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USMLE Step 1 Random Facts > Renal > Flashcards

Flashcards in Renal Deck (90):
1

nephrotic synd

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

2

nephritic synd

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

3

FSGS

-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

4

membranous nephropathy

-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

5

minimal change dz

-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)

6

MPGN

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

7

diabetic glomerulonephropathy

-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!!

8

acute post-strep GN

-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!

9

RPGN

-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

10

Goodpasture's synd

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

11

DPGN

-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

12

Berger's dz (IgA nephropathy)

-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

13

Alport synd

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

14

early prox tubule reabsorb/secrete?

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

15

PTH function in prox tubule

inhib Na/phosphate cotransport --> phosphate excretion

16

thin descending LOH function?

passive reabsorp of water (via medullary hypertonicity)
concentrating segment --> makes urine HYPERTONIC!

17

thin desc LOH impermeable/permeable to?

imperm to Na
perm to urea

18

thick ascending LOH reabsorb?

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

19

thick ascending LOH impermeable to?

WATER
makes urine LESS concentrated as it ascends

20

early distal convoluted tubule (DCT) reabsorb?

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

21

PTH effect on DCT?

increase Ca/Na exchange --> Ca reabsorb

22

DCT impermeable to?

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

23

collecting ducts reabsorb?

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

24

Potter synd?

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

25

most bladder cancers are?

transitional cell carcinoma aka UROTHELIAL carcinoma

26

GFR calc measured by?

inulin
(creatinine can estimate)

27

PAH best measure of?

RPF; underestimated by ~10%

28

horseshoe kidney trapped under what artery?

IMA

29

RBF =

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

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

30

no ureteric bud =

bilat kidney agenesis

31

horseshoe kidney ass w/ what?

Turner's synd

32

what property of glomerular filtration barrier lost in nephrotic synd?

charge barrier

33

what keeps negative charge barrier?

BM + heparan sulfate

34

renal clearance =

(U x V)/P

35

FF =

GFR/RPF

normally 20%

36

filtered load =

GFR x plasma concentration

37

glucose reabsorpt?

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

38

Hartnup disease is?

deficiency of tryptophan --> decreased vit B3 --> pellagra

39

in PCT, ATII action is?

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

40

TF/P > 1 when

solute absorbed less quickly than water
ex. PAH, Creatinine, inulin, urea, Cl

41

TF/P = 1 when

solute + water reabsorbed @ same rate
ex. K, Na

42

TF/P < 1 when

solute reabsorbed faster than water
ex. HCO3, AA, glucose

43

functions of ATII

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

ANP effect in kidney

increase GFR
decrease renin

45

JG cells are modified what?

modified SM of afferent arteriole

46

in renal artery stenosis what happens to JG cells

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

47

what part of kidney converts to active vit D

PCT

48

afferent arteriole mediators

prostaglandins - vasodil
NSAIDS - oppose prostaglandins

49

efferent arteriole mediators

AT II - vasoconstriction
ACE inhib - oppose AT II

50

protein effects in glomerulus

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

impt function of ATII to prevent further decrease in vol loss

compensatory Na reabsorp. @ PCT and DCT!!!

52

increased serum Mg levels -->

decreased DTRs, bradycardia, lethargy, etc.

53

winter's formula

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

54

anion gap =

Na - (Cl + HCO3)

normal = 8-12 mEq/L

55

increased anion gap metab acidosis

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

56

normal anion gap metab acidosis

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

57

RTA type 1

"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

RTA type 2

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

59

RTA type 4

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

60

what 2 synd can present as both nephritic/nephrotic

DPGN
MPGN
SLE

61

diff b/w IgA neph + PSGN

IgA neph - few DAYS after URI infection
PSGN - few WEEKS after infection

62

complications of kidney stones

hydronephrosis (expansion of renal pelvis)
pyelonephritis

63

all kidney stones are radiopaque EXCEPT

Uric acid stones = radiolUcent (not seen on x-ray)
view on CT or US

64

lowest pH in nephrons is @

DCT
collecting tubules

65

2 factors that prevent crystallization of stones

-citrate (binds free Ca --> facilitates its excretion)
-fluids!

66

calcium phosphate stones

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

67

calcium oxalate stones

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

common kidney stone presentation

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

69

ammonium magesium phosphate stones (struvite)

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

70

uric acid stones

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

71

cystine stones

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

72

RCC originates from what cells

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

73

RCC spread =

hematogenously by invading renal vein --> IVC

74

RCC ass w/ what paraneoplastic synd

ectopic EPO
ACTH
PTHrP
prolactin

75

Wilm's tumor (nephroblastoma) contains what cells

embryonic glomerular structures (blastema)

76

acute pyelonephritis histo + casts

neutrophilic infiltrate
WBC casts

77

chronic pyelonephritis histo + casts

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

78

drugs implicated in drug-induced interstital nephritis

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

79

diffuse cortical necrosis ass w/?

obstetric complic (ex. placenta abruptio)
septic shock
ARDS

80

acute tubular necrosis features?

-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

in ATN, death occurs usually in what phase

inciting

82

maintenance phase of ATN =

oliguria
risk of hyperkalemia
1-3 wks

83

recovery phase of ATN =

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

84

renal papillary necrosis ass w/

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

85

prerenal azotemia =

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

86

intrinsic renal failure =

-cause = ATN or ischemia/toxins
-patchy necrosis
-epith/granular casts in urine
-DECREASED BUN/creatine ratio

87

postrenal azotemia =

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

88

features of uremia

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

89

histo in renal osteodystrophy

subperiosteal thinning of bones

90

medullary cystic disease

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