Robbins Ch. 20 - The Kidney I Flashcards

1
Q

CVA location

A

T12-L1

-location of renal colic

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2
Q

tubules and interstitium

A

toxic/infection

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3
Q

glomeruli

A

immunologic

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4
Q

acute kidney injury

A

most damage - proximal tubules

rapid decline in GFR**

reversible

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5
Q

chronic kidney disease

A

GFR decreased to <60 for at least 3 months
OR persistant albuminuria

irreversible

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6
Q

nephrocalcinosis

A

calcification of the renal parenchyma

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7
Q

ESRD

A

GFR < 5% normal

end stage

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8
Q

podocyte

A

in lamina rara externa of BM

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9
Q

subendothelial

A

cations - cross BM

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10
Q

subepithelial

A

anions - cannot cross BM

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11
Q

GFR reduce to 30-50% of normal

A

slow progression to ESRD

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12
Q

cycle of FSGS

A

pocodyte loss > increased proteins in mesangium > proliferation of mesangium > ECM accumulation > segmental sclerosis > global sclerosis

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13
Q

TGF-beta

A

mediator of sclerosis

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14
Q

better correlate with kidney fxn

A

tubulointerstitial damage

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15
Q

subendothelial deposits?

A

lupus nephritis

MPGN

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16
Q

epimembranous deposits?

A

membranous nephropathy

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17
Q

subepithelial deposits?

A

acute GN

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18
Q

mesangial deposits?

A

IgA nephropathy

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19
Q

group A beta hemolytic strep

A

post-strep GN

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20
Q

SpeB

A

post-strep GN antigen

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21
Q

granular subepithelial humps, IgG/C3, hypocomplementemia

A

post-strep GN

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22
Q

post-strep GN treatment?

A

95% children recover with salt/water balance

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23
Q

non-streptococcal GN

A

Hep B/C, malaria, staph

24
Q

staph ?

A

IgA deposits

25
Q

untreated RPGN

A

death within weeks to months

26
Q

crescent formation

A

RPGN

-proliferation of parietal and visceral epithelium

27
Q

prognosis of RPGN

A

with steroids - many still need dialysis

28
Q

alpha4 of collagen IV

A

goodpastures

-cross react with alveolar tissue

29
Q

HLA-DRB1

A

associated with goodpasture

30
Q

Tx of goodpasture

A

plasmapharesis

31
Q

IgG/C3 linear deposits

A

anti-GBM antibody mediated disease

  • goodpastures
  • type of RPGN
32
Q

immune complex deposition RPGN

A

postinfectious GN, lupus nephritis, IgA nephropathy, henocy schonlein

granular deposit

Tx - underlying disease

33
Q

ANCAs

A

pauci immune

-type of RPGN

34
Q

50% of RPGN

A

have type 3 - pauci immune

35
Q

oval fat bodies

A

in urine - nephrotic syndrome

36
Q

majority of nephrotic in children

A

caused by primary disease (95%)

37
Q

majority of nephrotic in adults

A

caused by secondary disease (systemic) - DM, SLE, amyloidosis

38
Q

nephrotic syndromes?

A

membranous glomerulopathy
minimal change disease
FSGS

39
Q

PLA2R

A

membranous glomerulopathy

40
Q

diffuse thickening of glomerular cap wall

A

membranous glomerulopathy

41
Q

subepithelial, granular, IgG/C3, spike appearnace

A

membranous glomerulopathy

42
Q

non-selective proteinuria

A

membranous glomerulopathyF

FSGS

43
Q

selective proteinuria

A

minimal change disease

44
Q

IgG4

A

membranous glomerulopathy

45
Q

HLA-DQ1

A

membranous glomerulopathy association

46
Q

thyroiditis

A

membranous glomerulopathy

47
Q

prognosis of membranous glomerulopathy

A

40% transplant recur
40% to ESRD

women, low proteinuria - best prognosis

48
Q

hodgkins lymphoma

A

minimal changes disease

49
Q

most common cause of nephrotic in children

A

minimal change disease

-no deposits - only effacement of foot processes

50
Q

minimal change disease Tx?

A

reversible with corticosteroid therapy

51
Q

most common cause nephrotic in adults?

A

FSGS, primary

52
Q

secondary FSGS

A

HIV, heroin, sickle cell, obesity, renal abloation

53
Q

FSGS prognosis

A

bad - 50% ESRD within 10 years

25-50% transplants recur

54
Q

mutations in slit diaphragm?

A

podocin
nephrin
alpha-actinin 4
TRPC6

55
Q

IgM/C3, non-selective proteinuria

A

FSGS

56
Q

HIV associated nephropathy

A

FSGS collapsing variant

  • bad prognosis
  • fical cystic tubule dilation - full of proteinacious material
57
Q

nephritic syndromes?

A

acute proliferative GN (post-strep, post-infectious)

RPGN