Tubulointerstitial Disease Flashcards

1
Q

osmotic nephrosis

A

reversible renal tubular injury seen after admin of agents used to induce osmotic diuresis

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2
Q

what is this?

A

osmotic nephrosis

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3
Q

what is this? what does it indicate?

A

hyaline droplet change = protein resorption droplets in proximal tubular epithelium (results from increased glomerular loss of filtered proteins)

seen in severe proteinuria or nephrotic syndrome

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4
Q

clinical definition of acute renal failure

A
  • acute drop in GFR
  • oliguria/anuria
  • elevated BUN and creatinine
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5
Q

pathologic appearance of ischemic AKI

which area is most susceptible?

A

swollen kidney w/ pale cortex and congested medulla

patchy and multifocal

most susceptible: prox tubule and TAL

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6
Q

which cells are most susceptible to toxic AKI

A

tubular epithelial cells

  • tubular reabsorption
  • active transport
  • concentrationg function
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7
Q

clinical course of AKI/ATN

A
  1. initiating phase - 1-2 days w/ mild decrease in urine output
  2. maintenance phase: less urine, salt and H20 overload, increased BUN and K, metabolic alkalosis
  3. recovery phase
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8
Q

2 types of tubulointerstitial disease

A
  1. pyelonephritis
  2. tubulointerstitial nephritis
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9
Q

which type of bacteria usually causes pyelonephritis

A

gram neg

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10
Q

pathogenetic sequence for ascending pyelonephritis

A
  1. colonixation of distal urethra and introitis
  2. introduction into bladder
  3. incompetence of vesico-ureteral orifice –> reflux
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11
Q

type of infection

A

ascending pyelonephritis - linear/streaking pattern

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12
Q

type of infection

A

hematogenous pyelonephritis - miliary pattern of microabcesses throughout kidney

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13
Q

complications of acute pyelonephritis

A
  1. papillary necrosis
  2. pyonephrosis
  3. perinephric abcess
  4. scarring: broad-basses and u-shaped
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14
Q

what is chronic pyelonephritis?

name 2 types

A

pelvi-calyceal damage

  1. obstructive
  2. non-obstructive (reflux)
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15
Q

sx of drug/toxin-induced tubulointerstitial nephritis

A

average onset ~15 days after exposure

fever, eosinophilia, skin rash (25%)

ARF w/ oliguria (~50% cases)

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16
Q

pathogenetic sequence of drug-induced interstitial nephritis

A
  1. drug acts as a hapten secreted by the tubule
  2. drug binds to tubular cell component –> becomes immunogenic
  3. IgE and cell-mediated immune reaction to tubular cells or their BMs
17
Q

what is this?

A

interstitial nephritis

patchy infiltrate w/ no polys (differentiates this from infection)

18
Q

what is this?

A

tubulointersitial nephritis - inflammatory infiltrate w/ eosinophils

19
Q

analgesic abuse nephropathy - causes

A

phenacetin, aspirin, caffeine, acetaminophen, codeine

additive dosing

20
Q

pathogenesis of analgesic abuse nephropathy

A

acetaminophen: covalent binding and oxidative damage
aspirin: inhibits prostaglandin, predisposing papilla to ischemia

21
Q

pathology of analgesic tubulointersitial nephritis

A

chronic tubulointerstitial nephritis and fibrosis

papillary necrosis

urothelial carcinoma (predisposed)

22
Q

3 types of urate nephropathy

A
  1. acute uric acid nephropathy
  2. chronic urate nephropathy
  3. nephrolithiasis (in gout)
23
Q

what is this?

A

myeloma kidney:

brittle casts w/ inflammation

multi-nucleated giant cells