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
untreated RPGN
death within weeks to months
26
crescent formation
RPGN | -proliferation of parietal and visceral epithelium
27
prognosis of RPGN
with steroids - many still need dialysis
28
alpha4 of collagen IV
goodpastures | -cross react with alveolar tissue
29
HLA-DRB1
associated with goodpasture
30
Tx of goodpasture
plasmapharesis
31
IgG/C3 linear deposits
anti-GBM antibody mediated disease - goodpastures - type of RPGN
32
immune complex deposition RPGN
postinfectious GN, lupus nephritis, IgA nephropathy, henocy schonlein granular deposit Tx - underlying disease
33
ANCAs
pauci immune | -type of RPGN
34
50% of RPGN
have type 3 - pauci immune
35
oval fat bodies
in urine - nephrotic syndrome
36
majority of nephrotic in children
caused by primary disease (95%)
37
majority of nephrotic in adults
caused by secondary disease (systemic) - DM, SLE, amyloidosis
38
nephrotic syndromes?
membranous glomerulopathy minimal change disease FSGS
39
PLA2R
membranous glomerulopathy
40
diffuse thickening of glomerular cap wall
membranous glomerulopathy
41
subepithelial, granular, IgG/C3, spike appearnace
membranous glomerulopathy
42
non-selective proteinuria
membranous glomerulopathyF | FSGS
43
selective proteinuria
minimal change disease
44
IgG4
membranous glomerulopathy
45
HLA-DQ1
membranous glomerulopathy association
46
thyroiditis
membranous glomerulopathy
47
prognosis of membranous glomerulopathy
40% transplant recur 40% to ESRD women, low proteinuria - best prognosis
48
hodgkins lymphoma
minimal changes disease
49
most common cause of nephrotic in children
minimal change disease | -no deposits - only effacement of foot processes
50
minimal change disease Tx?
reversible with corticosteroid therapy
51
most common cause nephrotic in adults?
FSGS, primary
52
secondary FSGS
HIV, heroin, sickle cell, obesity, renal abloation
53
FSGS prognosis
bad - 50% ESRD within 10 years | 25-50% transplants recur
54
mutations in slit diaphragm?
podocin nephrin alpha-actinin 4 TRPC6
55
IgM/C3, non-selective proteinuria
FSGS
56
HIV associated nephropathy
FSGS collapsing variant - bad prognosis - fical cystic tubule dilation - full of proteinacious material
57
nephritic syndromes?
acute proliferative GN (post-strep, post-infectious) | RPGN