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USMLE Step 1 Random Facts > Renal > Flashcards

Renal Flashcards

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USMLE® Step 1 flashcards
1
Q

nephrotic synd

A 
massive proteinuria (>3.5g/day, frothy urine), hyperlipidemia, fatty casts, edema; ass. w/ thromboembolism (bc of ATIII loss in urine; present w/ flank pain + hematuria), increase risk of infection
NO RBC OR RBC CASETS IN URINE
FSGS
membranous nephropathy
minimal change dz (lipoid nephrosis)
amyloidosis - ass w/ chronic conditions
MPGN
diabetic glomerulonephropathy
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2
Q

nephritic synd

A

inflammatory!! (hypercellular, inflamed glomeruli from immune-complex dep)
hematuria, RBC casts in urine, azotemia, oliguria, HTN, mild proteinuria

PSGN
RPGN
DPGN
Berger's dz (IgA nephropathy)
Alport synd
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3
Q

FSGS

A
  • segmental sclerosis + hyalinosis (LM)
  • effacement of foot processes (EM)
  • adults (Hisp, Af Am)
  • NO response to steroids
  • ass w/ HIV, heroin abuse, obesity, sickle cell dz
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4
Q

membranous nephropathy

A
  • diffuse capillary + GBM thickening (bc immune-complex dep) (LM)
  • “spike-and-dome” appearance w/ SUBEPITHELIAL deposits [b/w epith cells + BM, under podocytes] (EM)
  • granular IF (w/ IgG + C3 dep)
  • SLE’s nephrotic presentation
  • idiopathic (85%)!!
  • also by use of NSAIDs/penicillamine, Hep C or B, DM
  • Caucasian adults
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5
Q

minimal change dz

A
  • NORMAL glomeruli (LM)
  • foot process effacement - bc of cytokine damage (EM)
  • selective loss of albumin, not Ig
  • may be triggered by recent infection/immune stim
  • children (usually idiopathic)
  • responds to steroids (ONLY ONE)
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6
Q

MPGN

A

type I:

  • granular IF (SUBENDOTHELIAL DEP)
  • tram-track appearance bc GBM splitting (from mesangial ingrowth)
  • thick capillary membranes
  • ass w/ HBV, HCV + subacute bacterial endocarditis

type II:

  • INTRAMEMBRANOUS DEP
  • ass w/ C3 nephritic factor (auto-Ab stabilizes C3 convertase)

**both have granular IF and LARGE HYPERCELLULAR GLOMERULI

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7
Q

diabetic glomerulonephropathy

A

-hyaline arteriosclerosis
-NEG of GBM –> increased permeability, thickening
NEG of efferent arterioles –> increases GFR
GBM thickening, Kimmelsteil-Wilson nodules (ovoid hyaline mass; eosinophilic nodular glomerulosclerosis)
ACE inhibitors slow injury process!!

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8
Q

acute post-strep GN

A
  • type III HST
  • “lumpy-bumpy” appearance (glomeruli enlarged and hypercellular, neutrophils) (LM)
  • SUBEPITHELIAL immune complex humps (EM)
  • granular IF (IgG, IgM, C3 deposition) - decreased C3, normal C4
  • children
  • periph + periorbital edema
  • dark urine
  • after group A-beta strep infection of SKIN (impetigo) or PHARYNX - WEEKS after! + resolves spontaneously
  • elevated ASO titers, or anti-DNase B!
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9
Q

RPGN

A
  • crescent-moon shape (consist of fibrin, plasma proteins like C3b, macrophages, glomerular parietal cells, monocytes) w/in BOWMAN’S SPACE (LM and IF)
  • poor prognosis

can result from:

  • Goodpasture’s synd (type II HST) - linear IF
  • Wegener’s granulomatosis (c-ANCA) - neg IF
  • microscopic polyangiitis, Churg Strauss (p-ANCA) - neg IF
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10
Q

Goodpasture’s synd

A

type II HST
Ab to GBM and alveolar BM
linear IF (C3 and IgG deposited along GBM)
hematuria/hemoptysis

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11
Q

DPGN

A
  • due to SLE (most common cause of death in SLE) or MPGN
  • “wire looping” of capillaries (LM)
  • SUBENDOTHELIAL OR INTRAMEMBRANOUS IgG based immune complexes often w/ C3 dep
  • granular IF
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12
Q

Berger’s dz (IgA nephropathy)

A
  • related to Henoch-Schonlein purpura
  • mesangial prolif (LM); mesangial IC dep (EM)
  • IgA-based immune complex dep in mesangium (IF)
  • NORMAL complement levels
  • presents/flares w/ URI or acute gastroenteritis
  • follows mucosal infection (bc excess prod of IgA)
  • most common nephropathy worldwide
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13
Q

Alport synd

A
  • mut in type IV collagen –> split BM
  • X-linked
  • GN, deafness, eye problems (cataracts, etc.)
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14
Q

early prox tubule reabsorb/secrete?

A

all of glucose and AA
most of bicarb, Na, Cl, phosphate, water (ISOTONIC absorption)
65-80% Na reabsorbed
secretes ammonia (to buffer H)

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15
Q

PTH function in prox tubule

A

inhib Na/phosphate cotransport –> phosphate excretion

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16
Q

thin descending LOH function?

A

passive reabsorp of water (via medullary hypertonicity)

concentrating segment –> makes urine HYPERTONIC!

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17
Q

thin desc LOH impermeable/permeable to?

A

imperm to Na

perm to urea

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18
Q

thick ascending LOH reabsorb?

A

active reabsorption of Na, K, Cl
indirectly reabsorb Mg, Ca (by + lumen potential from K backleak) - paracellular
10-20% Na reabsorbed

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19
Q

thick ascending LOH impermeable to?

A

WATER

makes urine LESS concentrated as it ascends

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20
Q

early distal convoluted tubule (DCT) reabsorb?

A

ACTIVE reabsorb of Na, Cl (urine hypotonic)
5-10% Na reabsorbed
MOST DILUTE SEGMENT

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21
Q

PTH effect on DCT?

A

increase Ca/Na exchange –> Ca reabsorb

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22
Q

DCT impermeable to?

A

water (unless vasopressin levels adeq to promote reabsorp) and urea

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23
Q

collecting ducts reabsorb?

A

Na in exchange for K, H secretion (reg by aldosterone)
3-5% Na reabsorbed
HYPERTONIC

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24
Q

Potter synd?

A 
clubfeet
flat face w/ low-set ears, other facial deformities
pulmonary hypoplasia (most common cause of death)

caused by bilat renal agenesis*** (mostly), ARPKD, posterior urethral valves

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25
Q

most bladder cancers are?

A

transitional cell carcinoma aka UROTHELIAL carcinoma

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26
Q

GFR calc measured by?

A

inulin

creatinine can estimate

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27
Q

PAH best measure of?

A

RPF; underestimated by ~10%

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28
Q

horseshoe kidney trapped under what artery?

A

IMA

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29
Q

RBF =

A

RPF/(1-hematocrit) = (PAH clearance)/(1-hematocrit)

or (renal artery pressure - renal vein pressure)/renal vascular resistance

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30
Q

no ureteric bud =

A

bilat kidney agenesis

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31
Q

horseshoe kidney ass w/ what?

A

Turner’s synd

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32
Q

what property of glomerular filtration barrier lost in nephrotic synd?

A

charge barrier

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33
Q

what keeps negative charge barrier?

A

BM + heparan sulfate

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34
Q

renal clearance =

A

(U x V)/P

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35
Q

FF =

A

GFR/RPF

normally 20%

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36
Q

filtered load =

A

GFR x plasma concentration

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37
Q

glucose reabsorpt?

A

prox tubule via Na/glucose co-transport
@160 mg/dL –> glucosuria (threshold)
@350 mg/dL –> all transporters fully saturated

38
Q

Hartnup disease is?

A

deficiency of tryptophan –> decreased vit B3 –> pellagra

39
Q

in PCT, ATII action is?

A

stim Na/H exchange –> increased Na, H2O, HCO3 reabsorption; secrete H
causes contraction alkalosis!

40
Q

TF/P > 1 when

A

solute absorbed less quickly than water

ex. PAH, Creatinine, inulin, urea, Cl

41
Q

TF/P = 1 when

A

solute + water reabsorbed @ same rate

ex. K, Na

42
Q

TF/P < 1 when

A

solute reabsorbed faster than water

ex. HCO3, AA, glucose

43
Q

functions of ATII

A

potent vasoconstrictor
constricts efferent arterioles –> maintains GFR by increasing FF
stim aldosterone prod, ADH release
increases PCT Na/H activity –> contraction alkalosis
stim hypothal –> thirst

44
Q

ANP effect in kidney

A

increase GFR

decrease renin

45
Q

JG cells are modified what?

A

modified SM of afferent arteriole

46
Q

in renal artery stenosis what happens to JG cells

A

JG cells of affected kidney(s) –> hypertrophy + hyperplasia bc increased release of renin

47
Q

what part of kidney converts to active vit D

A

PCT

48
Q

afferent arteriole mediators

A

prostaglandins - vasodil

NSAIDS - oppose prostaglandins

49
Q

efferent arteriole mediators

A

AT II - vasoconstriction

ACE inhib - oppose AT II

50
Q

protein effects in glomerulus

A

if increased - increases glomerular capillary oncotic pressure –> decreased GFR, FF; no change RPF

if decreased - decreases glomerular capillary oncotic pressure –> increased GFR, FF; no change RPF

51
Q

impt function of ATII to prevent further decrease in vol loss

A

compensatory Na reabsorp. @ PCT and DCT!!!

52
Q

increased serum Mg levels –>

A

decreased DTRs, bradycardia, lethargy, etc.

53
Q

winter’s formula

A

PCO2 = 1.5(HCO3) + 8 +/- 2

54
Q

anion gap =

A

Na - (Cl + HCO3)

normal = 8-12 mEq/L

55
Q

increased anion gap metab acidosis

A 
MUDPILES!
Methanol (formic acid)
Uremia
DKA
Propylene glycol
INH or Iron tablets
Lactic acidosis (ex. in shock)
Ethylene glycol (oxalic acid)
Salicylates (LATE)
56
Q

normal anion gap metab acidosis

A 
HARDASS!
Hyperalimentation (ex.overeating, parenteral nutrition)
Addison's dz
Renal tubular acidosis
Diarrhea
Acetazolamide
Spironolactone
Saline infusion
57
Q

RTA type 1

A

“distal”
defect in collecting tubule ability to EXCRETE H+ [intercalated cells]
urine pH > 5.5
hypokalemia
increased risk for Ca phosphate kidney stones bc of increased urine pH + bone resorption

58
Q

RTA type 2

A 
"proximal"
urine pH < 5.5
defect in PCT reabsorption of HCO3
hypokalemia
increased risk of hypophosphatemic rickets
may be ass w/ Fanconi synd
59
Q

RTA type 4

A

“hyperkalemic”
HYPOALDOSTERONISM or collecting tubule lack of response to aldost
hyperkalemia –> impairs ammoniagenesis in PCT –> decreased buffering capacity + urine pH decreased

60
Q

what 2 synd can present as both nephritic/nephrotic

A

DPGN
MPGN
SLE

61
Q

diff b/w IgA neph + PSGN

A

IgA neph - few DAYS after URI infection

PSGN - few WEEKS after infection

62
Q

complications of kidney stones

A

hydronephrosis (expansion of renal pelvis)

pyelonephritis

63
Q

all kidney stones are radiopaque EXCEPT

A

Uric acid stones = radiolUcent (not seen on x-ray)

view on CT or US

64
Q

lowest pH in nephrons is @

A

DCT

collecting tubules

65
Q

2 factors that prevent crystallization of stones

A
  • citrate (binds free Ca –> facilitates its excretion)

- fluids!

66
Q

calcium phosphate stones

A

alkaline pH
causes: hypercalcemia (cancer, increased PTH, sarcoidosis), Crohn’s
tx = citrate, thiazide diuretics

67
Q

calcium oxalate stones

A

acidic pH
**can result from ethylene glycol (antifreeze) or vit C abuse
other causes: hypercalcemia (cancer, increased PTH, sarcoidosis), Crohn’s
tx = citrate, thiazide diuretics

68
Q

common kidney stone presentation

A

calcium oxalate stones in pt w/ hypercalciuria + normal serum calcium (idiopathic hypercalciuria)

69
Q

ammonium magesium phosphate stones (struvite)

A

alkaline pH
infection w/ urease-positive bugs (Proteus, Staph, Klebsiella)
staghorn calculi (nidus for UTIs)

70
Q

uric acid stones

A

acidic pH
radioLUCENT
from hyperuricemia (gout); seen in dz w/ increased cell turnover like LEUKEMIA
tx = alkalinization of urine

71
Q

cystine stones

A

acidic pH
HEXAGONAL crystals - of sulfur-containing compounds!
2ndary to cystinuria
tx = alkalinization

72
Q

RCC originates from what cells

A

PCT cells - clear cells! (filled w/ lipids + carbs)

73
Q

RCC spread =

A

hematogenously by invading renal vein –> IVC

74
Q

RCC ass w/ what paraneoplastic synd

A

ectopic EPO
ACTH
PTHrP
prolactin

75
Q

Wilm’s tumor (nephroblastoma) contains what cells

A

embryonic glomerular structures (blastema)

76
Q

acute pyelonephritis histo + casts

A

neutrophilic infiltrate

WBC casts

77
Q

chronic pyelonephritis histo + casts

A 
lymphocytic infiltration + corticomedullary fibrosis (scarring)
eosinophilic casts (thyroidization of kidney)
78
Q

drugs implicated in drug-induced interstital nephritis

A

1-2 wks after: penicillin derivatives, diuretics, sulfonamides, rifampin
months after: NSAIDS
chronic interstitial nephritis: lithium, cyclosporine

79
Q

diffuse cortical necrosis ass w/?

A

obstetric complic (ex. placenta abruptio)
septic shock
ARDS

80
Q

acute tubular necrosis features?

A
  • 3 stages (inciting, maintenance, recovery)
  • inj + necrosis of tubular epith cells
  • ass w/ aminoglycosides, cisplatin, amphotericin B, foscarnet, heavy metals, ethylene glycol, crush injury (myoglobiuria), toxins, renal ischemia (shock, sepsis)
  • granular “muddy brown” casts seen**
  • w/ drugs/toxins –> PCT suscept; w/ renal ischemia –> PCT + medullary segment of thick ascending limb suscept
81
Q

in ATN, death occurs usually in what phase

A

inciting

82
Q

maintenance phase of ATN =

A

oliguria
risk of hyperkalemia
1-3 wks

83
Q

recovery phase of ATN =

A

polyuria
risk of hypokalemia (bc of high vol + hypotonic urine)
BUN + serum creatinine fall

84
Q

renal papillary necrosis ass w/

A

DM
acute pyelonephritis + UT obstruction
chronic phenacetin use (ex. acetominophen)
sickle cell anemia/trait

85
Q

prerenal azotemia =

A
  • bc of decreased RBF (ex. hypotension, NSAIDs)
  • Na/H2O and urea retained to conserve vol
  • INCREASED BUN/creatinine ratio
86
Q

intrinsic renal failure =

A
  • cause = ATN or ischemia/toxins
  • patchy necrosis
  • epith/granular casts in urine
  • DECREASED BUN/creatine ratio
87
Q

postrenal azotemia =

A
  • due to outflow obstuction (stones, BPH, neoplasia, etc.) - forces BUN back into blood
  • ONLY w/ bilat obstruction
  • INCREASED BUN/creatinine ratio
88
Q

features of uremia

A 
pericarditis
N/V
asterixis
encephalopathy
platelet dysfunt (qualitative dysfunct; NORMAL platelet count)
INCREASED BUN/creatinine ratio
89
Q

histo in renal osteodystrophy

A

subperiosteal thinning of bones

90
Q

medullary cystic disease

A
  • AD
  • tubulointerstital fibrosis (cysts in medullary CD)
  • inability to conc urine
  • SHRUNKEN KIDNEYS on US

USMLE Step 1 Random Facts (35 decks)

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