing CO and P back up
iii. Chemoreceptors: in aortic arch, arteries, and medulla; sensitive to blood pH, CO2, and O2 and
important to respiratory control (no influence on heart rate)
12. Effects of Chemicals
a. Glucagon, thyroid hormone, and epinephrine (binds to SA node): increase heart rate
b. Hyperkalemia: too much potassium outside the cell causes the heart to stop mid-systole  can’t relax

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c. Hypokalemia: too little potassium outside the cell causes excess hyperpolarization and heart may not
be able to depolarize again  heart stops in diastole
d. Hypercalcemia: too much calcium outside the cell causes increases contractibility of the heart
e. Hypocalcemia: too little calcium outside the cell causes weakening of the heart

Circulatory System: Blood Vessels and Circulation

1. General Anatomy and Mechanisms
a. Arteries (efferents): vessels of distibution
b. Veins (afferents): collecting and storage vessels
i. Mechanism of Venous Return
1. Pressure generated by the heart is the most important force; when blood volume
increases, the pressure gradient increases and more blood is returned to the
heart; widespread vasoconstriction also raises blood pressure and flow
2. Skeletal muscles surrounding the veins contract and pump blood up the veins and
valves ensure blood only travels in one direction
3. Respiratory pump aids flow from abdominal to thoracic cavity and back to the
heart; inhale the pressure in abdomen increases and throracic cavity drops
pushing blood up
4. Exercise increases venous return because skeletal muscles contract, cardiac
output and blood pressure increase, respiratory rate increases
5. Blood pooling occurs when body is at rest for long periods or when you stand for
long periods of time
c. Capillaries: connect small arteries to small veins, where exchange occurs i.e. fluids, gases,
nutrients, wastes
i. Precapillary sphincter muscles: control blood flow to capillaries using local control and
hormones
1. Dilated when O2 pressure is low, CO2 is high, lots of wastes, acidic environment
i.e. during exercise
ii. Types of Capillaries
1. Continuous: held together by tight junctions, lack clefts only allow small molecules
i.e. glucose to pass through
2. Fenestrated: contain filtration pores and allow for rapid passage of small
molecules but not proteins, important in glands, kidneys, choroids plexus of brain,
small intestine
iii. Capillary Exchange: two way movement of fluid
1. Routes: clefts, cell cytoplasm, filtration pores
2. Mechanisms
a. Diffusion: concentration gradient (glucose, oxygen, carbon dioxide, waste)
b. Transcytosis: receptor mediated endocytosis across membrane (fatty
acids, albumin, insulin)
c. Filtration and reabsoprtion: fluid filters out of arterial end and reenters at
venous end
i. Hydrostatic pressure: force exerted by a liquid against capillary
wall that draws water out of capillary; greater at arterial end
ii. Oncotic pressure: force opposing hydrostatic pressure that draws
water into capillary; greater at venous end
iii. More capillaries at venous end with larger diameter account for
lower pressure at venous end in re-uptaking fluid
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3. In: CO2, ammonia, waste

4. Out: O2, glucose, water, nutrients, amino acids, lipids, white blood cells
(diapedisis), steroids, vitamins, electrolytes
d. Portal System: blood flows through two consecutive capillary beds before returning to the heart i.e
hypothalamus and pituitary, liver, kidneys

e. Vessel Wall Layers

i. Tunica interna/intima: simple squamous endothelial layer that is closest to the lumen
overlying a basement membrane; selectively permeable to materials entering and exiting
bloodstream
ii. Tunica media: smooth muscle layer that allows for changing in diameter
iii. Tunica externa: connective tissue with elastic fibers (esp. in arteries)
1. Vasa vasorum: vessels of the vessels; supply blood to wall of vessels
2. Blood Pressure, Flow, and Resistance
a. Variables in Blood Pressure
i. Cardiac output
ii. Blood volume
iii. Resistance to flow: influenced by blood viscosity, vessel length, and vessel radius
b. Local Control
i. Autoregulation: vasodilatation occurs when tissues are inadequately perfused
1. Platelets, endothelial cells, and tissues can secrete vasodilators (histamine, nitric
oxide)
c. Neural Control
i. Medulla Oblongata: Vasomotor Center
1. Sympathetic control over blood vessels (precapillary sphincters not affected)
through negative feedback control
a. Baroreflex: response to changes in blood pressure, short term regulation
b. Chemoreflex: respond to changes in blood chemistry, respiration changes
d. Vasomotion: raising or lowering of blood pressure through the body or selectively modifying the
perfusion of a particular organ and rerouting blood from one region of the body to another’
i. Centralized control: medulla vasomotor center or hormones affect blood vessels
everywhere
ii. Central or local control: rerouting blood flow of individual organs i.e. reduce flow to kidneys
and digestive tract and increase flow to skeletal muscles during exercise
3. Special Circulatory Routes
a. Brain: blood flow fluctuates less than any other organ to maintain oxygen levels to the brain
b. Skeletal muscles: receive highly variable flow of blood depending on state of exertion; vasodilation
from NE and epinephrine from adrenal medulla and sympathetic nerves, precapillary sphincters
dilate from increased waste and lactic acid, etc
c. Lungs: blood flows more slowly to increase gas exchange and oncotic pressure overrides
hydrostatic pressure so capillaries involved more in absorption

The Lymphatic and Immune Systems

1. Functions
a. Fluid recovery: reabsorb excess fluid and return it to the bloodstream

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b. Immunity: picks up foreign cells and chemicals from tissues and immune cells in lymph nodes activate
immune response
c. Lipid absorption: digestive process for dietary lipids
2. Lymph and Lymphatic Vessels
a. Lymph: fluid that has been taken up by lymphatic vessels
i. Flows under low pressure and from lymphatic contractions of the vessels themselves, skeletal
muscle contractions and arterial pulsations
b. Lymphocytes: divide and spur chemotaxis and enter circulation upon contact with toxin
c. Lymphatic tissue: made of reticular fibers that hold tissue together and anchor lymphocytes
3. Lymphatic Cells
a. Natural Killer (NK) cells: attack and destroy bacteria and cells that have become infected with viruses
or are cancerous; responsible for immune surveillance
b. T cells: mature in the thymus and depend on thymic hormones
c. B cells: differentiate into plasma cells that secrete antibodies; mature in bone marrow
d. Macrophages: phagocytotic cells that develop from monocytes that have moved into the bloodstream;
phagocytize debris, dead neutrophils, bacteria, and foreign matter; alert immune system
e. Dendritic cells: branched, mobile antigen-presenting cells that alert immune system and egulf bacteria
by receptor-mediated endocytosis
f. Reticular cells: branched, stationary cells that act as antigen-presenting cells in the thymus
4. Lymphatic Organs
a. Lymph nodes: most numerous lymphatic organs that cleanse the lymph and act as a site for T and B
cell activation
i. Subcapsular sinus: contains reticular fibers, macrophages, and dendritic cells
ii. Lymph flows from one node to another to become cleansed of impurities
iii. Lymph nodes become swollen when under attack from foreign antigen
b. Red bone marrow: supplier of lymphocytes
c. Thymus: houses premature T lymphocytes and secretes hormones to regulate their activity
i. Secretes thymosin to activate T lymphocytes
ii. Role in specific immunity: memory of virus, toxins, etc
d. Tonsils: first line of defense during swallowing and breathing (guard against inhaled and ingested
pathogens)
i. Tonsillar crypts: contain white blood cells that can be activated to release cytokines and set up
immune response
1. Act as macrophages and alert other defenses
e. Spleen: largest lymphatic organ that reconditions the blood
i. Destroys and recycles red blood cells: porous capillaries capture worn out red blood cells and
they are broken down by white blood cells and macrophages and their heme and protein are
recycled
ii. Removes waste and byproducts (cell debris)
iii. Stores iron and platelets
f. Peyer’s patches: nodules under intestinal mucosa found in small intestine where they protect the
digestive tract from toxins when food is absorbed
5. Immunity
a. Lines of Defense
i. First: external barriers
ii. Second: nonspecific defense mechanisms; leukocytes and macrophages, antimicrobial
proteins, immune surveillance, fever, and inflammation
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iii. Third: immune system  direct cell attack, chemical secretion, antibody formation
1. Leaves a memory to help future encounters
b. Nonspecific Resistance: immediate and always prepared; general attack
i. External Barriers: skin and mucous membranes (endothelium) that keep out foreign invaders
1. Contain chemical barriers: sweat, saliva, salts, urea, acids, enzymes (lysozymes),
mucus, tears that kill or trap bacteria
ii. Leukocytes and Macrophages: phagocytes that digest foreign matter
iii. Natural Killer Cells: specific to one’s body that polices cancer; activates upon finding DNA
damage (cancer)

iv. Antimicrobial Proteins: perforate cell membranes

1. Interferons: proteins secreted by cells when they are infected by viruses that alert
neighboring cells
a. Bind to surface receptors and cause second messenger system that causes
synthesis of proteins that will defend cells against infection
b. Also activate NK cells and macrophages to destroy infected cells
2. Compliment System: group of globulins that are synthesized by the liver
a. Once activated they cause inflammation, immune clearance, phagocytosis,
and cytolysis
v. Immune Surveillance: NK cells continually patrol body for pathogens and diseased cells
1. Release perforins which create holes in membrane allowing rapid flow of water and
salt into enemy cell to kill it along with secreting enzymes that induce cell death
(apoptosis); dead cells eaten by macrophages
vi. Fever: elevation of body temperature initiated by pyrogens which stimulate hypothalamus to
raise set point for body temperature
1. Onset: body temperature rises and person shivers to generate heat and blood vessels
constrict to reduce heat loss
2. Stadium: body temperature oscillates around new set point as long as pathogen is
present
3. Defervescence: pathogen dies, pyrogen secretion stops causing hypothalamus to
return body to its normal set point
4. Benefits of Fever
a. Promotes interferon activity
b. Elevates metabolic rate and accelerates tissue repair and leukocyte division
c. Inhibits reproduction of bacteria and viruses by denaturing enzymes
5. Disadvantages of Fever
a. Get too hot, own enzymes denature causing hallucinations
b. Dehydration requires lots of water (problematic in babies due to high surface
to volume ratio)
vii. Inflammation: local defensive response, characterized by redness, swelling, heat, and pain
from increased blood supply and cytokine production in the area as a way to bring substances
to the area in order to heal and repair tissue
1. Limits spread of pathogens and ultimately destroys them
2. Removes debris of damaged tissue
3. Initiates tissue repair
c. Specific Immunity
i. Immunity is directed against a particular pathogen; immunity to one pathogen does not grant
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immunity to other pathogens

ii. When reexposed to the same pathogen, the body reacts more quickly
iii. Active or Natural Immunity: body makes its own antibodies or T cells against a pathogen due
to natural exposure
iv. Artificial Immunity: body acquires antibodies or T cells from another human or animal that has
developed immunity to a pathogen such as a vaccination (dead strain that induces response)
v. Antigens: any molecule that triggers an immune response; can be free molecules or surface
proteins
vi. T Lymphocytes: develop surface antigen receptors that can recognize antigens presented to
them by antigen-presenting cells
vii. B Lymphocytes: respond to self antigens undergo clonal deletion or produce surface receptors
for antigens and divide to produce immunocompetent B cell clones which disperse
viii. Antigen-Presenting Cells (APCs): contain surface proteins (MHC protein) that act as ID tags
for every cell in your body.
1. Encounters antigen and digests it via endocytosis
2. Breaks down antigen and fragments are send to MHC protein
3. If it’s a self-antigen, T cells ignore it; if it’s a nonself-antigen, T cells initiate an immune
attack
ix. Cellular (cell-mediated) immunity: employs lymphocytes that directly attack and destroy
foreign cells or diseased cells and the immune system remembers the antigens of the
invaders and prevents disease in the future; rids body of pathogens not accessible to
antibodies
1. Cytotoxic T cells: seek out and attack on enemy cells
2. Helper T cells: secrete cytokines and stimulate more cells to create an “army” of a
specific type to recognize a specific pathogen
3. Regulatory T cells: inhibit multiplication and cytokine secretion by other T cells to limit
immune response to prevent it from getting out of control
4. Memory T cells: responsible for memory in cellular immunity against a pathogen
(typically good for 2-40 years)
5. Three Stages of Cellular Immunity
a. Recognition
i. APC encounters and processes antigen and displays to Cytotoxic or
Helper T cells
ii. Activated T cells undergo cloning (mitosis) to identical T cells
programmed against same pathogen to carry out immune attack and
along with memory cells
b. Attack
i. When cytotoxic cell recognizes enemy cell, it delivers chemicals to
destroy it and searches for other enemy cells
c. Memory
i. Memory cells are able to become activated more quickly when they
respond to antigens during reexposure
x. Humoral (antibody-mediated) immunity: mediated by antibodies which do not directly destroy
pathogen but tag them for destruction; more indirect method of defense
1. Three Stages of Humoral Immunity
a. Recognition
i. Antigen binds to B cells with complementary receptors
ii. Antigen digested and presented on cell surface (antigen presentation)

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iii. Helper T cell binds to B cell triggering B cell mitosis (clonal selection)
iv. Cloned B cells are programmed against same antigen
v. Clones differentiate into plasma cells which contain lots of
endoplasmic reticulum which produce and secrete antibodies
b. Attack: antibodies use mechanisms to render antigen harmless
i. Netrualization: neutralize antigen by masking active regions
ii. Lysis if cell membrane: disrupt cell membrane
iii. Agglutination: stick cells together to prevent spreading
iv. Precipitation: link antigen molecules together to prevent dissolvation
c. Memory
i. Primary response when exposed to antigen for first time
ii. Clonal selection produces memory B cells as well which will cause
quick secondary response if exposed again