Urinary Pathology Flashcards

(38 cards)

1
Q

What are mesangial cells?

A
  • phagocytose macromolecules and immune complexes
  • contract to autoregulate glomerular blood flow
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2
Q

What are examples of non-urinary lesions associated with renal failure?

A
  • gastric ulcers/uremic gastritis
  • ulcerative glossitis/stomatitis
  • mineralization of intercostal pleura - ‘uremic frosting’
  • uremic pneumonitis - pulm edema/mineralization
  • parathyroid hyperplasia
  • anemia
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3
Q

Why does parathyroid hyperplasia occur with renal failure?

A
  • phosphate retention –> decr ionized Ca++ –> PTH release
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4
Q

Describe polycystic kidney disease in cats

A
  • autosomal dominant, defect of PKD1 gene
  • Persians predisposed
  • can dx @ 10 mo via U/S
  • cysts can arise from any segment of nephron
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5
Q

Describe polycystic kideny disease in other species

A
  • congenital PKD w/ an unknown inheritance can occur in all domestic mammals
  • animals are typically stillborn or die of renal failure in first few weeks of life
  • enlarged kidneys w/ numerous 1-5 mm diameter cysts
  • can have concurrent biliary and/or panc cysts
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6
Q

Describe papillary necrosis

A
  • common in horses (esp in dehydrated horses treated w/ bute)
  • NSAIDs inhibit COX–>decr PGE2 production
    • PGE2 maintains vasodilation in arterioles, loss of this –> ischemia and subsequent necrosis
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7
Q

Describe hydronephrosis/hydroureter

A

Hydronephrosis- dilation of renal pelvis/calyces

Hydroureter - dilation of ureters

  • typically occurs secondary to obstruction
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8
Q

What is glomerulonephritis?

A
  • alteration of structure of glomerulus involving one or more of the following: basement membranes, mesangial matrix, mesangial cells, immune complex deposition
  • end result: alter the filtration barrier–> protein loss, decr GFR –> renal failure
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9
Q

Characterization of glomerulonephritis is dependent on what?

A
  • which parts of the glomerulus are affected
  • whether there is immune complex deposition
  • where immune complexes are deposited
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10
Q

What is the pathogenesis of immune complex glomerulonephritis?

A
  • circulating immune complexes deposited in/adjacent to glomerular b.m. or antibodies formed against the glomerular b.m.
    • immune complexes may be deposited subendothelially, in the b.m. or subepithelially
  • complement fixation, leukocytic infiltration and production of inflammatory mediators by mesangial cells may contribute glomerular injury
  • filtration barrier becomes compromised –> protein loss
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11
Q

What are some conditions commonly associated with immune complex glomerulonephritis?

A
  • viral dz
  • chronic bacterial infections
  • parasitic and protozoal dz
  • autoimmune dz
  • neoplasms
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12
Q

What might you see histologically with glomerulonephritis?

A
  • thickened basement membranes
  • increased #s of mesangial cells
  • synechiae - adhesions b/t the glomerular tuft and the capsule
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13
Q

What are the clinical features of acute renal failure?

A
  • good body condition
  • smooth, enlarged kidneys (+/- painful)
  • PCV normal to incr
  • K+ normal to incr
  • more severe metabolic acidosis
  • relatively severe clinical signs relative to bloodwork
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14
Q

What are the clinical features of chronic renal failure?

A
  • poor body condition
  • small irregular kidneys
  • nonregenerative anemia
  • K+ normal to decr
  • less severe metabolic acidosis
  • relatively mild clinical signs relative to bw
  • longstanding PU/PD
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15
Q

What is the clinicopathologic finding the most suggestive of glomerular disease?

A

proteinuria in the absence of hemorrhage or inflammation

*most sensitive way to measure is the urine protein to urine creatinine ratio

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16
Q

Describe glomerular amyloidosis

A
  • often reactive systemic amyloidosis
  • assoc w/ chronic inflammation
  • common in Shar Peis and Abyssinian cats
  • extensive glomerular amyloid deposition leads to compromise of the filtration barrier and proteinuria
    • develop progressive renal insufficiency and proteinuria
17
Q

Describe embolic nephritis

A
  • bacteria lodge mainly in glomerular and peritubular capillaries
    • Horses: Actinobacillus equuli
    • Pigs: Erysipelothrix rhusiopathiae
    • Cattle: Trueperella pyogenes
18
Q

What might you see histologically with tubular degeneration?

A

vacuolation of epithelial cells

19
Q

Waht might you see histologically with tubular necrosis?

A
  • loss of cellular detail
  • nuclear karyorrhexis, karyolysis, pyknosis
  • incr cytoplasmic eosinophilia
  • sloughing of epithelial cells
20
Q

What might you see histologically with tubular regeneration?

A
  • increased cytoplasmic basophilia
  • piling/crowding of epithelial cells
  • nuclei with an open chromatin pattern and prominent nucleoli
  • mitotic figures
21
Q

Describe acute tubular (ischemic) injury

A

Due to hypotension; mild - degeneration/necrosis of primarily tubules; prolonged ischemia- renal cortical necrosis, affects all cortical structures; disruption of b.m can occur —> no scaffolding for tubular epithelial regeneration

22
Q

Describe acute tubular toxic injury

A

Histologic lesions: extensive necrosis of predominantly proximal tubules, distal tubules sometimes; b.m may be preserved (scaffolding)

23
Q

List some examples of nephrotoxic substances

A

Animal venom, antimicrobials, chemo, cantharadin, contrast media, ethylene glycol, heavy metals, plants, mycotoxins

24
Q

Describe oxalate necrosis

A

Can be d/t ethylene glycol or oxalate containing plants (ie halogeton, greasewood, rhubarb, sorrel)

25
Describe ethylene glycol toxicosis
Major component of antifreeze; fluorescein dye added to it to help detect a radiator leak - urine of animals with acute toxicosis might fluoresce w/ black light; calcium oxalate crystals precipitate in renal tubules and cause tubular necrosis
26
What is pigment nephrosis?
Myoglobin and hemoglobin can cause tubular injury - myoglobin from mm damage and hemoglobin from hemolytic anemias; cannot distinguish Hb and Mb casts in kidney on light microscopy
27
Describe interstitial (tubulointerstitial) nephritis
acute cases - edema, leukocyte infiltration, focal tubular necrosis; chronic cases - leukocytic (usually lymphoplasmacytic) infiltrate, interstitial fibrosis, tubular atrophy
28
What causes “white-spotted kidney” disease in calves?
Thought to be due to a prior bacteremia, usually E. Coli; nonsuppurative interstitial nephritis w/ fibrosis
29
Describe the pathogenesis of leptospirosis
Caused by serovars of L. Interrogans, contact w/ infected fluid (often urine), bacteria can enter via mucous membranes or wet skin —\> abortion, stillbirth, hepatitis, nephritis, meningitis, septicemia; renal failure most common in dogs, pigs - extensive interstitial nephritis (not renal failure); histo: tubular degeneration/necrosis, interstitial/tubulointerstitial nephritis
30
Describe canid herpesvirus 1
* often fatal for newborn puppies, can also cause abortion and stillbirth * puppies generally need to be exposed before 2 wks of age - die within 2d of showing signs * C/S: anorexia, vomiting, abd pain * Gross lesions: foci of hemorrhage and necrosis in mult. organs, esp kidney
31
Describe pyelonephritis
* **inflammation of the renal pelvis and parenchyma** * usually results from ascending infection from lower urinary tract, so patients typically have _concurrent ureteritis and cystitis_ * vesiculouerteral reflux - retrograde flow up ureters during micrturition
32
What are two parasites involved in renal disease?
* **Stephanurus dentatus** - kidney worm in swine that encyst in perirenal tissue * these cysts communicate w/ the renal pelvis to allow for passage of eggs * **Dioctophyma renale** - giant kidney worm, usually in piscovorous mammals (mink, dogs, cats); adults live in renal pelvis and are very destructive * cause progressive destruction of renal parenchyma
33
What are examples of renal neoplasms?
* Adenomas: benign tumors of tubular epithelium * Adenocarcinomas: **most common primary renal tumors in horses, cattle and dogs**; usually well-demarcated, compress remaining renal parenchyma, located at one pole * Nephroblastomas: **most common primary renal tumor of pigs and chickens**, usually occurs in young animals * Histo: primitive glomeruli, tubules and mesenchyme, may contain cartilage, bone or fat * Metastatic lymphoma very common
34
What are a few examples of congenital urinary tract abnormalities?
* Ectopic ureters - ureters can empty into bladder neck, urethra, vagina, vas deferens or seminal vesicles; may be uni- or bilateral; certain predisposed breed * Patent urachus - failure of closure of the urachal lumen results in dribbling of urine from the urachus; _most common in foals_
35
Describe urolithiasis
* calculi in urinary passages, may be located from renal pelvis to urethra * calculogenic substances must be present in sufficient concentration * predisposing factors: * urine pH (precipitation) * water intake * hereditary factors (dalmatians) * dietary factors * UTIs * male sex
36
Describe bacterial cystitis
* bacteria from ascending infection from urethra, _almost always rectal flora_ * predisposing factors: * female * loss of normal voiding mechanisms * loss of acidic urine pH (carnivores) * glucosuria * proteinuria * mucosal trauma
37
What is emphysematous cystitis?
* seen rarely in diabetic animals d/t bacterial fermentation of urinary glucose into carbon dioxide; E. coli most common
38
What are some neoplasms of the lower urinary tract?
Papilloma - covered by well-differentiated transitional epithelium, May undergo malignant transformation to TCC in dogs; transitional (urothelial) cell carcinoma - most often in bladder neck or trigone, 50% met.; botyroid rhabdomyocsarcoma - young (usually \<18 mo) large or giant breed dogs