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GU Flashcards

1
Q

Development of male and female genitalia

  • what determines sex
  • what determines gonadal and external genitalia differentiation
A
  • genetic, wither XX or XY

- SRY gene

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2
Q

Gonadal Stage

  • primitive gonads: what are they, how are they formed
  • SRY gene
A
  • germ cells; primordial germ cells

- influences gonads to secrete testosterone and Mullerian inhibiting factor

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3
Q

Ductal stage

  • MIF causes
  • mesonephric ducts develop into
  • what is not produced in female embryo
  • what does estrogen do
A
  • regression of he paramesnopehric ducts
  • epididymus, ductus deferens, seminal vesicles
  • MIF and testosterone
  • paramesonephric duct gives rise to uterine tubes, uterus, cervix, and upper vagina
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4
Q

Male and Female equivalents

  • genital tubercle
  • UG folds
  • labioscrotal swellings
  • UG sinus: bot sexes, female, male
A
  • glans penis, clitoris
  • ventral portion of penis, labia minor
  • scrotum and labia majora
  • give rise to the bladder, urethra; skenes ducts (in lower part of urethra that drains alkaline fluid into urethra)/ prostate duct, bartholins glans (in labia majora and produce muco protein secretion through duct) /cowpers glands at base of penis, and lower vagina
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5
Q

Male Vs Female Development

  • mullerian inhibiting factor
  • if not present
A
  • mesnophric persists and paramensonephric die

- paramesonephric persists

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6
Q

Mullerian Inhibiting Factor

  • produced at, by
  • leydig secrete
  • testosterone vs DHT
  • 5- alpha reductase def
A
  • around 8th week gestation, sertoli cells
  • testosterone
  • t: internal genitalia, D: external genitalia
  • normal internal but female outside when born; will be able to develop 2nd sex characteristics at puberty bc of increase of testosterone
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7
Q

Development of Kidney

  • perfusion
  • increases susceptibility
  • division of blood supply
A
  • rate 3-5x of other organs
  • to ischemia and infarcts
  • 90% to cortex and 10% at medulla
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8
Q

Embryo of Kindey

  • metanephros
  • urteric bud
  • vitillene duct
  • allantois
A
  • adult kidney
  • outpouching of mesonephric duct
  • communication between yolk sac and mid gut
  • gas exchange and waste elimination
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9
Q

Phases of development of kidney

  • derived from
  • glomerulus produced by
  • functional by
  • maturation
A
  • nephrogenic chord from urogenital ridge
  • precursors of vasc endo cells position themselves at tip of renal tubules to diff into glomerulus
  • 32-36 wks
  • ascend and elongate the urters as body grows
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10
Q

Metanephros

  • when
  • made from
  • when is renal tubule development signaled
A
  • 5th wk gestation
  • metnephrogenic mesoderm and urteric bud
  • after ureteric bud starts to form it will signal metanephros to begin renal tubule development
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11
Q

Vitelline Duct

  • what is it
  • appears
  • obliterated by
  • vitelline fistula
  • meckels diverticulum: what is it, rule of 2
A
  • long narrow tube joins yolk sac to midgut lumen
  • 4th wk gestation
  • 9th week gestation
  • if duct fails to close, will have digested food and bilious fluid come out of umbilicus
  • persistence of proximal part of vitelline duct; 2 types tissue -> pancreatic and gastric, 2:1 male to female; 2 feet away from illeum
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12
Q

Allantois

  • what is it
  • becomes -> function
  • patent
  • urachal cyst
  • urachal sinus
  • urachal diverticulum
A
  • connects bladder to hindgut and allows for waste elimination of fetus
  • urachus; connection between bladder and umbilicus
  • open communication between bladder and umbilicus -> expel urine from umbilicus
  • failure of central portion of allontois to be obliterated causes extraperitoneal mass located between umbilicus and suprapubic region
  • failure of closure at level of urachus and will get infected
  • failure of close by bladder and urine will get into diverticulum allowing for stone formation
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13
Q

Location of kidneys

  • left
  • right
A
  • L1

- L2, bc of liver

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14
Q

Cortex

  • what is it
  • contains
  • function
  • blood supply
A
  • outermost layer of kidney
  • glomerulus, PCT and DCT
  • isotonic urine
  • 90%
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15
Q

Medulla

  • what is it
  • contains
  • function
  • blood supply
A
  • inner layer kidney
  • LOH, papilla, caylexes, renal pelvis, ureters
  • hypertonic urine
  • 10% blood supply
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16
Q

Ureter blood supply

  • abdominal
  • pelvic
A
  • renal or gonadal -> from aorta

- superior and inferior vesical a -> from internal illiac a

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17
Q

Ureter course

  • abd: begins, UPJ, continues, level of pole of kidney, medial, lateral
  • pelvic: enters, crosses, under, lateral, medial
A
  • retroperitoneal; begins at level of renal a and v but is posterior to them, uretero pelvic junction at 2nd vertebrae; continues ant to psoas and at level of pole of kidney goes under gonadal v; head medially to SI then laterally once they get into pelvis
  • enters pelvis and crosses ant to illiac A, then goes under ovarian vessels laterally to iliac vessels, then go laterally to ischial spines then go medial to get to bladder
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18
Q

Ureter constriction

  • 1
  • 2
  • 3
A
  • uretero pelvic junction
  • mid ureter
  • bladder entrance
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19
Q

Blood supply of kidneys

  • pathway
  • left renal v: size, drains
  • right renal v location
A
  • aorta -> renal a -> segmental a -> interlobar -> arcuate a -> cortical radiate a -> afferent arteriole -> glomerulus -> efferent arteriole -»»>IVC
  • left is longer than r bc has to travel further to ge to to IVC, into renal v and then renal v goes to IVC (predisposed to vericocele) while right goes straight into IVC
  • ant to abd aorta
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20
Q

Filtration membrane

  • endothelial cells
  • GBM
  • podocyte
A
  • fenestrated epi w/ small openings to prevent proteins from getting out
  • type 4 collagen, negatively charged
  • line outer side of basement membrane, have foor processes that also help w filtration
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21
Q

JG apparatus

  • function
  • macula densa: location, function
A
  • detects changes in renal blood flow and produces renin if slower than it should be
  • located in DCT, detects Na and leads to increase of renin release when NaCl detected is decreased
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22
Q

GFR

  • what is it
  • how much reabsorbed
  • how is it calculated
  • what is clearance
  • filtration factor
  • renal plasma flow
A
  • volume of fluid filtered by glomerulus and sent into bowmans capsule / time
  • 99% filtrate will be reabsorbed in nephron
  • clearance of inulin; bc inulin will get filtered but cannot be reabsorbed or secreted
  • [ ] urine * urine vol / [ ] plasma
  • GFR/ renal plasma flow -> should be 20%
  • clearance of PAH -> filtered by glomerulus, cannot be reabsorbed but can be secreted -> represents everything in blood
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23
Q

Glomerular Forces

  • Kf
  • hydrostatic pressure in glomerulus
  • hydrostatic pressure in bowmans capsule
  • oncotic pressure in vessel
  • oncotic pressure in bowmans capsule
A
  • constant due to number of fenestrations in endothelial cells of glomerulus
  • blood being pushed forward in vessel and out into bowmans capsule
  • fluid being pushed back into glomerulus -> pathologic
  • proteins in glomerulus trying to pull fluid back into glomerulus -> pathologic
  • pull fluid into bowmans capsule -> pahtologic
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24
Q

Dilation and constriction of arterioles

  • dilation of afferent art: what does it do, what causes it
  • constrict efferent art: what does it do, what causes it
  • constrict afferent: what does it do, what causes it
  • dilate efferent: what does it do, what causes it
A
  • increases flow in -> increases GFR; prostgalndins, low dose dopamine, ANP, NP
  • decreases flow out -> increase GFR; angiotensin II low dose
  • decrease flow in -> decrease GFR; angiotensin II at high doses, NorEpi, ADH, prostaglandin blockaid (NSAID)
  • increase flow out -> decrease GFR; angiotensin II blockade (ACE i)
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25
Q

Normal Clearance Valuse

  • glucose
  • inulin
  • PAH
A
  • completely reabsorbed
  • not reabsorbed or secreted
  • filtered and then completely secreted
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26
Q

Transport max

- what is it

A
  • once concentration of solute reaches point that all carrier proteins are saturated, then can no longer reabsorb and it will be excreted
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27
Q

What happens in nephron

  • PCT
  • descending LOH
  • ascending LOH
  • DCT
  • CT: what kind of cells and what do they do
A
  • most active reabsorption -> glucose, AA, water, Na, bicarb, potassium, Ca, mg, phosphate, vitamins, and secretion of ammonia
  • permeable to water
  • only permeable to electrolytes (Na, K, 2 Cl, Ca, Mg)
  • Na and water permeability -> reg by aldosterone and ADH; if PTH around then increase Ca and Bicarb reabsorption
  • alpha intercalated (secrete H+ and reabsorb HCO3), beta intercalated (secrete HCO3 and reabsorb H)
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28
Q

Structures involved in osmostic gradient

  • loop
  • vasa recta
  • collecting ducts
A
  • created gradient
  • preserves gradient
  • use gradient
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29
Q

Aldosterone

  • function
  • how
A
  • increase Na and H2O re absorption and secrete K

- increase synthesis and concentration of Na/K pumps

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30
Q

ADH

  • function/ how
  • what kind of pathway is used
  • effect of EtOH
A
  • stimulates V1 (vasoconstriction) and V2 (production and insertion of AQ2 through Gs pathway -> increased water reabsorption)
  • supresses release -> produce high volume of dilute volume -> peeing out lots of water -> dehydrating -> makes you want to drink more
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31
Q

Diuretics

  • carbonic anhydrase inhibitors
  • osmostic
  • loops
  • Thiazides
  • ADH antagonist
A
  • in PCT
  • PCT
  • LOH
  • DCT
  • CT
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32
Q

Carbonic anhydrase inhibitor

  • MOA
  • examples
  • indications: mountain sickness, glaucoma, stones
  • SE
A
  • prevent H and bicarb from being made from carbonic acid -> H cant get pushed into lumen and exhanged for Na -> if Na stays in lumen so will water -> Na combines with Bicarb in lumen and alkanalizes it causing acidosis in body
  • acute mountain sickness -> the hypoxia causes edema and resp alkalosis -> will get rid of water and cause met acidosis balancing out the resp alkalosis and causing normal pH
  • bicarb needed for production of aq humor
  • met acidosis, renal stones (Ca and PHosphate bc of alkanalized urine), renal K wasting (bc Na-Biacarb formation causes decreased Na which increases renin); inhibits conversion of NH3 to NH4 -> hepatic encelopahty
  • Acetazolamide
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33
Q

Loops

  • MOA
  • examples
  • indications
  • tox: OH DANG
  • Bartter syndrome: what is it, looks like, BP
A
  • blocks triple transporter -> osmotic gradient for water reabsorption decreased; also stimulate release of prostaglandins
  • furosemide, torsemide, bumentanide or ethacrynic acid (non sulfa)
  • CHF, pulm edema, edema, hypercalcemia, severe htn, forced diuresis for drug/chemical intoxication
  • ototox, hypokalemia (both from triple transporter and renin), dehydration, allergy (sulfa -> also for preg bc of kernicterus), nephritis, gout (not peeing out uric acid); hypokalemic met alkalosis (bc once K gets too low it will trade K for H)
  • triple transporter doesnt work, looks as if on loop but not, BP will be normal or low
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34
Q

Mannitol

  • MOA
  • where it works
  • indication
  • central pontine myelinolysis
A
  • osmostic diuretic, pulls fluid from interstitum and intracellular spaces and moves back into lumen
  • PCT and descending LOH
  • increased intracranial pressures
  • if given too fast will cause fluid to leave cells to go into vasc and if too fast will cause demyelination of pons -> locked in syndrome
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35
Q

Thiazides

  • examples
  • kind of drug
  • secretion and location they work
  • MOA
  • electrolyte effects
  • AE: effect on DM, affect on lipids
  • indication
A
  • HCTZ, chlorothiazide
  • sulfa drug
  • secreted into PCT but exert effects on DCT
  • block Na-Cl symporter -> decrease water reabsorption
  • increase Na/ Cl excretion, decrease Ca excretion, inhibit uric acid secretion (watch out for gout), increase Mg excretion
  • sex dysfunction, worsening of DM (Na/ Cl not reabsorbed -> low Na -> increase in renin -> low K -> no depolarization in beta cells -> Ca not allowed into cell and no insulin release); insulin blocks hormone sensitive lipase and since there is decrease in insulin then will have release of stored triglycerides
  • HTN, CHF, edema, nephrogenic diabetes insipidus
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36
Q

Potassium Sparing Diretics

  • MOA
  • aldosterone antagonist
  • when are they used
  • benefit of spironolactone
  • indications
  • contraindications
  • AE
A
  • Na channel inhibitor -> Na and water excretion -> K spared; amiloride, triaterne
  • no increase in Na/ K atpase; spironolactone
  • in combo w/ other diuretic bc it is weak diuretic, just helps to stop hypokalemia
  • prevents myocardial hypertrophy and myocardial fibrosis
  • heart failure, aldosteronism caused by cirrhosis
  • can never be taken with ACE i, and ARB (increase K by inhibiting RAAS), NSAID (decrease renin secretion), K+ supplementation
  • hyperkalemia, gynecomastia, menstrual disturbances, decreased libido
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37
Q

SIADH

  • what is it
  • common cause
  • effects on blood
  • effect on urine
  • TX
A
  • increase ADH -> excessive water reabsorption in kidneys
  • small cell lung CA; produces similar to ADH w/o negative feedback
  • dilute blood -> hyponatremic, hypervolemic
  • hypervolemia causes decrease of RAAS -> decrease reabsorption of Na and water -> so water begins to balance out but Na will still be low
  • ADH antagonist -> conicaptan (v1 and v2) other vaptans only block V2; demeclocyline and lithium will inhibit action of ADH at some point distal to cAMP
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38
Q

Diabetes Inspidus

  • sxs
  • psychogenic: cause, dx, tx
  • nurogenic: caused by, dx
  • nephrogenic: caused by,
  • managment
  • tx
A
  • polyuria and polydipsia
  • excess fluid intake causing them to be hypervolemic and suppresses release of ADH (bc of defect in thirst mech of hypothalamus), restricting fluid for 24 hr will concentrate urine,
  • post pit -> cannot secrete ADH; give synthetic ADH and will concentrate urine
  • kidney cannot respond to ADH (lithium);
  • admit -> do basline UA -> restrict water (if concentrates then psychogenic) -> give desmopressin (if [] then neurogenic but if no concentration then nephrogenic)
  • thiazide -> pee out Na and water so slowly decrease serum Na and serum osmolarity so no more trigger for thirst
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39
Q

Compartments for water

  • intracellular
  • extracellular: includes
A
  • 60%

- interstitial and plasma, 40%

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40
Q

Dehydrated pts

  • never give
  • correct tx
  • when to give hypertonic
A
  • hypertonic solution
  • normal saline: push fluid into cell
  • hyponatremic w/ sxs
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41
Q

How to answer body water questions

  • loss of isotonic fluid: ex, what is affected
  • gain of isotonic fluid: ex, what is affected
  • loss hypotonic fluid: ex, what happens, fix
  • gain of hypotonic fluid: ex, what happens
  • gain of hypertonic fluid
  • loss hypertonic fluid
A
  • vomiting, diarrhea, hemorrhage; only vascular volume is decreased, concentration remains the same -> since concentration remains same fluid will not move
  • administration of isotonic saline; only vascular space affected
  • dehydration, DI, alcohol; osmolarity increases of blood -> water from cell move out to help, shrinkage of cells, give isotonic fluid
  • water intoxication or giving hypotonic saline; fluid gain in vascular space, dilute blood, water moves into cell -> cellular swelling
  • hypertonic saline, mannitol use; increase osmolarity in vasculature, fluid pulled from ICF into vascular -> cell shrinkage
  • loop diuretics, thiazide diuretics, addisons dx; intravascular decreased and osmolality decreased, intracellular is more concentrated -> cell swelling
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42
Q

RAAS

  • regulated by
  • pathway
  • when
A
  • macula densa, intra-renal baro receptore, beta adrenergic pathway (B1)
  • renin makes angiotensinogne turn into angiotensin I -> angiotensin I goes to lungs and is turned into angiotensin 2 by ACE -> angiotensin II will cause vasoconstriction and release of aldosterone (retention of Na, Cl and water)
  • when in low fluid or low pressure state
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43
Q

Renal artery stenosis

  • what is it
  • sequalae
A
  • chronic low flow to kidney causing atrophy and fibrosis -> activates RAAS and always on
  • secondary HTN
44
Q

ACE i

  • suffix
  • MOA
  • AE
  • heart effects
  • indication
  • contraindication
A
  • pril
  • block angiotensin converting enzyme; will also dilate efferent arteriole
  • no aldosterone so holding on to K; cough (bc accumulation of bradykinin), rise in creatinine (because decreases GFR)
  • increase in cardiac output and stroke vol
  • started in all diabetics with proteinuria, HTN, CHF, renal failure, left ventricular hypertrophy (to decrease resistance and amnt work heart has to do)
  • never give to someone with bilateral renal a stenosis bc will drop GFR too mcuh and will go into kidney failure
45
Q

ARB

  • suffix
  • MOA
  • uses
A
  • artan
  • angiotensin 2 receptor antagonist
  • HTN, CHF, diabetic nephropathy
46
Q

Acidosis

  • causes
  • anion gap vs non
A
  • low HCOs or high PCO2

- MUDPILES or HARDASS

47
Q

Alkalosis

- causes

A
  • low PCO2 or high HCO3
48
Q

Anion Gap

  • what is it
  • normal value
  • what happens in met acidosis w/ anion gap
  • what happens in met acidosis w/o anion gap
  • increased
  • normal
A
  • diff between anion and cation in blood
  • (Na+K) - (Cl+HCO3)
  • 12-16
  • increase in acid -> bicarb being used -> incerase in anion gap
  • increase in acid -> bicarb being used but chlorine compensates
  • MUDPILES
  • HARD ASS
49
Q

acute vs chronic resp acidosis

  • what happens
  • compensation during acute
  • compensation during chronic
  • caused by
A
  • increase in CO2
  • cells -> not good, can only make 1 bicarb for every 10 pts that pCO2 has gone up
  • kidneys compensating -> better bc can make 1 bicarb for every 3 pCO2
  • opiates, stroke to brain stem, head injury w/ increased ICP, infection that affects movement of diaphragm; foreign body aspirated, mechanical hypoventilation
50
Q

metabolic alkalosis

  • what happens
  • compensation
  • ratio
  • causes
  • Conns syndrome: what is it, management
  • thiazide / loop
  • saline responsive
  • saline unresponsive
A
  • increase in bicarb -> losing H+ ions making it look like increase in HCO3
  • decrease resp rate -> resp acidosis
  • for every 2 bicarb made, 1 pCO2 exhaled
  • vomiting, or NG tube that sicks out gastric contents
  • hyper aldosteronism -> alodosterone is causing to reabsorb Na and kick out K -> hypo kalemia -> start reabsorbing K and trade it for H+ -> loss H+ -> met alk; aldosterone receptor block, remove tumor
  • same mech -> work through RAAS
  • if associated w/ RAAS (low volume) -> then saline will stop problem
  • CONNs syndrome bc saline will not stop the secretion of aldosterone
51
Q

resp alkalosis

  • caused by
  • acute compensation
  • chronic compensation
A
  • hyperventilation -> decrease in pCO2
  • buffering from cells -> can only decrease bicarb 1 pt for every 5 pCO2 dropped
  • kidney now comepnsating -> beta intercalated cells getting rid of bicarb
52
Q

Increase anion gap acidosis

  • M
  • U
  • D
  • P
  • I
  • L
  • E
  • S
A
  • Methanol
  • Uremia
  • DKA
  • Paraldehyde
  • Isoniazide
  • Lactic acid
  • Ethanol, ehtylene glycol
  • Salicylates
53
Q

Non anion gap met acidosis

  • H
  • A
  • R
  • D
  • A
  • S
  • S
  • i
A
  • hyperalimentation -> total parental nutrition
  • addisons
  • renal tubular acidosis
  • diarrhea
  • acetazolamide
  • spironolactone
  • saline
  • illeostomy -> not able to reabsorb bicarb in colon
54
Q

Aldosteone Escape

  • Conns syndrome chronically
  • ACEi
A
  • over time aldosterone stops having effect bc receptors stop responding
  • ACEi can’t block aldosterone anymore -> 40% pts -> will have to switch drugs
55
Q

Mixed acid base disorder
- what is it
when to expect

A
  • indicated simulataneous presence of > 1 acid/ base disturbances
  • inadequate or extreme compensation, pCO2 and HCO3 move in opp directions
56
Q

Aspirin

  • overdose causes
  • compensation
  • tx
A
  • met acidosis and lungs respond w/ resp alkalosis
  • kidneys will compensate to the resp alkalosis by excreting bicarb but acid still on board so then develop met acidosis
  • activated charcoal and alk urine
57
Q

Renal Tubular Acidosis

  • type 1: what is it, what happens to HCO3 and K, urinary pH, urine anion gap
  • type 2: what is it, what happens to HCO3 and K, urinary pH, urine anion gap
  • type 4: what is it, what happens to HCO3 and K, urinary pH, urine anion gap
  • urine anion gap
A
  • impaired distal H+ excretion -> alpha intercalated cells do not work -> increase in H+ -> bicarb low bc need to neutralize H -> also have to get rid of positive charges someway so will excrete K+; urinary ph > 5.5; + urine anion gap
  • reduced bicarb reabsorption in PCT -> bicarb is really low; k is low (only if fanconi syndrome because reabsorption in PCT would be affected) or normal; urinary pH < 5.5 bc can secrete H+; no anion gap bc shouldnt be elevated levels of Na or K
  • aldosterone resistance or decrease in secretion -> elevation in K levels; mild acidosis bc decrease ability to secrete H -> looks like elevated bicarb; yes
  • suggests low NH4 bc suggests low levels of Cl
58
Q

Acute Kidney injury

  • pre renal: BUN:CR, urine Na, FENa; epi
  • renal
  • post renal
  • acute interstitial nephritis
  • renal insuff + HTN tx
  • initiation phase
  • maintenance phase
  • recovery phase: what is it; managment
A
  • something wrong with blood flow; BUN: CR ratio > 20; urine Na<20; Fractional excretion of Na <1; most common -> usually bc dehydration
  • something wrong with kidney parenchyma; BUN: CR ratio < 20; urine Na>20; Fractional excretion of Na > 2
  • obstruction of urine outflow; BUN: CR ratio < 20; urine Na>20; Fractional excretion of Na > 2
  • fever, maculopapular rash, sxs of acute renal failure after starting on beta-lactam antibiotic
  • fenoldopam -> domapine 1 receptor agonist -> dilation of afferent a and naturesis + peripheral dilation (drop BP)
  • GFR falls and urine decreases
  • GFR stabilizes. lasts 1-2 wks
  • epithelial cells replace themselves, polyuria (bc medulla is messed up) and gradual normalization of GFR; will need tons of IV fluid to keep up with urine output and don’t get dehydrated
59
Q

Urine output

  • oliguria
  • anuria
A
  • below 400 cc day

- below 100cc/day

60
Q

Acute Tubular Necrosis

  • what is it
  • sequlae
  • findings
A
  • ischemia triggers hypoxic changes in tubular epi cells especially in PT and thick ascending ascending limb
  • decrease functional capacity of kidney
  • muddy brown cast -> consists of dead epithelial cells
61
Q

Pre-Renal Azotemia

- causes: volume, cardio, decreased oncotic, renal a vasoconstriction, decrease vasc resistance

A
  • dehydration, burns, diarrhea; hypotension, CHF, tamponade, low albumin, nephrotic syndrome, cirrhosis, NSAIDS, ACEi’s, shock
62
Q

Significance of BUN:CR

  • what is BUN
  • what is creatinine
  • normally
  • what happens when blood flow down
A
  • by product of protein metabolism
  • by product of muscle metabolism
  • more creatinine absorbed
  • absorb lots more BUN than creatinine
63
Q

Intra-renal azotemia

  • caused by
  • difference
  • drugs
  • crystals
  • other
A
  • acute tubular necrosis
  • damage to tubules is less severe than pre-renal
  • ampho B, aminoglycoside, cisplatin,
  • uric acid crystals, oxalate stones,
  • crush injuries -> release myoglobin which can damage kidneys by precipitating in kidney tubules
64
Q

Post renal azotemia

- what is it

A
  • outflow obstruction -> bot must be affected
65
Q

Renal Failure Tx

  • 1
  • 2
  • dialysis w/
A
  • correct and balance fluids and electrolytes
  • discontinue all offending meds
  • acidosis, K > 6.5, lithium intoxication, fluid overload, uremic sx of encephalopathyh and pericarditis
66
Q

NSAID nephropathy

  • caused by
  • how
A
  • prolonged use of NSAIDs
  • NSAID concentrated in medulla -> inhibit prostaglandin cause constriction of medullary vasa recta -> interstitial nephritis
67
Q

Nephrotic VS Nephritic

  • urine casts
  • proteinuria
  • hematuria
  • why is proteinuria important
A
  • nephrotic: fatty, nephritic: RBC
  • more than 3.5 g/ day; less than 3.5
  • maybe; definitely
  • liver can only make up to 3.5 g/ day so liver has to go into over drive in nephrotic syndrome
68
Q

Nephritic

  • sxs
  • dx
  • managment
  • syndromes
A
  • HTN, Macro/micro hematuria, oliguria, edema
  • UA (hematuria), biopsy of kidney, check for AI process (complement, ANCA, Anti-GBM)
  • diuretics / dialysis; fluid and salt restriction; corticosteroid if AI
  • post strep, good pastures, rapidly progressive, IgA, membranproliferative
69
Q

Post Strep

  • caused by
  • prognosis
  • specific sxs
  • labs
  • MS: light, electric
A
  • step pyo, seen with either strep throat or strep skin ifection
  • 95% will recover
  • peripheral and peri-orbital edema
  • anti- strep O titers or anti-DNAse B titers, decreased C3 and complement
  • hypercellularity with PMNS, sub epi lumps and bumps (made from immune complexes and complement)
70
Q

Good pastures

  • what is it
  • progresses to
  • LM
  • IF
A
  • anti-glomerular BM dx -> type 4 collagen
  • RPGN
  • hyperccelularity
  • linear deposits on BM
71
Q 
Wegners Granulomatosis
- affects
- causes
- marker
-
A

kidney, lung, nose/sinuses

  • epistaxis, rhinitis, perforation, pulm infiltrates, cavitary lesion, pulm hemmorrhage
  • cANCA -> targets protinase 3 on PMNs
72
Q

IgA nephropathy

  • presentation
  • Diff from Henoch-Schonlein purpura
  • LM
A
  • painless hematuria 2-3 days after URI
  • HCP will have abd pain and pruritic skin lesions
  • hypercellularity and mesangial proliferation
73
Q

Membranoproliferative

  • what is it
  • appearance
  • type 1
  • type 2
  • type 3
A
  • mesangial deposits and thickening of GBM
  • tram track appearance
  • most common, immune complexes deposited sub-endothelial and mesangial
  • similar to type 1 but with alt pathway
  • rare
74
Q

Nephrotic Syndromes

  • proteinuria: amount, leads to
  • sxs
  • caused by
  • management
A
  • greater than 3.5 -> albumin is lost -> liver tries to compensate for protein loss by making more lipids -> hyperlipidemia
  • edema, ascites, foamy urine, hypercoagulable
  • DM, lupus, amyloidosis
  • salt restriction, protein restriction with mild or protein supplementation with severe, diuretics, ahti-hyperlipidemic drugs, ACEi for diabetics, pneumo vaccine
75
Q

Membranous glomerulonephritis

  • what is it
  • secondary causes
  • EM
A
  • immune complexes get deposited in subepithelial space -> IgG or antibodies
  • SLE, Hep B, syphilis, meds, CA
  • spikes and domes
76
Q

Minimal Change

  • epi
  • what happens
  • EM
  • TX
A
  • children
  • loss of foot processes that normally repel albumin
  • loss of foot processes
  • Prednisone and ACEi -> decrease proteinuria
77
Q

Focal Segmental

  • what is it
  • associated w
  • sequale
A
  • small foci of glomerulus affected
  • AIDS and sickle cell
  • collapsing -> high risk ESRD; glomerular tip lesion -> low risk ESRD
78
Q

Amyloidosis

  • what is it
  • LM
A
  • amyloid proteins deposit in mesangium and GBM

- congo red stain of the proteins

79
Q

Nodular glomerulosclerosi

  • hx of
  • KW nodules
  • LM
  • TX
A
  • DM
  • pink eposits in glomeruli bc of hyaline atherosclerosis
  • nodular sclerosis of glomerulus with BM thickening
  • ACEi and ARB -> slow down proteinuria
80
Q

UA

  • eosinophils
  • RBC
  • WBC/ bacteria
  • Crystals
  • bence- jones
    • blood, - RBC
  • fat
  • abrupt onset of gross hematuria in Sickle Cell
A
  • drug induced hypersensitivity -> cepahlosporin
  • glomerulonephtitis
  • infection
  • bifringent -> gout;
  • mult myeloma
  • myoglobinuria -> coca cola urine -> crush injury, reperfusion injury, someone exercised too much
  • nephrotic
  • papillary (where CT enters kidney) necrosis -> can also be caused by DM, pyelonephritis or NSAID
81
Q

Casts

  • WBC
  • RBC
  • Eosinophil
  • Fat
  • Waxy
  • hyaline and epi cells
  • crescent shaped
A
  • acute pyelonephritis
  • glomerulonephritis
  • interstitial nephritis
  • nephrotic syndrome
  • chronic end stage renal dx
  • normal
  • RPGN, good pastures
82
Q

Kidney Stones

  • calcium
  • struvite
  • uric acid
  • cysteine
  • presentation
  • dx
A
  • radiopaque, colorless; octahedrone; 70-80% of time; thiazide diuretic and acidify urine
  • Mg ammonium sulfate; radio paque; coffin lid; form stagohorn claculi; urease + bacteria
  • radiolucent; diamond and rhombus shapes; rapid cell division (CA, burns, trauma)
  • radiopaque; flat, yellow, hexagon; reduce salt and protein from diet and alkanalize urine
  • painful hematuria, flank pain that radiates down to groin
  • xray w/o contrat or US for uric acid stone
  • saline and opiate for pain;
  • < 5mm pass on own , litho tripsy 5-10, >1cm surgery
83
Q

Horshoe Kidney

  • genetics
  • what is it
  • sxs
  • sequalae
A
  • congenital
  • central portion of kidneys remain fused during embryogenesis
  • asymptomatic usually; can have abd discomfort, UTI and kidney stones
  • cannot ascned correctly bc get caught on IMA
84
Q

Pelvic Kidney

  • what is it
  • sxs
  • dx
  • problem
A
  • kidney does not ascend properly during development
  • asymptomatic
  • incidental
  • less protection of kidney, be careful w/ sports
85
Q

Size discrepancies

  • normal
  • too small
  • too large
A
  • renal a stenosis

- polycystic kidney

86
Q

Renal A stenosis

  • caused by
  • fibromuscular dysplasia
  • side
  • when do sxs present
  • dx
  • Tx: use, avoid
A
  • atheroclerosis (smoking, HTN, dyslipidemia, DM)
  • fibrotic tissue in renal a -> will see stenosis and then dilation of a
  • unilateral
  • 50% stenosis
  • ultrasoundST, MRA, angiography
  • CCB, statins, angioplasty, bypass, avoid ACEi,
87
Q

Polycytic Kindey Dx

  • adult: inheritance, genes, sxs, risk, progresses
  • infantile: inheritance, side, sxs,
  • DX
  • Management
A
  • AD, PKD1, 2,3 genes, presents with HTN and renal failure; high risk subarrachnoid hemm bc it is associated w/ berry aneursyms, will progress to renal failure
  • AR, unilatera, no HTN or renal failure
  • US
  • supportive; kidney transplant
88
Q

Medullary Cystic Kidney

  • childhood
  • adult
  • what happens
  • side
  • sxs early
  • sxs late
  • dx
  • tx
A
  • AR; growth retardatoin and ESRD before 20 yrs old
  • AD
  • cystic dilation of CT
  • bilateral
  • polyuria, pallor (cortex fibrotic -> decrease in EPO), lethargy
  • HTN
  • US, show small, scarred kidney
  • have renal salt wasting so diet high in salt and water; no therapy will prevent progression to renal failure
89
Q

Medullary sponge dx

  • inheritance
  • gene
  • what happens
  • sxs
  • dx
  • tx
  • prognosis
A
  • AD
  • MCKD 1 or 2
  • cysts in medullary collucting duct, cortex is spared
  • polyuria, polydipsia, nephrocalcinosis, type 1 distal renal tubular acidosis
  • US or CT
  • thiazide (for hypercalciuria) to prevent kidney stones
  • excellent
90
Q

Pyelonephritis

  • what is it
  • how
  • histo
  • sxs
  • caused by
  • tx uncomplicated cystitis
  • tx uncomplicated pyelonephritis
  • severe pyelonephritis
A
  • infection of kidney
  • ascending
  • massive interstitial infiltration of PMNs
  • dysuria, frequency, urgency, suprapubic pain, fever, pain, flank pain, CVA tenderness
  • E. coli and E. faecalis
  • nitrofurantoin or TMP-SMX
  • fluoroquinolones
  • IV fluoroquinolones, cephalosporin, penicillin
91
Q

Hydronephrosis

  • what is it
  • acute caused by
  • chronic sxs
  • newborn caused by
  • children MCC
  • teenager MCC
  • adult male MCC
  • adult female MCC
  • hysterectomy
A
  • urine outflow obstructed
  • kidney stones
  • asymptomatic
  • posterior urethral valves -> retrograde flow and ejaculation or malimplantation of ureters
  • UTI
  • urethral valve stricture from STD
  • BPH
  • cystocele or uterine prolapse
  • when ligating uterine a also catch ureter -> kidney will continue to make urine but cant drain; flank pain that radiates to groin w/ hx of recent surgery
92
Q

BPH

  • what is it
  • caused by
  • sxs
  • epi
  • DX
  • TX
  • androgenic alopecia
A
  • hyperplasia of prostate stroma
  • androgen and 5 alpha reductase -> forms DHT -> stimulates prostate growth
  • urinary hesitancy, frequency, retention and increased risk of UTI
  • men > 70 yrs old
  • sits between pubic bone and anal canal
  • compresses prostatic urethra
  • DRE -> symmetrically nodular prostate
  • 5-alpha reductase blockers -> prevent formation of DHT or trans-urethral resection of prostate
  • DHT causes baldness -> blocking will allow for hair growth
93
Q

Prostatic CA

  • sxs
  • DRE
  • staging
  • tx
A
  • urinary urgency, frequency, nocturia and hesitancy, w/ chronic lower back pain
  • asymmetric nodular enlargement of prostate, will find dominant nodule with boggy prostate
  • 1: located one side prostate, 2: located on both sides prostate, 3: tumor has spread through capsule of prostate, 4: mets, regional nodal involvement
  • removal of prostate, radiation, hormonal therapy, chemo
94
Q

TURP AE

  • TURP syndrome
  • Pudendal N
  • Urinary incontenence
  • retrografe ejaculation
A
  • hyponatremia caused by water intoxication bc water is reabsorbed though prostatic sinusoids
  • injured -> impotence
  • damage to external sphincter
  • damage to internal sphincter
95
Q

Renal Cell CA

  • epi
  • sxs
  • known as
  • histo
  • tx
A
  • male, smokers
  • gross hematuria w/ falnk pain, palpable mass, hematuria, feverm secondary polycythemia
  • clear cell CA bc CA cells have hogh lipid content
  • round or polygonal shape
  • resection of mass
96
Q

Wilms Tumor

  • epi
  • sxs
  • histo
  • WAGR dx
  • TX
A
  • children
  • large palpable flank mass
  • epi cells, blastema cells (solid sheets, smal blue round cells; least differentiated and most malignant), stromal cells
  • wilms tumor, aniridia, GU malformation, retardation
  • nephrectomy w/ chemo or radiation
97
Q

Bladder CA

  • cell type
  • sxs
  • dx
  • staging
  • risks
  • tx
A
  • transitional epi
  • painless hematuria
  • cytoscopy to see mass
  • based on involvment of detrussor muscle; 1: no muscle involvement, 2: muscle invovled but not all way through, 3: all way through muscle but not into fat, 4: through muscle and into fat and involves LN
  • smoking, aflatoxin, cyclophosphamide
  • surgery, radiation
98
Q

exstrpohy of bladder

  • what is it
  • what happens
  • t x
A
  • congenital anomaly
  • failure of abd wall to close
  • bladder exteriorized; pt cannot get rid of urine and will need to be cathed
  • surgery
99
Q

cystocele

  • what is it
  • sxs
  • why
  • dx
  • 1: what is it, tx
  • 2: what is it, tx
  • 3 : what is it, tx
A
  • bladder herniate posterior into vagina
  • urinary leakage or incomplete bladder empyting
  • pubocervical ligament gets stretched with mult vaginal deliveries allowing for bladder to tilt back
  • voiding cystourethrogram -> series of xrays while pt voiding urine
  • mild herniation into vagina -> no sxs; kegel exercises to strengthen muscle of pelvic floor to support bladder
  • bladder sinks into vag opening; pessary pushes bladder anterior
  • bladder bulges out of vaginal opening; surgical correction to reconstruct pelvic floor in order to keep bladder in correct position
100
Q

Micturition reflex

  • what is it
  • sacral micturition center
  • pontine micturition center
  • cerebral cortex
A
  • coordinated contraction of detrussor muscle at same time that urinary sphincter have relaxed
  • s2-4, PNS, M3 receptor, contraction of detrssor muscle
  • located in pontine reticular formation -> coordinates relaxation of external urethral sphincter with bladder contraction to void
  • inhibits pontine micturition center
101
Q

Incontinence

  • urge: what is it, caused by, specail tx kids/ adults; also need
  • normal pressure hydrocephalus: what happens, epi, sxs
  • stress: what is it, caused by, tx
  • overflow: what is it, what happens, sxs, tx
  • tx
A
  • feel like they need to urinate all time; caused by increased detruser acticity -> spasticity of bladder; imipramine: TCA w/ anticholinergic properties decreasing ladder contraction; oxybutynin -> blocksAch at receptor to decrease contraction of bladder; urination schedule
  • decreased CSF absorption causes increase in vol of CSF causing symmetric enlargement of all ventricles -> push on periventricular pathways causing disruption of pathways from cortex to central micturition reflex; elderly pts; wet, wacky wobbly
  • weak pelvic floor causes leakage w/ increased abd pressure; obesity; kegel exercises of pseudoephedrine to stimulate sphincter constriction
  • anatomical obstruction; bladder ca pacity decrease, detrussor activity decreased, sphinter pressure increased; weak urinary steream w/ driblling and urgency/frequency; surgical correction
  • kegel exercises
102
Q

Cystitis

  • seen in
  • most common causes
A
  • females, elders, catheters
  • E. coli and S. saprophiticus or enterococcus if nitrite negative
  • dysuria, urgeny, lower abd pain
  • TMP-SMX (bactrim) of fluoroquinolone
103
Q

Hemmorrhagic cytitis

  • caused by
  • prevent w
A
  • chemo meds bc produce acrolein which is toxic to epi of bladder and leads to death of tissues
  • stay hydrated and use MESNA which inactivates acrolein
104
Q

Penis development

  • begins and ends
  • early termination causes; sequale; tx
A
  • dorsally to ventrally and then fuses

- hypospadius ; UTI; surgery

105
Q

Common penile inflammatory prblems

  • balantitis
  • phismosis
  • paraphimosis
  • tx
A
  • inflammation of foreskin and head of penis; s aureus
  • scarring of foreskin and adheres to head; unable to retract foreskin
  • scarring of foreskin and adheres to base; unable to return foreskin
  • urology consult
106
Q

urethritis

  • most common cause
  • sxs
A
  • chlamydia and gonorrhea

- dysuria

107
Q

cryptochordism

  • what is it
  • managment
  • damages
A
  • undescended tetsicle
  • give them to 1 yr old to see if it will descen by itself, if not will have to remove
  • increased temp will damage semineferous tubules

Boards II (20 decks)

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