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Pathophys II - Exam 3 > Schoenwald - Renal > Flashcards

Schoenwald - Renal Flashcards

1
Q

fxn’s of the kidneys (3)

A

primary regulators of internal environment

fluid regulation

filtration/urine concentration

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2
Q

kidneys filter __ L of fluid/day

and produce __ L of urine/day

A

180

1.5

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3
Q

what is used to determine kidney pathology

A

microscopy

bx

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4
Q

3 types of ARF/AKI

A

prerenal

renal

postrenal

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5
Q

azotemia involves elevated

A

BUN

Creatinine

+/- anuria

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6
Q

pathology behind prerenal ARF

A

low volume stimulus

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7
Q

causes of prerenal aRF

A

hypovolemia

heart failure

sepsis

renal vascular pathology → stenosis, atherosclerosis

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8
Q

kidney function is not impaired in prerenal ARF, but responds to low volume by (3)

A

reabsorption of Na, water, urea

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9
Q

in ARF, __ is secreted by the tubules

but __ is reabsorbed

resulting in __

A

Cr

BUN

BUN:Cr ratio > 20:1

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10
Q

renal ARF originates __

and indicates __

A

within the kidney

kidney dysfxn

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11
Q

causes of renal ARF (3)

A

ATN

glomerular dz

AIN

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12
Q

impaired tubular fxn is indicated by what lab values (2)

A

FENa > 1%

BUN:Cr ratio < 20:1

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13
Q

postrenal failure is caused by __

and the major cause is __

A

obstruction

stones

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14
Q

obstruction causes __

and __ is the preferred evaluation test

A

hydronephrosis

US

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15
Q

sx of ARF/AKI (5)

A

lyte disturbances

decreased urine output

lethargy

fatigue

nausea

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16
Q

lab summary of pre vs post ARF/AKI

A
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17
Q

mc causes of CKD

A

DM

HTN

glomerulonephritis

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18
Q

sx of CKD

A

same as AKI/ARF but longer duration →

fatigue, n/v, edema

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19
Q

stages of CKD (CRF)

A

diminished renal reserve

renal insufficiency

renal failure

esrd

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20
Q

sx of renal insufficiency (3)

A

htn

anemia

polyuria

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21
Q

sx of renal failure

A

edema

metabolic acidosis

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22
Q

GI complications of CKD/CRF

A

n/v

anorexia

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23
Q

cardiac complications of CKD/CRF (3)

A

htn

CHF

pericarditis

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24
Q

hematologic complications of CKD/CRF

A

normocytic, normochromic anemia (anemia of chronic dz)

platelet dysfxn

increased infxn

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25
Q

CNS complications of CKD (2)

A

polyneuropathy

encephalopathy

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26
Q

glomerular d.o can be __ (4)

A

segmental

global

focal

diffuse

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27
Q

a portion of the glomerulus is involved in dz

A

segmental

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28
Q

some of the gomeruli are involved in CKD

A

focal

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29
Q

3 techniques to evaluate glomeruli

A

light microscopy

immunofluorescence (IgG, IgM, IgA)

electron microscopy

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30
Q

types of light microscopy technique

A

periodic acid schiff (PAS)

trichrome

silver

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31
Q

type of light microscopy that highlights the basement membrane and mesangium

A

periodic acid schiff (PAS)

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32
Q

type of light microscopy that highlights fibrosis

A

trichrome

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33
Q

type of electron microscopy that highlights the basement membrane

A

silver

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34
Q

types of immunofluorescence (2)

A

linear pattern

granular pattern

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35
Q

type of immunofluorescence rxn directed against antigen in glomerular basement membrane

A

linear pattern

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36
Q

what do you think when you see goodpasture syndrome

A

linear pattern immunofluorescence

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37
Q

type of immunofluorescence rxn that is against Ag/Abs immune complexes in glomerular basement membrane

A

granular pattern

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38
Q

what condition do you think of when you see linear pattern immunofluorescence

A

SLE

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39
Q

electron microscopy shows (2)

A

structure

immune complex deposition

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40
Q
A

linear pattern → Good Pasture

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41
Q

granular pattern

A

SLE

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42
Q

clinical manifestations of glomerular dz (5)

A

nephrotic syndrome

nephritic syndrome

rapidly progressive glomerulonephritis

CKD/CRF

asymptomatic hematuria

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43
Q

most glomerular dz’s are __ in nature

and are the result of either __

or __

A

immunologic

immune complex deposition

Abs-Ag binding

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44
Q

what do immune complexes activate

A

complement

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45
Q

short lived immune complexes cause __

long lived immune complexes cause __

A

infxn

CKD/chronic failure

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46
Q

damage of glomeruli results in leakage of protein (mainly albumin) → hypoalbuminemia

A

nephrotic syndrome

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47
Q

how does nephrotic syndrome cause edema

A

hypoalbuminuria → decreased osmotic pressure → edema

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48
Q

how does edema affect blood pressure

A

decreased fluid in vascular space → decreased bp

49
Q

how does decreased bp worsen edema

A

decreased bp → simulates renin → aldosterone causes Na and water retention → worse edema

50
Q

in response to hypoalbuminuria, the liver produces __

to compensate for decreased __,

which causes __

A

apolipoprotein

osmotic pressure

hyperlipidemia

51
Q

why does infxn risk increase w. nephrotic syndrome

A

decreased Ig production

52
Q

quad of nephrotic syndrome

A

proteinuria

hypoalbuminemia

anasarca

hyperlipidemia

53
Q

in nephrotic syndrome, proteinuria is > __/day

A

3.5 g

54
Q

sx of nephrotic syndrome (3)

A

n/v

periorbital edema

frothy urine

55
Q

UA findings of nephrotic syndrome besides proteinuria (2)

A

waxy casts

oval fat bodies

56
Q

lipid droplets in urine for nephrotic syndrome have __ appearance w. polarized light microscopy

A

maltese cross

57
Q

preferred dx test for nephrotic syndrome to find specific cause

A

kidney bx

58
Q

what is this showing

A

light microscopy

lipid droplet → maltese cross

59
Q

4 specific causes of nephrotic syndrome

A

minimal change dz

focal segmental glomerulosclerosis

membranous glomerulonphropathy

diabetic nephropathy

60
Q

mc cause of nephrotic syndrome in kids 2-8 yo; 2:1 m:f

A

minima change dz

61
Q

minimal change dz causes __ proteinuria

and is treated w. __

A

selective

steroids

62
Q

in adults, minimal change dz is associated w. (3)

A

lymphomas

leukemias

NSAIDs

63
Q

light microscopy findings of minimal change dz (2)

A

no abnormalities in glomeruli → “minimal change”

PCT laden w. lipid and protein

64
Q

immunofluorescence findings of minimal change dz

A

no abnormalities → “minimal change”

65
Q

2nd mc cause of nephrotic syndrome in kids

and mc cause of nephrotic syndrome in adults

A

focal segmental glomerulosclerosis

66
Q

focal segmental glomerulosclerosis is NOT __ in origin

A

immunologic

67
Q

pathophys of focal segmental glomerulosclerosis

A

IgM and C3 are trapped → injury to epithelial cells

68
Q

what pt population is 30x higher risk for focal segmental glomerulosclerosis

A

IV heroin users

69
Q

is there a tx for focal segmental glomerulosclerosis

A

no! → leads to esrd in w.in 10 years

70
Q

light microscopy findings of focal glomerulosclerosis

A

segmental sclerosis of a few glomeruli

71
Q

immunofluorescence for focal segmental glomerulosclerosis

A

(+) IgM and C3

72
Q

electron microscopy findings for focal segmental glomerulosclerosis

A

no immune complexes

73
Q

type of nephrotic syndrome that is 2/2 to other processes

A

membranous glomerulonephropathy

74
Q

membranous glomerulonephropathy causes __ proteinuria

A

selective

75
Q

common causes of membranous glomerulonephropathy (7)

A

syphilis

malaria

hep B or C

lung carcinoma

melanoma

SLE

drugs → NSAIDs

76
Q

85% of cases of membranous glomerulonephropathy are

A

idiopathic

77
Q

membranous glomerulonephropathy outcomes:

⅓:

⅓:

⅓:

A

⅓: remission

⅓: proteinuria w. stable renal fxn

⅓: esrd in 5-10 years

78
Q

light microscopy findings of membranous glomerulonephropathy

A

silver stain:

thickened basement membrane btw immune complexes

spike and dome formation

79
Q

immunofluorescence findings of membranous glomerulonephropathy

A

granular pattern

(+) IgG

80
Q

electron microscopy findings of membranous glomerulonephropathy

A

subepithelial immune complexes

81
Q

mc cause of esrd in US

A

diabetic nephropathy

40% of esrd pt’s have DM

82
Q

diabetic nephropathy causes __ albuminuria,

__,

and decrease in __

A

persistent

htn

GFR

83
Q

what test predicts development of diabetic nephropathy

A

microalbumin

84
Q

mc light microscopy findings of diabetic nephropathy

A

diffuse glomerulosclerosis → thickening of basement membrane

85
Q

increased BUN/Cr, oliguria, htn, hematuria

A

nephritic syndrome

86
Q

__ and

__ are present w. nephritic syndrome, but less severe

A

proteinuria

edema

87
Q

__ is much more severe w. nephritic syndrome than nephrotic syndrome

A

damage of glomeruli

88
Q

nephrotic syndrome involves leakage of __

nephritic syndrome involves leakage of __

A

protein

RBC

89
Q

in nephritic syndrome, __ deposition triggers proliferation of glomerular cells

and stimulates __

A

immune complex

neutrophils

90
Q

clinical presentation of nephritic syndrome

A

edema

oliguria

htn

hematuria

proteinuria

91
Q

cola colored/smoky brown urine

A

nephritic syndrome

92
Q

nephritic syndrome casts are

A

RBC

93
Q

serum complement will be low w. __ glomerulonephritis, including (3)

A

postinfectious:

SLE

bacterial endocarditis

membranoproliferative glomerulonephritis

94
Q

complement will be normal w. nephritic syndrome caused by (2)

A

IgA nephropathy

antiglomerular basement membrane dz

95
Q

antiglomerular basement membrane dz is same-same

A

goodpasture syndrome

96
Q

3 causes of nephritic syndrome

A

postinfectious

rapidly progressive

membranoproliferative

97
Q

mc occurs 1-4 weeks after GAS or impetigo infxn

A

postinfectious glomerulonephritis

98
Q

other infxns associated w. postinfectious GN

A

staph

mumps/measles

hep B or C

chickenpox

99
Q

post infectious GN can progress to

__,

which causes __

A

rapidly progressing GN

chronic GN

100
Q

2 tests for past GAS infxn

A

ASO titer

antiDNAse B

101
Q

lumpy bumpy appearance from basement membrane growing around immune complexes

A

light microscopy silver stain findings of post infectious GN

102
Q

immunofluorescence findings of post infectious GN

A

granular pattern

(+) IgM and complement

103
Q

electron microscopy findings of post infectious GN

A

immune complex deposition

104
Q

__ can occur alone,

but is one of mc of nephritic syndrome

A

rapidly progressive GN

105
Q

crescent cells in bowman capsules

A

rapidly progressive GN

106
Q

rapidly progressive GN is classified in to

A

types I-III

107
Q

type I rapidly progressive GN

A

IgG binds directly to glomerular basement membrane

good pasture syndrome

108
Q

type II rapidly progressive GN

A

immune complex related

post infectious GN, IgA nephropathy, SLE, henoch-schonlein purpura

109
Q

type III rapidly progressive GN

A

no immune complexes

wegener granulomatosis

110
Q

abs directed against the glomerular basement membrane

lung hemorrhage

severe rapidly progressing GN

A

anti-glomerular basement membrane dz - good pasture

111
Q

immunofluorescence findings of goodpasture shows __ distribution of complement

and __ along basement membrane

A

linear pattern

IgG

112
Q

membranoproliferative GN is classified in to

A

typeI and II

113
Q

which type of membranoproliferative GN is associated w. hep B/C and SLE

A

type I

114
Q

which type of membranoproliferative GN is associated w. hypocomplementemia

A

type II

115
Q

__% of membranoproliferative GN progresses to renal failure w.in 10 years

A

50

116
Q

sclerosis of glomeruli, sx of renal insufficiency

A

chronic GN

117
Q

pale, swollen cortex dt lipid deposition and interstitial edema

A

chronic GN

118
Q

5 common causes of chronic GN

A

DM

SLE nephritis

RPGN

FSGS

membranoproliferative GN

119
Q

nephrotic vs nephritic syndromes

A

Pathophys II - Exam 3 (8 decks)

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