Endocrinology Flashcards
What is the amount of water intake in ml/kg/day for cats and dogs that is considered as polydipsia?
Dogs > 100 ml/kg/day
Cats > 50 ml/kg/day
Normal 50-60 ml/kg/day
Amount is affected by: environmental temperature, exercise, diet type (dry vs wet, salt content, protein content)
How do we ensure that PU/PD is present, how do we measure it?
Measure:
- Water intake
- Urine specific gravity (serial)
- Urine output (weigh cat litter)
What are the 5 steps in diagnosing PU/PD in a dog or a cat?
Step 1: Ensure PU/PD is present
Step 2: Review signalment, history and physical examination
Step 3: CBC, serum biochemistry, urinalysis, urine culture
Step 4: Additional tests as dictated by differential list
Step 5: Modified water deprivation test or desmopressin trial
Primary polydipsia (psychogenic polydipsia) is secondary to?
- Hyperthyroidism
- Liver failure
What are the causes of primary polyuria?
-> Central diabetes insipidus - lack of vasopressin (ADH) production
- neoplasia, trauma, surgery, inflammation, infection, etc.
-> Nephrogenic diabetes insipidus - problem with response to vasopressin
- primary (mutation in V2 receptor gene) rare!
- secondary (group of diseases causing this: hyper and hypoadrenocorticism, hyperthyroidism, etc.)
-> Loss of osmotic gradient
- osmotic diuresis (diabetes mellitus, chronic renal failure, etc.)
- loss of medullary tonicity (medullary washout, low urea/sodium)
Investigation: Step 1 - ensure PU/PD is present, what is involved in this step and what are the DDx?
DDx: incontinence, pollakiuria
Objective assessment:
- quantify water intake
- weigh cat litter
- urine osmolality or USG measurement
Cats: USG values decrease with age, lower values can be associated with health or PU/PD especially in renal disease, hyperthyroidism, diabetes mellitus, USG is not affected by timing of samples
Dogs: USG is variable within and between individuals, >1.025 makes PU/PD unlikely, decreases with age, varies with time of the day (higher in the morning)
Generally: take serial samples for USG, low values can be normal, collet samples at home (morning in dogs), values usually higher in cats
What is involved in step 2 of the investigation of PU/PD in dogs and cats?
Signalment, history & physical exam
- History
- Breed
- Age
- Sex
- Drugs
- Physical examination findings
Examples: physical exam findings that would indicate Cushing’s (pot belly, hair loss), plantigrade stance in cats or cataracts in dogs (diabetes), cachexia, ascites, goitre
What is involved in step 3 of the investigation of PU/PD in dogs and cats?
CBC, Biochemistry, UA, +/- culture - may confirm:
- Diabetes mellitus
- Hypercalcaemia
- Kidney disease
- Hypokalaemia
May provide evidence of disease:
- Hyperadrenocorticism (dogs) = increased ALP, ALT, cholesterol
- Hypoadrenocorticism (dogs) = azotaemia, increased K, decreased Na
- Hyperthyroidism (cats) = increased ALT, ALP
- Liver failure = decreased liver products, +/- increased ALT,ALP
What is involved in step 4 of the investigation of PU/PD in dogs and cats?
Additional tests as dictated by differential list (as identified in step 2)
Common tests:
- Abdominal ultrasound (adrenal disease, renal disease, liver disease)
- Adrenal function test - ACTH response test (hyperadrenocorticism, hypoadrenocorticism)
- Total T4 (cats) (hyperthyroidism)
- Bile acid stimulation test or ammonia (liver failure)
- SDMA (early kidney disease)
- Advanced imaging (CT, MRI)
What is involved in step 5 of the investigation of PU/PD in dogs and cats?
Modified water deprivation test
- the MWDT and desmopressin trial are very rarely necessary
- the MWDT differentiates between central diabetes insipidus, primary (congenital), nephrogenic diabetes insipidus and primary polydipsia, but can only be interpreted when all other causes have been excluded.
What is the treatment for central diabetes insipidus?
Tx: Desmopressin
- intranasal (eye drops)
- oral (tablet)
- Subcutaneous (especially cats)
Tx at night alone an option
- less expensive
- controls nocturia
- ensure free access to water
What are the most common causes of canine hypothyroidism?
Primary (>95%)
- Lymphocytic thyroiditis (50%)
- Idiopathic atrophy (50%)
- less common congenital or neoplasia
Secondary (congenital or acquired) rare, Tertiary (lack of TRH = lack of TSH) exceptionally rare
Was is the typical signalment for canine hypothyroidism?
Middle aged dogs
- rare in dogs < 2 years of age
- mean age 6-8 years (younger with lymphocytic thyroiditis)
Either sex
Any breed
- Mid to large pure breeds
- Dobermans, Hovawarts, Gordon setter, Old English sheepdogs, Retrievers, Ridgebacks, Spaniels, Shelties, Setters, Giant schnauzer
What are the clinical features of canine hypothyroidism?
Insidious in onset
Variable - many clinical signs possible
Dermatological features in 70-80% of cases
- poor quality coat
- dry
- failure to regrow
- non-inflammatory alopecia
- hyperpigmentation
- tragic facial expression (myxoedema)
Metabolic features (signs may be subtle) in >80% of cases
- lethargy
- weight gain
- exercise intolerance
- cold intolerance
What are some of the less common features of canine hypothyroidism?
Reproductive
- infertility (bitch)
- prolonged parturition
- increased puppy mortality
- galactorrhoea
Neuromuscular
- myopathies
- neuropathies
Cardiovascular
- bradyarrhythmias
Ocular
- corneal lipidosis
- reduced tear production
Gastrointestinal
- constipation
- vomiting
- diarrhoea
- gall bladder mucocele
Neurological
- myxoedema coma
- central vestibualar disease
What are the indications for testing with a suspected canine hypothyroidism case?
Supportive:
- metabolic (lethargy, weight gain)
- dermatologic (non inflammatory alopecia)
- clinical pathology (increased cholesterol)
- specific conditions (vestibular, gall bladder mucocele)
Not supportive:
- Polyuria and polydipsia
Which diagnostic testing is recommended and in which order once we have supportive indication for testing in a dog with suspected hypothyroidism?
- Perform routine clinical pathology
- supportive: mild non-regenerative anaemia, increased cholesterol, increased triglycerides, mild increase in ALT/ALP - Avoid thyroid function testing if external factors will impair interpretation of results
- nonthyroidal illness syndrome
- thyroid suppressive medications (prednisolone, phenobarbitone)
- consider breed effects (sighthounds) - First line testing: Total T4 and circulating TSH
- Decreased total T4; increased TSH = primary hypothyroidism
- Total T4; TSH WRL = euthyroid
- Total T4 WRL; TSH increased = subclinical hypoT4, recovery from NTIS/drugs, hypothyroidism with autoantibody interference
- Decreased total T4; TSH WRL = hypothyroidism, NTIS/drug therapy, breed (e.g. sighthound)
Additional Diagnostic tests: (if first line non diagnostic)
- Second line testing: Free T4
- less affected by NTIS, but can be decreased with severe disease - Third line testing (rarely needed):
- scintigraphy (limited availability)
- ultrasound (operator dependant, does not directly assess function)
- TSH-ST (gold standard but very expensive unless performing frequently)
When NOT to test a dog for hypothyroidism?
- Severe non-thyroidal illness
- Thyroid suppressive medications
Wait until:
- recovery from illness
- removal from thyroid suppressive drugs
Variable time to recovery of function
- often 4-6 weeks
Why is endogenous TSH high in primary hypothyroidism?
Because the thyroid glands are unable to produce any T4 or T3 so the feedback loop keeps going and more and more TSH is being produced to try and make up for the loss of T4 and T3.
How do we treat hypothyroidism in a dog?
Levothyroxine
- physiological prohormone, normalises T4 and T3
Dosing regimen: once or twice daily, same time each day, absorption is decreased by food so either always with or without food, avoid administration with other meds
Monitoring therapy:
- clinical signs: metabolic days to weeks, derm weeks to months
- monitor TSH: high values may indicate poor control long-term
- body weight: will decrease but diet and exercise change needed
What is the most common endocrinopathy in cats?
Hyperthyroidism - excess production of T4 and T3
Would you expect feline hyperthyroidism in a cat <6 years of age?
Very unlikely! it is extremely rare in cats younger than 6.
Feline hyperthyroidism is extremely common in older cats, and signs of mild disease can be subtle (e.g. weight loss alone). Testing should be considered in older cats with non-specific signs.
What is usually the first general clinical sign of feline hyperthyroidism?
Weight loss
What are the common clinical signs of feline hyperthyroidism?
- Weight loss despite an increase in appetite
- PU/PD
- Vomiting/diarrhoea
- Tachypnoea, tachycardia
- Heart murmur or identification of HCM
- Goitre, hyperactivity
- Increased ALT/ALP, decreased K, USG <1.035
- Unkempt/overgroomed
- Increased temperature (from increased metabolic rate)
How do we investigate feline hyperthyroidism?
-> Routine clinicopathological tests
- support a diagnosis
- eliminate other diseases with similar signs
- important in treatment decisions
-> Confirmatory
- Hormone analysis
-> Diagnostic imaging
- if required
What might we see on clinpath with feline hyperthyroidism?
-> Increased liver enzyme activity
- ALT, AST, ALP, GGT in over 90% of cases (may not be increased in mild or early cases)
- Most common cause of increased liver enzyme activities in older cats
+/- hypokalaemia
+/- decreased USG
+/- proteinuria
If hyperthyroidism is present in a cat but total T4 is normal, what can be the reason? and How do we diagnose these cats?
Usually mildly affected
- early disease
- concurrent illness (non-thyroidal illness suppresses total T4)
If cat has significant non-thyroidal illness:
Total T4 in high reference interval is inappropriate - Hyperthyroidism likely
If cat does not have significant non thyroidal illness:
Early hyperthyroidism or euthyroidism likely - options: retest total T4 later (min 4-6 weeks) values may remain in grey range, free T4 (expensive), TSH (species specific assay not widely available), scintigraphy (gold standard)
Can free T4 be used to diagnose feline hyperthyroidism?
yes but no..
free T4 concentrations are increased in almost all hyperthyroid cats but increased can also be seen in non thyroidal illness (sensitive, but not specific if non thyroidal illness present)
We are doing a hormone assay on a cat where we suspect hyperthyroidism, the result comes back as increased total T4 what is the diagnosis? and what would the diagnosis be if the result came back with decreased total T4?
Increased total T4 = hyperthyroidism - treat
Decreased total T4 = Non thyroidal illness - investigate further
Feline hyperthyroidism: If the total T4 on diagnostics comes back as: total T4 in lower reference interval what is the diagnosis?
Euthyroid
Feline hyperthyroidism: If the total T4 on diagnostics comes back as: total T4 in upper reference interval what is the diagnosis?
-> Euthyroidism OR
-> Hyperthyroidism - mild or with concurrent non thyroidal illness
Treatment of feline hyperthyroidism is either palliative or curative what are these treatments broadly?
Palliative: medical, dietary
Curative: surgical thyroidectomy, radioactive iodine administration
Sort of like definitive vs non definitive
What are the treatment options for feline hyperthyroidism?
Medical management:
- Antithyroid drugs: Methimazole or Carbimazole (metabolised to methimazole), decreases the hormone production but is non-curative (prior to surgery or lifelong therapy), adverse reactions (uncommon), high long-term cost
Dietary Management:
- Iodine restricted: Hill’s y/d, useful in mildly hyperthyroid cats, useful in old cats where other treatment options are not feasible, indoor cats only, is less effective, high long-term cost
Surgical thyroidectomy:
- Parathyroid has to be left and saved during surgery - possible post op hypocalcaemia
- Requires skill, high upfront cost but cure possible, persistence/recurrence possible
Radioiodine:
- Curative, no hypocalcaemia risk, no anaesthesia, limited availability, long hospital stay, high upfront cost, persistence possible
What are some of the complications that can occur after a thyroidectomy to treat feline hyperthyroidism?
- Hypoparathyroidism (hypocalcaemia)
- Laryngeal paralysis
- Haemorrhage
- Voice change
- Horner’s syndrome
- Hypothyroidism
Feline hyperthyroidism can have an affect on the heart and kidneys, what are they?
Hyperthyroidism can contribute to HCM
- reversible HCM
Hyperthyroidism can increase GFR (capable of masking kidney disease)
- If azotaemia develops start therapy for kidney disease and avoid development of hypothyroidism (worsens azotaemia and survival)
What is canine hypoadrenocorticism and what are the two types?
Addison’s disease - lack of glucocorticoids, mineralocorticoids, or both.
Secondary: (< 5%) pituitary
- Iatrogenic
- Pituitary neoplasia
- Idiopathic
- Glucocorticoid deficiency alone
Primary: (>95%) adrenal
- Immune-mediated
- Typical = glucocorticoid & mineralocorticoid deficiency
- Atypical = glucocorticoid deficiency alone
What is the typical signalment for canine hypoadrenocorticism?
- Young dogs (median 4 years)
- Females predisposed
- Any breed, mostly purebred (great dane, rottweiler, white terrier, wheaten terrier, poodle, portuguese water dog, bearded collie)
Historical features:
- Non-specific illness
- Anorexia
- Depression/lethargy
- GI signs
- Waxing and waning
- Response to symptomatic therapy
- Crisis precipitated by stressful event
What are the clinical signs and reasons for investigation of canine hypoadrenocorticism?
Supportive clinical signs:
- Collapse/weakness/hypovolaemia
- Vomiting/diarrhoea/melena
- Waxing/waning illness
- Rapid response to IVTF/glucocorticoids
- Often acute deterioration
- PU/PD, bradycardia
- May be preceded by stressful event
Supportive clinical pathology:
- Absence of a stress leukogram in a sick dog
- Eosinophilia/lymphocytosis
- Hyponatraemia/hyperkalaemia
- Azotaemia with inappropriate dilute urine
- Hypoglycaemia
- Hypercalcaemia
- Hypocholesterolaemia
Which haematological and biochemical features could be present in canine hypoadrenocorticism?
Haematological:
- Anaemia (lack of cortisol can lead to anaemia - severely volume depleted from loss of sodium therefore loss of water - lack of red cell count)
- Erythrocytosis
- Lymphocytosis
- Eosinophilia (reverse stress leukogram)
Lack of cortisol = lack of stress response
Biochemical: often look like they have renal disease
- Azotaemia
- Hyperphosphataemia
- Increased ALT,ALP (mild)
- Hypoglycaemia (can be severe) = no glucocorticoid = no hepatic gluconeogenesis
- Hypoalbuminaemia
- Hypocholesterolaemia
What is the obvious sign for canine hypoadrenocorticism when we should investigate?
-> Dull, collapse with supportive electrolyte changes or immediate response to IVFT/glucocorticoids however generally non-specific!
Electrolyte changes:
- Hyperkalaemia
- Hyponatraemia
- Hypochloraemia
- Hypercalcaemia
Other:
- GI disease
- Bradycardia
- Hypocholesterolaemia
- Azotaemia in a young dog (major differential for azotaemia with reduced concentrating ability)
Hypoadrenocorticism is often overlooked - misdiagnosed as renal failure or GI disease!
What could the urinalysis features be of a dog with hypoadrenocorticism?
They are unable to concentrate their urine
- Inappropriately dilute urine (SG<1.030 despite hypovolaemia)
- May lead to inappropriate diagnosis of renal failure
What are some other investigations that can be done to diagnose canine hypoadrenocorticism?
Electrocardiography
- potassium induced changes
Radiography
- Hypovolaemia associated changes
Ultrasonography
- Adrenal glands small
How do we confirm a diagnosis of canine hypoadrenocorticism?
Firstly ensure that there is no exogenous glucocorticoid administration!
ACTH response test (preferred):
- Adequate stimulation = excludes hypoadrenocorticism
- Inadequate stimulation = confirms hypoadrenocorticism
-> response test is done by injecting synthetic ACTH ideally IV then sample 0.5-2 hours later
Basal cortisol measurement: this can’t be used to confirm alone!
- Cortisol > 55 nmol/L excludes hypoadrenocorticism
- Cortisol <55 nmol/L = hypoadrenocorticism or normal function -> perform ACTH response test
How do we treat canine hypoadrenocorticism? (differentiate between GC deficiency alone and GC & MC deficiency together)
GC deficiency alone:
- Supportive therapy
- Prednisolone/cortisone
- Atypical cases may later develop MC deficiency
GC & MC deficiency:
- Emergency: IVFT (isotonic crystalloids and glucose if necessary) and Hydrocortisone or dexamethasone
- Chronic: DOCP* (Desoxycortisone pivalate) SC and prednisolone/cortisone OR Fludrocortisone^ (with prednisolone or cortisone at times of stress)
- DOCP is given SC but needs additional glucocorticoid (oral) as DOCP is a mineralocorticoid only
^ Fludrocortisone has mineralocorticoid and glucocorticoid activity
What are the two types of canine hypercortisolism?
ACTH dependant
- Pituitary dependant 80-85% of cases
ACTH independent
- Functional adrenal tumour 15-20% of cases
What is the signalment for canine hypercortisolism?
Middle aged - older dogs, almost all > 6 years, median 10-11 years
Breeds: poodles, dachshunds, terriers
No sex predisposition
What are the clinical signs seen with canine hypercortisolism?
- PU/PD, panting
- Pendulous abdomen, pot belly
- Fat redistribution, muscle atrophy
- Dermatological changes (alopecia, comedones, skin atrophy (loss of elasticity, prominent veins, striae, scar breakdown), easy bruising, calcinosis cutis, coat colour changes
- Thromboembolic disease, GB mucocele
What would we see on clinical pathology in a suspected canine hypercortisolism case?
^^^ ALP (corticosteroid induced)
^ ALT, decreased urea
^ cholesterol, triglycerides
Stress leukogram
^ PCV, platelets
Decreased USG, proteinuria, bacteriuria
DO not investigate based on clinical pathology changes alone!
Which of the dermatological features seen with canine hypercortisolism is very specific for the disease?
Calcinosis cutis
- 10% of cases
- High specificity
What is the most common combination of tests used to diagnose canine hypercortisolism?
LDDST and ACTH response test
- LDDST is sensitive, not specific
- ACTH response test is specific, not sensitive
Other test would be Urine cortisol to creatinine ratio (UCCR): most sensitive, least specific
Once canine hypercortisolism is confirmed, what is the next step?
Test to differentiate AT and PDH (Adrenal tumour or pituitary dependant hypercortisolism)
LDDST
- Anything but a lack of suppression pattern supports PDH
- Lack of suppression pattern = equal likelihood of PDH or AT
Abdominal ultrasound
- Two symmetric, commonly enlarged = PDH
- One large, one atrophic = Adrenal tumour
Endogenous ACTH
- Decreased = AT
- Not decreased = PDH
HDDST
- Not recommended
- Limited additional value over LDDST
- Administering GC’s to dog with GC excess = risk
Which additional tests can be done for a dog with hypercortisolism in selected cases?
Abdominal/thoracic CT
- Adrenal masses
- Pre-operative planning
- Staging (metastasis)
- Vessel invasion
Brain MRI/CT
- Confirm macro-tumour (neurological signs)
- Pre-operative/radiation (rarely performed)
Abdominal radiography
- May identify mass +/- calcification of mass
- Very limited value
You see a dog where you are suspecting hypercortisolism, the dog doesn’t have clinical signs but there are clinical pathology changes, should you test for canine hypercortisolism?
No!
Only test appropriate cases with clinical signs, not clinical pathology changes alone!
IF testing for a dog with clinical signs:
- Perform multiple tests (typically combine ACTH stimulation and LDDS test)
- Discriminate using LDDS test, abdominal ultrasound, ACTH measurement
Dogs with hypercortisolism are at increased risk of which conditions?
- UTI
- Pyelonephritis
- Urolithiasis
- Diabetes mellitus
- Gallbladder mucocele
- Pancreatitis
- Other infections
- Thromboembolic disease
How do we treat canine hypercortisolism?
Medical management:
Trilostane: (impairs cortisol production)
- Daily treatment
- Titrated to effect
- Absorption enhanced by food
- Care with kidney and renal disease
- Care with ACE-i, telmisartan, spironolactone
- Risk of hypocortisolaemia, hypoadrenocorticism
Mitotane (low dose):
- Less commonly used
- Daily induction then weekly maintenance
Surgical management:
Adrenalectomy: (removing adrenal gland)
- Treatment of choice for adrenal tumours
- Require short term GC (unilateral) or long term GC and MC (bilateral) supplementation
Hypophysectomy: (removing pituitary)
- Rarely performed in Australia
What are the contraindications for use of Trilostane in a dog with hypercortisolism?
- Primary hepatic disease
- Chronic renal disease
- Pregnancy
- Concurrent medications: potassium sparing diuretics, ACE-inhibitors, Angiotensin 2 receptor antagonist
How do we monitor medical therapy in a dog with hypercortisolism?
- Pre pill cortisol
- ACTH-ST 4 hours post pill
- Titrate to effect
What are the clinical signs that would give enough reason to investigate a disorder of calcium homeostasis?
- PU/PD
- Lethargy, weakness
- Renal failure, urolithiasis
- Vomiting, anorexia, constipation, pancreatitis
May be serendipitous finding on routine screening
What are the causes of hypercalcaemia? (HARD IONS)
- Hyperparathyroidism (primary)
- Addison’s disease
- Vitamin D toxicity
- Idiopathic
- Osteolytic disease
- Neoplasia
- Spurious
Which tests can we do to detect disorders of calcium homeostasis?
Total calcium:
- widely available
- cheap
- does not accurately predict ionised calcium
Ionised calcium:
- biologically active
- sensitive to pH
Phosphate:
- PTH increases circulating calcium but decreases circulating phosphate
Parathyroid hormone:
- normal is inversely related calcium increase = PTH decrease and vice versa
- primary hyperparathyroidism = PTH increase -> calcium increase
- primary hypoparathyroidism = PTH decrease -> calcium decrease
PTH-rp:
- low concentrations in adults
- produced by certain neoplasms
Vitamin D:
- increases circulating calcium and circulating phosphate -> vit D toxicity
What are the 3 most common reasons for hypercalcaemia in a dog and a cat (in order)?
Dogs:
1. Neoplasia (50%)
- anal sac adenocarcinoma
- lymphoma
- Kidney disease
- Hyperparathyroidism
Cats:
1. Neoplasia (30%)
- Kidney disease
- Idiopathic (possibly diet related)
How do we investigate hypercalcaemia, what is the diagnostic approach?
- Assess signalment, history, and physical examination, may permit more rapid diagnosis e.g. lymphadenomegaly -> FNA -> lymphoma
- Complete CBC, biochemistry and urinalysis
- ideally total and ionised calcium
- assess phosphate: if decreased = PTH/PTH-rp mediated process more likely, if increased makes vitamin D mediated process more likely
- perform ACTH-ST if hypoadrenocorticism suspected - Neoplasia most common
- so palpate anal sacs
- abdominal and thoracic imaging - Assess PTH and PTH-rp
- if PTH increased -> neck ultrasound may identify gland enlargement - If cause not identified, consider vitamin D measurement
How do we treat hypercalcaemia?
Treat underlying disease!
Non-specific treatment:
Intravenous fluids
- normal saline
Furosemide (hypocalcaemia can be a rare side effect)
- increases calcium excretion
Prednisolone
- increases calcium excretion
- may mask underlying disease
Bisphosphonates e.g. pamidronate
- infusion
- osteoclast inhibitor (stops bone from being broken down and calcium being released)
- prolonged decrease in calcium
- side effects: hypocalcaemia, jaw osteonecrosis (rare)
How do we treat idiopathic hypercalcaemia in cats?
Dietary change
- fibre, renal, oxalate)
- chia seeds
Prednisolone
Alendronate (Bisphosphonate, that inhibits osteoclasts)
How do we treat hypocalcaemia?
Acute therapy:
- 10% calcium
- slow IV
- ideally monitor ECG
- stop if bradycardia develops
- continue supplementation with continuous rate infusion
What is the aetiology of diabetes mellitus in dogs?
Insulin dependant diabetes mellitus:
- immune-mediated beta cell destruction
Resistance may also occur with:
- pancreatitis
- urinary tract infection
- obesity
- hypercortisolism
- dioestrus/pregnancy
What is the aetiology of diabetes mellitus in cats?
Insulin resistance due to:
- obesity/inactivity
- genetics
- altered diet/feeding habits
- hypersomatotropism (acromegaly)
- pancreatitis
Decreased insulin secretion
- occurs secondary to glucose toxicity
What are the possible clinical signs of diabetes mellitus that give an indication to investigate?
- PU/PD
- Polyphagia
- Weight loss
- Exercise intolerance
- Hepatomegaly
- Ketosis
- Cataracts (dogs)
- Plantigrade stance (cats)
What are the common routine clinical pathology changes seen with diabetes mellitus?
- increased glucose (consider stress, especially in cats)
- increased cholesterol
- increased triglycerides
- increased ALT/ALP
- urinary tract infection
Confirm:
- repeated fasting hyperglycaemia, glucosuria, ideally home sample (avoid stress)
- ketones
- fructosamine
What are additional diagnostic tests to investigate diabetes mellitus?
- urine culture
- abdominal ultrasonography
- pancreatic lipase / DGGR lipase
- IGF-1 (cats) 2-3 weeks after insulin commences
What are the three main areas to control in the treatment of diabetes mellitus in dogs and cats?
- Insulin
- porcine lente (Caninsulin) (dogs) 40 units/mL
- glargine (cats) 100 nits/mL - Diet
- cats = low carbs, high protein
- dogs = high fibre, protein; low calorie, (low carb, high protein) - Exercise
- regular, not at time of peak activity, commensurate with animals ability
Owner education essential, treatment plan needs to consider owner’s lifestyle.
When considering diabetes mellitus, what is the signalment in dogs?
- middle aged to old
- more common in females
- variable breed predisposition (samoyed, poodles, terriers, schnauzers)
Apparently boxers never get diabetes (the random shit I write on my slides sometimes)
When considering diabetes mellitus, what is the signalment in cats?
- older cats (>10 years)
- obese cats
- male cats
- burmese cats
What are the steps involved in dealing with a difficult case of treating a dog or cat for diabetes mellitus?
- First check for any problems with:
- insulin (dose, syringe, storage)
- diet (correct type, amount)
- exercise - If no issues identified, examine owner factors closely (number of people injecting, compliance, skill, timing)
- Explore & treat concurrent disease
- UTI and pancreatitis common
- hypercortisolism (dogs)
- acromegaly (cats)
- dioestrus (dogs) - Explore individual animal factors e.g.
- long/short duration insulin action (by continuous glucose monitoring)
