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Renal Final > Nephritis Pathology > Flashcards

Nephritis Pathology Flashcards

1
Q

clinical manifestations of nephritic syndrome

A
  • hematuria
  • urine RBC casts
  • proteinuria (usually less than 3 g/24 hrs, less than NS)
  • sometimes HTN
  • varying renal failure, stages: asymptomatic w/ hematuria/proteinuria, acute GN, rapidly progressive GN, chronic GN
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2
Q

6 DDx for nephritic syndrome

A
  • membranoproliferative GN
  • IgA nephropathy
  • lupus nephritis
  • acute post infectious GN
  • ANCA GN
  • anti GBM GN
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3
Q

why is MPGN unique for nephritis (2)

A

often presents w/ both NS and GN

can be either immune complex or C3 glomerulopathy

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4
Q

histo LM changes w/ MPGN

A

thickened walls AND hypercellularity- some in lumen, some in mesangium

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5
Q

4 broad GN mechanisms

A

all immune dysfn:

  1. immune complex GN
  2. C3 glomerulopahty
  3. anti GBM GN
  4. ANCA GN
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6
Q

how to distinguish two types of MPGN

A

IF-
immune complex will have Ig AND C3 deposits in granular pattern

C3 MPGN will have C3 deposits but no Ig

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7
Q

causes for different types of MPGN

A

immune complex- infection, autoimmunity, neoplasia

C3- complement dysregulation (alternate pathway)

can have overlap! infectious provocation and complement dysfn

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8
Q

describe the general progression of glomerular injury patterns (4), along w/ clinical manifestations

A
  1. mesangial hypercellularity- mesangioproliferative GN, asymptomatic to mild nephritis
  2. endocapillary hypercellularity -focal/diffuse proliferative or necrotizing GN, moderate to severe nephritis (maybe RPGN)
  3. extracapillary hypercellularity (crescentic)- severe to RPGN
  4. sclerosis (sclerosing GN)- chronic nephritis
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9
Q

way to separate 4 GN mechanisms by IF

A

immune complex- granular w/ Ig and C3

C3 GN- granular for C3 and little/no Ig

anti GBM- linear GBM Ig

ANCA- paucity of staining for Ig and complement

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10
Q

2 main causes of immune complex GN, populations

A

lupus nephritis (AA females) and IgA (whites/asians)

both the predominant causes in younger pts (under 50)

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11
Q

why biopsy w/ SLE and GN?

A

assess severity and chronicity- often not used for Dx w/ other signs/ Sx of lupus

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12
Q

classes 1-6 of lupus GN

A

based on patho pattern

1- normal histo

2- mesangioproliferative

3- focal prolferative/ necrotizing (mesangial and subendothelial deposits, endocapillary leukocytes)

4-diffuse proliferative/ necrotizing

5- membranous GN (subepithelial deposits)

6- sclerosing

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13
Q

clinical note of stage 5 lupus nephritis

A

membranous lupus GN causes nephrotic proteinuria

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14
Q

by far most common GN for asians

A

IgA

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15
Q

patho pattern for IgA nephropathy

A

IgA mesangial deposits- hypercellularity and more matrix in mesangium w/ LM

IgA stain on IF

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16
Q

progression of IgA compared to lupus

A

more on the left end of the spectrum (further from crescentic and sclerosing)- more common w/ mesangioproliferative, proliferative

slower progressing, does not need as aggressive Tx

17
Q

manifestations of IgA vasculitis (henoch schonlein purpura)

A

systemic variant of IgA nephropathy- affects skin (purpura, raised and palpable) and GI tract

18
Q

mechanisms for acute postinfectious GN (PIGN)

A

immune complex and/or C3 GN

19
Q

clinical key for acute PIGN

A

most often follows strep or staph infection- pay attention to past illnesses, rashes, etc

20
Q

pathological pattern of PIGN (think 3 modalities- LM, EM, IF)

A

diffuse proliferative GN

PMN infiltration and sub-epithelial humps of deposit visible by EM

granular deposits by IF, IgG and/or C3

21
Q

2 categories of anti-GBM disease

A

w/ lung hemorrhage- goodpasture

w/o- anti GBM GN

22
Q

IF and LM presentation of anti GBM

A

linear deposition in IF- b/c anti GBM Abs target type IV collagen antigens, deposit in line along GBM

LM often has crescentic to sclerosing pattern

23
Q

detection of ANCA

A

IF microscopy assay for PMN cytoplasm autoAb

can specify b/w MPO ANCA and PR3-ANCA

24
Q

ANCA population

A

older pts- 50-80

25
Q

ANCA vasculitis effect on different vessel types

A

arteries: abdominal pain, skin nodules/ ulcers
capillaries: GN, pulm capillaritis
venules: purpura (leukocytes in dermis)

26
Q

3 patterns of pulm inflammation from ANCA vasculitis

A

MPA- hemorrhagic capillaritis

GPA- necrotizing, granulomatous vasculitis w/ giant cells

eGPA- GPA w/ eosinophils

27
Q

4 possible ANCA diseases

A

RLV - renal limited, nothing systemic

MPA- vasculitis w/o granulomas or asthma

GPA- vaculitis w/ granulomas, no asthma

eGPA- vasculitis w/ granulomas and asthma

Renal Final (13 decks)

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