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VET 409: Renal > Tubulointerstitial Disease > Flashcards

Tubulointerstitial Disease Flashcards

1
Q

causes of acute renal failure

A

pre-renal
renal (tubular, glomerular, vascular)
post-renal

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2
Q

causes of tubular ARF

A
  1. acute tubular injury (ischemic or toxic)
  2. inflammatory
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3
Q

what nephron segments are the most susceptible to acute tubular injury

A

PCT and thick ascending loop of Henle

due to HIGH O2 demand

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4
Q

ischemic ATI

A

decreased perfusion of renal parenchyma caused by vasoconstriction

segmental distribution

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5
Q

what part of the kidney is most susceptible to ischemic ATI

A

outer medulla

LOW O2 availability

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6
Q

toxic ATI

A

nephron exposure to endogenous/exogenous toxins

diffuse distribution

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7
Q

what part of the kidney is most susceptible to toxic ATI

A

renal tubules

high surface area, active transport systems, high O2/energy demands, high toxin exposure

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8
Q

what is the maladaptive response to injury in the nephron

A
  1. tubular activation
  2. histologic cell changes
  3. cell swelling
  4. cell detachment
  5. de-differentiation
  6. proliferation
  7. differentiation
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9
Q

tubular activation

A

increased demand on tubular cells –> release of cytokines –> recruitment of inflammatory cells and fibroblasts –> fibrosis + necrosis –> tubule loss

occurs in response to ischemia/hypoxia, glomerular injury, and tubular injury

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10
Q

what is the main sign of glomerular dysfunction

A

proteinuria

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11
Q

how is glomerular dysfunction related to tubular injury

A

glomerular dysfunction causes proteinuria

proteins in urine cause tubular damage –> tubular activation

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12
Q

what histologic changes occur to tubular epithelial cells during maladaptive response to injury

A

loss of polarity
loss of microvilli/brush border –> decreased absorptive capacity –> high Na in filtrate reaching DCT –> increased vasoconstriction

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13
Q

why do cells start to swell in maladaptive response to injury

A

leukocyte infiltrate and vesiculation –> increased intracellular pressure

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14
Q

what happens when cells detach from basement membrane

A

dead tubular cells slough off into lumen –> increase intratubular pressure and decreased GFR –> wrinkled basement membrane (tubular atrophy)

formation of casts –> can obstruct distal tubules

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15
Q

what is de-differentiation

A

simplification (stretching out) of surviving epithelial cells to cover the exposed segments of the basement membrane; causes cells to become undifferentiated

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16
Q

what is required in order for cells to regenerate

A

INTACT basement membrane

17
Q

what happens if the basement membrane is not intact OR cells don’t regenerate

A

chronic nephron loss –> CKD

18
Q

what happens once cells completely cover the basement membrane

A

cells proliferate across the basement membrane and re-differentiation (reestablish polarity)

19
Q

what are the classes of inflammatory diseases

A
  1. tubulointerstitial nephritis
  2. interstitial nephritis (acute and chronic)
  3. pyelonephritis (acute and chronic)
20
Q

what is the pathogenesis of tubulointerstitial nephritis

A

infectious
sterile (glomerular disease)
idiopathic
chronic

21
Q

pathogenesis of leptospirosis

A
  • bacteria is shed in urine
  • enters through MM or abraded skin
  • moves through the blood to the kidney, liver, uterus, and eye and migrates through endothelium
22
Q

what kind of disease does leptospirosis cause

A
  1. interstitial nephritis
  2. tubulitis
23
Q

interstitial nephritis

A

lymphocyte and plasma cell infiltrate/inflammation

24
Q

tubulitis

A

neutrophil infiltrate in renal tubules

25
Q

what is chronic nephritis

A

loss of nephrons that get replaced by fibrosis

26
Q

gross and histologic lesion of chronic nephritis

A

scalloped edges

interstitial inflammation, fibrosis, tubular atrophy w/ intact glomeruli

27
Q

what is the sign of tubular atrophy

A

wrinkled basement membrane

28
Q

what histologic lesion does FIP cause

A

perivascular pyogranulomatous interstitial nephritis/vasculitis (neutrophils + lymphocytic infiltrate)

causes pressure necrosis –> tubule loss

29
Q

pyelonephritis

A

ascending infection from lower urinary tract to kidneys

ONLY infectious etiologies

neutrophilic infiltrate

30
Q

chronic pyelonephritis gross lesion

A

pale, fibrotic, irregular margins, irregular renal crest

linear scars from ascending necrosis

31
Q

mechanism of NSAID toxicity

A
  • NSAIDs inhibit COX 1 and 2
  • decreased production of prostaglandins
  • decreased vasodilation –> increased vasoconstriction
  • vasoconstriction –> medullary ischemia –> renal papillary necrosis
32
Q

renal papillary necrosis

A

death of renal parenchyma in the region of the renal papilla

caused by ischemia due to low perfusion of papillary vessels

33
Q

mechanism of copper toxicity

A

chronic low-level copper exposure –> massive hepatic copper storage –> stressful event triggers hepatocellular necrosis –> copper releases into the blood –> damages RBCs (intravascular hemolysis) –> anemia + hemoglobinuria –> ischemia + tubular necrosis

occurs in sheep

34
Q

gross lesion of copper toxicity

A

gun metal blue kidneys

VET 409: Renal (21 decks)

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