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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 |
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What is considered oliguria
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under 0.25ml/kg/hour or 5-6ml/kg/day
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What is normal osmolality of plasma
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280-320mosm/kg
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Why does creatinine reflect GFR better than urea?
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because urea increases with diet protein intake and liver disease
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when does renal azotaemia occur?
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when more then 3/4 nephrons lost - will be isosthenuric
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What are some of the uraemic toxins (6)?
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ammonia, PTH, amines, gastrin, aromatic amino acids, urea
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How are ulcers formed in uraemia?
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urea in saliva/intestine --> bacterial action converting it to ammonia: injury to oral and intestinal epithelium
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What is the radiographic size of kidney in cat and dog
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cat: 2-3x length of L2
dog: 2.5-3.5xlength of L2 |
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At what % of nephron loss does poor urine concentrating ability occur?
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at 67% loss
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what are the normal values of urine protein:creatinine in dogs and cats
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dog: under 0.5
cat: under 0.4 |
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How much protein must be lost in urine until dipstick detects it?
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when over 30mg/dl
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List causes of acute renal failure
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hypovolaemia, hypotension, shock, anaesthesia, pancreatitis, sepsis, DIC, NSAID, ethylene glycol, heavy metals, grapes, raisins, lily, hypercalcaemia, haemoglobin, myoglobin, immune mediated glomerulonephritis, leptospirosis, pyelonephritis
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what are the main biochemical abnormalities detected in arf?
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hyperkalaemia, metabolic acidosis and sudden increase in urea and creatinine?
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what are some of the clinical signs (2) of arf aside from V, anorexia, dehydration, renal encephalopathy, neuropathy and lethargy?
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pericarditis and pneumonitis
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what mineral should be administered if life threatening hyperkalaemia?
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calcium
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when is CKD considered chronic?
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when been goingon for more than 2 weeks
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what are some of the consequences and clinical signs of CKD?
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poor platelet function and immunity
anorexia, vomiting, halitosis, GI ulcers lethargy and weight loss (protein catabolism) - small kidneys and non regenerative anaemia |
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when is renal biopsy indicated?
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if renomegaly with proteinuria or haematuria of unkown aetiology
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how is CKD staged?
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on plasma creatinine, proteinuria and blood pressure
- note that proteinuria may decrease as dysfunction worsens |
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what are the 4 main causes of CKD progression?
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- disease initiating CRF
- systemic complciations - metabolic complications - single nephron GFR (supernephrons) --> glomerulosclerosis: disease progresses even if inciting cause is removed |
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list the 4 main complications of CKD?
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- renal secondary hyperparathyroidism
- systemic hypertension - anaemia - metabolic derangements: dehydration, hypokalaemia and acidosis |
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why does secondary renal hyperparathyroidism occur and how is it treated?
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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 |
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how is CKD systemic hypertension addressed?
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amlodipine besylate, ACE inhibitors
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what is the ideal diet for CKD?
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low salt, K supplementation if cat, B vits (excreted in urine), wet food with restricted protein of high quality, omega 3 fatty acids
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what are the predisposing factors of upper urinary tract infections (3)?
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obstructions, renal calculi and veiscoureteral reflux
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how long are upper UTI treated?
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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
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where are most small proteins reabsorbed?
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in proximal tubules
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how do you treat glomerulosclerosis?
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steroids and ace inhibitors
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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 |
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which breeds is renal amyloidosis familial?
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sharpei and abyssinian
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what is the nephrotic syndrome?
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- proteinuria
- hypoalbuminaemia . hypercholesterolaemia - ascites/oedema/effusion may see thromboembolism due to loss of antithrombin III in urine |
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how is PLN treated?
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- restricted protein diet (increase protein, increase proteinuria)
- ace inhibitors: decrease proteinuria and decrease rate of CRF progression low dose aspiring if hypercoagulable state |
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What is Fanconi syndrome? what are the clinical signs and which breeds are predisposed?
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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 |
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what is renal glucosuria?
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disorder of proximal tubule resorption of glucose so get glucosuria and PUPD but without hyperglycaemia
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what condition can result in glucosuria?
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pyelonephritis occasionally can
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what is renal tubular acidosis? what are the two types?
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= 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 |
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name 8 causes of acquired nephrogenic diabetes insipidus
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- CRF
- pyelonephritis - HAC - hypercalcaemia - hyperthyroidism - liver failure - pyometra - steroid treatment |
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how long does it take for uraemia to develop in blocked bladder cases?
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if obstructed for more than 48 hours will develop uraemia
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why is crystalluria not god to diagnose presence of urolith?
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because can have urolithis without detectable crystalluria or crystalluria of one type and urolith of another
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name 2 urease producing bacteria
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proteus and staphylococcus
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in what situations are acidifying diets contra-indicated when treating struvite uroliths?
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when young: as they will buffer acid with calcium from bones
when in renal failure |
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how do you treat calcium oxalate uroliths?
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- 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 |
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what is special in patients with cystine uroliths?
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they have an inborn error of metabolism: an abnormal transport of cystine by renal tubules = not resorbed at glomerulus
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how do you treat cystine uroliths?
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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 |
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what are dantrolene, prazosin and phenoxybenzamine?
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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 |
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what are the most common bacteria found in UTIs in dogs (5)?
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E. Coli, proteus, klebsiella, staph, strep
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what are the bladder's natural defense mechanisms
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- urethral sphincter
- epithelial folds in proximal urethra - GAGs - flushing of urine - endogenous flora - competition - high osmolality of urine - immunoglobulin in vaginal mucus |
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how long a course of antibiotics are usually used in cystitis? when do you culture?
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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 |
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what can cause persistent or recurrent UTIs? how long may these need antibiotic cover?
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- 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 |
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what are the most common causes (in order of most to least common) of feline cystitis if under 10yo?
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1) idiopathic (55%)
2) urolithiasis (15-20%) 3) urethral plug (20%) 4) anatomical defect/neoplasia 10% 5) behavioral 10% 6) bacterial, 2% |
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what is the most common cause of feline cystitis in a pati9ent over 10 years?
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bacterial - if negative on culture perform radiographs and ultrasound for uorliths, tumours, etc
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how do you treat idiopathic feline cystitis?
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wet diet (want SG under 1.035), amitriptyline, GAGS, feed happy and prazosin
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where are polyps found on bladder cf. TCC? how do you treat them?
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polyps on ventral border - surgically remove or treat with piroxicam (decrease size)
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where do cystic tumours met to?
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regional and pelvic/iliac lymph nodes, prostate, pelvic bones, lung, liver, etc
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what CS of bladder tumours do you get in cats but not in dogs?
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tenesmus, rectal prolapse, anorexia and palpable abdominal mass
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why are canine bladder tumour antigen dipsticks not usually used?
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get false positives with proteinuria and haematuria
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how is bladder neoplasia diagnosed?
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- aspirate via urinary catheter, cystoscopy, ex lap
DON'T FNA --> SEEDING IN ABDOMEN |
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what are the treatment options for bladder neoplasia?
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surgery (removal) or reconstructive (e.g. uretocolonic anastamosis)
mitoxantrone and piroicam/metacam |
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what may you see in GSD with renal tumours?
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may see cystadenocarcinoma and nodular dermatofibrosis
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what is the origin of most prostatic tumours? how do you treat them?
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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 |
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what type of tumours do cryptorchids usually have (2)? Where do these met to?
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seminoma or sertoli cell tumours
these met to liver, lungs, spleen, kidneys, adrenal gland, pancreas |
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what are some of the clinical signs of sertoli cell tumours?
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all due to hyperoestrogenism
attracted to males flank alopecia preputial oedema gynecomastia aplastic anaemia squamous metaplasia of prostate |
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what is the treatment of choice for testicular tumours?
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castration with scrotal ablation
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what proportion of granulosa cell tumours produce oestrogen? benign or malignant in cat vs dog?
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50% produce oestrogen. tend to be malignant in cat and benign in dog
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what tends to cure transmissible venereal tumours?
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chemotherapy has a high cure rate
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what proportion of mammary tumours are malignant in dogs?
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50%
- mixed tumours most common in bitch |
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what factors are associated with good prognosis in mammary tumours in dog
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- if under 3cm large
- well circumscribed - no met - well differentiated - oestrogen and progresteron Rc +ve - if male |
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what are poor prognostic factors in mammary tumours of dog?
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- if mass over 3cm
- invasive - met - anaplastic - oestrogen Rc -ve - ulceration - vascular or lymphatic invasion on biopsy |
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which lymph node do you remove when performing mammectomy?
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superficial inguinal lymph node with 5th gland - only remove axillary lymph node if enlarged
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what treatments can result in mammary tumour development in cats?
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progesterone like drugs
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if you spay a cat before 6months of age what is its risk to develop mammary cancer?
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91% decreased risk
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what does MST in cats with mammary tumours depend on?
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size (most important), time of diagnosis, histological grade and surgical margins
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what should you not confuse mammary tumours in cats with?
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do not confuse with benign fibroepithelial hyperplasia that young cats get after silent oestrus
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how do you treat feline mammary tumours?
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surgery - radical mammectomy with bilateral LN removal. can also administer doxorubicin or cyclophosphamide or mitoxantrone
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what are poor prognostic indicators in feline mammary tumours?
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- big, old, vascular or lymphatic invasion or if surgical excision is poor
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