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Renal Path MC > Renal 4 > Flashcards

Renal 4 Flashcards

1
Q

characterizes diabetes kidney problems (early on)

A

glomerulosclerosis (hyaline deposits)

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2
Q

3 syndromes associated with glomerulosclerosis in diabetes

A

non-nephrotic proteinuria, nephrotic syndrome, CRF

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3
Q

changes other than glomerulosclerosis that is associated with diabetes

A

afferent/efferent arteriolar sclerosis, papillary necrosis (increased infection), tubular lesions

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4
Q

responsible for thickening of BM in diabetes

A

increased collagen IV and fibronectin

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5
Q

hallmark of diabetic nephropathy; what is stain for matrix deposits?

A

nodular glomerulosclerosis (Kimmelstiel-Wilson disease); PAS

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6
Q

clinical features of diabetic nephropathy

A

microalbuminemia, overt proteinuria, progressive loss GFR

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7
Q

most common type of GN worldwide

A

IgA nephropathy (Berger’s disease)

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8
Q

vasculitis from IgA deposition -> purpuric skin lesions, renal disease also

A

Henoch-Schnolein purpura

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9
Q

renal manifestations of HSP

A

hematuria, proteinuria, nephrotic syndrome

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10
Q

what is defective in Alport syndrome?

A

type IV collagen synthesis -> defective BM

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11
Q

this causes hyalinosis and sclerosis in FSGN

A

entrapment plasma proteins with increased ECM deposition

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12
Q

hyaline thickening of what in FSGS?

A

afferent arterioles

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13
Q

glomerular disease characterized by nonselctive proteinuria, hematuria, reduced GFR, HTN -> no response to corticosteroids, no immune complexes

A

focal segmental glomerulosclerosis

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14
Q

condition in which you see sub-epithelial spikes

A

membranous GN

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15
Q

irregular dense deposits that occur in membranous GN with loss of foot processes

A

sub-epithelial spikes

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16
Q

seen on immunofluorescence of membranous GN

A

granular deposits containing Ig

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17
Q

these are present in granular deposits of membranous GN

A

Ig

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18
Q

where are granular deposits located in membranous GN

A

between BM and epithelium (sub-epithelial spikes)

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19
Q

Ab to these structures is responsible for idiopathic membranous GN

A

podocyte membrane antigens

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20
Q

causes of membranous GN

A

Ab podocyte membrane antigens, SLE, hep B, drugs, malignant tumors, diabetes/thyroiditis

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21
Q

this occurs in mixed nephrotic and nephritic disease (membranoproliferative GN)

A

thickened BM, increased mesangial cells and matrix

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22
Q

varying degrees of membranoproliferative GN

A

asymptomatic hematuria, nephrotic syndrome w/ hematuria, decreased GFR/azotemia and HTN

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23
Q

morphology of major changes seen in membranoproliferative GN

A

BM alterations, proliferation glomerular cells, leukocyte infiltration, proliferating mesangial cells and increased matrix

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24
Q

what is present in granular deposits in Type I of membranoproliferative GN

A

complement w/ or w/o Ig

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25
Q

where are granular deposits seen in type 1 membranoproliferative GN

A

subendothelial

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26
Q

this renal disease causes “tram tracking” and sub endothelial deposits

A

type I MPGN

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27
Q

mesangial cells interspersed between old and new BM (as result of reduplication of membranes)

A

tram-tracking

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28
Q

morphology of type II MPGN

A

dense deposition w/in BM proper, complement (NOT in deposits), no IgG

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29
Q

this glomerular disease causes profound hypocomplementemia (activation of classic and alternative pathway)

A

MPGN

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30
Q

major cause of MPGN

A

SLE

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31
Q

causes of MPGN

A

idiopathic, chronic immune complex disorder, SLE, hepatitis, HIV, malignant disease, hereditary complement deficiency

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32
Q

glomerular diseases that are primarily nephritic

A

acute proliferative GN, focal proliferative and necrotizing GN, RPGN

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33
Q

nephritic disease characterized by mesangial infiltration of cells and deposition of protein

A

acute proliferative GN

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34
Q

morphology of acute proliferative GN

A

immune complex deposition, proliferation glomerular cells, influx leukocytes, granular deposits Ig/complement

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35
Q

this causes hypercellularity of acute proliferative GN

A

leukocyte infiltration, proliferation endothelial and mesangial cells

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36
Q

most common cause of acute proliferative GN

A

post-strep GN

37
Q

signs/symptoms of acute proliferative GN

A

red cell casts, mild proteinuria, periorbital edema, moderate HTN, oliguria

38
Q

condition with sub epithelial humps

A

acute proliferative GN

39
Q

kind of deposits present in acute proliferative GN

A

subepithelial humps

40
Q

onset of post-strep GN in adults

A

sudden HTN, edema, elevated BUN

41
Q

can cause focal proliferative and necrotizing GN

A

SLE, Henoch-Schonlein purpura, Goodpasture’s, IgA nephropathy

42
Q

these make up crescent that fills Bowman’s space in rapidly progressive GN

A

infiltrating leukocytes and proliferating epithelial cells

43
Q

morphology of RPGN

A

obliteration Bowman’s space, fibrinogen/fibrin strands/scaffold, ruptures of BM, infiltrating leukocytes, proliferating epithelial cells

44
Q

antibodies in micro-polyarteritis nodosa (can cause type 3 RPGN)

45
Q

most common type of RPGN in 40+ age group

A

type 3 (pauci immune…micro-PAN or Wegener’s)

46
Q

most common type of RPGN in 10-40 age group

A

type 2 (immune complex)

47
Q

these glomerular diseases commonly progress to chronic GN

A

focal sclerotic and RPGN

48
Q

morphology of chronic GN

A

contracted/scarred kidneys, hyaline obliteration glomeruli, afferent arterial sclerosis, tubule atrophy, interstitial fibrosis, lymphocyte infiltration

49
Q

immunofluorescence of Goodpasture’s

A

linear deposits Ig and complement

50
Q

manifestation of renal Goodpasture’s; lung manifestation

A

proliferating GN; necrotizing hemorrhagic interstitial pneumonitis

51
Q

Ab against this in Goodpasture’s disease

A

non-collagenous part BM collagen type IV

52
Q

environmental exposures that act as co-factors in Goodpastures’ disease

A

hydrocarbon solvents, virus infection, smoking

53
Q

this is treatment for Goodpastures -> removes circulating Ab and inflammatory cytokines

A

plasma exchange

54
Q

GN associated with URT infections/manifestations

55
Q

associated findings with focal lesions of Wegener’s

A

hematuria and proteinuria

56
Q

treatment for Wegener’s

A

immunosuppressive meds

57
Q

2 forms of Wegener’s renal disease

A

focal necrotizing GN OR diffuse necrosis, proliferation, and crescent formation

58
Q

SLE Ab associated with renal disease

59
Q

signs/symptoms of combination of nephrotic/nephritic most commonly seen in SLE

A

recurrent hematuria, acute nephritis, CRF, HTN

60
Q

3 kinds of renal lesions seen in SLE

A

focal, diffuse proliferative, or diffuse membranous GN

61
Q

key pathologic features of renal SLE

A

mesangial and endocapillary proliferation, membranous change -> membranous GN or MPGN I (sub endothelial deposits Ig and complement)

62
Q

morphology of glomerular membrane change in diabetes

A

BM thickening, decreased heparan sulfate (loss negative charge), non enzymatic glycosylation proteins

63
Q

3 main components of pathogenesis of renal involvement in diabetes

A

thickened/leaky BM, increased mesangial matrix, progressive GS (hemodynamic abnormalities)

64
Q

result of sclerosis (as seen in diabetic nephropathy)

A

decreased GFR, increased glomerular filtration area, increased glomerular capillary pressure, glomerular hypertrophy

65
Q

nephropathy in which mesangial area expands to fill entire glomerulus, ovoid/spherical hyaline masses in periphery of glomerulus, matrix deposits continuous w/ hyaline thickening of arterioles

66
Q

late lesions of diabetic nephropathy

A

ischemic tubular atrophy, interstitial fibrosis, contraction of kidney, papillary necrosis with increased pyelonephritis

67
Q

these can slow progression of diabetic nephropathy

A

ACE inhibitors

68
Q

characteristic of Henoch-Schonlein purport and IgA nephropathy

A

mesangial IgA deposits

69
Q

precedes IgA nephropathy/Berger’d disease in children/young adults

A

respiratory, GI infection, lower urinary infection

70
Q

associated conditions with IgA nephropathy/Berger’s disease -> increased IgA synthesis

A

mucosal infections, celiac disease

71
Q

morphology of IgA nephropathy/Berger’s disease

A

mesangial hypercellularity, increased mesangial matrix with IgA and C3

72
Q

where are purpura located in HSP? what causes them?

A

extensor surface arms/legs, buttocks; necrotizing vasculitis

73
Q

signs/symptoms of Henoch-Schonlein purport (after infection…mostly 3-8 y.o)

A

purpuric skin lesions, GI pain/vomiting/bleeding, non migrating arthralgia, hematuria/proteinuria/nephrotic syndrome

74
Q

Alport syndrome renal manifestations

A

glomerular segmental proliferation or sclerosis, hematuria (varying progression to end stage renal disease)

75
Q

this is defect in hereditary nephritis/thin membrane disease

76
Q

glomerular disease with subepithelial spikes

A

membranous

77
Q

glomerular disease with subepithelial humps

A

immune complexes (acute proliferative, post-strep)

78
Q

glomerular disease with sub endothelial deposits

A

SLE, MP type I

79
Q

glomerular disease with sub endothelial deposits w/ duplication of the membrane (tram tracking)

A

MP type II

80
Q

glomerular disease with effacement of podocyte foot processes

A

minimal change disease/lipoid nephrosis

81
Q

glomerular disease with areas of thickened and thinned basement membrane

A

Alport’s disease

82
Q

conditions with increased mesangial matrix

A

diabetes, IgA nephropathy

83
Q

Ab present in MPGN type II

A

C3NeF Ab to C3 convertase

84
Q

stain for crescentic disease

A

fibrinogen

85
Q

condition with ANA antibody

86
Q

condition with c-ANCA antibody

A

Wegener’s

87
Q

Ab present in post-streptococcal GN

A

anti-streptolysin O

88
Q

hepatitis B surface antigen associated with this glomerular disease

A

membranous GN

Renal Path MC (5 decks)

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