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5 Patho > Glomerular > Flashcards

Glomerular Flashcards

1
Q

Glomerular syndrome:

Hypertension and hematuria

A

nephritic

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2
Q

Pathogenesis of hematuria in nephritic syndrome?

A

Compression of capillaries –> wall damage –> RBC leakage

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3
Q

Pathogenesis of hypertension in nephritic syndrome?

A

Compression of capillaries –> low blood flow –> renin release –> vasoconstriction

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4
Q

Glomerular syndrome with more proteinuria

A

nephrotic syndrome

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5
Q

A deposit in the basement membrane would result in what clinical gluomerular syndrome?

A

nephrotic

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6
Q

Glomerular syndrome: proteinuria < 3.5/day

A

nephritic

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7
Q

Glomerular syndrome: lipiduria

A

nephrotic

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8
Q

Pathogenesis of lipiduria in glomerular disease?

A

liver compensation due to protein loss

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9
Q

Azotemia is characterized by

A

increased BUN and creatinine levels

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10
Q

Type of azotemia due to hypoperfusion of kidneys without parenchymal damage

A

prerenal

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11
Q

Type of azotemia where urine flow is obstructed at ureter or lower level

A

postrenal

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12
Q

Nephritic syndrome with rapid decline in GFR

A

RPGN

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13
Q

Oliguria or anuria with recent onset of azotemia is a sign of

A

acute renal failure

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14
Q

Renal tubular defect signs

A

polyuria, nocturia, electrolyte disorders

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15
Q

Stage of chronic renal failure: GFR <20-25% of normal
Edema, metabolic acidois and hyperkalemia
Uremia with neuro, GIT, CV complications

A

Stage III (CRF)

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16
Q

Stage of chronic renal failure: GFR <50%
Serum BUN and creatinine normal.
Asymptomatic

A

Stage I (Diminished renal reserve)

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17
Q

Stage of chronic renal failure: GFR 20-50%

Azotemia, HTN, anemia, polyuria

A

Stage II (renal insufficiency)

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18
Q

Stage of chronic renal failure: GFR <5%

A

Stage IV (end stage renal disease)

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19
Q

Size of molecules that will not pass through glomerulus in healthy kidney

A

70 kDa (size of albumin)

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20
Q

Charge that more permeable to filtrating membrane

A

positive

albumin is anionic so it won’t be filtered

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21
Q

Molecules responsible for barrier charge

A

proteoglycans and sialoglycans

maintain negative charge on membranes

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22
Q

Hematuria and RBC casts in urine

Azotemia.

A

acute nephritic syndrome

history of sore throat and/or child means post strep GN

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23
Q

Formation of crescents indicates what histological change?

A

hypercellularity

crescent = accumulation of cells composed of proliferating parietal epithelial cells + leukocytes

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24
Q

What stain is best used to see BM thickening

A

PAS stain

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25
Q

Two forms of BM thickening:

A

1) increased synthesis of protein components as seen in diabetic glomerulosclerosis
2) Deposition of amorphous electron-dense material (imune complexes) on endothelial and epithelial side or within GBM itself

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26
Q

Accumulation of homogenous and eosinophilic material on light microscopy signifies this histological change

A

hyalinosis

accumulation of plasma proteins

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27
Q

Accumulation of extracellular collagenous matrixrial on light microscopy signifies this histological change

A

sclerosis

accumulation of ECM

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28
Q

Mechanism of glomerular injury where the Ig reacts directly with intrinsic kidney tissue Ag

A

In situ immune complex deposition

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29
Q

Mechanism of glomerular injury where immune complexes become trapped and activate complement

A

Circulating immune complex

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30
Q

PSGN shows this pathological pattern of kidney disease

A

acute diffuse GN

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31
Q

PSGN antigenic determinants

A

exotoxin B and zymogen precursor

SpeB and zSpeB

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32
Q

PSGN etiological agent

A

GABHS (strep pyogenes) types 12, 4, 1

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33
Q

Protein of cell wall used to identify GABHS

A

M protein

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34
Q

When does PSGN appear?

A

1-4 weeks after strep throat or impetigo

35
Q

Other causes of acute diffuse proliferative GN

A

bacteria
viruses
parasites
systemic diseases (SLE or PAN - polyarteritis nodosa)

36
Q

Diagnostic feature of acute diffuse proliferative GN

A

neutrophil and monocyte infiltration, proliferation of endothelial and mesangial cell

37
Q

Lab studies done for acute diffuse proliferative GN to confirm infectious agent?

A

ASO titres

low serum complement

38
Q

Immunofluorescence is done on a PSGN patient. What is seen?

A

Granular deposites of IgG and C3 (also IgM)

39
Q

What is seen on EM of PSGN?

A

subepithelial humps (immune complex deposits)

NOT within membrane – otherwise it would be nephrotic

40
Q

Complication of characterized by rapid loss of renal function.

Crescent formation seen. Crescentic GN.

A

RPGN

41
Q

Anti-GBM Ig-induced disease (Type I RPGN)

A

Goodpasture syndrome

42
Q

Immune-complex mediated diseases (Type II RPGN)

A

PSGN complication
SLE
Henoch-Schonlein purpura
IgA nephropathy (Berger’s)

43
Q

ANCAs are associated with what Type of RPGN?

A

Pauci-immune (Type III)

ANCA = vasculitis.

44
Q

RPGN type with little to no evidence of immune complexes or antibodies on immunofluorescence

A

Type III (vasculitis syndromes like Wegener granulomatosis, microscopic polyangiitis, or Churg-Strauss syndrome)

45
Q

RPGN type with linear pattern on immunofluorescence

A

Type I (Goodpasture syndrome)

46
Q

RPGN type with granular pattern on immunofluorescence

A

Type II (systemic lupus erythematosus, acute proliferative glomerulonephritis, Henoch-Schönlein purpura, and IgA nephropathy)

47
Q

Characterized by the diffuse thickening of capillary walls

A

MGN

48
Q

Characterized by diffuse flattening of podocytes

A

Minimal change disease

49
Q

Characterized by sclerosis of selected affectation of glomeruli involving only a portion of the glomerular tuft

A

Focal segmental glomerulosclerosis

FSGS

50
Q

Mixed nephrotic/nephritic with low C3

A

MPGN

51
Q

Immune dysfunction –> elaboration of cytokine-like circulating substance –> visceral epithelial cells affected –> heavy proteinuria

A

MCD (lipoid nephrosis)

52
Q

Nephrotic presentation seen in all ages, and more common in African Americans

A

FSGS

53
Q

Dense deposit disease

A

Type II MPGN

54
Q

Most common nephrotic syndrome in adults

A

MGN

55
Q

MPGN type with low C3, normal C1 and C4, low factor B and properdin

A

Type II

56
Q

Heymann nephritis pathgenesis

A

antibody to megalin antigenic complex

57
Q

MPGN type with activation of both classic and alternative complement pathways

A

Type I

58
Q

MPGN type with activation of alternative complement

A

Type II

59
Q

Secondary form is associated with AIDS, heroin use, sickle cell

A

FSGS

60
Q

EM reveals effacement of podocytes

A

MCD (lipoid nephrosis)

61
Q

MCD in adults usually associated with

A

Hodkin’s lymphoma

62
Q

Secondary MCD may follow use of these drugs

A

NSAIDs

63
Q

Similar lesion to MGN

A

Heymann nephritis

64
Q

In its secondary (non-idiopathic) form, a secondary event such as IgA nephropathy may reflect scarring of previously actie necrotizing lesions.

Superimposed on other glomerular diseases.

A

FSGS

65
Q

IgG antibody against alternative pathway C3 convertase (C3bBb)

A

C3 nephritic factor (seen in DENSE DEPOSIT DISEASE or TYPE II MPGN)

The binding of this autoantibody to C3bBb stabilizes the enzyme thus reduces the actions of C3b inactivators

66
Q

xx

A

x

67
Q

Initial involvement in FSGS

A

juxtamedullary glomeruli

proceeds to generalized involvement

68
Q

IF and LM reveals normal glomeruli.

A

MCD (lipoid nephrosis)

69
Q

Slit diaphragm complex affected –> epithelial damage

A

FSGS

70
Q

x

A

x

71
Q

On IF: granular pattern of C3 with IgG, C1q, and C4

On EM: subendothelial and mesangial immune complex deposits

A

Type I MPGN

72
Q

Nephrotic syndrome usually following infection or prophylactic immunization

A

MCD (lipoid nephrosis)

73
Q

x

A

x

74
Q

Degeneration and focal disruption of visceral epithelial cell

A

FSGS

75
Q

IgM and C3 seen in IF at mesangium or sclerotic areas

A

FSGS

76
Q

Nephrotic syndrome with dramatic response to corticosteroid therapy

A

MCD (lipoid nephrosis)

77
Q

Double-contour or tram-track capillary wall. in silver or PAS stain (splitting of GBM).

A

MPGN

78
Q

On LM: lipid droplets and foam cells

A

FSGS

79
Q

Causes of MGN (secondary MGN)

A

D-rugs
I-nfections (Hep, syph)
S-ystemic diseases SLE, DM)
C-arcinoma (lung, colon)

80
Q

Most common nephrotic syndrome in children

A

MCD (lipoid nephrosis)

81
Q

Spikes seen on silver stains in LM

A

MGN

82
Q

On IF: granular and linear pattern of C3

On EM: Dense deposits within GBM

A

Type II MPGN

83
Q

IgG and C3 seen in IF (nephrotic syndrome)

No C1q or C4

A

MGN

5 Patho (2 decks)

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