Quick nephritic Flashcards

1
Q

triad of nephritic?

A

hypertension+hematuria+oliguria

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2
Q

Why hypertension?

A

due to retention of salt

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3
Q

how looks glomeruli?

A

hypercellular/inflamed glomeruli on biopsy

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4
Q

Acute poststreptococcal GN in what age?

A

most frequently seen in children 3-12y/o

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5
Q

Acute poststreptococcal GN after infection when occur?

A

~2-4 weeks after group A streptococcal infection

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6
Q

What infections on A streptococcus? 2

A

pharynx (1-2 sav) and skin (3-4sav)

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7
Q

Acute poststreptococcal GN. Result in children and adult?

A

in children resolves spontaneously;

in adults may progress to renal insufficiency.

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8
Q

Acute poststreptococcal GN. What type of hypersensitivity?

A

type III

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9
Q

Lab? What titers and C? Acute poststreptococcal GN

A

positive strep titers/serologies;

decr. C3 due to consumption.

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10
Q

LM - glomeruli enlarged and hypercellular

A

Acute poststreptococcal GN

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11
Q

IF - (starry sky) granular appearrance (lumpy-bumpy) due to IgG, IgM and C3 deposition along GMB and mesangium

A

Acute poststreptococcal GN

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12
Q

IF - starry sky?

A

Acute poststreptococcal GN

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13
Q

IF - lumpy bumpy

A

Acute poststreptococcal GN

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14
Q

IF - granular appearrance due to IgG, IgM and C3 deposition along GMB and mesangium

A

Acute poststreptococcal GN

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15
Q

EM - subepithelial IC deposits (humps)

A

Acute poststreptococcal GN

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16
Q

LM - crescent moon shape

A

Rapidly progressive (crescentic) GN

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17
Q

crescent moon shape consists of?

A

Fibrin and plasma proteins (eg C3b) with glomerular parietal cells, monocytes, macrophages

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18
Q

Rapidly progressive (crescentic) GN prognosis?

A

Poor prognosis, rapidly deteriorating renal function (days to weeks) [ESRD]

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19
Q

Rapidly progressive (crescentic) GN Age?

A

60-85y/o

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20
Q

What diseases results in Rapidly progressive (crescentic) GN pattern?

A

IF pattern

Linear: Goodpasture syndrome (anti-GBM disease)

Granular (immune complex RPGN):

a) Poststreptococcal GN
b) Diffuse proliferative glomerulonephritis (most common with SLE)

Negative (pauci-immune RPGN):

a) Granulomatosis with polyangiitis (wegener)
b) Microscopic polyangiitis
c) Eosinophilic granulomatosis with polyangiitis

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21
Q

Goodpasture syndrome (anti-GBM disease) IF pattern?

A
Rapidly progressive (crescentic) GN
LINEAR
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22
Q

Poststreptococcal GN IF pattern?

A
Rapidly progressive (crescentic) GN
Granular (immune complex RPGN)
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23
Q

Diffuse proliferative glomerulonephritis (most common with SLE) IF pattern?

A
Rapidly progressive (crescentic) GN
Granular (immune complex RPGN)
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24
Q

Granulomatosis with polyangiitis IF pattern?

A
Rapidly progressive (crescentic) GN
Negative (pauci-immune RPGN)
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25
Q

Microscopic polyangiitis IF pattern?

A
Rapidly progressive (crescentic) GN
Negative (pauci-immune RPGN)
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26
Q

Eosinophilic granulomatosis with polyangiitis IF pattern?

A
Rapidly progressive (crescentic) GN
Negative (pauci-immune RPGN)
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27
Q

Linear IF pattern patho?

A

antibodies to GBM and alveolar basement membrane (anti-GBM disease)

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28
Q

Goodpasture manifestation and hypertensitivity?

A

hematuria/hemoptysis.
Typer II.
Treatment - plasmapheresis

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29
Q

Negative IF/Pauci-immune patho?

A

no Ig/C3 depositions

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30
Q

Granulomatosis with polyangiitis (wegener) kokie yra ANCA?

A

PR3-ANCA/c-ANCA

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31
Q

Microscopic polyangiitis kokie ANCA?

A

MPO-ANCA/p-ANCA

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32
Q

PR3-ANCA/c-ANCA

A

Granulomatosis with polyangiitis (wegener) kokie yra ANCA?

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33
Q

MPO-ANCA/p-ANCA

A

Microscopic polyangiitis kokie ANCA?

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34
Q

Microscopic polyangiitis vs Granulomatosis with polyangiitis (wegener)? microscopy

A

In Microscopic polyangiitis there are no granulomatous inflammation

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35
Q

Goodpasture against what collagen?

A

colagen IV

36
Q

SLE most commonly cause what GN?

A

Diffusive proliferative GN

37
Q

Diffusive proliferative GN crescent IF pattern?

A

Granular (immune complex RPGN):

38
Q

LM - ‘‘wire looping” of capillaries? aka Thickening of glomerular capillaries

A

Diffusive proliferative GN

39
Q

IF - granular?

A

Diffusive proliferative GN

40
Q

EM - suENDOTHELIAL and sometimes intramembranous IgG-base IC often with C3 deposition?

A

Diffusive proliferative GN

41
Q

Diffusive proliferative GN what EM deposits?

A

suENDOTHELIAL and sometimes intramembranous IgG-base IC often with C3 deposition

42
Q

lupus cause what nephrotic and what nephritic?

A

Nephrotic - membranous nephropathy

nephritic - diffuse proliferative GN

43
Q

IgG+C3+C1q?

A

Diffusive proliferative GN

44
Q

C3 in Diffusive proliferative GN?

A

decreased

45
Q

what markers may be found in Diffusive proliferative GN?

A

ANA and anti-dsDNA - due to lupus. Because Diffusive proliferative GN often due to lupus.

46
Q

Characterized by increased glomerular cellularity in more than half of the glomeruli?

A

Diffusive proliferative GN

47
Q

Episodic hematuria concurently with respiratory of GI infections?

A

IgA nephropathy (Berger disease)

48
Q

LM - mesangial proliferation?

A

IgA nephropathy (Berger disease)

49
Q

IF - IgA based IC depostis in mesangium?

A

IgA nephropathy (Berger disease)

50
Q

EM - mesangial IC deposits?

A

IgA nephropathy (Berger disease)

51
Q

in what diseases the main location is mesangium?

A

IgA nephropathy (Berger disease) (mesangial deposits!)

52
Q

when (days) manifest IgA nephropathy (Berger disease)?

A

2-3 days after mucus membrane infection

53
Q

Most common type of idiopathic glomerulonephritis worldwide?

A

IgA nephropathy (Berger disease)

54
Q

↑ Serum IgA?

A

IgA nephropathy (Berger disease)

55
Q

Normal C3 complement levels?

A

IgA nephropathy (Berger disease)

56
Q

C3 in postreptococcal?

A

decreased

57
Q

IgA nephorpathy (berger). in kidney - IgA vasculitis (HSP)

A

.

58
Q

Type IV hypersensitivity reaction?

A

Granulomatosis with polyangiitis (wegener)

59
Q

Renal biopsy: segmental necrotizing glomerulonephritis?

A

Granulomatosis with polyangiitis (wegener)

60
Q

Type II hypersensitivity reaction?

A

Goodpasture

61
Q

Hemosiderin-filled macrophages in sputum

and Iron deficiency anemia?

A

Goodpasture

62
Q

X-linked dominant disease?

A

Alport

63
Q

mutation in gene coding type IV collagen?

A

Alport

64
Q

eye problems (retinopathy and lens dislocation) in wgat disease?

A

alport

65
Q

sensineural deafness in what disease?

A

alport

66
Q

cant see cant pee cant hear a bee. what disease?

A

alport

67
Q

EM - basket-weave?

A

alport

68
Q

Severe disease typically manifests during adolescence?

A

alport

69
Q

Most common type of hereditary nephritis?

A

alport

70
Q

Persistent microhematuria with intermittent gross hematuria?

A

alport

71
Q

mutation in type IV collagen how changes GBM?

A

mutation –> thinning and splitting of GBM (lamellated and basket-weave appearance)

72
Q

what two GN manifest as both nephritic and nephrotic?

A

Diffuse proliferative and membranoproliferative GN

73
Q

Type 1 MPGN mechanism?

A

IG-mediated

74
Q

Type 2 MPGN mechanism?

A

Complement-mediated

75
Q

Hepatitis B and C what membranoproliferative GN?

A

type 1

76
Q

IF - subendothelial and mesangial IgG immune complex deposits with granular appearance?

A

Type 1 MPGN

77
Q

Type 1 MPGN C3 level?

A

↓ Serum C3 complement levels

78
Q

IF - Intramembranous C3 deposits (dense deposit disease) on basement membrane?

A

Type 2 MPGN

79
Q

Type 2 MPGN C3 level?

A

↓ Serum C3 complement levels

80
Q

Dense deposit disease? what is that?

A

Type 2 MPGN, because Intramembranous C3 deposits

81
Q

Tram-track appearance?

A

both Type 1 and 2 MPGN

82
Q

LM with H&E or PAS stain shows mesangial ingrowth, which leads to thickening and splitting of the glomerular basement membrane (tram-track appearance)?

A

both Type 1 and 2 MPGN

83
Q

IgG against C3 convertase?

A

Type 2 MPGN

84
Q

IgG against C3 convertase effect?

A

stabilizes C3 convertase –> persistent complement activation –> decr. C3 levels.

85
Q

What is C3NeF?

A

C3 nephritic factor (IgG against C3 convertase)

86
Q

characterized by deposition of antibodies between podocytes and the basal membrane?

A

MPGN