Renal

Question 1

protein losing nephropathy

Answer 1

damage to glomerulus –> barrier becomes less selectively permeable –> leaks protein in and loses it in urine

Question 2

methods of kidney injury

Answer 2

infection - ascending or hematogenous
inflammation
toxins - direct (aminoglycosides), toxic metabolites (ethylene glycol), or intrinsic (myoglobin)
congenital
neoplasia
ischemia -
- acute - sepsis, heatstroke, shock, thromboembolism - sudden large drop in blood pressure
- chronic - congestive heart failure
- drugs affecting blood flow to kidneys (prostaglandins, COX)
- hydronephritis secondary to obstruction downstream

Question 3

rhabdomyolysis

Answer 3

excessive muscle use –> destruction of muscle tissue –> myoglobinuria

signs -
tachycardia
tachypnoea
darkened urine

differentiate haematuria/haemaglobinuria/myoglobinuria - spin blood, whole cells form sediment, then differentiate myoglobin and haemoglobin with ammonium sulfate (haemoglobin forms precipitate at 80% saturation, myoglobin needs 100%)

Question 4

red maple poisoning

Answer 4

destruction of RBCs –> haemoaglobinuria

signs -
depression
jaundice
ataxia
loss of appetite
colic
red-brown urine

Question 5

oak poisoning

Answer 5

signs -
diarrhoea
colic
inappetence
ventral oedema
straining to urinate
red-brown urine

Question 6

ragwort poisoning

Answer 6

signs -
liver related - jaundice, photosensitisation, abdominal pain
weight loss
neurological signs - head pressing, circling, seizures

Question 7

sycamore poisoning

Answer 7

atypical myopathy

muscle stiffness and tremors
reluctance to walk
dark urine
death

Question 8

rhododendron poisoning

Answer 8

diarrhoea
hypersalivation
collapse
death

Question 9

AKI

Answer 9

types -
pre-renal - impaired blood flow to kidneys
renal - within kidney itself
post-renal - urinary obstruction

pathophysiology -
failure to eliminate waste - azotemia
inability to regulate acid-base homeostasis - metabolic acidosis
inability to maintain blood pressure - hypertension

azotemia –> uremia

uremia -
systemic changes associated with azotemia
elevated urea and creatinine
endothelial damage from toxin build up
toxins leached into saliva and gastric secretions - metabolised to ammonia, mucosal ulceration and hallitosis

Question 10

CKD

Answer 10

pathophysiology -
damage to one nephron –> gradual damage of more
damage replaced by fibrosis
eventual uremia

inactivated vitamin D –> less calcium absorption in intestine
hypocalcemia –> increased phosphate

hypertension, non-regenerative anemia, calcium deposition in soft tissues, secondary hyperparathyroidism

Question 11

CKD –> secondary hyperparathyroidism

Answer 11

hypocalcemia –> increased PTH release –> secondary hyperparathyroidism –> more calcium released from bones –> weak bones, calcium replaced by fibrosis (rubber jaw)

Question 12

progressive juvenile nephropathy

Answer 12

congenital renal dysplasia - usually in glomerulus
defect in collagen forming genes

common in samoyeds

Question 13

polycystic kidney disease

Answer 13

2 types -
1 - autosomal dominant - persian cats, english bull terriers
2 - autosomal recessive - westies, cairn terriers, sheep

cysts present from birth - slowly grow - signs at 7-10 years old
eventual kidney failure
enlarged or shrunken kidneys at post mortem depending how far along

Question 14

common kidney tumours

Answer 14

in kidneys - renal cell carcinoma, urothelial cell carcinoma

metastasis - lymphoma