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then add one week

If the womans menstrual cycle varies from 28


days, then you add/subtract the difference at
the end
Some Rules
Term pregnancy: 37 to 42 weeks
Average birth weight: 2500gms to
3500gms (5 to 7 pounds)
Preterm: birth prior to 37 weeks
Postterm: birth after 42 weeks
SGA: small for gestational age
LGA: large for gestational age
Naegles rule also allows us to
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Oogenesis
Begins in-utero at about 5mo gestation
At birth, a female ovary contains about
400k eggs
Beginning at puberty, 8 to 10 follicles
begin development; but, only ONE egg will
ovulate
The eggs that do not finish development will
turn into small white nodules (corpus
albicans)
Oogenesis: The Steps
One round of mitosis first: 2n to 4n (occurs in
utero)
Primary oocyte
Enters meiosis 1 and arrests in Prophase (cells
still at 4n)
Eggs remain arrested in meiosis 1 in prophase
until ovulation occurs
If egg ovulates, it will complete meiosis 1, give
off first Polar Body, and enter meiosis 2,
arresting again in Metaphase(4n to 2n)
Secondary oocyte
Oogenesis: The Steps
If fertilization occurs, egg will complete
meiosis 2, give off the second Polar Body,
and form a zygote (2n to 1n)
Tertiary oocyte
Because moms eggs remain
arrested for SO long
You can trace 80% of
chromosomal mutations to MOM

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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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Spermatogenesis

One round of mitosis: 2n to 4n


Primary spermatogonium
Meiosis 1: 4n to 2n
Secondary spermatocyte
Meiosis 2: 2n to 1n
Tertiary spermatid

One spermatogonium gives rise to 64 spermatids

As spermatogonia mature, they move from the basal


layer into the epididymus to finish maturing
Spermatogenesis, cont
Each day 20 to 40 million sperm mature
Complete spermatogenesis takes 41 to 72
days
Sperm can live for 5 days in fallopian tube
while an egg can live for only 3 days
Virility
20 to 40 million sperm per cc of semen
4 to 5cc of semen per ejaculate
No more than 40% abnormal forms
30 to 60% of sperm must still be motile
after 5 minutes on a glass slide
The pH is basic
Infertility
50% male factor
Always do sperm analysis first
30% female factor
Mcc is PID
20% miscellaneous
Before Sperm Can Leave
Seminal vesicles: semen; fructose
Bulbourethral ( Cowpers ) gland: HCO3
Prostate: Zn ; acid phosphatase;
hyaluronidase
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Sexual Response
Sexual Dysfunction

In young men: premature ejaculation


In older men: stress induced impotence
In the elderly: vascular impotence
Atherosclerosis decreases blood flow
Takes longer to establish an erection
Harder to maintain an erection
Need for more direct stimulation
Longer refractory phase

The Difference Between the Sexes


Men have a longer refractory phase; short
excitement phase
Women have a longer excitement phase;
short refractory phase
To Address Premature

Ejaculation
Apply the SQUEEZE TECHNIQUE
Gently squeeze the head of the penis; it starts
retrograde peristalsis in the ejaculatory duct
and epididymus
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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

Zygote: 2 cell stage


90% fertilizations occur in the ampulla
It must now migrate into the fallopian tubes
Ectopic pregnancy: mcc is PID (forms scars)
Morula: 16 cell stage
This stage enters the uterus
Blastula: 256 to 512 cell stage
This is the stage that implants

Formation of the Placenta Placental Hormones


HCG
PROGESTERONE
ESTRIOL
HUMAN PLACENTAL LACTOGEN
INHIBIN
RELAXIN

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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

Fundal height rises 1cm per week


Pubic symphasis = 12 weeks
Umbilicus = 20 weeks
HCG doubles every 2days
Estriol level rises linearly

If fetus dies: estriol level falls first


Think of Molar Pregnancy if
Fundus growing higher than predicted
HCG rising faster than predicted
HTN in first trimester
Complete mole
Incomplete mole
Progesterone
Increase RR from pons
Increase appetite
Pica
Increase RBC mass by 30%
Causes acne
Hyperpigmentation

Cloasma or malasma
Helps increase plasma volume by 50%
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Estrogen

Smooth muscle relaxation


Stimulates protein synthesis in the liver
High ESR
Hyperlipidemia
Increased TBG
Increased angiotensinogen
Increased clotting factors

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

Ureteric bud must make contact with the


metanephros or kidney will NOT develop
Renal
Pelvis
Metanephros
URETERIC BUD
Calyx
Gives rise to the GENITALIA in MALES
Has kidney
Develops into the testes, seminal vesicles, vas
deferens and epididymus
To develop, you need a Y chromosome and MIF
H kid
function prior
to kidney
formation
Gives rise to female genitalia
Paramesonephros
(never functional) (never functional)
as a kidney
Develops into the ovaries, fallopian tubes, uterus and
upper vagina
A female can develop either by DESIGN or by DEFAULT
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Vitelline Duct: Allantois:
Omphalomesenteric duct
IN MALES: prostate, prostatic urethra and
bulbourethral ( Cowpers) glands
IN FEMALES: lower vagina, and labia minora
Urogenital Sinus
IN MALES: becomes the PENIS
IN FEMALES: becomes the CLITORIS
Urogenital
Tubercle

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

Medulla- first place to infarct in a low volume


state leading to medullary necrosis
Consist of visceral epithelial cells
(foot processes-podocytes)
Glomeruli
Glomular basement membrane
(electron dense-type 4 collagen)
Parietal epithelium lines bowman s space
Fenestrae (in the endothelium)
Most glomerular diseases are immunologically
mediated.
Proximal convoluted tubule (80% of reabsorption)
Tubules
Loop of Henely (triple transport)
Distal convoluted tubule
Collecting tubule (for concentrating the urine).
Most tubular diseases are frequently
caused by toxic or infectious agents
In the cortex, comprising mostly of fenestrating
Interstitium
capillaries (so any change in space, i.e. edema is
abnormal).
Most interstitial disorders are
frequently caused by toxic or infectious
agents.
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Patient presents with polyuria and
polydyspia
You rule out diabetes based on glucose
What next?
Diagnosis Cause Labs
Psychogenic DI

Excessive fluid intake


i.e. As much as 10-12 gallons
of H2O a day
Uosm/Posm > 0.7
Restrict H2O for 24 hours
Urine will concentrate
Central DI
Posterior pituitary does not
release the stored ADH
Uosm/Posm < 0.7
ADH is t tt, but t Central DI
i.e. Infarction of the pituitary
gland
ADH i not presen b
when you give it, expect
the urine to concentrate
Nephrogenic DI
Renal kidneys are
unresponsive to ADH
i.e. Renal failure, lithium,
low volume state infracting
the medulla of the kidney
Uosm/Posm < 0.7
ADH is present and wants
to work, but its a receptor
problem
Urine will not concentrate
For burn patients: Parkland formula
( to calculate fluid deficit only)
4cc x Wt (Kg) x % burned areas
Never calculate more than 50% of burned
body area
Replace fluids:
within the first 8 hrs ( from time of trauma)
Remainder over the next 16 hrs
Head and neck: 9%
Each arm: 9%
Front of torso: 18%
Back of torso: 18%
Back of torso: 18%
Each lower extremity: 18%
Genitalia: 1%
For newborns: subtract 9% from each lower
extremity and add it to the head and neck
Head 27%, legs 9%

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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)

Increased anion gapp Normalmal anion gapp Increased anion ga


MUD PILES
M- methanol
U- uremia
D- DKA
P- paraldehyde or phenformin
I- iron tablets or INH
L- lactic acidosis
E- ethylene glycol
S- salicylates
Nor anion ga
Diarrhea
Renal tubular acidosis
Hyperchloremia
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Diuretics
PCT
Acetazolamide, Dorzolamide:
Mannitol:
Ethacrynic Acid (no sulfa)
Furosemide (sulfa) Hydrochlorothiazide (sulfa)
Indapamine (no hyperlipidemia)
Spironolactone:
Amiloride:
Triamterene: (no anti-androgenic effects)
Intra- Renal
Pre- Renal Post-Renal
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Kidneys stop functioning properly: increase in
Creatinine
BUN and/ or
Decreased urine output
Oliguria i decrease in iine ( 400 /d/day) ) Oli : d i ur output ( < 400 cc
Anuria ( < 100 cc/day)
Volume depletion
Dehydration (nausea, vomiting)

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

toxins that could be nephro-toxic.


Myoglobin is a normal intracellular proteins:
- toxic to the kidneys
- intra-renal damage
If youu suspectspect arteroemboli,teroemboli, look for If yo su ar look for
subcutaneous nodules
digital ischemia or immobility
With Glomerulonephritis:
red cast
edema (protein loss)
hypertension (renin pathway)
If you suspect a post-renal problem,
check for
prostate disease (Prostitis, BPH, Prostatic CA)
all can lead to an enlarged bladder with pain
radiating to the flanks
Check the urine (RBC s, WBC s, cast,
eosinophils), Electrolytes
FeNa+ can destinguish between prerenalenal and renalenal problemsoblems r and r pr
DRE, urinary cath as well as ultrsound
can rule out an obstruction
Renal biopsy only when the cause of
intra-renal can not be determined
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Dialysisysis if necessaryy- Hyperkalemiakalemia,
Attempt to balance fluids and
electrolytes
Discontinue medications if they are the cause of the
renal disease
Dial if necessar Hyper
Metabolic acidosis, Fluid overload, Pericarditis,
Encephalopathy
Urinalysis CLUES
Eosinophils
(Most common causeCephlosporins)
Drug induced

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

Blood chemistry- decreased albumin


(<3g/dL), hyperlipidemia
Always look for secondary causes
Renal biopsy (definitive): LM, IF, EM
Diuretics and antihyperlipidemicsyperlipidemics
Diet restrictions of salt and protein
Vaccinate (PPV 23)- patients at risk of Streptococcus
pneumoniae infections
If the patient is a diabetic- put them on an ACE-I for it
decreases the prograssion of the disease
Diuretics and antih
Nephrotic Syndrome
Mcc in children: minimal change disease
Mcc in adults:: membraneousaneous nephropathyopathy Mcc in adults membr nephr
Mcc in Blacks and Hispanics: FSGN
Fat cast
1.Membranous GN
2.Minimal change disease
3.Focal Segmental GN
4. Amyloidosis
5.Nodular Glomular Sclerosis
Block aldosterone
Have sulfur in them- anaphylaxis, hapton to RBCs
Angioedema- block C1 esterase inhibitor
Serum inc., ( )
Capto pril
Liseno pril
Enalo pril

S Na- dec. , K -i pH dec (hangs onto H+)

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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

(Lab) use inulin


Pa Pb
FLOW
X
If you increase resistance at X
Pa pressure will increase
Pb pressure will decrease
Flow will decrease throughout
GC
Glomerular
cap pressure
Peritubular
cap pressure
Renal
plasma flow
1. Constrict efferent
GFR Post- efferent Efferent
2. Dilate efferent
3. Constrict afferent
4. Dilate afferent
E A
GC
E A
GC
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E A
GC
E A
GC
Rate at which plasma is filtered into
bowmans capsule.
Units of filtration:
(Volume filtered per unit of time)
e.g. ml/min, L/day
Glomerula Filtration Rate (GFR)
= Oncotic
ydration

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

Carriers are easily saturated


Carriers have high affinity for the substrate
Low back leak
The entire filtered load is reabsorbed until the
carriers are saturated, then the excess is excreted.
Morning glucose is 6 00 mg/1 00ml,
how much will leave the kidneys?
120 (GFR) x 6 = 720mg
will be filtered
How much will leave
in the urine?
(normal carrier Tm 375 mg/min)
So urine dipstick will measure
345 mg/min
Tubular Secretion (PAH):
(para-amino-hippurate)
Secreted from the peritubular
capillaries into the PCT.
There are enough carrier to
secrete 4 times the amount
filtered.
If you inject 100 mg of PAH into
a patient, how much will be
excreted?
100 mg
(20% filtered and 80% secreted)
Protein
Lipid soluble
Inulin
Manitol
(filtered, not
secreted or
reabsorbed)
Glucose
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Theoretical volume of plasma from which a substance is removed over a
period of time
Calculate the clearance ?
V = 2ml/min

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

Medullar spong kidne

Polycystic Kidney Disease


ADULT TYPE
AD
Bilateral, HTN, RF
SAH - berry aneurysms
INFANTILE TYPE
AR
Unilateral
NO HTN
In posterior
communicating artery
CN 3- blown pupil
Worst headache
Tx: Transplant
NO HTN
NO RF
Medullary Cystic Kidneys
Multiple cysts destroy the medulla
Polyuria
Polydypsialydypsia
Low volume state

Po

Occasional kidney stone


Dx: Sonogram (bubbles)
Medullary Sponge Kidneys
Many holes develop in the medulla
Polyuria
Polydypsialydypsia
Low volume state

Po

Multiple kidney stones


Dx: Sonogram (holes)
Ureters: 3 anatomical narrowings
Hilum
Mid ureter: caused by going
overer the iliac bones ov the iliac bones
Ureteropelvic junction
( where it enters the bladder)
Kidney stones
Most common type: calcium
MCC: hypercalciuria

Tx: Normal saline


Opiates for pain
Thiazides decrease hypercalciuria
by forcing the PCT and Loop to
increase Ca2+ absorption
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Kidney stones
Struvite stones (Staghorn calculus)
Triple phosphate stones
Ca-Mg-NH4-Phosphate M NH4 Ph h t

MCC: urease positive UTIs


Tx: normal saline; opiates for pain
Urease Positive Bugs
P roteus
P seudomonas
U reoplasma
N dia
N ocardi
C ryptococcus
H elicobacter Pylori
S taph Saprophyticus
Brucellosis
Kidney stones
Uric acid stones
The only stone NOT visible on xray
(radiolucent)adiolucent) (r
Associated with rapid cellular death
(burn pt, CA, massive trauma)
Tx: normal saline
opiates for pain
Kidney stones
Cystine stones
CYSTINURIA
C ysteine
O rnithine
L ysine
A rginine
AD
Coffin lid, enveloped
Defective renal transport of amino acids

Tx: normal saline; opiates for pain


Kidney stones
Oxalate stones
Due to malabsorption in GI tract
When you have malabsorption, calcium gets
trapped in the malabsorbed fat (saponification) and
do not therefore bind oxalates from proteins
breakdown. Oxalate get absorbed in the GI
Can be hexagonal
Kidney Stones: management
IV normal saline
Opiates for pain
< 5mm ( cm)
Let it pass
Let it pass
5mm to 1cm
Lithotripsy (whorl pool)
> 1cm
Open laparotomy (i.e. struvate)
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-Street- Heroin (short acting)
-For withdraws- Methadone (long acting)
-Kidney stones- Morphine Kidney stones Morphine
-Abdominal pain- Meperadine
(no contraction of sphincter of odi)
Kidney Stones: management
If pyelonephritis develops:
percutaneous nephrostomy stent placement
to drain the pus
Dx: KUB; spiral CT; IVP;
Sonogram (if with hydronephrosis)
Ureteroscopy- if stone is in the middle or
lower 1/3 of ureter
HYDRONEPHROSIS
Newborns:
(1)malimplantation of the ureters (lack 2 90)
(2) posterior urethral valves

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

Tx: terazosin or doxazosin


(alpha 1 blockers) loosen sphinctor
Tamsulosin (Flomax)- least side effects
2nd line - Fenesteride (block 5 alpha recductase)
Sx TURP (transurethral resection of prostate)
HYDRONEPHROSIS
UNILATERAL
Kidney stones
BILATERAL
Retroperitoneal
fibrosis
Methysergideysergide Meth
(seretonin Rx for
migranes)
Nitrofurantoins
Bladder
Allantois develops into
Urachus develops in the
abdomen and descends into the
pelvis
forming the Bladder
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Urachal Cyst
Urachus retains attachment to the
umbilicus
Clue:e: urineine drainsains fromom the umbilicus
Tx: surgery

Clu ur dr fr the umbilicus

Exotrophy of the Bladder


Bladder was caught outside the abdominal
cavity
Predisposes to bladder cancer (MC
complication)
Risk for bladder cancer persists even after
surgery (UA and CT every year)
Tx: surgery
MCC: Atherosclerosis
Location: 90% occur below the renal arteries
Presentation:
1. Ripping, tearing pain down the lower back
2. Pulsating abdominal mass
(can only feel if they are thin)
Dx: Sono, CT scan
< 4 cm diameter
- control HTN
- follow
> 6 cm in diameter
- control HTN
-surgery
4 6 cm (surgery is the doctors call)
MCC: 1# Trauma , 2# Collagen disease
Presentation:
1. Ripping, tearing pain between the shoulder blades
Diagnosis: Spiral CT
Treatment: Type A control HTN, surgery
Type B- control HTN, pray
(not much connective tissue)
Incontinence
The involuntary loss of urine
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Urge Incontinence
Detrusser muscle activity is increased.
A spastic bladder ( UMN lesion)
Bladder capacity is low due to repetitive

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
-

hourlyly forr 2 to 3 daysys, - hour fo 2 to 3 da


then every 2 hours for 2 to 3 days,
then every 3 hours for 2 to 3 days,
then every four hours (normal)

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

Sphincter pressure is increased


Sx: a weak urine stream; dribbling after urination;

urgency; frequency
Tx: surgically remove the obstruction
Overflow Incontinence, cont
Causes:
In newborns: posterior urethral valves
In children: stricturesictures

In children: str

In adult men: BPH


In adult women: uterine prolapse and
cystoceles
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Urethra: Penis
Develops dorsal (top) to ventral
(bottom)
Fuses fromom the tip to the base of penis or
is or
clitoris
Hypospadiayp p

Fuses fr the tip to the base of pen

The most common congenital genitourinary abnormality!


Hypospadia ( still zipping)
Located at the base of the penis just next
to the anus
Predisposesedisposes to UTIs

Pr to UTIs

Tx: surgical correction immediately to


prevent UTIs
Circumcision
Done primarily for cosmetic reasons
UTI argument
Penile cancer argument
Should be done in first 48 hours
Clean by pulling the foreskin up, then
clean; pull the foreskin back, then clean
Inflammatory Problems
Phimosis: foreskin is scarred and

adherent to the head of the penis


Paraphimosisaraphimosis: foreskinreskin is scarredred and
adherent to the base of the penis

P : fo is scar and

Tx: urology consult


Infections
Ballanitis ( head of the penis )
Staph Aureus
Urethritis ( dysuria)- infectionection of urethraethra
of ur
Chlamydia Trachomatis # 1 (90% asymp.)
Nisseria Gonorrhea # 2 (90% symp. Men)
(50% symp. Women)
Actinomyces Israelii
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Azythromycin 1gm or 2gm (Chlam + GC)
Ceftriaxone (250 IM)
Cefixemeixeme ( 400 PO)
Cefoxitin (250 IM)

Cef ( 400 PO)

Quinolones (400 PO)


Ciprofloxacin
Ofloxacin
Gatifloxacin
Infections, cont
Cystitis: ( urgency and frequency)
Pyelonephritis: ( WBC Casts)- only nephron
can formrm cast can fo cast
Causes:
E. Coli
Proteus
Klebsiella
Enterococcus: nitrite negative
Nephritis
Pyelonephritis: WBC Casts; sepsis
Interstitial nephritis: drug allergy;
collagenen vascularscular disease collag va disease
Glomerulonephritis: RBC Casts; hematuria
Casts

Urethritis ( dysuria) inf

WBC casts: nephritis


RBC casts: glomerulonephritis
Eosinophil casts: interstitial nephritis
Fat casts: nephrotic syndrome
Waxy casts: chronic renal failure
Hyaline and epithelial casts: normal findings;
represent sloughed off cells, most from the PCT
Crescents: RPGN. Goodpastures or Wegeners
RTAs
Type I: distal H/K exchange is defective
Urine pH is very high; renal stones; UTIs
Type II: proximal CA does not work
Urine pH is very high ( distal H/K exchange still
works)
Can not reabsorb HCO3TYPE III: combines the above two
Urine pH is normal
Type IV: hyporenin-hypoaldosterone syndrome
Seen in diabetics; JG apparatus is infarcted
THE END ! THE END !
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218
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Mking The Connections i Maki Th C
Embryology of the Brain
Primitive Streak
Spinal cord
Notochord
In the first trimester
y Notochord: visible by 3 weeks
y Brain: fully formed by 8 weeks
y Brain is active early with movements,
especially reflexes
y Brain is active in formation of amniotic fluid
Amniotic Fluid

y 80% of amniotic fluid is filtrate from moms


plasma
y Fetus SUBTRACTS by swallowing the y Fetus SUBTRACTS by swallowing the
fluid
y Fetus must absorb and digest the fluid
y 20% is added by the fetus
y Fetus then urinates the additional fluid into
the sac
Polyhydramnios
y AFI
Neuromuscular l disease y N di
y Autonomic dysfunction: dry eyes- Riely Day syndrome
y Muscle disease: in a newborn fasciculation- Wernig
Hoffman syndrome
y GI obstruction
Oligohydramnios
y Renal agenesis
y Urinary outlet obstruction
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Spinal Cord
y Develops from the notochord
y Goes down as far as L-1 or L-2
y End : Conus Medullaris
y Nerves: Cauda equina
y Filum terminalis: anchors
Vertebral Arches
y Fuse ventral to dorsal
y Begins at the cervical level g
y Proceeds bi-directionally
y If child born prematurely, a hole can
be still present at either end
Upper- vertebral arch defects
y Anencephaly no contact to the brain
y Only has the medulla
y Breath 8-10 ipm y Breath 8-10 ipm
y Encephalocele

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 >

spinal canal >


dural sinuses >
back into plasma
CSF Flow
Vomiting Centers
y Chemotactic Trigger Zone: located on
the floor of the 4th ventricle
y Responds to any increase in ICP
y Stimulated by dopamine
Vomiting Centers
y Area Postrema: located on the blood
side of the blood brain barrier (BBB)
y Responds to offensive smells or
taste
y Stimulated by dopamine
Hydrocephalus
y Non-communicating:
y due to an obstruction
y Communicating:
y overproduction of CSF
Communicating Hydrocephalus
y Newborns: mainly premature newborns
y Intraventricular hemorrhage
y Children: due to inflammation
y Meningitis (posterior fossa) CN 3,
9,10,11,12
y Adults: over ingestion of vitamin A
y Pseudotumor Cerebri
Communicating Hydrocephalus
y Elderly: due to brain atrophy
y Normal Pressure Hydrocephalus
y Ventricles enlarge
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Normal Pressure Hydrocephalus
y Ventricles expands as the brain atrophies

y Enlarged ventricles then compress the long midline


fibersibers that go to the bladderadder and legs f that go to the bl and legs
y Triad:
y Dementia
y Incontinence
y Ataxia
y Tx: VP shunt
Noncommunicating Hydrocephalus
y Due to some form of obstruction
y In newborns:
y MCC: Aqueductal stenosis y MCC: Aqueductal stenosis
y 2nd Dandy-Walker cyst
y In children: meningitis, especially TB
y In adults: cancer
y In elderly: cancer
The role of CSF
y To add cushion for the brain
y Shock absorption
y Head Injury
y Coup lesions
y Contracoup lesions worst than the
coup (brain makes CSF for repair)
Neurocutaneous Syndromes
Sturge Weber Syndrome:
y Benign port wine stain- capillaries
y Opthalmic branch of CN V
y Mental retardation
y Seizure
Neurocutaneous Syndromes
Osler-Weber Rendu Syndrome
y Small aneurysmal telangiectasia on
he kin d brane th sk and mucus memb
y Causes GI bleeding
y Pulmonary AV fistula
Neurocutaneous Syndromes
Tuberous sclerosis: benign tumors
y AD
Mental l dation i y M retard
y Seizure
y Retinal angiomyolipoma
y Cardiac rhabdomyoma
y Pancreatic cyst / Coloboma
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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

Amblyopia: difference in visual acuity


Lazy eye
Tx: Patch the eye up to age 5
Weak muscles- CN: 3,4,6

Abnormalities of the Eyes


y Strabismus: misalignment of the eyes
y Isotropia
y Exotropia y Exotropia
Weak muscles of the eye.. Tx. Patch good eye
y
y
y
y

Stigmatism: corneal defect


Straight line card (pt will see a blip in the line)
Convex or a concave defect in the cornea
Laser keratotomy

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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6
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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7
Optic Radiation
Meyers Loop

Monocular Visual Loss


Optic Nerve
L
L
R
R
Monocular blindness
Monocular blindness
y Newborns: cataracts or retinoblastoma
y Children: optic nerve gliomas
y Neurofibromatosis
y MEN III
y Adults: embolic phenomena
y TIA (Amaurosis Fugax)
y Acute retinal artery occlusion
y (white retina, macula has its own blood supply)
y Acute retinal vein occlusion (bluish retina)
y Elderly: macular degeneration
y Receives the smallest arteries of the retina - atherosclerosis
Bitemporal Hemanopsia
L
L
R
R
Optic Chiasm Lesions
Optic Chiasm Lesions
y Pituitary tumors: 90%
y Pituitary sits just beneath the chiasm
y Pineal tumors
y Pineal gland sits just lateral to the
chiasm
y Circadian rhythm - Responds to light
Contralateral
Homonymous
Hemianopia
L
L
R
R

Optic Tract Lesions


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8
Optic Tract Lesions
Mcc: y M
cancers or tumors
Contralateral Superior
Quadrantanopia
L
L
R
R
Contralateral Inferior
Quadrantanopia
L
L
R
R
Contralateral
Homonymous
Hemianopia with
Macula Sparing
L
L
R
R
Quadranopsia
y Can get such a lesion in
the Optic radiation or
Meyers loop Meyer s loop
y Pie in the sky
Frontal Lobe ( Precentral Gyri)
y CST (corticospinal tract) motor fibers
originates from here
y Unique information:
y Personality is stored in the frontal lobe
y Abstract reasoning
y (dont cry over spilled milk)

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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

toward the lesion


Median Midbrain Syndrome
(Weber)
Occlusion of posterior cerebral
artery
CST- contralateral spastic
hemiparesis (upper limb)
Corticobulbar tract- lower face
(contra)
CN3- eye (down and out)
Epidural Hematoma
y Middle meningeal
artery
y Fracture of
temporal bone
y Lucid interval
y Lenticular shape
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Subdural Hematoma
y Bridging vein
y Venous bleed
y Delayed onset
y Shaken baby
y Elderly
y Crescent shape
Subarachnoid Hemorrhage
y Aneurysm rupture
y Worst headache of y Worst headache of
their life
y Bloody spinal tap
THALAMI- SENSORY
y Epithalamus