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Pathology high yield Flashcards

buzz words, pathognomonics, from every lecture with a nichols handout

1
Q

Foot process effacement

A

Minimal change disease

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2
Q

Spike and dome

A

Membranous nephropathy (new GBM represent the spikes that project between the subepithelial immune complexes (domes))

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3
Q

Subepithelial humps

A

Post infectious glomerulonephritis

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4
Q

Tram tracks

A

MPGN

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5
Q

Basketweave

A

Alport syndrome

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6
Q

Wire loops

A

Lupus nephritis

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7
Q

Onion skin appearance

A

Hypertensive nephropathy (glomeruli) OR scleroderma (glomeruli) OR thrombotic microangiopathies (vessels)

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8
Q

Proteinuria

A

Nephrotic syndrome

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9
Q

RBC casts

A

Glomerular inflammation (nephritic syndrome)

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10
Q

Fatty casts

A

Nephrotic syndrome (due to hyperlipidemia)

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11
Q

Flea bitten kidney

A

malignant hypertension

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12
Q

mutations in Apolipoprotein L1 (APOL1)

A

increased risk for hypertensive nephropathy, FSGS, HIV nephropathy

provides resistance to Trypanosoma b. rhodesiense (african sleeping sickness)

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13
Q

antibodies to noncollagenous (NC) domain of alpha3 chain of type 4 collagen in the GBM

A

Goodpasture’s syndrome (anti-GBM)

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14
Q

how to treat anti-GBM disease

A

plasmapheresis

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15
Q

rapidly progressive glomerulonephritis

A

crescentic glomerulonephritis

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16
Q

proliferation of parietal epithelial cells

A

crescentic glomerulonephritis

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17
Q

nephrin and podocin mutations

A

congenital nephrotic syndromes

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18
Q

glomerular cells that provide structural support and have phagocytic and contractile properties

A

mesangial cells

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19
Q

immune complex deposition in mesangium

A

IgA nephropathy

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20
Q

subendothelial deposition of immune complexes against the GBM with a linear IF pattern

A

Goodpastures (anti-GBM)

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21
Q

antibodies against podocyte cell membranes

A

membranous nephropathy

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22
Q

granular deposits on IF

A

Any disease with immune complex formation

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23
Q

example of a subendothelial deposition of immune complexes

A

Lupus

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24
Q

no IF detection

A

pauci-immune GN

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25
Q

advanced glycation end-products (AGE)

A

diabetic nephropathy

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26
Q

arterionephrosclerosis

A

globally sclerotic glomeruli seen in hypertensive nephropathy

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27
Q

fibrinoid necrosis of arterioles

A

malignant hypertension (fibrinoid necrosis is characteristic but not specific for malignant HTN)

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28
Q

hyperplastic arteriosclerosis

A

malignant HTN/onion skin appearance (hyperplastic arteriosclerosis is characteristic but not specific for malignant HTN)

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29
Q

muddy brown casts

A

ATN

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30
Q

maltese cross, oval fat bodies

A

nephrotic syndrome due to hyperlipidemia

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31
Q

xanthelesma

A

nephrotic syndrome due to hyperlipidemia

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32
Q

first clinical sign in diabetic nephropathy?

A

microalbuminuria

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33
Q

overflow proteinuria

A

multiple myeloma

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34
Q

albuminuria

A

glomerular disease

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35
Q

low MW proteinuria

A

tubular disease

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36
Q

values for nephrotic range proteinuria?

A

> 3.5 g/day and spot urine protein/creatinine ratio >3.5

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37
Q

elevated suPAR

A

FSGS

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38
Q

hyalinosis

A

FSGS

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39
Q

FSGS subtype with rapid onset of nephrotic syndrome and rapid progression to renal failure

A

collapsing glomerulopathy type (e.g. HIV)

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40
Q

steroid-sensitive nephrotic syndrome

A

MCD

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41
Q

steroid-resistant nephrotic syndrome

A

FSGS

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42
Q

antibodies against neural endopeptidase (NEP)

A

congenital MN

43
Q

antibodies against M-type PLA2 receptor

A

primary (idiopathic) MN

44
Q

in primary MN, PLA2R co-localizes with ___ and deposits in ____

A

IgG4, subepithelial layer

45
Q

smoky urine, low C3

A

post-streptococcal GN

46
Q

Hepatitis C

A

think MPGN (type 1) or cryoglobulinemia (mixed)

47
Q

dysregulation of complement system

A

dense deposit disease

48
Q

C3 nephritic factor

A

dense deposit disease

49
Q

ribbons of dense material in GBM

A

dense deposit disease

50
Q

IgA nephropathy has _____ deficient IgA deposition in mesangium

A

galactose-deficient IgA

51
Q

use ___ to differentiate IgA nephropathy from other forms of glomerulonephritis

52
Q

use ____ to differentiate DDD from other forms of glomerulonephritis

53
Q

what distinguishes anti-GBM from Goodpastures

A

pulmonary involvement in Good-pastures but essentially the same thing

54
Q

mutation in alpha5 chain of collagen type 4

A

alport syndrome

55
Q

nephritis + deafness + lens disorders

A

alport syndrome

56
Q

defects in alpha3 or alpha4 of type 4 collagen

A

thin basement membrane disease

57
Q

nocturia

A

indicated tubular damage due to inability to concentrate urine

58
Q

BUN:creatinine >20

A

pre-renal issue (most sensitive marker)

59
Q

abnormal fundoscopic exam

A

malignant hypertension, diabetic nephropathy

60
Q

crescentic formation associated with?

61
Q

septic shock and ischemia

62
Q

K+ > ____ is a medical emergency

A

> 7 mmol/L

63
Q

most vulnerable portions of the kidney to hypoxic injury?

A

straight portion of PT and TALH

64
Q

loss of brush border and blebbing

65
Q

myoglobin casts

A

rhabdomyolysis, releases myoglobin which can contribute to ATN

66
Q

ATN with vacuolization and formation of oxalate crystals in tubular lumen due to?

A

ethylene glycol poisoning

67
Q

tx when K+> 7mmol/L

A

IV calcium gluconate

OR insulin + glucose

68
Q

most common cause of acute pyelonephritis

69
Q

neutrophil infiltration with liquefactive necrosis and abscess formation

A

acute pyelonephritis

70
Q

pyonephrosis

A

when infected pus fills and distends the renal calyces, pelvis and ureter (seen in acute pyelonephritis)

71
Q

thyroidization

A

acute pyelonephritis (tubules become atrophic and distended with urine causing them to resemble thyroid follicles)

72
Q

classic triad of interstitial nephritis

A

fever, rash, eosinophilia

73
Q

new onset azotemia with oliguria, fever, skin rash, and eosinophilia think…

A

interstitial nephritis

74
Q

polycystin1 or 2 mutations

A

adult polycystic kidney disease (autosomal dominant)

75
Q

fibrocystin mutation

A

childhood polycystic kidney disease (autosomal recessive)

76
Q

medullary cystic disease complex that is the most common genetic cause of ESRD in children

A

Nephronophthisis

77
Q

C-ANCA

A

Granulomatosis with polyangiitis (Wegener’s)

78
Q

anti-proteinase 3 antibodies

A

C-ANCAs, seen in granulomatosis with polyangiitis (Wegener’s)

79
Q

anti-myeloperoxidase antibodies

A

microscopic polyangiitis

80
Q

sinopulmonary renal syndrome

A

granulomatosis with polyangiitis (Wegener’s)

81
Q

shiga toxin

82
Q

inactivation of factor H

83
Q

sudden onset of irritability, lethargy, weakness, pallor and oliguria in a small child, 5-10 days following gastroenteritis

84
Q

ADAMTS13

85
Q

tx of TTP

A

plasmapheresis

86
Q

tx of HUS

A

plasmapheresis

87
Q

ANAs

88
Q

class 1 lupus

A

minimal mesangial (rare)

89
Q

class 2 lupus

A

mesangial proliferative

90
Q

class 3 lupus

A

focal proliferative

91
Q

class 4 lupus

A

diffuse proliferative (severe, most common), wire loop lesions and hyaline thrombi

92
Q

class 5 lupus

A

membranous

93
Q

class 6 lupus

A

advanced sclerosing

94
Q

full house immunoflourescence

A

Lupus (IF staining for IgG, IgM, IgA, C3, C4)

95
Q

scleroderma renal crisis

A

new onset of accelerated arterial hypertension and/or rapidly progressive oliguric renal failure

96
Q

non-proliferative, non-inflammatory glomerulopathy

A

amyloidosis

97
Q

apple green birefringence

A

amyloidosis

98
Q

hemosiderin depositis

A

sickle cell nephropathy

99
Q

what type of amyloidosis is the main target for the kidney? presentation?

A

AA, nephrotic syndrome

100
Q

what kind of amyloidosis do you get with long-term dialysis?

A

AB2microglobulin

101
Q

collapsing form of focal segmental glomerulosclerosis

A

HIV nephropathy

102
Q

syncytium formation

A

seen in AL amyloidosis as tubular epithelial cells can form a syncytium around the bence jones proteins

103
Q

deposition of material that looks like “silt” on EM

A

light chain disease

104
Q

Most common cause of ESRD?

A

Diabetic nephropathy

Renal (11 decks)

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