Feline diabetes mellitus Flashcards
(59 cards)
1
Q
Signalment
A
- 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
2
Q
Clinical Signs - typical CS
A
- polyuria
– the renal threshold for glucose is ~14-16 mmol/l - polydipsia
- weight loss, but the cat might still be obese initially
- lethargy
- polyphagia
3
Q
Clinical Signs - less common
A
- weakness
- plantigrade stance
- depression/anorexia
– suggests DKA - muscle loss
4
Q
Which cats is pre-diabetes / subclinical diabetes common in?
A
- obese cats
5
Q
Physical exam findings in diabetic cats
A
- Variable BCS: poor, obese
- Poor hair coat
- Dehydration?
- Abdominal pain if concurrent pancreatitis
- Evidence of peripheral neuropathy?
- Breath smelling of ketones?
6
Q
What causes type I diabetes in cats?
A
- 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
7
Q
What causes type II diabetes in cats?
A
- an inability to respond to insulin
– cats often still have functioning beta cells at the time of diagnosis - (+/- relative insulin deficiency)
8
Q
Glucose toxicity
A
- hyperglycaemia -> amylin deposition in islets -> beta cell apoptosis -> permanent IDDM
- beta cell apoptosis -> hyperglycaemia
9
Q
How can pancreatitis/obesity/glucocorticoids/megoestrol acetate/infecyion cause glucose toxicity & how can they be resolved?
A
- 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
10
Q
Consequences of insulin deficiency/resistance
A
- Persistent hyperglycaemia and glucosuria
- Fat mobilisation is favoured leading to
- hepatic lipidosis
- hepatomegaly
- hypercholesterolaemia
- hypertryglyceridaemia
- increased catabolism
Failure to intervene→ketonaemia, ketonuria→DKA
10
Q
Why must pts have type I diabetes to have ketotic breath?
A
- 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
11
Q
Is type I or II more common in cats?
A
- type II
12
Q
Diagnosis - things to document
A
- persistent hyperglycaemia and glucosuria
- AND appropriate clinical signs
13
Q
Diagnosis - things to rule out
A
- stress hyperglycaemia and glucosuria
- usually BG is < 16mmol/l, but not always
- usually resolves within a few hours, but not always
14
Q
Diagnosis - considering concurrent dz, esp if CS not typical
A
- 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?
15
Q
Diagnosis: Urinalysis
A
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
16
Q
Glucosuria differentials
A
Common
* DM
* Stress hyperglycaemia
Rare
* Renal tubular disease
* Fanconi syndrome
* Primary renal glucosuria
* Nephrotoxin exposure
17
Q
Fructosamine
A
- 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
18
Q
Problems with relying on fructosamine
A
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
19
Q
Diagnostic plans: what else you need to consider
A
causes
* pancreatitis
* acromegaly
consequences
* UTI
* peripheral neuropathy
contributing factors
* obesity
concurrent disease
* airway disease? +/- treatment
* inflammatory disease (dental disease)
20
Q
What are the aims of treating diabetes in cats?
A
- 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
21
Q
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?
A
- 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
22
Q
The ideal diabetic diet for cats
A
- 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
23
Q
Insulin treatment in diabetic cats - licensed products
A
- Caninsulin
– “BG<20 mmol/l start on 1IU bid”
– “BG> 20 mmol/l start on 2 IU bid” - ProZinc
– “o.2-0.4 IU/kg bid”
24
Insulin treatment in diabetic cats - unlicensed products (cascade)
* glargine
-- rapid onset/long duration
* determir
* most cats start on 1 IU bid
25
Insulin treatment in diabetic cats - syringes
- use the correct insulin syringe for the insulin being used
26
Insulin treatment in diabetic cats - dose changes
* Dose changes are usually 0.5 IU
* smaller changes aren’t feasible or accurate
* never dilute insulin
27
Insulin treatment in diabetic cats - dose increase
* Dose increase not more often than every 7 days
* rapid increase in dose increases risk of hypoglycaemia→rebound hyperglycaemia
28
Starting insulin treatment: Day 1
* Morning: check BG, feed and give insulin dose
* is there an ideal time to feed?
* Check BG every 2-4 hours
-- assess response to insulin
-- monitor for hypoglycaemia
-- try to establish the nadir
-> might take 10-12 hrs or more
* Review dose based on BG results
-- nadir <4.5mmol/l→↓ dose by 0.5IU
What next?
* Send your patient home
-- it can take at least 3 days to equilibrate to any dose change
* Review after 5-14 days
* Discharge with detailed
written information/instructions as well as a discharge appointment
-- provide a point of contact at the practice
29
The ideal BG curve
* BG < 14 mmol/l throughout
-- limits osmotic diuresis
-- ↓ risk of glucose toxicity
* Nadir between 4.5-8 mmol/l
* Time of nadir ideally between 6-10 hours
* Duration of action ~ 12 hours
30
What is important if aiming for remission?
- rapid/early tx
* glucose toxicity: high BG → glycogen deposition in the pancreas→ apoptosis of beta cells
* breaking the cycle might prevent irreversible DM
31
Is timing of diabetic remission predictable?
- no
* warn owners about possibility of hypoglycaemia
32
Indicators of diabetic remission
* hypoglycaemia despite low dose insulin
* no glucosuria
* “too good to be true”
33
What to do after diabetic remission
* continue dietary management
* monitor closely
-- relapse is quite common → IDDM
* Non-absorbing litter (hydrophobic sand)
* Litter in plastic bags
* In-litter detection systems (now discontinued)
34
Are oral hypoglycaemic drugs useful in cats?
* Owners may ask about drugs that are used in Type II DM in people
Glipizide:
* has evidence to support beneficial effects (? in 40% cats?)
* promotes insulin secretion from the pancreas
* adverse effects can include
-- cholestasis
-- hypoglycaemia
-- vomiting
* might contribute to progression of DM and pancreatic amyloidosis
* seldom used
35
New addition to oral hypoglycaemics
* Sodium-glucose cotransporter 2 (SGLT2) inhibitors
* Velagliflozin - Senvelgo - Boehringer Ingelheim EU/UK
* Bexagliflozin - Bexacat – Elanco USA
-- Promotes renal losses of glucose
-- Depends on reversible glucotoxicity as underlying pathogenesis
-- Can’t use as sole therapy in IDDM
-- May use as adjunctive and in NIDDM (monitor ketones)
-- Not all cats Type II and not all Type II reversible
-- eDKA risk within first week – more complicated to manage than DKA
-- May increase polyuria initially- osmotic diuresis
-- Polyuria may resolve if assists sufficiently with reversible gluco-toxicity to restore sufficient islet function.
36
Human vs feline DM
* Strict glycaemic control is not as essential in cats as in people
-- long term complications in people are a major concern
-> cats don’t have similar issues
* We know that people with DM feel less well if they have low normal BG than if they have a slightly high BG
37
Monitor the clinical signs
* General demeanour
* Water intake
* Appetite
* Weight/BCS
* Owner’s diabetic diary
-- off days?
-- check compliance
-- time of insulin injections
* Careful evaluation of clinical history and physical exam can be more useful than a BG curve
* BG curves are for unstable not stable patients
-- significant day to day variability
-- situation at home won’t be the same as in the practice
-> stress
-> variable food intake and exercise
-- a BG curve day (even at home) is not a “normal” day for a diabetic cat
38
Urinalysis for monitoring
* Most diabetic cats will have glucosuria
* Persistent absence of glucose in urine could mean risk of hypoglycaemia
-- insulin overdose?
-- diabetic remission?
* Ketonuria can indicate DKA
* Blood or change in pH can indicate UTI
39
Diabetic monitoring: can we use fructosamine?
* Trends are more useful than individual results
-- variability in lab results esp in-house
-- doesn’t give indication of degree of hypo or hyperglycaemia
* Beware of relying on the reference range to compare results
-- fructosamine > reference range
-> even a well controlled diabetic will have periods of hyperglycaemia each day
-> may not need a change in dose
* fructosamine in reference range
-> could indicate periods of hypoglycaemia even if owner unaware
-> may need dose reduction
* Less useful in monitoring than in diagnosis
* Always interpret fructosamine in light of the clinical signs
40
When should we use blood glucose curves?
* To detect hypoglycaemia
-- more helpful in decisions about reducing insulin dose than increasing
-- may need to do hourly BG rather than every 2-3 hours
* If BG is consistently high there is likely no point in continuing that curve for the full 12 hours
41
The Freestyle Libre
* Starter pack comes with the reader and 2 sensors
* The sensors last up to 14 days each
* No need for calibration
* Sensor is water resistant
* Smartphone App to enable glucose readings to be downloaded and analysed
* £160 for the starter pack
The future?
42
What are the likely causes of unstable diabetes in cats?
* Compliance issues
-- is the owner giving the right dose of the right insulin at the right time?
-- is only ONE owner doing this?
-- how do the owners record what they are doing
* UTI
-- often without clinical signs of lower urinary tract disease
* Pancreatitis
-- common comorbidity in cats and not always easy to manage
* Significant dental disease
43
Is insulin more common in cats than dogs?
- cats
44
Diabetogenic hormones
* glucocorticoids (iatrogenic more likely than Cushing's disease in cats)
* growth hormone (acromegaly)
-- 95% of acromegalic diabetic cats have insulin resistant DM
-- up to 25% of cats with DM might have acromegaly? (but don't know what population of cats this data came from)
* progestogens
* adipokines/cytokines
* adrenaline/noradrenaline * glucagon
45
Diabetogenic scenarios
* inflammatory conditions
46
What is insulin resistance?
- no response to insulin at a dose of >2.2IU/kg/dose
47
General approach to suspected insulin resistance
* Review the history for clues
-- poor compliance?
-- any GI signs?
* Thorough physical exam
-- dental status?
-- abdominal pain?
-- any mass lesions?
* Blood tests:
-- Haematology
-> markers of inflammation/infection?
-> anaemia suggesting comorbidity?
-- Biochemistry
-> any evidence of other organ involvement?
* fPLI
* Urinalysis
-- stix
-- sediment
-- culture
-- (SG less useful in diabetic cats)
* Diagnostic imaging
-- abdominal ultrasound?
-> check liver/GI tract/pancreas
* Blood test for IGF1
-- could the cat be acromegalic?
48
Cycle of insulin resistance
Insulin Resistance -> Increased demand on insulin secretion -> beta−cell exhaustion -> Failure of glycaemic control -> Uncontrolled hyperglycaemia -> Insulin Resistance -> ...
49
Hypoglycaemia in cats
* BG < 3-3.5mmol/l
* Mild hypoglycaemia is well tolerated and easily missed by owners
* Severe hypoglycaemia is life threatening
* Detection of hypoglycaemia or a strong clinical suspicion of hypoglycaemia are the only reasons why an insulin dose might be changed more often than every 5-7 days
-- ie we may reduce a dose but never increase a dose in this time
50
Hypoglycaemia - CS to look out for (i.e. for O)
* lethargy
* muscle tremors
* anorexia and vomiting
* ataxia
* recumbency
* vocalisation
* seizures
51
Hypoglycaemia - action at home
* apply honey or glucose to oral mucous membranes
-- advise to keep a dextrose gel available
* feed a proper meal ASAP
52
Hypoglycaemia - action in clinic
* 25% dextrose solution
-- 2-4 mls slow iv over 5-10 minutes
* continue with a 5% dextrose CRI
* monitor clinical signs and BG
Review treatment for diabetes
53
When should an owner contact the vet/nurse?
Seek urgent advice if
* any signs suggesting hypoglycaemia
* anorexia
* vomiting
* lethargy/weak
But also need to seek advice if
* weight loss
* polydipsia
* polyphagia
* plantigrade stance developing
54
Myths about diabetes in cats - anti-insulin antibodies
* in the past thought to be a cause of insulin resistance but no evidence to support this even though we are injecting “foreign proteins”
55
Myths about diabetes in cats - discarding open bottles after 4-6w (even if in date)
* this might not be necessary if insulin is stored in the fridge, handled carefully and doesn’t become discoloured or flocculant
56
Myths about diabetes in cats - timing is crucial and never miss a dose
* be kind to owners and allow them to give injections every 12 +/- 2 hours
* missing the occasional injection completely is unlikely to be a problem
57
Myths about diabetes in cats - stabilisation is quick, and afterwards just needs to be maintained
* management of diabetic cats with insulin is an ongoing challenge
* changes should always be done slowly and with time for the patient to adapt
58
Possible new treatment
* Extended-release glucaogon-like peptide-1 [GLP-1] analogs such as exenatide
* Secreted from the GI tract in response to ingestion of nutrients
* enhances insulin secretion
* decreases glucagon secretion
* induces satiation
* slows gastric emptying
