PRACTICAL: Pathology of the urinary tract

Question 1

Pathogenesis - hydronephrosis

Answer 1

• urine outflow obstruction increases pressure in renal pelvis –> compression of delicate tissue
• interstitial BVs collapse and RBF decreases –> hypoxia and ischaemic necrosis
• tubules degenerate and/or atrophy and necrosis –> replaced by interstitial fibrosis –> pale radiating columns/ rays

Question 2

What does bilateral hydronephrosis suggest?

Answer 2

blockage affects both ureters or was at level of bladder neck or urethra. More serious than unilateral as causes renal failure.

Question 3

Factors leading to hydronephrosis?

Answer 3

Obstructionofurineoutflowcausedby:

• intraluminal occlusion of urinary tract (calculi, mucous plugs, blood clots, neoplasia, inflammatory cells)
• external compression (neoplasia, inflammation, circumferential fibrosis, vaginal and/or uterine prolapse)
• congenital abnormalities (ureter aplasia, ectopic ureters)
• trauma
• bladder paralysis

Question 4

What do indistinct pale striations in the inner zone of the cortex represent?

Answer 4

tubular degeneration and necrosis

Question 5

What can polarised light show inside cells?

Answer 5

intratubular crystals (e.g. caused by antifreeze containing ethylene glycol)

Question 6

Pathogenesis - antifreeze toxicity

Answer 6

• EG absorbed from GIT
• oxidised in liver (by alcohol dehydrogenase) to toxic metabolites including glycolic acid and oxalate
• these are filtered by glomeruli and directly cuase acute tubular necrosis
• formation and precipitation of calcium oxalate crystals in renal tubular lumens, tubular epithelial cells and the interstitium causes intrarenal obstruction and mechanical damage

Question 7

How may herbivores succumb to similar condition as EG toxicity?

Answer 7

by consumption of oxalate-containing plants

Question 8

Gross appearance - bovine pyelonephritis

Answer 8

renal calyces contain suppurative exudate bordered by red rim of haemorrhage

Question 9

Pathogenesis - bovine pyelonephritis

Answer 9

• ascending infection (bladder)
• trauma during parturition
• stresses of parturition, peak lactation and a high-protein diet (latter increases urine pH which is conducive to bacterial colonisation of urinary tract)

Question 10

Which infectious agents are associated with pyelonephritis in cattle?

Answer 10

• E. coli
• A. pyogenes
• C. renale
• Others (opportunisitc and environmental possible, including Staph and Strep)

Question 11

What is urease?

Answer 11

• produced by E.coli and C. renale

- causes hydrolysis of urea releasing excessive ammonia which damages urinary tract mucosa and increases urine pH

Question 12

Which spp are commonly affected by post-partum pyelonephritis?

Answer 12

• cattle

- sows

Question 13

What is acute tubular necrosis?

Answer 13

necrosis of the tubular epithelial cells without reactive inflammation or scar tissue indicating recent death of cells

Question 14

Causes - acute tubular necrosis

Answer 14

• ischaemia
• nephrotoxins
• inflammation
• certain infectious agents

Question 15

T/F: tubular BMs are retained more consistently after toxic than ischaemic insults and are necessary for repair of necrotic tubules

Answer 15

True

Question 16

How can cysts form in kidneys?

Answer 16

where fibrous CT compresses tubules causing dilation proximal to the obstruction

Question 17

What is the toxic syndrome associated with chronic renal failure?

Answer 17

uraemia

Question 18

Name lesions associated with chronic renal failure

Answer 18

• ulcerative stomatitis, gastritis, colitis
• mineralisation of gastric mucosa, intercostal parietal pleura and pulmonary parenchyma
• uraemic pneumonitis
• fibrous osteodystrophy
• parathyroid hyperplasia
• non-regenerative anaemia

Question 19

What happens to glucose molecules in the bladder of DM animals?

Answer 19

• glucose split by bacteria (E.coli and C.perfringens) with release of CO2 into bladder lumen and subsequent absorption into bladder lymphatics

Question 20

Which cystitis syndrome are cats particularly prone to?

Answer 20

• feline urologic syndrome (fine struvite crystals (sand) in a mucoid protein matrix fill the urethra and can cause obstructive urolithiasis

Question 21

Define anisokaryosis

Answer 21

variation in nucleus size

Question 22

Define anisocytosis

Answer 22

abnormal variation in size of RBCs

Question 23

What might a TCC mass do if enlarged obstructing urine outflow?

Answer 23

• urine retention
• cystitis
• hydroureter
• hydronephrosis
• pyelitis
• pyelonephritis

Question 24

What can infarcts occlude?

Answer 24

interlobar, arcuate or interlobular arteries –> obstructing blood supply to local parenchyma –> coagulative necrosis consequent to peracute ischaemia

Question 25

What might precipitate renal infarcts?

Answer 25

thromboemboli could have formed from vegetative endocarditis affecting the mitral or aortic valves of the heart.

Question 26

Gross appearance - suppurative glomerulitis or embolic nephritis

Answer 26

multifocal small pale white or red necrotic foci randomly scattered throughout the capsular surface and cortical surface

Question 27

What are the necrotic foci in suppurative glomerulitis/ embolic nephritis?

Answer 27

microabscesses centered on glomeruli comprising bacteria, neutrophils and necrotic debris

Question 28

What can cause microabscessation in foals, pigs and small ruminants?

Answer 28

• FOALS: Actinobaciullus equuli
• PIGS: Erysipelothrix rhusiopathie
• SMALL RUMINANTS: Corynebacterium pseudotuberculosis

Question 29

Pathogenesis - suppurative glomerulitis or embolic nephritis

Answer 29

• causative bacteria enter the kidney via vasculature (bacteraemia) and lodge in capillaries of glomeruli, replicate, induce necrosis and inflammation
• in young animals, environmental bacteria could enter and disseminate from umbilicus or in lambs, from docking or castration wounds
• bacterial thromboemboli could form in any animal from bacterial endocarditis

Question 30

If animal survives microabscessation of kidney, what will happen to the kidney?

Answer 30

microabscesses persist or gradually replaced by chronic inflammation (lymphocytes, PCs, macrophages) and eventually fibrous CT.