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D&T 3 Test 3 > Glomerular Disease > Flashcards

Glomerular Disease Flashcards

1
Q

what are all possible patterns seen on light microscopy?

A
  1. normal
  2. too many cells
  3. too many cells plus inflammatory cells
  4. sclerosed
  5. thickened membrane
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2
Q

What are possible patterns seen in IF

A
  • linear GBM
  • finely granular
  • coarse on mesangium
  • coarse on GBM
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3
Q

what is the classical clinical symptom for nephritic

A

hematuria

red cell casts

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4
Q

name 3 diseases presenting as primarily nephritic syndrome

A
  1. acute proliferative (poststreptococcal) glomerulonephritis
  2. non-streptococcal acute glomerulonephritis
  3. rapidly progressive glomerulonephritis
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5
Q

When does acute proliferative (poststreptococcal) glomerulonephritis occurs

A

1-4 weeks post strep skin or pharynx infection

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6
Q

who does acute proliferative (poststreptococcal) glomerulonephritis occur in

A

6-10 yr old

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7
Q

What immune response is mediated in acute proliferative (poststreptococcal) Glomerulonephritis? what are anti–streptococcal Abs and complement levels

A

immune-Complex

  • elevated anti-streptococcal Abs
  • low complement levels
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8
Q

What is seen in light microscopy for acute proliferative (poststreptococcal) glomerulonephritis

A

Proliferation - enlarged hypercellular glomeruli

neutrophil and monocyte infiltration

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9
Q

What is seen in IF for acute proliferative (poststreptococcal) glomerulonephritis?

A

Granular deposits of IgG, IgM, C3, mesangium along GBM

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10
Q

What is seen in electron microscopy for acute proliferative (poststreptococcal) glomerulonephritis

A

“humps”

epithelial side of basement membrane (subepithelial)

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11
Q

What are some symptoms seen in children with proliferative (poststreptococcal) glomerulonephritis

A

fever, malaise, nausea, oliguria, hematuria

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12
Q

prognosis for children with proliferative (poststreptococcal) glomerulonephritis

A
  • 95% recover with conservative toxicity, Na, and water balance
  • 1% develop rapidly progressive glomerulonephritis
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13
Q

what are signs and symptoms for adults with proliferative (poststreptococcal) glomerulonephritis

A

sudden hypertension
edema
elevated BUN

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14
Q

What is type I rapidly progressive Glomerulonephritis ? correlated disease?

A

Anti- GBM antibodies

Goodpastures syndrome

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15
Q

What is type II rapidly progressive glomerulonephritis? Correlated Disease?

A

Immune complex deposition

  • SLE
  • Henoch-Schoenlein Purpura ( IgA nephropathy)
  • post infectious glomerulonephritis
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16
Q

What is type III rapidly progressive glomerulonephritis

A

Pauci-Immune

  • Wegener granulomatosis
  • Microscopic polyangiits
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17
Q

What does rapidly progressive glomerulonephritis look like under light microscopy

A

Crescents

  • infiltration of monocytes and macrophages
  • proliferation of parietal epithelial cells lining Bowman’s capsule
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18
Q

What is the IF for rapidly progressive IF for

Type I, II, and III

A

I: linear GBM, Ig and complement

II: granular immune deposits

III: little or no deposition

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19
Q

What is electron microscopy for rapidly progressive glomerulonephritis

A

ruptures in GMB

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20
Q

What are symptoms for goodpasture

A

hemoptysis and pulmonary hemorrhage

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21
Q

What antibody is circulating with goodpasture

A

anti-GBM abs

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22
Q

What antibody is circulating with Wegener

A

c- ANCA

PRC

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23
Q

What antibody is circulating with SLE

A

anti-nuclear abs

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24
Q

What are general signs and symptoms for rapidly progressive glomerulonephritis

A

hematuria

RBC casts

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25
Q

What happens in nephrotic syndrome Pathophysiology

A
  • increased basement membrane permeability
  • urinary loss of plasma protein
  • proteinura greater than 3.5 gm/day
  • edema
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26
Q

Name 4 diseases that are nephrotic syndromes

A
  • membranous nephropathy
  • minimal-change disease
  • focal segmental glomerulosclerosis
  • membranoproliferative glomerulonephritis
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27
Q

What is the most common nephrotic syndrome in Caucasian adults

A

membranous nephropathy

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28
Q

what is the pathogenesis of membranous nephropathy

A

immune-complex mediated

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29
Q

What happens to Glomeruli in membranous nephropathy

A

diffuse thickening of glomerular capillary wall

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30
Q

What is IF for membranous nephropathy

A

Granular IgG and C3

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31
Q

What does membranous nephropathy look like in EM

A

immune-complex deposits between GBM and epithelial cells

“spikes and Domes”

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32
Q

What are clinical features of membranous nephropathy

A

insidious onset

  • hematuria
  • mild hypertension
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33
Q

What is the most common cause of nephrotic syndrome in children

A

minimal-change in disease

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34
Q

what is etiology and pathogenesis of minimal-change disease

A

immunologically mediated although lacks immune-complex mechanisms

35
Q

What is a good treatment for minimal-change disease

A

steroids

36
Q

If a child had this then they might get minimal-change disease

A
  • previous respiratory infection

- immunization

37
Q

what is the light microscopy for minimal-change disease

A

no change

38
Q

what is the IF for minimal-change disease

A

No Ig or complement deposits

- maybe weak staining

39
Q

What is Em for minimal change disease

A

effacement of foot processes of visceral epithelial cells

- no electron dense deposits

40
Q

What is a clinical feature for minimal change disease

A

massive proteinuria

41
Q

what is treatment responds rapidly with minimal-change disease

A

corticosteroid

42
Q

Focal segmental glomerulosclerosis is associated with other sytmptoms

A

HIV
heroin addiction
sickle-cell disease
morbid obesity

43
Q

What is the pathogenesis of focal segmental glomerulosclerosis

A

visceral epithelial damage

44
Q

What genes are involved with focal segmental glomerulosclerosis

A

NPHS1

NPHS2

45
Q

What is the light microscopy for focal segmental glomerulosclerosis

A
  • sclerosing some glomeruli ( focal)
  • segmental
  • affected capillary loops collapse
  • segmental hyalinosis
46
Q

What if the IF for focal segmental glomerulosclerossi

A

IgM and C3 in sclerotic areas

47
Q

What is the EM for focal segmental glomerulosclerosis

A
  • effacement of foot processes

- detachment of epithelial cells and denudation of GBM

48
Q

What can be used to treat focal segmental glomerulosclerosis

A

poor response to corticosteroid

49
Q

who has better prognosis with focal segmental glomerusclerosis

A

children

50
Q

Secondary membranoproliferative glomerulonephritis is associated with what disease

A 
SLE
HepB
HepC
endocarditis
HIV
alpha 1 antitrypsin deficiency
51
Q

What is the pathogenesis for Type I membranoproliferative glomerulonephritis

A
  • immune complexes

- activation of classical and alternative complement pathways

52
Q

what is the pathogenesis for Type II membranoproliferative glomerulonephritis

A

alternative complement pathway

53
Q

What is seen in Light microscopy for membranoproliferative glomerulonephritis

A
  • hypercellular: proliferation of mesangial cells and proliferation of capillary endothelium
  • glomerular capillary wall “tram-track” apperance
54
Q

What is seen in IF for membranoproliferative glomerulonephritis Type I

A
  • C3 in granular pattern

- IgG, C1q and C4

55
Q

What is seen in IF for membranoproliferative glomerulonephritis Type II

A

C3 - irregular granular pattern or linear

NO IgG or C1 or C4

56
Q

What does membranoproliferative glomerulonephritis Type I look like in EM

A

subENDOthelial electron-dense deposit

57
Q

What does membranoproliferative glomerulonephritis Type II look like in EM

A
  • dense material into GBM

- ‘ribbon-like’

58
Q

who does membranoproliferative glomerulonephritis usually occur in

A

children, adolescents and young adults

59
Q

Name 3 isolated glomerular abnormalities

A
  1. IgA nephropathy
  2. Alport syndrome
  3. think basement membrane lesion
60
Q

What is the pathogenesis of IgA nephropathy

A
  • genetic or acquired abnormality of immune regulation
61
Q

Where does IgA deposit in IgA nephropathy

A

mesangium

62
Q

What is the light microscopy for IgA nephropathy

A
  • Mesangial widening due to proliferation and endocapillary proliferation
63
Q

What is IF for IgA nephropathy

A
  1. Mesangial deposition of IgA

2. C3, IgG, IgM often

64
Q

What is IgA nephropathy look like on EM

A

dense deposits in mesangium

65
Q

what is another name for IgA nephropathy

A

Berger syndrome

66
Q

What is the classical symptoms for IgA nephropathy

A

hematuria

67
Q

How is Alport syndrome inherited

A

X-linked

68
Q

what are clinical symptoms of Alport syndrome

A
  1. hematuria with progression to chronic renal failure
  2. nerve deafness
  3. Eye disorders
69
Q

what is the pathogenesis for alport sydnrome

A
  • Abnormal alpha3, alpha4 or alpha 5 chains in collagen IV

- defective assembly of collagen IV

70
Q

What is the EM for alport syndrome

A

Early lesion: GBM thinning

Fully developed: GBM alterating thick and thin; splitting and layering of lamina densa

71
Q

What are clinical symptoms for alport syndrome

A

Hematuria

red cell casts

72
Q

what are clinical symptoms of thin basement membrane lesion? prognosis

A

-asymptomatic hematuria +/_ proteinuria

  • renal function preserved
  • prognosis excellent
73
Q

what disease shows subepithelial humps

A

acute proliferative glomerulonephritis

74
Q

what disease shows epimembranous deposists

A

membranous nephropathy

75
Q

what disease shows subendothelial deposists

A

membranoproliferative glomerulonephritis

lupus nephritis

76
Q

what disease has mesangial deposists

A

IgA nephropathy

77
Q

what happens to the kidney in end stage renal disease

A
  • sclerotic glomeruli
  • interstitial fibrosis and inflammation
  • hyalinized sclerotic vessels
  • atrophy of tubules
78
Q

what is a potential cause chronic glomerulonephritis

A

dialysis change

79
Q

who and when does Henoch-Scholein purpura show up

A
  • children 3-8 yrs

- follows an upper respiratory infection

80
Q

what is pathogenesis for Henoch-Schoenlein purpura

A

IgA deposited in glomerular mesangium

81
Q

What is the clinical feature for Henoch-Schoenlein Purpura

A

skin: purpuric lesions on arms, legs, buttocks

82
Q

what happens to the proteins in diabetic nephropathy

A
  • nonenzymatic glycosylation of proteins
83
Q

Where does amyloids deposit in amyloidosis

A

mesangium and glomerular capillary walls

D&T 3 Test 3 (7 decks)

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