Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

USMLE Renal > Nephritic Syndromes > Flashcards

Nephritic Syndromes Flashcards

You may prefer our related Brainscape-certified flashcards:
USMLE® Step 1 flashcards
1
Q

What are the characteristics of nephritic syndrome?

A
  • Limited proteinuria (<3.5g/day)
  • Oliguria and azotemia
  • Salt retention w. periorbital edema and hypertension
  • RBC casts and dysmorphic RBCs in urine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What will a biopsy show in nephritic syndrome?

A
  • Hypercellular, inflamed glomeruli
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What does C5a attract?

A

Neutrophils

- Mediate damage in nephritic syndromes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What does PSGN arise after?

A

Group A (B hemolytic) strep infection

  • Of skin
  • Or pharynx
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What do nephritogenic strains of strep carry as a virulence factor?

A

M protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How long after infection does PSGN usually present?

A

2 - 3 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What do patients with PSGN usually present with?

A
  • Hematuria (cola-coloured urine)
  • Oliguria
  • Hypertension
  • Periorbital edema
  • Usually seen in children, but may occur in adults
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What kind of hypersensitivity reaction is PSGN?

A

Type 3 - immune complex deposition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What happens to complement levels in PSGN?

A

Decreased (esp C3)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What can be seen on histology in PSGN?

A
  • LM - Glomeruli enlarged and hypercellular
  • IF - starry sky granular appearance lumpy bumpy due to IgM, IgG and C3 deposition along BM and mesangium
  • EM - Subepithelial IC humps
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the treatment for PSGN?

A

Supportive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What can PSGN progress to in adults?

A

Rapidly Progressive (crescentic) Glomerulonephritis (RPGN)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How quickly can RPGN progress to renal failure?

A

days to weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is Rapidly progressive (crescentric) GN characterized by?

A

Crescents in Bowman space

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the crescents in RPGN comprised of?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Why is immunofluoresence often required in RP (crescentric) GN?

A

To resolve etiology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What will Goodpasture syndrome show on IF

A

Linear IF

- Antibodies to GBM and alveolar BM this creates a sharp line on IF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What type of hypersensitivity reaction is Goodpasture syndrome?

A

Type II

19
Q

What are classic signs of a patient with RP (crescentric) GN secondary to Goodpasture’s?

A
  • Young adult male presents with hemoptysis and hematuria
20
Q

What is Goodpastures RPGN treated with?

A

Plasmapheresis

21
Q

What would cause a negative or Pauci-immune (no Ig/C3 deposition) IF finding in a aptient with RPGN?

A
  • Granulomatosis w. polyangitis (aka Churg-Strauss syndrome)
  • Eosinophilic granulomatosis w. polyangiitis
  • Microscopic polyangiitis
22
Q

What is the most common cause of death in SLE?

A

Renal failure

  • RP(crescentic)GN
  • > granular IF, Diffuse proliferative
23
Q

What cause would Granular IF findings in RP(crescentric)GN be due to?

A
  • PSGN

- Diffuse Proliferative (often due to SLE)

24
Q

Negative/Pauci-immune IF in RPGN with PR3-ANCA/c-ANCA is caused by what?

A

Granulomatosis with polyangiitis

25
Q

Negative/Pauci-immune IF in RPGN with MPO-ANCA/p-ANCA is caused by what?

A
  • Eosinophilic granulomatosis w. polyangiitis OR

- Microscopic polyangiitis

26
Q

What will Diffuse Proliferative GN show on Light Microscopy?

A

Wire looping of capillaries

27
Q

What will immunofluoresence show in diffuse proliferative GN?

A

Granular

28
Q

What will Electron Microscopy show in Diffuse Proliferative GN?

A

Subendothelial, sometimes subepithelial or intramembranous IgG-based Ics often w. C3 deposition

29
Q

What will IgA nephropathy (Berger disease) present with?

A

Episodic hematuria that usually occur concurrently w. resp or GI tract infections (IgA is secreted by mucosal linings)
- Renal pathology of IgA vasculitis

30
Q

What will histology show in IgA nephropathy (Berger disease)?

A

LM - Mesangial proliferation
IF - IgA-based IC deposits in mesangium
EM - Mesangial IC deposition

31
Q

What is Alport syndrome due to a mutation in?

A

Type IV collagen

32
Q

How is Alport Syndrome inherited?

A

X-linked dominant

33
Q

What happens to the glomerular BM in Alport syndrome?

A

Irregular thinning and thickening and splitting of GBM

34
Q

What other issues are associated with Alport syndrome (type IV collagen mutation)?

A
  • Eye problems (e.g retinopathy, anterior lenticonus)
  • GN
  • Sensorineural deafness

Can’t see, pee or hear a bee!

35
Q

What will EM show in Alport Syndrome?

A

“Basket-weave” appearance due to irregular thickening of GBM

36
Q

How can Membrano-proliferative GN be subdivided?

A

Type I and II

37
Q

What can type I Membrano-proliferative GN be secondary to?

A

Hep B or C infection

- May also be idiopathic

38
Q

What will be seen on histology in type 1 membrano-proliferative GN?

A

Subendothelial IC deposits w. granular IF

39
Q

What will be seen on histology in type 2 membrano-proliferative GN?

A

Intramembranous deposits, also called dense deposit disease

40
Q

What is seen on both types of Membrano-proliferative GN?

A

Mesangial ingrowth

  • GBM splitting
  • Tram-track on HandE and PAS stains
41
Q

What autoantibody is type 2 Membrano-proliferative GN associated with?

A

C3 nephritic factor (IgG autoantibody that stabilises C3 convertase -> persistent complement activation -> decreased C3 levels

42
Q

What condition may be seen with Churg-Strauss and not microscopic polyangitis?

A

Asthma

43
Q

What is the most common cause of nephropathy worldwide?

A

IgA nephropathy

44
Q

What nephritic syndromes often co-present with nephrotic?

A
  • Membrano-proliferative GN

- Diffuse Proliferative GN (crescentic, rapidly progressive w. granular IF)

USMLE Renal (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions