Feline diabetes mellitus Flashcards
Signalment
- Cats >7 years of age are at greatest risk
- M and MN cats > F and FN
- Breeds:
– Burmese cats have a higher risk in the UK and in Australia, NZ and Europe * think about other breeds such as Tonkinese, Norwegian Forest - Obesity: can increase risk of diabetes up to 4 x compared with optimal weight cats
- Indoor and inactive cats
- Cats on treatments such as:
– glucocorticoids
– progestagens
Clinical Signs - typical CS
- polyuria
– the renal threshold for glucose is ~14-16 mmol/l - polydipsia
- weight loss, but the cat might still be obese initially
- lethargy
- polyphagia
Clinical Signs - less common
- weakness
- plantigrade stance
- depression/anorexia
– suggests DKA - muscle loss
Which cats is pre-diabetes / subclinical diabetes common in?
- obese cats
Physical exam findings in diabetic cats
- Variable BCS: poor, obese
- Poor hair coat
- Dehydration?
- Abdominal pain if concurrent pancreatitis
- Evidence of peripheral neuropathy?
- Breath smelling of ketones?
What causes type I diabetes in cats?
- a deficiency of insulin
– pancreatic β cell loss - destruction of cells
– chronic pancreatitis, +/- EPI
-> inflammatory mediators may contribute to insulin resistance ie Type I→Type II
– pancreatic amyloidosis
– glucose toxicity
– immune mediated disease - congenital lack of β cells
– very rare in cats
What causes type II diabetes in cats?
- an inability to respond to insulin
– cats often still have functioning beta cells at the time of diagnosis - (+/- relative insulin deficiency)
Glucose toxicity
- hyperglycaemia -> amylin deposition in islets -> beta cell apoptosis -> permanent IDDM
- beta cell apoptosis -> hyperglycaemia
How can pancreatitis/obesity/glucocorticoids/megoestrol acetate/infecyion cause glucose toxicity & how can they be resolved?
- Carbohydrate intolerance → hyperglycaemia ->
- Glucose toxicity inhibits beta cell insulin production ->
- Induction of apparent IDDM ->
- Hyperglycaemia controlled or cause of peripheral insulin resistance resolves ->
- Glucose toxicity resolves, beta cells resume insulin production ->
- Diabetic Remission: Hypoglycaemia develops, Ability to maintain normoglycaemia is restored
Consequences of insulin deficiency/resistance
- Persistent hyperglycaemia and glucosuria
- Fat mobilisation is favoured leading to
- hepatic lipidosis
- hepatomegaly
- hypercholesterolaemia
- hypertryglyceridaemia
- increased catabolism
Failure to intervene→ketonaemia, ketonuria→DKA
Why must pts have type I diabetes to have ketotic breath?
- it only takes a small amount of insulin for ketone production to be shut down
- if ketotic = no insulin made, so must be a production problem
Is type I or II more common in cats?
- type II
Diagnosis - things to document
- persistent hyperglycaemia and glucosuria
- AND appropriate clinical signs
Diagnosis - things to rule out
- stress hyperglycaemia and glucosuria
- usually BG is < 16mmol/l, but not always
- usually resolves within a few hours, but not always
Diagnosis - considering concurrent dz, esp if CS not typical
- could the cat have pancreatitis or even “triaditis”
– abdominal ultrasound
– blood tests including fPLI - could your cat be hyperthyroid?
– is there any overlap in clinical signs between hyperT4 and DM? What are the main differences?
Diagnosis: Urinalysis
USG:
* affected by glucosuria in some situations
* not always quite as low as you think it will be for a polyuric cat
Dipstick:
* confirms glucosuria
* rules out ketonuria
* any changes that suggest UTI?
Sediment analysis
* often no active sediment even if there is a UTI
Culture and sensitivity
Glucosuria differentials
Common
* DM
* Stress hyperglycaemia
Rare
* Renal tubular disease
* Fanconi syndrome
* Primary renal glucosuria
* Nephrotoxin exposure
Fructosamine
- Indicates the average BG during the preceding 1-3 weeks
- Often not affected by transient stress hyperglycaemia
- Might be normal in recent or mild diabetics
– repeat if persistent glucosuria at home?
– if you think the cat has DM don’t rule it out too quickly: cats become diabetic over a period of time so there can be some waxing and waning of clinical signs - Might be affected by hypoglycaemia induced periods of hyperglycaemia (the Somogyi effect) if they are prolonged
– less useful for monitoring diabetic cats on treatment than for initial diagnosis
– fructosamine might be high even though the cat has had episodes of hypoglycaemia
Problems with relying on fructosamine
Fructosamine concentrations are variable depending on:
* individual cats
* different labs and methodology
* age
* gender
* serum protein concentrations
* hydration status
* thyroid status and conditions that modify protein turnover, eg fructosamine tends to be lower in hyperthyroid cats
Diagnostic plans: what else you need to consider
causes
* pancreatitis
* acromegaly
consequences
* UTI
* peripheral neuropathy
contributing factors
* obesity
concurrent disease
* airway disease? +/- treatment
* inflammatory disease (dental disease)
What are the aims of treating diabetes in cats?
- Resolve or at least reduce clinical signs
– maintain or improve QOL - Select a treatment protocol suited to the owners and their cat
- Minimise risk of complications
– hypoglycaemia
-> diabetic remission can occur
-> insulin induced hypoglycaemia
– DKA - Optimise body weight
- Increase exercise
Weight loss as a treatment for diabetes in obese cats - what can it lead to? what do we need to be aware of in cats re rapid weight loss? how to do it?
- Can lead to diabetic remission
– temporary
– permanent? - Rapid weight loss in cats is not a good idea (hepatic lipidosis)
– aim for 2% weight loss/month - Wet food
– tends to reduce calorie intake
– helps maintain hydration - Diabetic cats can continue grazing rather than having strict timed feeds but ensure not > daily food allowance
- Consider environmental enrichment to encourage activity
– feeding puzzles
The ideal diabetic diet for cats
- High protein
– normalises fat metabolism and provides a consistent energy source (gluconeogenesis)
– limits the risk of hepatic lipidosis during weight loss
– prevents loss of lean muscle mass - Restricted carbohydrate
– helps relieve tendency to hyperglycaemia and glucose toxicity - Wet formulation
– improves satiety - Results: higher diabetic remission rates and improved glycaemic control
- BUT if a cat is on a different therapeutic diet for a concurrent illness that diet should be continued. For example:
– continue a renal support diet for an older cat with CKD that becomes diabetic
– feed for IBD if you suspect the cat has triaditis
