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Systems 1 Part 2 > Renal Pathology I > Flashcards

Renal Pathology I Flashcards

1
Q

4 histologic alterations due to glomerular injury

A

hypercellularity, BM thickening, mesangial expansion, sclerosis

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2
Q

where can new cells grow in response to injury?

A

glomerular capillaries, urinary space, mesangium

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3
Q

BM thickening aka

A

duplication or double contours

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4
Q

mesangial widening due to –

A

increased mesangial matrix and cells (mesangial proliferation)

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5
Q

crescents

A

cellular proliferation in urinary space

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6
Q

crescents in urinary space is due to –

A

basement membrane rupture

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7
Q

what cells are present in crescents?

A

macrophages, neutrophils, epithelial cells

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8
Q

T/F: crescents contain fibrin and are seen in severe glomerular injury

A

true

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9
Q

pathogenesis of glomerular injury (immunologic injury)

A

immune complex-mediated injury, cytotoxic antibodies, cell mediated autoimmunity

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10
Q

how can you detect immune complex deposits?

A

immunofluorescence (most sensitive method)

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11
Q

immunofluorescence can be used to characterized – of immune complex deposits

A

type of immunoglobulin

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12
Q

How can you determine the precise location of immune complex deposits?

A

electron microscopy

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13
Q

what color is immune complex deposits in immunofluorescence?

A

green

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14
Q

where can immune deposits be found?

A

subepithelial, subendothelial, mesangial

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15
Q

which type of immune deposits elicits more inflammation?

A

subendothelial

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16
Q

deposits activate – which lead to inflammation

A

complement

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17
Q

4 types of glomerular syndromes

A

asymptomatic hematuria and/or proteinuria, nephrotic syndrome, acute nephritic syndrome, chronic renal failure

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18
Q

T/F: most glomerular diseases present with one particular syndrome

A

true

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19
Q

T/F: some patients present with a mixed syndrome

A

true

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20
Q

T/F: some diseases have variable presentation

A

true

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21
Q

features of nephrotic syndrome

A

proteinuria (at least 3.5 g/day)
hypoalbuminemia
generalized edema
hyperlipidemia, hyperlipiduria

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22
Q

hypoalbuminemia

A

low albumin in blood because you lost albumin to urine

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23
Q

edema in nephrotic syndrome is the result of –

A

lost albumin

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24
Q

major causes of nephrotic syndrome

A

membranous nephropathy, minimal change nephropathy, focal and segmental glomerulosclerosis

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25
Q

nephrotic syndrome is due to – abnormality

A

podocyte (visceral epithelial cell)

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26
Q

what causes membranous nephropathy (one cause of nephrotic syndrome)?

A

immune complex formation on subepithelial side of BM

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27
Q

in membranous nephropathy (one cause of nephrotic syndrome), epithelial cells respond to injury by –

A

making more BM in form of spikes

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28
Q

why do epithelial cells make spikes in membranous nephropathy?

A

try to wall off immune complex deposits

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29
Q

immunofluorescence of membranous nephropathy show –

A

granular deposits of IgG and complement along BM

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30
Q

types of membranous glomerulonephritis

A

primary (idiopathic) or secondary

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31
Q

features of minimal change nephropathy (one cause of nephrotic syndrome)

A

most common cause of proteinuria in children, can develop at any age, normal glomeruli by lumen, diffuse loss of podocytes by EM

32
Q

how to treat minimal change nephropathy?

A

steroids

33
Q

focal affects

A

some but not all glomeruli

34
Q

segmental affects

A

only a portion of glomerulus

35
Q

focal and segmental glomerulosclerosis (one cause of nephrotic syndrome) is often found in –

A

older kids, young adults

36
Q

types of focal and segmental glomerulosclerosis

A

primary (idiopathic) or secondary

37
Q

FSGS –>

A

leaky glomeruli

  • -> lose ability to filter blood
  • -> need more compensatory nephrons
38
Q

features of nephritic syndrome

A

hematuria, oliguria (decreased urine), hypertension, proteinuria (less than nephrotic syndrome)

39
Q

types of nephritic syndrome

A

acute proliferative or rapidly progressive glomerulonephritis

40
Q

acute proliferative glomerulonephritis is – process

A

immune complex mediated

41
Q

causes of acute proliferative GN

A

exogenous or endogenous antigens

42
Q

exogenous antigens of acute proliferative GN

A

post infectious/post-streptococcal

43
Q

endogenous antigens of acute proliferative GN

A

lupus (autoimmunity)

44
Q

in acute proliferative GN, – are trapped in the glomerulus

A

circulating immune complexes

45
Q

acute proliferative GN: circulating immune complexes –

A

bind/fix complement

46
Q

acute proliferative GN: complement and cytokines –

A

recruit leukocytes

47
Q

acute proliferative GN: proliferations of –

A

endothelial and circulating cells in capillaries (may include mesangial and epithelial cells)

48
Q

most post infectious GN (acute proliferative GN) cases are resolves with –

A

supportive care

49
Q

deposits of post infectious GN (acute proliferative GN) resolve within –

A

a few months

50
Q

is there scarring in post infectious GN (acute proliferative GN)

A

no

51
Q

who easily recovers from post infectious GN (acute proliferative GN)?

A

children

52
Q

most adults with post infectious GN (acute proliferative GN) develop –

A

end stage renal disease

53
Q

post infectious GN (acute proliferative GN) prevalence

A

developing countries

54
Q

If circulating immune complex mediated GN is transient then –

A

deposits are phagocytized and/or degraded and inflammatory changes resolve

55
Q

if circulating immune complex mediated GN is continuous then –

A

chronic progressive GN

56
Q

lupus is – circulating immune complex mediated GN

A

continuous

57
Q

post streptococcal GN is – circulating immune complex mediated GN

A

transient

58
Q

all rapidly progressive glomerulonephritis are have this morphological characteristics

A

crescents

59
Q

crescent is – within urinary space

A

fibrin

60
Q

crescent: fibrin within urinary space incites –

A

marked proliferation/accumulation of macrophages and epithelial cells

61
Q

isolated hematuria – nephropathy

A

IgA and thin basement membrane nephropathy

62
Q

most common primary glomerular disease

A

IgA nephropathy

63
Q

IgA nephropathy prevalence

A

Asian and Hispanic patients

64
Q

most common presentation of IgA nephropathy

A

hematuria

65
Q

1/3 of patients with IgA nephropathy

A

progress to end stage renal disease

66
Q

IgA has variable appearance in light microscopy but the most common finding is –

A

mesangial proliferation

67
Q

T/F: when extensive loss of nephrons occurs, end stage renal disease continues to progress regardless of initial cause of injury

A

true

68
Q

progression of renal disease results in glomerular injury which morphologically resembles –

A

FSGS and tubulointerstitial scarring

69
Q

tubulointerstitial scarring includes

A

tubular atrophy and interstitial fibrosis

70
Q

renal disease progression to FSGS results in –

A

proteinuria

71
Q

features of renal disease progression to FSGS

A

segmental scarring and eventually global scarring

72
Q

as more glomeruli become sclerotic –> GFR

A

decreases

73
Q

T/F: hyperfiltration increases as renal disease progresses to FSGS

A

true

74
Q

what causes nephritic syndrome?

A

endothelial cell injury

75
Q

what causes nephrotic syndrome?

A

podocyte injury

76
Q

diseases that potentially cause endothelial injury

A

post-infectious GN
lupus nephritis
RPGN

Systems 1 Part 2 (27 decks)

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