Path Kidneys Flashcards
Outline species differences between renal anatomy
> horse - love heart shaped - mucus glands (urine more cloudy and viscous) - unilobar > dog - unilobar > cat - external blood vessels - unilobar > cow - lobulated - both on RHS > pig - flat - multilobar (but cant see this externally)
What does each lobe of a kidney represent?
a renal pyramid
Normal ratio of cortex: medulla?
1:2
Where are kidneys located?
Retroperitoneum
What is the urinipherous tubule?
nephron and collecting ducts
Is it easy to tell inciting causes of kidney damage at PM?
With chronic kidney disease all path will look the same - fibrosed and hard to ID inciting cause
Where are different sections of nephron located?
- glomeruli cortex
- tubules loop into medulla
- collecting ducts pass through medulla
Outline vascular system of the kidney? How does this pdf pathology?
- renal artery -> afferent glomerular arteriole -> glomerular capillaries -> efferent glomerular arteriole -? peritubular capillary netowork and vasa recta
- end arterial blood supply so thrombus wipes out whole section of kidney*
What are the portals of entry of pathogens to the kidney?
> serosal spread - or direct penetration > ureters - GIT content, genital tract contamination eg. pyo, dermal contamination > haematogenous - septic embolic nephritis/infarction > glomerular infiltrate - secreted into glomerular fitrate causing local trauma or toxins
What are the defence mechanisms of the kidney?
- basement memebrane prevents entry organisms into interstitium
- provide scaffold for re-epithelialisation of tubule after necrosis
3 main endocrine fucntions of the kidney
> EPO - maturation of RBCs d/t v O2 tension > Calcitriol - facilitates Ca absorption SI > Renin - Blood pressure
3 functional types of renal failure
> pre-renal
- compromised renal perfusion -> vRBF -> renal ischaemia
- hypotension
- shock
- obstruction of vasculature (embolism etc)
intra-renal -> compromised kidney function
- tubular necrosis (infectious gaents, toxins eg ethylene glycol, NSAIDs)
- embolic dz/pyelonephritis
post-renal -> obstruction of urine outflow
- urolithiasis
- inflammation/damage (ascending infections)
- masses
What is acute renal failure and what causes it? Clinical signs?
> 75% renal function capcity abruptly impaired
failure to excrete waste products and maintain fluid/electrolyte homeostasis
- abrupt azotaemia
- retention of K+ -> cardiac arrhythmias and arrest
- retention of phosphates -> binds Ca hypocalcaemia -> muscular tremors and coma
- disturbance of electrolytes and v pH -> metabolic acidosis
- hypertension
oliguria or anuria
Is acute renal fialrue reversible?
Yes often
What is chronic kidney failure? Clinicla signs?
- end point of many kidney pathologies
- not reversible
> signs - PU, isosthenuria, PD
- halitosis, dribbling, lank coat, weightg loss
- at PME: fibrosis and atrophy of kidney, ^ irregularilty of surface
Path findings of acute renal failure?
- ^ cortex:medulla ratio
- red
- smooth capsule
- softer
Histo findings with chronic renal failure?
- ^ interstitial connective tissue
- renal tubules absent, atrophic/compressed
- hyperplastic/hypertrophic tubules
- intraluminal protein
- thickened hyalinised BM
- calcification of vessels and BM
- cysts (d/t blockage of flow dilating tubules)
- glomerulosclerosis
- foci of interstitial lymphocytes and plasma cells
What is uraemia?
- urea in the blood
- clinical syndrome of renal failure
- often accompanied by extra-renal signs d/t toxins
Clinical signs with uraemia?
- renal dz (pain/pyuria)
- effects of v renal function (metabolic acidosis/dehydration)
- compensatory responses to renal dysfunction (hyperPTH)
Outline 4 stages of renal failre. When is uraemia seen?
- “DIminished renal reserve” GFR 50% normal, animal asymptomatic but susceptible to renal insults
- “Renal insufficiency” GFR 20-50^ normal, animal azotemic and becomes PU
- “Renal failure” GFR 20-25% normal, kidneys cannot maintain homeostasis, uraemia ensues (GI, CV, resp, skeletal effects)
- “End stage” renal disease, GFR
Systemic effects of uraemia? Clinical signs.
- v GFR -> azotaemia and progressive retention of nitrogen metabolites
- failure tubular function -> NaCl and water retention, metabolic acidosis, electrolyte imblanaces (esp hyperK)
- plasma protein los
- hyperphosphataemia, 2* renal hyperPT
- v EPO -> non-regenerative anaemia
- hypertension
PME signs of uraemia
- uraemic ulcers on lateral edges of tongue
- drooling marks
- parathyroid (cheif cell) hyperplasia
- calcium deposits/mineralisation esp intercostal region
- fibrous osteodystophy (rubber jaw)
Why does 2* renal hyperPT occour?
- v Vit d v intestinal absorption Ca
How are non-renal lesions of uraemia formed? egs.
> endothelial degeneration and necrosis -> vasculitis with 2* thrombosis and infarction (GIT etc)
caustic injury (oral cavity epithelium ulcers often symmetrical, stomach ulcers/gastritris -> V+ black stuff) bacteria split urea -> ammonia
uraemic encephalopathy (white matter spongiform degeneration)
uraemic pneumonitis (vasculitis affects alveolar capillaries ^ vascular permeability -> pulm oedema, fibrin exudation, mild infiltrate of macrophages and neutrophils)
intercostal mineralisation (calcification of subpleural connective tissue intercostal spaces)
fibrinous pericarditis (carcium deposits epicardium)
arteritis (finely granular plaques in LA and prox aorta/pulm trunk)
- loss of anticoagulant by glomerular leakage -> ^ risk large mural thrombi at sites of arteritis
2 types of calcification
- metastatic mineralisation (deposits)
- dystrophic mineralisation d/t cell damage
4 structural componenets of kidney when looking at renal disorders?
- glomerular
- tubular
- interstitial
- vascular system
4 diseases of glomeruli? Mechanism of glomerular injury? LOOK UP EXTRA READING
- immune mediated glomerulonephritis
- glomerular amyloidosis
- acute supparative glomerulitis
- glomerulosclerosis
What is ultrafiltrate (glomerular filtrate) determined by?
Size and charge of molecules
Outline responses of the glomeruli to injury
- necrosis
- proliferation cells aand membranes
- infiltration of leukocytes
- v vascular perfusion
- ^ vascular permeability (protein leakage)
- continued/severe injury -> atrophy and fibrosis of glomerulus (sclerosis) and 2* atrophy renal tubules (blood supply to entire nephron affected)
Path findings with glomerular injury
- ^ cortex
- nodular appearance of cortex (glomerulitis/thickened BM)
Casues of glomerular damage
- damage filtration barrier by immune complexes
- entrapment thromboelboli/bacterial
- viral or bacterial infection of glomerular componenets
- damage to other parts of nephron
- v blood flow
- chronic loss tubular function
- amyloid deposition
How does damage to the glomerulus affect renal function?
> Affects... - plasma ultrafiltration - BP regulation - peritubular blood flow regulation - tubular metabolism regulation - circulating macromolecule removal > Causes... - protein losing nephropathy (leakage albumin overwhelms reabsorption capabilities of PCT -> proteinuria and hypoproteinaemia) -> NEPHROTIC SYNDROME (hypercoaguability d/t loss of antithrombin 3, v plasma oncotic pressure causing ascites/oedema, liver attempting to regenerate antithrombin 3 -> ^ cholesterol production, wt loss)
2 main diseases of the tubules
- inherited abnormalities
- acute tubular necrosis
How can PCT and DCT be differentiated on histo?
- PCT more metabolically active so ^ vacuoles in cytolplasm, larger, more likely to be damaged by toxic injury) PCT has brush border
Causes of tubular disease
- blood borne infection (innocent bystander)
- ascending infection (intratubular pathogens)
- direct damage fromt oxins (intratubular effects)
- ischeamia/infarction (MOST COMMON)
- Tubular obstruction
- interstitial fibrosis
- external compression
> toxic and hypoxic insults can be difficult to differentiate
Resoponses of the tubules to injury
- degeneration, necrosis, apoptosis, atrophy -> PCT more vulnerable
- cells slough into lumen -> cellular cast s
- remaining tubules undergo compensatory hypertrophy -> attempt to maintain overall renal function
> NO REGENERATION OF NEPHRONS
What 2 ways do cells die and how can these be differentiated?
> apoptosis
- nuclear pyknosis, cytoplasm shrinks
- no inflammatory response (cell membrane not damaged so no inflammatory cytokines released)
necrosis
- cell swells first, BM damage -> Na/H2O balance, pyknosis and karyolysis/karyorhexis of nucleus
How does toxic and ischaemic damage differ?
- toxins only damage epithelium: BM intact so repair by proliferation of remaining viable epithelial cells
- ischaemia damages all layers so no regernation possible -> fibrosis
Main disease of interstitium
- interstitial nephritis
Causes of interstitial disease?
> 1* interstitial didsease or 2* to tubular damage -> tubulointerstitial dz
caused by…
- haematogenous infection tubules and interstitium (E. COli, Leptispira, canine adenovirus)
- ascending infection -> pyelonephritis
- 2* injurty of vasculature or tubules or glomeruli
Responses of interstitium to injury
- oedema
- haemorrhage
- inflammation
- fibrosis
Gross and histo findings with interstitial disease?
- coalescing grey foci on capsule and cut surface
> histopath (dependant on acute v chronic stages) - initially oedema, haemorrhage and neutrophilic infiltration
- later lymphocytes and plasma cells
- tubular epithelial degernation
- vascular compromise
- fibrosis
Disease of the vascular system that affect renal?
- hyperamiea and congestion
- haemorrhage and thrombosis
- infarction
Defence mechanisms of inteact endothelium
- prevents access by intravascular pathogens
- antithrombotic (prevents activation of clotting cascade)
Responses of the vasculature to injury?
- hyperaemia and congestion
- haemorrhage and thrombosis
- infarction
- papillary (medullar crest) necrosis
- embolic nephritis
Sources of renal emboli?
- ardiac mural or valvular thrombi
- endarteritis in parasitic diseases eg. equine strongylosis
- neoplastic cell emboli
- any bacterial/septic emboli
