186 185
3
OCPs
Norethindrone
Mestranol
Depo-provera
Estrone
Estradiol
Estriol
HRT
Decreases symptoms
Decreases osteoporosis ( decreases
osteoclastic activity)
Decreases risk of CAD ( increase HDL;
vasodilator)
Controversy!!
Other Hormonal Drugs
Clomiphene
Leuprolide
RU-486 (mifeprostone)
Now, introducingTYRONE!
Spermatogenesis
Begins at puberty
First sign of puberty in a male is testicular
enlargement
Controlled by testosterone
LH > testosterone > spermatogenesis
FSH > Sertoli cells > produce inhibin
Sertoli Cells
Produce inhibin
Maintain the blood-testes barrier
Protect and nourish the sperm to maturity
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4
Spermatogenesis
Ejaculation
Apply the SQUEEZE TECHNIQUE
Gently squeeze the head of the penis; it starts
retrograde peristalsis in the ejaculatory duct
and epididymus
189 188
6
Once the sperm are deposited in
the vagina
Sperm hide under the semen
HCO3 is released to neutralize lactic acid
Zn is used for the Capacitation Reaction
Fructose is used for energy
70% of sperm are dead before reaching
the cervix
Acid phosphatase is used to eat through
cervical mucus
Once the sperm are deposited in
the vagina
Sperm enter the uterus
They swim through the fallopian tubes
By the time the sperm approach the egg,
only a few thousand sperm remain
Sperm surround the egg
They dart in and out, opening their heads
to release enzymes ( Acrosomal Reaction)
Once the sperm are deposited in
the vagina
Once one sperm head fuses with egg, a
wall forms behind the sperm (
Crystallization Reaction)
This prevents Polyspermy
A ZYGOTE is formed when egg (1n) and the
sperm head (1n) fuse
Stages to Know
190 189
7
HCG
Detectable in BLOOD one week after
fertilization; in the URINE two weeks after
Has the same alpha subunit as FSH. LH,
and TSH ( check the beta-HCG)
Maintains the corpus luteum
Increases GI motility and absorption
Sensitizes the TSH receptor
HCG, cont
Maintains corpus luteum production of
progesterone
Can lead to Hyperemesis Gravidarum
DES
Cervical incompetence
Adenomyosis
Clear cell carcinoma of the vagina
Increases BMR
HCG, cont
Doubles every 2 days until week 12
HCG of 600: viable fetus
HCG of 2000: fetus visible on abdominal
ultrasound
How to Follow the First Trimester
Cloasma or malasma
Helps increase plasma volume by 50%
191 190
8
Estrogen
Inhibin
Inhibits FSH
Prevents another menstrual cycle from
beginning
Human Placental Lactogen
BLOCKS moms Insulin receptors
Creates insulin resistance
Gestational diabetes
Relaxin
Relaxes tendons and ligaments
Stretches the pelvis
The END
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At different points of gestation, various
organs are embryologically developed.
For example:
- Notochordd at 2wks
Renal Embryology:
Notochor at 2 wks
-Brain at 4 wks
- Renal system is formed at 12 wks
METANEPHROS - give rise to the kidney
URETERIC BUDD ives ise to the tire
URETERIC BU - gi ri t th enti
collecting system
Collecting duct, major and minor calices, papillae,
hilum and ureters
L1 and L2 levels:
right kidney is positioned
li htly lower than the left ft slightl l th th l
kidney
Why?
Cortex: outermost layer of the kidney.
It contains the nephrons, PCT, and DCT
Cortical nephrons are shorter in length
compared to the medullary nephrons
Functions to maintain an isotonic urine
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Medulla: deeper layer of the kidney
Pyramids collect urine from the collecting
ducts that drain into each renal papilla pp
From the papilla > calyces > ureters
Responsible for hypertonic urine
Why do we sweat in different regions?
In hot places, we sweat and lose water.
In cold do t t d thus do I cold areas, we d not sweat and th d
not need to preserve this water.
The nephrons elongate after 3-4 days
Allows for more water conservation
(hypertonic urine) and fluid replacement lost
Renal Blood Supply
Right renal artery
Right renal vein
Renal Blood Supply
Right gonadal vein
directly drains into the y
IVC. Right sided
infection or cancer has
a worse prognosis
Left gonadal vein
drains into the left
renal vein
Healthy
Kidney
Sodium and
water
removal
Unhealthy
Kidney
Fluid
overload
Waste
removal
Hormone
production
Renin
Erythropoietin s
Prostaglandins
Elevated
waste- Urea,
Creatinine,
Potassium
Changes in
hormone levels
Blood pressure
Making red blood
cells
Uptake of calcium
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Divide the kidney into 4 regions.
When one of the 4 are affected, ultimately it will affect the others
Tubules Glomeruli
Blood
vessels Interstitium
20% f blood d from the CO is ing to the kidneys
Blood
Vessels
20% of bl f th CO i goi t th kid
90% of it, supplys the cortex
Only blood supply for the medulla - vasa recta
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A 36 y/o fire fighter (70 kg),was trapped in a
burning building and suffered 2nd and 3rd degree
burns to over 65% of his body. What will be the
fluid replacement management?
Urine output : 1cc/kg/hr
70 kg x 50 % = 3500 x 4cc = 14,000 ml (14L)
7 L first 8 hrs : 7 L remaining 16 hrs
2nd day that, 3rd day nothing
Urine Output: 1cc/kg/hr (70 kg male)
A. 15, 20, 15 ml/hr
B. 300, 250, 270 ml/hr
C. Over 48 hrs, urine output has been
between 50-100 ml/hr. Now on day 3,
urine output 250, 300. Next step in mgt.?
Never give a hypertonic solution this will pull fluids out of the
extracellular fluid to help fill the vascular space, which will be
replaced by the intracellular fluid.
H 2 O
Ok great job on getting patient Xs blood pressure back to the normal range, but
at what cost. the tissue (oops!!!)
Cell
H 2 O
H 2 O
Intracellular
Extracellular
Exception to the rule:
Hyponatremic patient ( Na <120) patients:
Use 3% (hypertonic) saline to get sodium
above 120
Body water is broken down into fluid compartments:
Intracellular fluid (2/3 of Body Water)
Extracellular fluid (1/3 of Body Water)
Interstitial fluid (ISF) 2/3 ECF
Vascular fluid (VF) 1/3 ECF
ICF ECF
ISF VF
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Loss of isotonic fluid:
Hemorrhage, Diarrhea, Vomiting
Osm
ICF ECF
Loss of hypotonic fluid:
Dehydration, Diabetes Insipidus, Alcoholism
ICF ECF
Gain of isotonic fluid:
Isotonic saline
ICF ECF
Gain of hypotonic fluid:
Hypotonic saline, Water intoxication
ICF ECF
Gain of Hypertonic fluid:
Hypertonic saline, Mannitol
ICF ECF
Renin
Angiotensinogenen Angiotensinog
Pathway
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Renin
(JG cells-afferent)
Liver
AT-II (stimulates)
alpha 1 vasoconstriction
Adrenals l (Z. Glomerlus)- l ) (Angiotensinogen)release AT-I
Lungs
(AT-I is converted
to AT-II via ACE)
Ad (Z Gl
Aldosterone release
Posterior pituitary- ADH release
CNS- thirst center
Bartter s syndrome:
JG cell hyperplasia with renin excess
No increase in blood pressure due to insensitivity
of the presser effects of AT-II
Defect in the kidney s ability to reabsorb
potassium p
Excessive amount of potassium is excreted from
the body. This is also known as potassium wasting
DKA metabolic acidosis, which causes a
switch in H+/K+ pumps leading to K+
leaving the cells and intering the serum.
Not a true hyperkalemia, just ions shifted in
the wrong place.
Kidneys illill ize the high h K+ dd ttart t Kid w recogni th hi K+ an s
to secrete it in the urine.
(Hyperkalemia to Hypokalemia)
Hypomagnesemia due to decreased
gastrointestinal (GI) absorption
(Diarrhea, malabsorption, diet)
or increased renal loss(diuresis due to
alcohol, thiazides and loop diuretics)
Always look a pH first, then HCO3 You should be able to differentiate
based off of these two
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For example
If the patients pH is acidic, you should
expect that patients HCO 3- to be low
(buffering)
If not, then the problem has to be
respiratory
Aidosis i
Respiratory
PaCO2
HCO 3-
(compensations)
HCO 3-normal
(non-compensation)
ACID / BASE Disorders:
Acid
Metabolic
HCO3-
PaCO 2
(compensation)
PaCO 2 normal
(non-compensation)
Alkalosis l i
Respiratory
PaCO 2
HCO 3-
(compensating)
HCO 3- normal
(non-compensation)
ACID / BASE Disorders:
Alk
Metabolic
HCO 3-
PaCO 2
(compensating)
PaCO 2 normal
(non-compensation)
Arterial pH 7.3
pCO2 30 mm Hg
pO2 95 mm Hg pO2 95 mm Hg
Serum HCO3- 14 mEq/L
What is the diagnosis?
Arterial pH 7.3 (ACID)
pCO2 30 mm Hg
pO2 95 mm Hg
Serumum HCO3-- 14 mEq/L (low)w) Ser HCO3 14 mEq/L (lo
What is the diagnosis?
Metabolic Acidosis
w/respiratory compensation
Metabolic acidosis
Check anion gap... Na+ -(Cl- + HCO 3-)
(N: 8-12 mEq/L)
Burns ( massive)
Third spacing (i.e. liver chirossis)
Diarrhea
Decrease in Aldosterone (Addisons)
Cardiovascular
Hypotension (CHF)
Coarctation / tamponade
PreRenal
Decrease in Oncotic pressure
Low Albumin
Nephrotic syndrome
Edematous states ( Cirrhosis)
Renal Artery Vasoconstriction
Medications ( NSAID s- block PG s, ACE-I)
Anatomical Renal Artery Stenosis
Decreased Vascular Resistance
Shock
(inflow to
the
kidneys)
Pre-Renal
BUN/Cr > 20/1
Urineine Na+ <10 Ur Na < 10
FeNa+ < 1%
UOsm > 500
Intra-renal problems
Drugs ( Gentamicin,
Amphoteracin B, Cisplatin) takes 5 to 7 days to damage
Crystals Uric acid tumor lysis Renal Uric acid - tumor lysis
Oxilate stones- antifreeze
or malabsorption
Crushing injuries-cell lysis
dipstick positive (NO RBC s)
Thromboembolism, ATN
(Kidneys)
Renal
BUN/Cr < 20/1
Urineine Na+ >20 Ur Na > 20
FeNa+ > 2%
Low specific gravity
(can not concentrate urine)
Bladder obstruction
Prostate enlargement
Pelvic tumors
Urethral strictures
(foley,retroperitoneal
PostRenal
(out flowow obstruction)truction) fibrosis)
Urethral obstruction
Tumor
Stones
( out fl obs
Both kindeys need
to be affected to
see any deficit
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Post- Renal
Obstruction
(hydronephrosis)
Increased post void
residual volume
If you suspect a pre-renal problemthe patients usually have
positive orthostatics
dry branes
d mucous memb
increase for thirst
rapid heart rate
skin tenting (turgor)
Consider (co-morbid) conditions that could
lead to their pre-renal problem
For a renal problem (intra-renal)consider drug history
Knowingwing the patients drugsugs could preventevent Kno the patients dr could p
r
unnecessary test for the patient and time
wasted in determining the cause.
Any recent history of exposure to possible
hypersensitivity
RBC cast Glomular RBC cast
nephritis
WBC s
Bacteria Infection
Crystals
Uric Acid (Gout)
Urinalysis CLUES
Proteinuria (bence
jones)
Multiple
myeloma
Blood dipstick +, but
no red blood cells Myoglobinuria
Proteinuria >
3.5gm/d
Fat cast
Nephrotic
syndrome
Glomerular Disease:
Have you ever noticed, that when you
wake up in the morning and urinate,
there is a soapy appearance to your
urine in the toilet bowl?
Why is it, that when a nurse is going to
do a morning U/A on a patient, you ask
her to get a mid-steam catch?
When we look at nephritic or nephrotic
syndromes, we need to decide what sets
them apart from each other.
Aside from a few details, it just comes down
to protein loss and the magical number is
3.5g/day. 5g/day 3
If less than 3.5 g/day then we name that
Nephritic and if greater than 3.5 g/day, we
call that Nephrotic.
Why 3.5 g/day?
Hypertension
Macroscopic /
Microscopic
hematuria
(smokey brown
urine)
Oliguria Edema
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24 hour U/A ( best initial test) - look
for hematuria, proteinuria
If GFR is decreasethink auto-immune If GFR is decreasethink auto immune
check complement, ANCA and anti-GBM
Renal biopsy (most definitive) - LM, IF, or
EM to help in the diagnosis
Treat any hypertension, fluid overload and
uremia with
Salt and water restrictions, diuretics and if
needed, dialysis
If the underlying cause is inflammation of the
glouerular, the give corticosteroids
1. Post Strep GN
2. Good Pasture GN
3. RPGN
4. IgA Nephropathy
5. Membranoproliferative GN
(can be both)
Proteinuria (> 3.5 g/day)
Generalized edema
Hypoalbuminemiauminemia Hypoalb
Hyperlipidemia.
Approximately one-third of all cases are
the result of systemic diseases such as
DM, SLE, or amyloidosis.
Generalized
Edema
Foamy urine
Ascites
Hypercoagulable
state
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U/A - proteinuria (>3.5 g/day),
lipiduria
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Acute Renal Failure
Renal Plasma flow
BUN
(lab) use PAH
GFR- look at Cr clearance:
Renal Blood Flow- assocated with Cr
clearance
Decreased in
pregnancy, liver
failure, over
hy
GFR = Kf [ (PGC-PBC)-(
GC-BC)]
P= Hydrstatic
Inreased in
kidney stone,
obstruction
Breakdown of
bowmans
capsule
PGC
GC
PGC is the main
factor that
determines GFR
(promotes filtration)
PBC
BC
PBC opposes filtration
Does not affect the
rate of filtration,
except in obstruction
Should not be a factor
The negative charge of the filtering
membrane inhibits the filtering of
proteinsoteins [anions (-)])] pr [anions (
If the negative charge is not
present, significant protein
filtration takes place
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Filtration fraction (FF) fraction of material that
enters the kidney, that is filtered normally (.20 or 20%)
GFR 140 ml/min
RPF 400 ml/min
.35 or 35% FF
Constrict Efferents
Px = 2mg/ ml
Ux = 2mg / ml
2 x 2 = 2 ml/ min
2
Each kidney measures about 3 to 7 inches
If kidneys too small
Renalenal Arterytery Stenosis
Kidneyy Pathologyathology Kidne P
R Ar Stenosis
If kidneys too large
Polycystic kidney disease
Medullary sponge kidneys
Medullary cystic kidneys
Renal Artery Stenosis
atherosclerosis
fibromuscular dysplasia
Unilateralal
If the kidneysys are too small If the kidne are too small
Unilater
Abdominal bruit
Low volume state
Dx: ultrasound; renal vein renin elevated
( higher renin output indicates stenosis)
Goldblat Kidney
Treatment
herectomy
Avoid ACE-inhibitors once HTN is severe
(AT-II Dependent)
RAS: most common cause of secondary
hypertention
Ipsilateral ath (or stent if not a surgical
candidate) and contralateral nephrectomy
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If you have large kidneys
Polycystic kidney disease
Medullaryy spongee kidneysys
Medullary cystic kidneys
Po
Po
Children: UTIs
Adolescents: urethral strictures ( from STDs)
Adult men: BPH
Adult women: uterine prolapse and cystocele
BPH
Most common cause of urinary obstruction in
adult men
Obstructionuction is periurethraliurethral (central)al) : Dx DRE
entr : Dx DRE
Obstr is per (c
bladder emptying
Sphincter pressure is normal
Gotta gogotta gogotta go
Tx:
Imipramine (in children) TCA
Oxybutynin (in adults) Blocks Ach (M)
(to decrease bladder contractions)
Urge Incontinence, cont
Tx: have patient urinate around the
clock beginning with
-
Stress Incontinence
Due to weak pelvic floor muscles
Estrogen connection
Any increase in abdominal pressure
( like from sitting down, laughing, coughing,
sneezing, etc) causes a sudden loss of urine
Detrussor muscle function is normal
Bladder capacity is normal
Sphincter pressure is decreased
Stress Incontinence, cont
MCC: obesity; estrogen connection
Tx: weight loss; Kegle exercises to
tighten up pelvic floorloor muscles tighten up pelvic f muscles
Use pseudoephedrine to tighten up the
sphincter (alpha adrenergic)
Suggest diapers or panty liners in the
meantime
Overflow Incontinence
Due to an anatomical obstruction
Detrussor muscle activity is decreased due to
stretching
Bladder dd itity is increased d
Bl capac i i
urgency; frequency
Tx: surgically remove the obstruction
Overflow Incontinence, cont
Causes:
In newborns: posterior urethral valves
In children: stricturesictures
In children: str
Pr to UTIs
P : fo is scar and
y Encephalo-meningocele
y Encephalo-meningo-myelocele
Lower vertebral arch defects
y Spina Bifida Occulta
y Spina Bifida Aperta
1. Meningocele
2. Meningomyelocele
y Arnold Chiari Malformation (Type I and II)
y Syringomyelia
AFP
y A filtrate of plasma
y Made by the Choroid Plexus in each ventricle
Now you need some CSF
y
y Requires Vitamin A
y Requires Carbonic Anhydrase
How CSF differs from plasma
y Less HCO3y More CLy Lower pH 7.34 (acidic)
y Up to 25 WBCs normal in first month of life normal
y >1 month, only up to 3 WBCs normal
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Lateral ventricles >
foramen of Munro >
3rd ventricle >
aqueduct of Sylvius >
4th ventricle >
foramina of Lushka & Magendie
subarachnoid layer >
Neurocutaneous Syndromes
Von-Hippel Lindau
y Cerebellar hemangioma g
y Retinal hemangioma
y Renal cell carcinoma
(increased EPOs)
Embryology of the Brain
Prosencephalon Telencephalon cerebrum
Diencephalon thalami and BG
Mesencephalon Mesencephalon midbrain
Rhombencephalon Metencephalon pons & cerebellum
Myelencephalon medulla
Visual Cortex
y Light must hit the retina by 3 months of age
or the child is blind for life
y You must verify that a child has a RED reflex
on eye exam at birth (retinal arteries, and if
you can see them- nothing is in the way)
Abnormalities of the Eyes
y Anisocoria: unequal pupil size
y MCC: Congenital (AD) check parents
y If it occurs in childhood- inc. ICP until proven
herwise i DCTx: LP oth D CT, LP
y
y
y
y
Vision Correction:
y 20/20 20/100 (5 times the difference)
20 ft. 4ft
y 20/200 legally blind (no drivers license)
y can not see details
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Abnormalities of the Eyes
y My-opia: near sightedness (can not see far)
y Focus of light is before the retina
y Tx: Concave lens- disperses light
y Hyperopia: far sightedness
y Focus of light is behind the retina
y Tx: Convex lens- focuses light earlier
y Presbyopia: loss of accommodation seen with aging
y Due to muscles weakening with age
y Ability to focus on objects coming close
Myopia-can not see far away
White Reflex
y Cataracts: opacification of the lens
y Does not allow light to hit the retina
y Must be removed
d dence h high h lucose y Increased incid with h gl or
galactose ( sorbitol or galactitol accumulates)
y Idiopathic: 90%
y Diabetes or galactosemia
y Rubella
White Reflex
y Retinoblastoma (rare)
y Rb gene y Rb gene
y Cancer
y High association with Ewings
sarcoma
Visual field deficits Visual field deficits
Optic Nerve
Optic Tract
Optic Chiasm
Meyers
Optic Radiation
Calcarine
Fissure
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Optic Radiation
Meyers Loop
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Frontal Lobe Lesions
y Atonic seizures- generalized (knock out CST)
y Dementias
Alzheimer s h i y Al
y Picks disease
y Schizophrenia: loss of asymmetry
y Frontal lobotomies
Temporal Lobe
y Hearing
y Balance
y Hallucinations ( released by serotonin) y Hallucinations ( released by seroton
in)
y PCP
y LSD
y Posterior temporal lobe: Wernickes area
Amphetamines
y Taken up presynaptically; cause release
of catecholamines
y Clue: vertical nystagmus
Amphetamines
y Used in ADD
y Methylphenidate (use in Narcolepsy)
y Pemoline y Adderal
y Dexadrine
y OTC for weight loss
y Dexatrim
y
y
y
y
Cause hallucinations
LSD
PCP
ECSTACY
SSRIs
y Fluoxetine
y Paroxetine
y Luvoxetine Depression, eating disorders
y Sertraline (MAOI- wait a month)
y Nefazadone
y Trazadone
Parietal Lobes
y Dominant lobe: long term memory; all the
things you learned since kindergarten
y left side is dominant in 90% of right- left side is dominant in 90% of right
handed and left-handed people
y Nondominant lobe: apraxia and hemineglect
y Right side is nondominant in 90% of righthanded and left-handed people
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Anterior Cerebral
Anterior
Communicating
Posterior Cerebral
Superior Cerebellar
Anterior Inferior Cerebellar
Posterior Inferior Cerebellar
Vertebrals
Lateral Pontine Syndrome
Occlusion AICA (anterior
inferiorerior cerebellarebellar artery)ery) inf cer art
CN 7- ipsilateral facial
paralysis
CN 8- hearing loss
Lateral Medullary Syndrome
( Wallenberg)
Occlusion of PICA (posterior inferior
cerebellar artery )
Cerebellar peduncle- ipsilateral limb
ataxia
Descending hypothalamicsipsilateral horners
Nucleus ambiguus- dysphagia
Medial Medullary
Syndrome
Occlusion of vertebral artery
Pyramid- contralateral spastic
hemiparesis
CN 12- tongue deviates