PRAC: Tarc Path Urinary Tract Flashcards Preview

Renal > PRAC: Tarc Path Urinary Tract > Flashcards

Flashcards in PRAC: Tarc Path Urinary Tract Deck (28)
Loading flashcards...

How does hydronephrosis appear PM?

- dilated thin pelvis with fibrosis of the tissue (d/t compression of interstitial BVs v renal blood flow -> ischaemic necrosis)
- Tubules undergo degeneration and/or atrophy and necorsis -> pale radiating columns or rays of fibrotic tissue


How may animals with hydronephrosis compensate?

- hypertrophy of the other kidney providing it is a unilateral disease
- if bilateral disease cannot compensate -> renal failure


Causes of hydronephrosis?

- intraluminal occlusion of UT by calculi, mucus plugs, blood clots, neoplasia, inflame cell s
- external compression by neoplasia, inflame, circumferential fibrosis, vaginal ± uterine collapse
- congenital (ureter aplasia, ectopic ureters etc.)
- trauma to urinary tract
- bladder paralysis


What would you suspect in a dog, died after short illness and near signs that was a guard dog in a breakers yard, drinks from puddles. On PME kidney has indistinct pale striations in inner zone of cortex (tubular degeneration and necrosis) but is not fibrotic. On histopath there is multifocal tubular dilation, degenerate tubular epithelial cells are distended with intracytoplasmic vacuoles, many tubules contain crystalline material. How can this be more definitively dx?

- ethylene glycol poisoning
- 2D image taken using polarised light shows presence of intratubular crystals


Outline pathogenesis of ethylene glycol toxicity

- oxidised by liver (alcohol dehydrogenase) to toxic metabolites inc glycol acid and oxalate
- filtered by glomeruli directly causing acute tubular necrosis
- formation and precipitation of calcium oxalate crystals in renal tubular lumens, tubular epithelial cells and the interstitium causes internal obstruction and mechanical damage


How may herbivores succumb to a similar condition to ethylene glycol toxicity?

eating oxalate containing plants


How does pyelonephritis present in cows?

- recently calved
- v milk yield
- passing small flecks of blood in last phase of urination
- stiff when walking and hunched back
- grunted with pain in rectal exam of lumbar area
- ^ temperature


What is seen PM with pyelonephritis?

- renal calyces contain supparative exudate bordered by rim of red hamaemorrhage


What pdf pyelonephritis in cows?

- it is an ascending bladder infection
- trauma @ parturition van compromise defence mechanisms of the ureters
- stress of parturition, peak lactation, high protein diet ^ risk (high protein ^ pH urine allowing easier colonisation of urinary tract)


What bacteria can cause pyelonephritis in cows?

- E. Coli
- Arcanobacterium pyogenes
- Corynebacterium renale
± opportunistic staph and strep
- Uropathogenic E. COli and corynebacterium renale produce urease (hydrolyses urea -> ammonia) dmaage to urinary tract mucosa and ^ urine pH


What other species are affected by pyelonephritis postpartum?



How does acute tubular necrosis appear histologically?

- deffuse degernation and encores of epithelial cells of convoluted tubules
- glomeruli and collecting ducts often spared
- BM may or may not be retained
- no reactive inflammation or scar tissue would indicate recent cell death


What can cause acute tubular necrosis?

- ischaemia
- nephrotoxins
- inflammation
- infectious agents


What determines how well the kidney heals after acute tubular necrosis?

- whether BM is intact
- if in tact, forms a scaffold for cellular regeneration potential for renal function to be maintained
- if lost, no scaffold -> fibrous scar tissue formation and v renal function


When is basement membrane damage most commonly seen?

- with iscaemic insults
- (cf. toxins which damage epithelium and may well leave BM in tact)


How do kidneys with CKD appear @ PM?

- capsular surface irregular with multifocal pitting
- multifocal small acquired cysts at corticomedullary junction(where fibrous tissue compresses tubules -> dilation proximally)


What is the name of the toxic syndrome that accompanies chronic kidney disease? How is this seen clinically?

> uraemia
- ulcerative stomatits, gastritis and colitis
- mineralisation of gastricmucosa, intercostal parietal pleura, pulmonary parenchyma
- uraemic pneumonitis
- fibrous osteodystrophy
- PT hyperplasia
- non-regenerative anaemia


How does DM appear on histo?

B cells in islets of the pancreas are vacuolated consistent with hydraulic degeneration
- develops d/t sustained stimulation because of peripheral insulin resistance (Type 2 DM)


How is DM linked to urinary dz? Esp cats.

- glucosuria pdf urinary tract infections and enhances bacterial growth
- @ PM bladder mucosa may contain multifocal coalescing reddened nodules (cystitis) and emphysema
- bacteria (E. COli, C. Perfringens) split glucose -> CO2 in bladder lumen which is absorbed by lymphatics


Which other cystitis syndrome are cats pdf?

> feline urologic syndrome
- fine struvite crystal formation (sand) in a mucoid matrix fills the urethra and causes obstructive urithroliasis


How do transitional cell carcinomas appear on histo?

- atypical epithelial cells in haphazard islands and nests
- moderate anisokaryosis and anisocytosis with prominent nucleoli consistant with malignancy


What can affect prognosis of TCC?

- if lymphatics invaded by nests of malignant cells, prognosis poor (^ risk mets to local lNs)


What 2* effects may bladder tumours have?

- occluding urine outflow
-> cystitis, hydroureter, hydronephrosis, hydropyelitis, pyelonephritis


How do renal infarcts appear @ PM?

- multifocal irregular pale areas pm capsule bordered by red rim
- pale areas extend into parenchyma


Pathogenesis of renal infarcts?

- emboli in vasculature occlude interlobar/interlobular/arcuate arteries

- emboli most commonly from vegetative endocarditis (mitral/aortic valves)
- end arterial supply


What causes suppurative glomerulitis/embolic nephritis?

- actinobacilus equuli (foals)
- erisipelothrix rhusiopathiae (pigs)
- corynebacterium pseudotuberculosis (small ruminants)


How does supportive glomerulitis/embolic nephritis appear @ PM?

- multifocal small pale white or red necrotic foci randomly scattered throughout capsular and cortical surface
- microabscesses centered on glomeruli (bacteria, neutrophils, necrotic debris)


Pathogensis of supportive glomerulitis?

- bacteraemia
- lodge in capillaries of glomeruli
- replicate -> inflam and necorsis
> young animals, bacteria can enter via umbilicus, tail docking or castration wounds
> bacterial thromboemboli can form in any animal from bacterial endocarditis
- as microabscesses persist will become gradually replaced by chronic inflame (lymphocytes, plasma cells, macrophages) and eventually fibrous tissue