Firecracker III Flashcards

1
Q

Pathologic changes in renal interstitium with acute drug-induced interstitial nephritis

A

acute inflammation of renal interstitium (edema + prominent mononuclear and eosinophilic infiltrate)

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2
Q

EM FSGN

A

diffuse podocyte effacement and focal detachment of visceral epithelial cells

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3
Q

strep that causes PSGN

A

group A β-hemolytic Streptococcus pyogenes

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4
Q

large hypercellular glomeruli due to WBC infiltrate and proliferation of mesangial and endothelial cells

A

PSGN

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5
Q

Sub-Endothelial Deposits

A

DPGN (SLE)

Type 1 membranoproliferative glomerulonephritis

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6
Q

Sub-Epithelial Deposits

A
PSGN (nephritic)
Membranous glomerulonephritis (spike and dome)
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7
Q

spike and dome

A

membranous glomerulonephritis (on silver stain)

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8
Q

Drug acts as a hapten by covalently binding to a carrier→ hapten-carrier conjugate serves as an immunogen, triggering a HSR (type I &/or type IV) → injury of tubular cells &/or their BM

A

Acute drug-induced interstitial nephritis

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9
Q

What makes people think that drug-induced interstitial nephritis is a type I hypersensitivity?

A

Some patients have ↑ serum IgE levels, suggesting Type I hypersensitivity

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10
Q

What makes peoples think that drug-induced interstitial nephritis is a type IV hypersensitivity?

A

Other patients have mononuclear/granulomatous infiltrate on renal biopsy and positive skin tests to drugs, suggesting Type IV hypersensitivity

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11
Q

Acute drug-induced interstitial nephritis may be caused by “Please Note All Drugs that Can Possibly Scar Renals”

A
PCN
NSAIDs
Allopurinol
Diuretics (thiazides, furosemid, acetazolamide)
Cephalosporins
Proton pump inhibitors
Sulfamide antibiotics . Sulfasalazine
Rifampin
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12
Q

ICs deposit on the glomerular epi BM → activation of complement cascade → C5b-C9 MAC damages glomerular epithelial & mesangial cells, causing their release of proteases & oxidants which further contribute to glomerular cap wall damage → nephrotic-range proteinuria.

A

Membranous nephropathy

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13
Q

In cases of PSGN (poststreptococcal glomerulonephritis), how long does it usually take for PSGN to develop after a streptococcal infection? Why?

A

1-4 weeks to make antibodies (↑ anti-DNAse B) and form immune complexes →

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14
Q

Drugs that can cause secondary membranous nephropathy

A
  • Penicillamine
  • Captopril
  • NSAIDs
  • Gold
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15
Q

Infections that can cause secondary membranous nephropathy

A
  • Hepatitis B
  • Hepatitis C
  • Syphilis
  • Malaria
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16
Q

AI diseases that can cause secondary membranous nephropathy

A
  • SLE (systemic lupus erythematosus)
  • RA (rheumatoid arthritis)
  • SS (sjögren’s syndrome)
  • Hashimoto thyroiditis
17
Q

What malignancies can cause secondary membranous nephropathy

A
  • Solid tumors—eg, colon carcinoma, lung carcinoma, melanoma

- Chronic lymphocytic leukemia

18
Q

Membranous nephropathy EM

A

Subepithelial (subpodocyte) IC deposits

19
Q

Membranous nephropathy LM

A

Normal-appearing glomeruli (early stages of the disease) or diffuse glomerular capillary wall thickening (later stages of the disease)

20
Q

Membranous nephropathy on silver stain

A

spike and dome pattern—the spikes are basement membrane material (colored black by the silver stain) and the domes are immune complex deposits (not colored by the silver stain).

21
Q

Intramembranous Deposits (within the GBM):

A

MPGN type I and II (dense-deposit disease) → EM may show “tram-tracking”, although this is only present in a minority of cases and is not diagnostic of MPGN type II by itself

22
Q
  • Fever, rash, joint pain
  • Eosinophilia, ↑ serum IgE
  • Hematuria, mild proteinuria, pyuria (eosinophiluria)
  • 50% of patients develop acute renal failure with azotemia (BUN:Cr ratio≤15) and oliguria
A

S/sx of acute drug-induced interstitial nephritis ~15 days after first dose of drug

23
Q

The most common nephrotic syndrome in the US

A

Membranous nephropathy (membranous glomerulopathy):

24
Q

LM PSGN

A

Large hypercellular glomeruli

25
Q

IF PSGN

A

Granular/coarse deposits of IgG, IgM, and C3 along the GBM (glomerular basement membrane) and in the mesangium

26
Q

EM PSGN

A

Large subepithelial (subpodocyte) electron-dense deposits—prominent “bumps and humps”

27
Q

Renal vein thrombosis is classically associated with which nephrotic syndrome subtype?

A

Membranous nephropathy

28
Q

C3 levels in PSGN

A

↓ serum C3 level; normal C1 and C4 levels

29
Q

EM shows alternating thickening and thinning of GBM with splitting →“Basket weave appearance”

A

Alport Syndrome (Hereditary Nephritis)

30
Q

Where do you see deposits in PSGN

A

sub-epithelial

31
Q

where do you see deposits in membranous glomerulonephritis

A

sub-epithelial