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Urinary & Renal > GN > Flashcards

GN Flashcards

1
Q

glomerular disease is diagnosed by?

A

biopsy! (pathological, not clinical dx)

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2
Q

three types of microscopy used to examine renal biopsies

A

light + staining, immunofluorescence, electron

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3
Q

three types of cells in the glomerulus

A

podocyte (epithelial), endothelial cell, mesangial cell (at the neck)

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4
Q

fenestrated endothelial cell is separated from the podocyte by?

A

glomerular basement membrane

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5
Q

primary sx of nephrotic syndrome

A

edema, proteinuria, hypoproteinemia, hyperlipidemia, lipiduria (with oval fat bodies in urine)

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6
Q

primary sx of nephritic syndrome

A

hematuria, azotemia, HTN, RBC casts

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7
Q

major causes of nephrotic syndrome

A

minimal change GN, FSGS, membranous glomerulopathy, diabetic nephropathy, amyloidosis, (membranoprolif, lupus)

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8
Q

major causes of nephritic syndrome

A

IgA nephropathy, lupus GN, IgA vasculitis, cryoglobulinemic vasculitis, anti-GBM GN, ANCA GN (membranoprolif)

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9
Q

what does minimal change glom look like on microscopy?

A

normal by LM, normal by IM, foot process effacement on EM

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10
Q

who gets minimal change glom?

A

children

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11
Q

tx of minimal change glom

A

corticosteroids (empiric in a kid, don’t need biopsy first)

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12
Q

what does membranous glom look like on microscopy?

A

thick capillary walls on LM, granular capillary wall staining on IM, dense subepithelial deposits on EM (these are immune complexes)

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13
Q

primary membranous glom is caused by?

A

anti-phospholipase A2 receptor auto-antibodies (antigen comes from podocyte)

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14
Q

secondary causes of membranous glom

A

SLE, infections (hep B, syph), metal drugs, malignancy

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15
Q

what does FSGS look like on microscopy?

A

parts of some glomeruli have consolidation of glomerular tufts

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16
Q

primary FSGS is _____; secondary causes include?

A

idiopathic; HIV, mutation in podocyte genes, drug toxicity (heroin, pamidronate, interferon-alpha), adaptive structural response (obesity, sickle cell, congenital heart disease)

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17
Q

what does membranoproliferative glom look like on microscopy?

A

thick capillary walls AND hypercellularity (from leukocyte infiltration), variable IM based on immune complex vs. dense deposit dz

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18
Q

causes of immune complex MPGN

A

chronic bacterial infection (osteomyelitis, endocarditis), hep C (cryoglob), malignancy

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19
Q

causes of dense deposit MPGN

A

abnormalities in alternative complement pathway activation (antibodies or mutations)

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20
Q

most common cause of ESRD in US

A

diabetic glomerulopathy

21
Q

signs of diabetic nephropathy

A

proteinuria, progressive decline in GFR, HTN

22
Q

what does DN look like on microscopy?

A

progressive thickening of GBM, increase in mesangial matrix, KW nodules

23
Q

which types of amyloid cause nephrotic syndrome?

A

AL amyloid, AA amyloid

24
Q

by EM, amyloid looks like?

A

randomly arranged fibrils

25
Q

name three types of glomerulonephritis that cause nephritic syndrome

A

immune complex (granular), anti-GBM (linear), ANCA (no IF)

26
Q

name the major patterns of glomerular injury

A

mesangioprolif, prolif (inside lumen), crescent (extracapillary), sclerosing (order of severity)

27
Q

order glomerulonephritis in order of severity

A

acute postinfectious, IgA < lupus (huge range) < ANCA, anti-GBM

28
Q

acute postinfectious GN most often presents with what pathological features

A

diffuse proliferative GN with PMNs inside the lumen, subepithelial humps, and granular staining on IF

29
Q

the primary reason for a renal biopsy of a patient with SLE is to?

A

assess disease severity and direct management

30
Q

class V lupus shows what histologic manifestations?

A

membranous GN, thick BM

31
Q

IgA nephropathy has IgA dominant ____ immune deposits

A

mesangial (so mesangioprolif GN is common presentation)

32
Q

when IgA vasculitis is systemic, it is called?

A

Henoch-Schonlein purpura

33
Q

systemic vasculitis from Hep C is called?

A

cryoglobulinemic vasculitis

34
Q

ANCA GN and vasculitis is due to antibodies against?

A

myeloperoxidase or proteinase 3 (proteins in cytoplasm of PMNs and monocytes)

35
Q

pathology of ANCA GN

A

capillary necrosis and rupture, leading to crescent GN

36
Q

ANCA associated pulm lesions

A

hemorrhagic (hemoptysis), granulomatous, or eosinophilic inflammation

37
Q

when ANCA strictly affects the kidneys only, it is called?

A

Pauci-Immune Crescentic GN

38
Q

why doesn’t ANCA-GN show up on IF

A

ANCA directly attacks cells rather than the membrane

39
Q

in anti-GBM disease, patients have antibodies against?

A

type IV collagen in the GBM (leads to linear IF staining)

40
Q

ANCA GN presents in a (younger/older) population

A

older

41
Q

measurement of proteinuria

A

24-hour urine collection, spot urine-creatinine ratio (should be less than 0.2)

42
Q

transient proteinuria can occur in the present of ?

A

fever

43
Q

proteinuria must be ____ in order to suspect glomerular disease

A

fixed

44
Q

complications of nephrotic syndrome

A

thrombosis! (due to loss of anticoag factors) – can be DVT or renal vein thrombosis; infection (due to loss of Ig); accelerated atherosclerosis

45
Q

clues that hematuria is glomerular

A

brown color, proteinuria, dysmorphic RBCs (acanthocytes especially), RBC casts, rash

46
Q

GN associated with low C3 (alternative pathway)

A

postinfectious, endocarditis, membranoprolif.

47
Q

GN associated with low C3 and C4 (classic pathway)

A

lupus, cryoglobulinemic

48
Q

GN associated with normal complement levels

A

ANCA, IgA nephritis, Henoch-Schonlein purpura, Goodpasture’s

49
Q

signs of necrotizing vasculitis

A

systemic, skin, respiratory, and ENT symptoms

Urinary & Renal (22 decks)

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