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75 Cards in this Set

  • Front
  • Back
What is considered PU?
What is considered PD?
PU: over 50ml/kg/day
PD: over 100ml/kg/day
What is considered oliguria
under 0.25ml/kg/hour or 5-6ml/kg/day
What is normal osmolality of plasma
280-320mosm/kg
Why does creatinine reflect GFR better than urea?
because urea increases with diet protein intake and liver disease
when does renal azotaemia occur?
when more then 3/4 nephrons lost - will be isosthenuric
What are some of the uraemic toxins (6)?
ammonia, PTH, amines, gastrin, aromatic amino acids, urea
How are ulcers formed in uraemia?
urea in saliva/intestine --> bacterial action converting it to ammonia: injury to oral and intestinal epithelium
What is the radiographic size of kidney in cat and dog
cat: 2-3x length of L2

dog: 2.5-3.5xlength of L2
At what % of nephron loss does poor urine concentrating ability occur?
at 67% loss
what are the normal values of urine protein:creatinine in dogs and cats
dog: under 0.5
cat: under 0.4
How much protein must be lost in urine until dipstick detects it?
when over 30mg/dl
List causes of acute renal failure
hypovolaemia, hypotension, shock, anaesthesia, pancreatitis, sepsis, DIC, NSAID, ethylene glycol, heavy metals, grapes, raisins, lily, hypercalcaemia, haemoglobin, myoglobin, immune mediated glomerulonephritis, leptospirosis, pyelonephritis
what are the main biochemical abnormalities detected in arf?
hyperkalaemia, metabolic acidosis and sudden increase in urea and creatinine?
what are some of the clinical signs (2) of arf aside from V, anorexia, dehydration, renal encephalopathy, neuropathy and lethargy?
pericarditis and pneumonitis
what mineral should be administered if life threatening hyperkalaemia?
calcium
when is CKD considered chronic?
when been goingon for more than 2 weeks
what are some of the consequences and clinical signs of CKD?
poor platelet function and immunity
anorexia, vomiting, halitosis, GI ulcers
lethargy and weight loss (protein catabolism)
- small kidneys and non regenerative anaemia
when is renal biopsy indicated?
if renomegaly with proteinuria or haematuria of unkown aetiology
how is CKD staged?
on plasma creatinine, proteinuria and blood pressure
- note that proteinuria may decrease as dysfunction worsens
what are the 4 main causes of CKD progression?
- disease initiating CRF
- systemic complciations
- metabolic complications
- single nephron GFR (supernephrons) --> glomerulosclerosis: disease progresses even if inciting cause is removed
list the 4 main complications of CKD?
- renal secondary hyperparathyroidism
- systemic hypertension
- anaemia
- metabolic derangements: dehydration, hypokalaemia and acidosis
why does secondary renal hyperparathyroidism occur and how is it treated?
increased phosphate results in increased PTH release. but hyperphosphataemia depresses enzyme that stimulates vitamin D activation in kidneys so results in decreased calcium absorption and can get hypocalcaemia further increasing PTH release: Calcium thereby taken from bone. The negative feedback of vitamin D and high calcium levels fail
- in advanced cases the parathyroids become ieven less esnsitive to calcium so even if hypercalcaemic and phosphate low hypercalcaemia develops -->ST calcification
- put on renal diet and aluminium hydroxide and vit D
how is CKD systemic hypertension addressed?
amlodipine besylate, ACE inhibitors
what is the ideal diet for CKD?
low salt, K supplementation if cat, B vits (excreted in urine), wet food with restricted protein of high quality, omega 3 fatty acids
what are the predisposing factors of upper urinary tract infections (3)?
obstructions, renal calculi and veiscoureteral reflux
how long are upper UTI treated?
antimicrobials 3-6 weeks: sediment should show no bacteria by day 4. repeat culture 7-10 days after completing course. if infection recurs most probably defective host defense mechanism
where are most small proteins reabsorbed?
in proximal tubules
how do you treat glomerulosclerosis?
steroids and ace inhibitors
where is amyloid deposited in kidneys in renal amyloidosis?

how is it treated?
periglomerular deposition - excess fibrillar protein (acute phase protein serum amyloid A). Can also deposit in medulla --> loss of urine concentrating ability
- treated with colchicine (decreases deposits) and DMSO
which breeds is renal amyloidosis familial?
sharpei and abyssinian
what is the nephrotic syndrome?
- proteinuria
- hypoalbuminaemia
. hypercholesterolaemia
- ascites/oedema/effusion

may see thromboembolism due to loss of antithrombin III in urine
how is PLN treated?
- restricted protein diet (increase protein, increase proteinuria)
- ace inhibitors: decrease proteinuria and decrease rate of CRF progression
low dose aspiring if hypercoagulable state
What is Fanconi syndrome? what are the clinical signs and which breeds are predisposed?
Noeweigian elkhound and basenji predisposed

= dysfuntion of resorptive properties of proximal tubules: lose glucose, amino acids, phosphate, potassium and bicarbonate in urine
--> PUPD, alkanuria despite metabolic acidosis, and glycosuria despite normal blood glucose
what is renal glucosuria?
disorder of proximal tubule resorption of glucose so get glucosuria and PUPD but without hyperglycaemia
what condition can result in glucosuria?
pyelonephritis occasionally can
what is renal tubular acidosis? what are the two types?
= chronic metabolic acidosis secondary to impaired tubular ability to excrete H or have excess bicarbonate loss.
- proximal RTA: cant resorb bicarb (alkalinuria and met acidosis)
- distal RTA: can't excrete H+ in distal tubule: alkalineuria and metabolic acidosis

since acid base homesostasis mainly done via distal tubule, metabolic acidosis is severe in distal RTA
name 8 causes of acquired nephrogenic diabetes insipidus
- CRF
- pyelonephritis
- HAC
- hypercalcaemia
- hyperthyroidism
- liver failure
- pyometra
- steroid treatment
how long does it take for uraemia to develop in blocked bladder cases?
if obstructed for more than 48 hours will develop uraemia
why is crystalluria not god to diagnose presence of urolith?
because can have urolithis without detectable crystalluria or crystalluria of one type and urolith of another
name 2 urease producing bacteria
proteus and staphylococcus
in what situations are acidifying diets contra-indicated when treating struvite uroliths?
when young: as they will buffer acid with calcium from bones
when in renal failure
how do you treat calcium oxalate uroliths?
- treat any underlying cause of hypercalcaemia
- canned food and diuretics if needed
- nephrocalcin inhibits its formation as do citrate and GAGs
- acidosis increases calcium released in urine to bufer acid
what is special in patients with cystine uroliths?
they have an inborn error of metabolism: an abnormal transport of cystine by renal tubules = not resorbed at glomerulus
how do you treat cystine uroliths?
2MPC in dog and u/d diet (alkalinise urine, decrease its concentration and decrease cystine excretion)
--> diet alone is often effective to prevent recurrence
- potassium citrate to maintain alkaline urine as sodium enhances cystinuria
what are dantrolene, prazosin and phenoxybenzamine?
dantrolene is a skeletal muscle relazant, while prazosin and phenoxybenzamine are smooth muscle relaxants
- these are often used in urethral obstruction cases to prevent urethral spasm
what are the most common bacteria found in UTIs in dogs (5)?
E. Coli, proteus, klebsiella, staph, strep
what are the bladder's natural defense mechanisms
- urethral sphincter
- epithelial folds in proximal urethra
- GAGs
- flushing of urine
- endogenous flora - competition
- high osmolality of urine
- immunoglobulin in vaginal mucus
how long a course of antibiotics are usually used in cystitis? when do you culture?
2 weeks - TMPS for gram -ve and amoxicillin for gram +ve

culture 1 week into treatment, follow up 1-2 weeks post treatment to ensure clearance
what can cause persistent or recurrent UTIs? how long may these need antibiotic cover?
- prostatitis, pyelonephritis, calculi, neoplasia, defense problems, systemic disease

- 6-8 weeks of ABs needed if e.g. pyelonephritis is involved. if chronic, 4-6months of antimicrobial treatment may be necessary
what are the most common causes (in order of most to least common) of feline cystitis if under 10yo?
1) idiopathic (55%)
2) urolithiasis (15-20%)
3) urethral plug (20%)
4) anatomical defect/neoplasia 10%
5) behavioral 10%
6) bacterial, 2%
what is the most common cause of feline cystitis in a pati9ent over 10 years?
bacterial - if negative on culture perform radiographs and ultrasound for uorliths, tumours, etc
how do you treat idiopathic feline cystitis?
wet diet (want SG under 1.035), amitriptyline, GAGS, feed happy and prazosin
where are polyps found on bladder cf. TCC? how do you treat them?
polyps on ventral border - surgically remove or treat with piroxicam (decrease size)
where do cystic tumours met to?
regional and pelvic/iliac lymph nodes, prostate, pelvic bones, lung, liver, etc
what CS of bladder tumours do you get in cats but not in dogs?
tenesmus, rectal prolapse, anorexia and palpable abdominal mass
why are canine bladder tumour antigen dipsticks not usually used?
get false positives with proteinuria and haematuria
how is bladder neoplasia diagnosed?
- aspirate via urinary catheter, cystoscopy, ex lap

DON'T FNA --> SEEDING IN ABDOMEN
what are the treatment options for bladder neoplasia?
surgery (removal) or reconstructive (e.g. uretocolonic anastamosis)

mitoxantrone and piroicam/metacam
what may you see in GSD with renal tumours?
may see cystadenocarcinoma and nodular dermatofibrosis
what is the origin of most prostatic tumours? how do you treat them?
most from ductal epithelium that lack androgen receptors:
also get adenocarcinoma, SCC, TCC; haemangiosarcoma, leiomyosarcoma
- treat with NSAID and mitoxantrone as surgery and radiotherapy result in incontinence - MST 7mo
what type of tumours do cryptorchids usually have (2)? Where do these met to?
seminoma or sertoli cell tumours

these met to liver, lungs, spleen, kidneys, adrenal gland, pancreas
what are some of the clinical signs of sertoli cell tumours?
all due to hyperoestrogenism
attracted to males
flank alopecia
preputial oedema
gynecomastia
aplastic anaemia
squamous metaplasia of prostate
what is the treatment of choice for testicular tumours?
castration with scrotal ablation
what proportion of granulosa cell tumours produce oestrogen? benign or malignant in cat vs dog?
50% produce oestrogen. tend to be malignant in cat and benign in dog
what tends to cure transmissible venereal tumours?
chemotherapy has a high cure rate
what proportion of mammary tumours are malignant in dogs?
50%

- mixed tumours most common in bitch
what factors are associated with good prognosis in mammary tumours in dog
- if under 3cm large
- well circumscribed
- no met
- well differentiated
- oestrogen and progresteron Rc +ve
- if male
what are poor prognostic factors in mammary tumours of dog?
- if mass over 3cm
- invasive
- met
- anaplastic
- oestrogen Rc -ve
- ulceration
- vascular or lymphatic invasion on biopsy
which lymph node do you remove when performing mammectomy?
superficial inguinal lymph node with 5th gland - only remove axillary lymph node if enlarged
what treatments can result in mammary tumour development in cats?
progesterone like drugs
if you spay a cat before 6months of age what is its risk to develop mammary cancer?
91% decreased risk
what does MST in cats with mammary tumours depend on?
size (most important), time of diagnosis, histological grade and surgical margins
what should you not confuse mammary tumours in cats with?
do not confuse with benign fibroepithelial hyperplasia that young cats get after silent oestrus
how do you treat feline mammary tumours?
surgery - radical mammectomy with bilateral LN removal. can also administer doxorubicin or cyclophosphamide or mitoxantrone
what are poor prognostic indicators in feline mammary tumours?
- big, old, vascular or lymphatic invasion or if surgical excision is poor