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Test 9 > Path 2 Glomerular Disease > Flashcards

Path 2 Glomerular Disease Flashcards

1
Q

Normal glomerular measurement

A

BM and podocytes are same width

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2
Q

Inside v outside lining gaps

A
  • Fenestrae inside between Endothelial cells

- Filtration slits outside between Epithelial cells (podocytes)

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3
Q

Nephrotic syndrome

A

Increased BM permeability

  • Proteinuria, hypoalbuminemia
  • Generalized edema
  • Hyperlipidemia and hypercholesterolemia
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4
Q

Minimal change disease

A

Lipoid nephrosis (nephrotic syndrome)

  • Age 2-6
  • No immune complex deposition
  • Tx with steroids
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5
Q

Minimal change disease gross appearance

A

Lipid laden cortices

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6
Q

Minimal change disease histology (3)

A
  • Normal glomeruli
  • Lipid accumulation in proximal convoluted tubules
  • Fusing of foot processes (epithelial)
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7
Q

Focal segmental glomerulosclerosis

A

Sporadic partial glomerular scarring

  • Same clinical as MCD
  • Older patients, can’t Tx with steroids
  • IgM and C3 immune complex deposition
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8
Q

Focal segmental glomerulosclerosis

A
  • Primary

- Secondary (HIV, heroin, IgA nephropathy)

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9
Q

Membranous GN

A

Nephrotic syndrome in teenagers and young adults

  • IgG, C3 immune complex deposition
  • Doesn’t respond to steroids
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10
Q

Membranous GN stain

A

PAS

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11
Q

Minimal Change Disease stain

A

Fat stain

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12
Q

Membranous GN histology (3)

A
  • Thickened capillary loops
  • Spike and dome appearance
  • Granular immunofluorescence
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13
Q

Membranous GN EM

A

Thickened BM with immune complex nodules

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14
Q

Membranous GN etiology

A
  • Idiopathic

- SLE, infections, drugs, malignancy

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15
Q

Diabetic nephropathy

A

Nephrotic syndrome

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16
Q

Diabetic nephropathy glomerulus histology (4)

A

Kimmelstiel-Wilson nodules

  • Fibrin caps
  • Increase in mesangial matrix
  • Diffuse glmerulosclerosis
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17
Q

Diabetic nephropathy extra-glomerulus histology (2)

A
  • Sclerosed afferent & efferent arterioles

- Armanni-Ebstein lesions (glycogen in tubules) in chronic hyperglycemia

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18
Q

Diabetic nephropathy EM (2)

A
  • Markedly thickened BM

- Mesangial matrix accumulation

19
Q

Amyloidosis

A

Nephrotic syndrome

-Subendothelial and mesangial deposits

20
Q

Amyloidosis EM

A

Criss-cross fibrillary pattern

21
Q

Amyloidosis histology (2)

A
  • Congo Red stain

- Birefringence under polarized light

22
Q

Lupus Nephropathy Class I

A

No observable renal involvement

23
Q

Lupus Nephropathy Class II

A

Mesangial glomerulonephritis

24
Q

Lupus Nephropathy Class III

A

Focal proliferative glomerulonephritis

-Less than half of glomeruli involved, but individual damage can be extensive

25
Q

Lupus Nephropathy Class IV

A

Diffuse proliferative glomerulonephritis

26
Q

Lupus Nephropathy Class V

A

Membranous glomerulonephritis

-Intra and extramembranous immune complex deposition

27
Q

Lupus Nephropathy histology (5)

A
  • Extensive inflammatory glomerular scarring
  • Subendothelial and mesangial immune complex deposition
  • Wire loop lesions
  • Tubular reticular structures
  • Fingerprint patterns pathognomonic
28
Q

Nephritic syndrome

A

Inflammatory rupture of glomerular capillaries

  • oliguria
  • hematuria (w/RBC casts)
  • azotemia
  • HTN
29
Q

Acute Proliferative Poststreptococcal GN

A

Prototypical nephritis

  • IgG/C3 Immune complexes between epithelial foot processes -> PMN attack -> hemorrhage
  • Complete recovery in all children, 60% adults
  • Analogous to rabbit “serum sickness”
30
Q

PSGN gross appearance

A

Petechial hemorrhages covering surface of kidney

31
Q

PSGN histology

A
  • Glomeruli enlarged, hypercellular (mesangial, endothelial, PMN), “bloodless”
  • Granular immunofluorescence
32
Q

PSGN EM

A

Subepithelial immune complexes

33
Q

PSGN lab levels

A
  • Decreased serum C3

- Increased ASO titer

34
Q

Rapidly Progressive GN

-mechanism, cause, prognosis

A

Cresentic GN

  • Proliferation of parietal epithelial cells of bowmans capsure
  • Can be complication of PSGN
  • Renal failure over weeks to months
35
Q

Crescentic GN (RPGN) types

A
  • ANCA positive
  • ANCA negative
    • Anti-GBM (Goodpasture)
    • Immune complex (ASO, SLE, IgA)
36
Q

Goodpasture syndrome

A

Antiglomerular BM antibodies

  • attacks glomeruli and alveoli
  • linear immunofluorescence for IgG
37
Q

Alport syndrome - cause, histology, clinical

A

Type IV collagen mutation (alpha-5 chain)

  • Rarefaction and splitting of BM lamina densa
  • Hereditary nephritis, nerve deafness, ocular disorders (cataracts, lens dislocation)
38
Q

Berger disease

A

IgA nephropathy

  • IgA deposits in mesangium
  • Recurrent hematuria in youth, often benign
39
Q

IgA nephropathy as a component

A

Henoch-Schonlein purpura

  • Skin purpura
  • GI pain & bleeding
  • Joint arthritis
  • Kidney IgA nephropathy
40
Q

Membranous GN v Membranoproliferative GN

A

BM v BM and Mesangium

41
Q

Membranoproliferative GN histology (4)

A
  • Tram-track BM (doubled)
  • Lobular pattern
  • Mesangial proliferation (hypercellular)
  • Collapse of capillaries
42
Q

Type 1 Membranoproliferative GN

A

Immune complex nephritis

  • unknown antigen
  • striking tram-track
43
Q

Type 2 Membranoproliferative GN

A

Dense Deposit Disease

  • C3 nephritic factor
  • Serum C3 markedly reduced
44
Q

Chronic GN

A

End-stage kidney

  • Marked renal failure
  • HTN
  • Small pale kidneys
  • Hyaline arteriolosclerosis
  • Interstitial fibrosis

Test 9 (17 decks)

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