Urinary Flashcards

1
Q

possible causes of glomerular amyloidosis (w path)

A
  • 1° (immunocytic) – seen in plasma cell dyscrasias

* 2° (reactive) – inherited or chronic hyperstimulation of immune system

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2
Q

glomerular amyloidosis: path & sequelae

A

amyloid deposited in glomeruli →
• protein leaks (= generalized hypoproteinemic edema)
• antithrombin III (= consumption coagulopathy → thrombosis & ↑ clotting time)

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3
Q

2 pathways by which glomerular damage causes tubular damage in same nephron

A
  • proteins that escape filtration are reabsorbed in prox tubules → tubular (hyaline droplet) epithelial degen & necrosis
  • ↓ in blood to post-glomerular vessels → degen & ischemic necrosis of tubular epithelium
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4
Q

7 nephrotox agents

A
  1. antimicrobials
  2. NSAIDs
  3. endogenous pigments
  4. heavy metals
  5. ethylene glycol
  6. plant toxins
  7. vit D & K
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5
Q

how do type II & III HS rxns contribute to glomerular damage

A
  • type II HS: immune response against kidney (generally glomeruli)
  • type III HS: immune complexes are deposited in glomerular capillaries → stimulate complement & neutrophils → glomerular damage → protein losing nephropathy → tubular degen & necrosis
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6
Q

4 sequelae (w path) of renal neoplasms

A
  1. space occupation → pressure necrosis
  2. compression of b.v. → ischemia & infarct
  3. impedence of normal urinary flow → hydronephrosis
  4. paraneoplastic syndromes: renal tumors secrete growth factors → fibrosis & leiomyomas in various sites
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7
Q

juvenile nephropathy in dogs: lesions & CS

A

familial renal dz in young dogs
• gross: shrunken, firm, tan, pitted surface; thin cortex w radiating linear scar, diffuse fibrosis in medulla
• micro: cystic dilatation of • Bowman’s space & tubules, end-stage kidneys (interstitial fibrosis, mineralization, lymphocytic infiltrate ± tubular hyperplasia)
CS: PU/PD, azotemia, uremia

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8
Q

causes of hydronephrosis

A
congenital malformation or acquired: 
• urinary calculi
• prostatic enlargement
• neoplasm
• urethral strictures
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9
Q

5 congenital malformations of lower UT in animals

A
  1. agenesis of ureter
  2. ectopic ureter
  3. urethra-rectal or recto-vaginal fistula,
  4. urethral diverticulum (normal in bucks)
  5. patent urachus
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10
Q

cystitis: predisposing causes

A
  1. stagnation d/t obstruction
  2. catherization or urinary incontinence
  3. Abx or corticosteroids,
  4. being female
  5. glucosuria or proteinuria
  6. hyperestrogenism
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11
Q

cystitis: 4 inciting causes (w path)

A
  1. ascending infxns
  2. ycotic cystitis (usually 2° to bacterial cystitis or immunosuppression)
  3. hemorrhagic cystitis (malignant catarrhal fever)
  4. toxic (blockage, Canthardin, cyclophosphamide, bracken fern)
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12
Q

5 predisposing factors for development of uroliths in animals

A
  1. Δ in urine pH
  2. infxn & inflam
  3. dehydration
  4. dietary factors
  5. hereditary defects
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13
Q

5 likely sequelae of urolithiasis

A
  1. hydrourethra
  2. hydroureter
  3. hydronephrosis
  4. uroperitoneum
  5. cystitis/uretitis/pyelonephritis
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14
Q

FLUTD: sequelae

A
  • inflam (urethritis, cystitis),

* chronic obstruction (hydroureter, hydronephrosis, rupture of bladder, uroperitoneum)

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