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ENI2 > Small animal endocrinopathies 2 > Flashcards

Small animal endocrinopathies 2 Flashcards

Diabetes, ketoacidosis

1
Q

What are the aims of treatment of feline diabetes mellitus?

A
  • Maintain adequate glycaemia control
  • Avoid side effects of hyperglycaemia
  • Use exogenous insulin to generate glycaemic control then rely on dietary treatment if possible depending on aetiology
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2
Q

What are common side effects of hyperglycaemia in cats?

A
  • Ketoacidosis
  • Cataracts
  • Pancreatitis
  • Nephropathy, retinopathy (both rare)
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3
Q

What treatment options are available for cats with diabetes mellitus?

A
  • Diet alone, can be very effective
  • ProZinc and Caninsulin (licensed)
  • Insulin glargine (lantus)
  • Oral hypoglycaemic agents, but rarely (glipzzide, metformin, chromium, vanadium)
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4
Q

What is the typical dose of Caninsulin used in cats?

A

0.25-0.5IU/kg BID (start at 0.25)

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5
Q

Outline the feeding of cats with diabetes mellitus

A
  • High protein diet improves glycaemic control
  • High fibre can be beneficial as long as low carb
  • Low cal/high fibre good in obese diabetic patients to aid weight loss, DO NOT USE for emaciated diabetics
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6
Q

Outline the use of insuin glargine in the treatment of diabetic cats

A
  • Lantus
  • Human recombinant insulin analogue, excellent in studies
  • Microprecipitate that dissipates of the day
  • Difficulty with cascade in EU
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7
Q

Outline the use of oral hypoglycaemia agents in cats with NIDDM

A
  • Very rare

- Only where diet and exogenous insulin are giving sub-optimal control

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8
Q

What is the mechanism of action of glipzide? What are the side effects? Dose?

A

Sulphonylurea durg, stimulates insulin secretion from functional beta cells (but body already doing this so may be physiologically detrimental)

  • Hypoglycaemia, vomiting, icterus, elevated liver enzymes
  • 2.5mg/cat
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9
Q

What is the mechanism of action of metformin, in the treatment of diabetic cats? Side effects? Dose?

A
  • Biguanide, no direct effect on beta cells, increases sensitivity of peripheral tissue and liver to insulin, inhibits gluconeogenesis and glycogenolysis
  • Side effects: V, D, anorexia
  • 25-50mg/cat
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10
Q

What is the mechanism of action of acarbose in the treatment of diabetic cats? Side effects?

A
  • Alpha glucosidase inhibitor, slows intestinal absorption of glucose (inhibits sucrase, maltase, isomaltase)
  • Side effects: diarrhoea, weight loss
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11
Q

What is the mechanism of action of chromium in the treatment of diabetic cats?

A

Increases insulin sensitivity

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12
Q

What is the mechanism of action of vanadium in the treatment of diabetic cats? Side effects?

A
  • Acts at post-receptor site to stimulate glucose metabolism
  • Side effects: anorexia, vomiting, renal toxicity
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13
Q

What parameters should be measured in the monitoring of the feline diabetes mellitus patient?

A
  • clinical examination, owner report of clinical signs
  • Blood glucose/fructosamine
  • Urine glucose
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14
Q

Why is home blood glucose monitoring best in cats with diabetes mellitus?

A

Removes stress aspect which can increase glucose result

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15
Q

Outline the frequency of monitoring of the feline diabetes mellitus patient?

A
  • Weekly for first 3-4 weeks-
  • Then every 2-3 weeks until 4 months
  • Then every 4 months
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16
Q

Why is frequent monitoring of feline diabetes mellitus patients important?

A
  • Need to ensure that diabetes is controlled and that the cat has not gone into remission
  • Allows checking of owner compliance
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17
Q

When is a cat describe as resistant to the insulin they are receiving?

A

When they are receiving >2.2 IU/kg BID

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18
Q

What should be investigated if a cat becomes resistant to the insulin being administered?

A
  • Owner compliance
  • Infection (e.g. UTI)
  • Concurrent endocrinopathy
  • neoplasia
  • Stress
  • True insulin resistance
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19
Q

What is the main risk of remission in diabetic cats?

A

Hypoglycaemia - will kill them faster than chronic glow grade diabetes

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20
Q

In what aspects of diabetic monitoring should a cat owner be educated?

A
  • Clinical signs, of both uncontrolled diabetes and remission
  • What to do in the even of a hypoglycaemic crisis
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21
Q

Outline the potential for remission in a feline diabetes mellitus patient

A
  • Not usually the aim and often only temporary
  • Occurs usually after aggressive early treatment (~26% of those in primary care, 60-67% of those in referral), usually occurs within 3 months of starting treatment
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22
Q

Outline the value of urine glucose measurement in the monitoring of diabetes mellitus in the cat

A
  • Only an average of what is occurring between urinations

- Should not be used to alter daily insulin dose

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23
Q

What is the typical signalment for canine diabetes mellitus?

A
  • Peak 7-9yo, generally older dogs

- Females more common than males

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24
Q

Which breeds of dog are predisposed to diabetes mellitus?

A

Australian terrier, Standard and miniature schnauzer, Bichon Frise, Spitz, fox terrier, miniature poodle, samoyed, cairn terrier, keeshond, maltese, toy poodle, lhasa apso, yorkie, collie, GSD

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25
Q

What are the clinical signs of diabetes mellitus in the dog?

A
  • PUPD
  • Polyphagia and weight loss
  • Exercise intolerance, lethargy, sleepy
  • Diabetic cataracts
  • Recurrent infections
  • Ketosis (acetone breath)
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26
Q

Why do recurrent infections occur with diabetes mellitus?

A
  • Neutrophil function reduced by high glucose

- Warm bladder filled with glucose, perfect for UTI

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27
Q

What are the acute signs of diabetic ketoacidosis?

A
  • Dull, depressed, weak, possibly comatose
  • Often vomiting
  • Dehydrated
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28
Q

What are the effects of insulin on carbohydrates?

A
  • Stimulates receptor mediated glucose uptake via GLUT4 in most cells
  • In liver, enhances uptake, phosphorylation, glycolysis, glycogen storage and inhibits glycogenolysis
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29
Q

What are the effects of insulin on fat

A
  • Excess glucose -> pyruvate -> AcoA and FFA

- Insulin activates lipoprotein lipase and inhibits hormone sensitive lipase

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30
Q

What is the effect of insulin on protein?

A
  • Increased protein anabolism

- Inhibits gluconeogenesis

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31
Q

Describe the pathology of type I diabetes mellitus

A
  • Beta-cell destruction leading to absolute insulin deficiency
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32
Q

What are potential causes of type I diabetes mellitus in the dog?

A
  • Can be immune mediated
  • Idiopathic
  • Pancreatitis
  • Glucose toxicity
  • Chemical toxicity
  • Beta loss due to exocrine pacreatic insufficiency/pancreatitis
  • Congenital beta-cell loss
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33
Q

Give examples of immune mediated causes of type I diabetes mellitus

A
  • LADA - latent autoimmune diabetes in adults

- Antibodies against islet Ag e.g. insulin, gAD-65, insulinoma antigen-2

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34
Q

What are potential causes of type II diabetes mellitus in the dog?

A
  • Can be mainly IR with relative insulin deficiency or primarily secretory defect +/- IR
  • Progesterone/agen leading to increased GH which inhibits insulin
  • IR due to glucocorticoids, glucagon, catecholamines, thyroid, obesity
  • HAC, exogenous corticosteroids
  • IGF-1/GH excess (acromegaly)
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35
Q

Explain how insulin resistance can eventually lead to insulin deficiency

A
  • Reduced response = increased release

- Beta-cell exhaustion and glucose toxicity = hypoinsulinaemia and hyperglycaemia

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36
Q

Explain how diabetes mellitus can develop in the bitch

A
  • Can develop in metoestrus
  • High progesterone, causes mammary development
  • Leads to increased mammary growth hormone, can leak out and inhibit insulin = hyperglycaemia
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37
Q

What are the potential outcomes for metoestrus diabetics?

A
  • If low basal insulin once presented then have lost insulin production and diabetic for rest of life
  • If high basal insulin and therefore maintained islet function, can go into remission and metoestrus diabetes will not return if spayed
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38
Q

Explain the pathophysiology of diabetic cataracts

A
  • Normally glucose in eye metabolised by hexokinase, becomes overwhelmed by hyperglycaemia
  • Metabolised by AR (aldose reductase) to sorbitol
  • Sorbitol stays in eye and draws in water via osmosis
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39
Q

What tests need to be included when working up a case of suspected canine diabetes mellitus?

A
  • Urinalysis
  • Haematology and biochem
  • Fructosamine
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40
Q

Explain the interpretation of glucosuria

A

Glucosuria can indicate diabetes mellitus, but only where hyperglycaemia is also present - where this is not the case, renal tubular disease should be investigated

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41
Q

What findings might be expected on haematology and biochemistry in a case of canine diabetes mellitus?

A
  • Increased ALP and ALT
  • Increased cholesterol and TAGs
  • Fasting hyperglycaemia
  • +/- hyponatraemia
  • +/- ketonuria/ketoanaemia
  • Fructosamine
42
Q

What (other than glucosuria) may be found in urinalysis in a case of canine diabetes mellitus?

A

Positive bacterial culture (i.e. UTI)

43
Q

What value is indicative of fasting blood hyperglycaemia?

A

> 12mmol/l usually (>5.5-12mmol/l more challenging to identify)

44
Q

Why may hyponatraemia occur in diabetes mellitus?

A

Hyperglycaemia may have osmotic effect, drawing water out of intracellular into extracellular compartment, diluting sodium

45
Q

What is the renal threshold for glucose?

A

~10-12mmol/l

46
Q

Compare the relative doses required to inhibit ketogenesis, stimulate glucose uptake and stimulate K+ uptake

A

If have enough insulin to stimulate glucose uptake, inevitably have enough to inhibit ketogenesis, and if have enough to stimulate K+ uptake, have enough to stimulate glucose uptake

47
Q

What are the following signs of in a diabetic canine patient?
Collapsed, vomiting, anorexia

A

Ketoacidosis

48
Q

What treatment is required in a diabetic canine patient with the following signs?
PUPD, ketonuria, eating and drinking

A

Healthy other than PUPD, start insulin therapy, routine management required only and intermediate dose of insulin

49
Q

What are the aims of diabetic treatment?

A
  • Prevent ketoacidosis
  • Abolish clinicla signs
  • Restore lost condition/weight
  • Reduce risk of complications
  • Complete control of blood glucose not necessary as long as is stable and otherwise healthy
50
Q

What factors need to be taken into consideration when treating a diabetic dog?

A
  • Insulin type and frequency of administration
  • Diet
  • Body condition
  • Lifestyle
  • Spaying of intact females
51
Q

Outline what factors need to be discussed with the owner regarding the treatment of a diabetic dog

A
  • Need to give full explanation of therapy
  • Financial commitment required is substantial
  • Stability of lifestyle as consistency is critical
  • Expectation management
  • Provide examples of resources available
52
Q

What product is licensed in the treatment of canine diabetes mellitus?

A

Only Caninsulin is licensed

53
Q

What are the 2 lente forms of insulin available for dogs?

A
  • Caninsulin is a lente insulin zinc suspension
  • Semi-lente = soluble crystal of insulin quickly absorbed
  • Ultra lente = less soluble form, slower release of insulin
54
Q

Outline the doses of insulin used in dogs

A
  • Usually given BID but can be SID
  • Initial dose 0.5IU/kg BID
  • Most required between 0.8-1.2 IU/kg/dose to stabilise
55
Q

Describe the storage of caninsulin

A
  • Ideally in fridge door (2-8degreesC)
  • Rolled gently prior to drawing up dose, not shaken
  • May be ineffectual after expiry date
  • Keep open for 28 days max
56
Q

What factors need to be controlled in order to establish a consistent dose of insulin?

A

Exercise and diet

57
Q

How should diet be controlled in a diabetic canine patient? How does this differ in obese and thin patients?

A
  • Dry/tinned food
  • Keep meal times at a set time and corresponding with insulin dosing
  • Calculate patient’s MER in kcal and weigh out food
  • Food should be high in complex carbs for minimised post-prandial glucose peaks, high fibre
  • Avoid semi-moist foods
  • Ideally use a glucomodulation diet
  • Increase cal intake gradually if low BCS, careful and monitored weight reduction if high BCS
58
Q

Outline the control of lifestyle for a diabetic patient

A
  • Consistent regular exercise at a similar time each day
  • Maintain lifestyle of owner
  • Can learn to adapt food volume for particularly active days
59
Q

Outline a basic treatment protocol for a canine diabetic patient

A
  • Start insulin 0.5 IU/kg SC BID
  • Ensure diet correct and consistent
  • Monitor water intake at home
  • See again in 7 days and perform 12 hour BG curve if poss
  • If control sub optimal, increase dose by 10% and repeat cycle until stable
  • If repeated BG curves not an option, use home diary and possibly fructosamine
  • Spay entire females
60
Q

What aspects should be monitored at home by the owner of a canine diabetic?

A

Water intake, appetite, weight, demeanour

61
Q

Outline the use of blood glucose cures in canine diabetic monitoring

A
  • Shows effect of insulin
  • Can be done at home in some patients
  • Identify effect, nadir, duration of action, occurrence of Somogyi
  • NB inconsistent curves may occur despite consistent management
62
Q

Explain the use of glycated haemoglobin in canine diabetic monitoring

A
  • Gives indication of glycaemic control over preceding 2-3 months (glucose non-enzymatically bound to Hb)
  • Usedinhuman medicine, value in veterinary unclear
63
Q

What is Somogyi?

A

Aka “overswing”, insulin too high, blood glucose drops too far, mechanisms activated to protect from hypoglycaemia (glucagon, cortisol, epinephrine), inducing hypeglycaemia

64
Q

On a blood glucose curve, what would lack of response to hypoglycaemia following insulin administration suggest?

A

Glucagon deficient form of pancreatitis as the origin of the diabetes mellitus

65
Q

On a blood glucose curve, what would a curve with reasonable shape but still hyperglycaemia indicate?

A
  • Insulin too low

- If already >2Iu/kg then curve indicates insulin resistance

66
Q

What is a possible complication of canine diabetes mellitus treatment? What are the clinical signs?

A
  • Hypoglycaemia

- Hunger, food seeking, altered judgement, ataxia, weakness, collapse, convulsions

67
Q

What is the treatment for hypoglycaemia in a diabetic patient?

A
  • Dextrose absorbed across gums (owner can do this in emergency by using glucose, jam, honey) - does not need to be ingested
  • IV glucose at clinic or glucagon injection if not debilitated
68
Q

What may be the cause of fluctuating insulin requirements in a canine diabetic patient?

A
  • Insulin related (bottle, batch, dilution)
  • Prolonged Somogyi
  • Inconsistent administration, absorption, diet, exercise
  • Dramatic dose changes
  • Unstable illness (sepsis, inflammation, cirrhosis, HAC treatment)
  • Spontaneous remission
69
Q

Give some potential complications in canine diabetic patients

A
  • Clinical hypoglycaemia
  • Fatal hypoglycaemia
  • GI disturbance
  • Bacterial infection
  • Pancreatitis
  • Keratoconjunctivitis
  • Cirrhosis
  • Neuropathy
70
Q

What factors may lead to persistently high insulin requirements in a canine diabetic patient?

A
  • Insulin (species, short acting)
  • Diet
  • Diabetogenic therapy
  • Hyperadrenocorticism
  • Hyper/hypothyroidism
  • Acromegaly
  • Azotaemia
  • Progesterone (metoestrus)
  • Obesity
  • Phaechromocytoma
  • Glucagonoma
71
Q

What is the prognosis for canine diabetic patients?

A
  • Median survival time 2.75 years

- If survive first 6 months post-diagnosis, life expectancy close to age matched controls

72
Q

What are the potential differentials for hyperkalaemia +/- hyponatraemia?

A
  • Addison’s
  • Sodium loss with V/D
  • Severe GI disease (incl. duodenal perforation, gastric torsion)
  • Renal and urinary tract disease (incl.intrinsic acute renal failure, end stage renal failure, uroabdomen, post-obstructive diuresis)
  • Severe liver failure
  • Parasitism (whipworms)
  • Congestive heart failure
  • Pleural effusion (chylothorax)
  • DKA, metabolic acidosis, respiratory acidosis
  • Tissue cruss injury/reperfusion injury
  • Pregnancy
  • Artefact
73
Q

What are the potential differentials for increased BUN?

A
  • Addison’s (pre-renal azotaemia)
  • Renal disease
  • Gastrointestinal disease
74
Q

What are the potential differentials for hypercalcaemia?

A
  • Neoplasia
  • Addison’s
  • Primary hyperparathyroidism
  • Renal failure,
  • Vitamin D toxicosis,
  • Hypercalcemia of growing dogs,
  • and granulomatous disease
75
Q

What are the potential differentials for hypoglycaemia?

A
  • Addison’s,
  • Sepsis,
  • Liver disease,
  • Starvation or severe maldigestion,
  • Puppy hypoglycemia,
  • Hunting dog hypoglycemia,
  • Insulin-secreting pancreatic tumors,
  • Other neoplasia,
  • Insulin overdose,
  • and artifact
76
Q

What are the potential differentials for hypoalbuminaemia?

A
  • Addison’s
  • Decreased hepatic synthesis
  • Increased renal loss
  • Increased gastrointestinal loss/decreased absorption
77
Q

What should be considered in a dog with increased liver enzymes and renal azotaemia?

A
  • Addisons

- Infectious disease such as Leptospirosis

78
Q

What are the differentials for elevated liver enzymes?

A
  • Diabetes mellitus
  • Addison’s
  • Primary hepatopathy (immune mediated, esp if with hypoglycaemia, hypoalbuminaemia and hypocholesterolaemia)
79
Q

What are the consequences of diabetic ketoacidosis?

A
  • Ketone body formation in the liver
  • Enters metabolic acidosis
  • Severe dehydration
  • Shock
  • Death
80
Q

What leads to a diabetic ketoacidotic crisis?

A

Combined insulin deficiency and excess diabetogenic hormones, +/- insulin resistance but does not usually occur due to mismanagement of diabetes, usually due to a second triggering condition/stressor on top of underlying DM

81
Q

What conditions commonly trigger ketoacidosis in a diabetic patient?

A

Infections, other endocrine diseases (e.g. hyperadrenocorticism), inflammatory disease (e.g. pancreatitis)

82
Q

Outline the physiology of diabetic ketoacidosis

A

High glucagon and low/resistance to insulin leads to increased FFA metabolism producing acetyl-coA which accumulates in the liver and converted to acetoacetyl-coA and ultimately ketone production

83
Q

How does low insulin contribute to diabetic ketoacidosis?

A
  • Increased lipolysis leading to increased release of FFAs

- Decreased ketone body metabolism

84
Q

Which ketone bodies are of most concern in dogs and cats?

A
  • Beta-hydroxybutyrate (first one)
  • Acetoacetic acid
  • Acetone
85
Q

How do dehydration and hypovolaemia occur in diabetic ketoacidosis?

A
  • Hyperglycaemia and ketonuria leads to severe osmotic diuresis
  • Renal loss of water and electrolytes
  • Vomiting also leads to fluid loss
  • Dehydration eventually leads to hypovolaemia
86
Q

How does nausea occur in diabetic ketoacidosis?

A
  • Circulating KBs act on the chemoreceptor trigger zone in the brain (CRTZ)
  • Leads to nausea which reduces the appetite and water intake
87
Q

Explain why dehydration exacerbates diabetic ketoacidosis

A
  • Dehydration leads to reduced renal excretion of glucose and ketones due to reduced GFR
  • Increased aggregation of ketones aggravating the CRTZ
88
Q

What are further complications of dehydration in diabetic ketoacidotic crises?

A
  • Hyperviscosity
  • Thromboembolism
  • Severe metabolic acidosis
  • Renal failure
  • Electrolyte abnormalities
89
Q

What conditions may precipitate ketoacidosis in a dog?

A
  • UTI
  • Pyometra/dioestrus
  • Pancreatitis
  • Endocrine disease
  • Pneumonia
  • Corticosteroid treatment
  • Neoplasia
90
Q

What conditions may precipitate ketoacidosis in a cat?

A
  • UTI
  • Cholangiohepatitis
  • Pancreatitis
  • Airway disease +/- respiratory disease
  • CKD
  • Endocrine disease
91
Q

In what scenario may a non- diabetic ketosis occur in cats or dogs?

A
  • Metabolic situations where there is high fat metabolism
    e. g. starvation, later stages of pregnancy-
  • Urine ketones +ve, urine glucose -ve, blood glucose normal
92
Q

What are the key clinical signs of diabetic ketoacidosis in cats and dogs?

A
  • PUPD
  • Vomiting
  • Anorexia
  • Profuse diarrhoea
  • Weak, lethargy, depression
  • Pyrexia, tachycardia, poor peripheral pulses
  • Tachypnoea
  • Prolonged CRT
  • Hepatomegaly
  • Cataracts (dogs)
  • Jaundice
93
Q

Describe the typical appearance of the vomit produced in diabetic ketoacidosis

A

Frothy, bilious, large volume

94
Q

Describe the typical appearance of the diarrhoea produced in diabetic ketoacidosis

A

Watery, yellow

95
Q

What specific sign of diabetic ketoacidosis may be seen in cats?

A

Diabetic neuropathy - plantigrade hindlimb stance, relevant to poorly controlled DM rather than DKA

96
Q

List potential differentials for a vomiting patient

A
  • Dietary indiscretion
  • Non-specific gastritis
  • Foreign body
  • Intussusception
  • Neoplasia
  • Infectious
  • Pancreatitis
  • Acute kidney injury
  • Pyometra
  • Hepatitis
  • Hypoadrenocorticism
  • Drugs/toxins
  • CNS disease
  • Peritonitis
  • DKA
97
Q

What causes the jaundice that may be seen in diabetic ketoacidosis in cats and dogs?

A
  • Dogs: underlying pancreatitis

- Cats: hepatic lipidosis

98
Q

What may cause the tachypnoea seen in diabetic ketoacidosis?

A
  • Reflects respiratory response to metabolic acidosis

- Potential aspiration pneumonia as a complication of vomiting/weakness

99
Q

What do you need to know when presented with a vomiting diabetic with a high resp. rate and a prolonged CRT?

A
  • Consider DKA
  • Need to know last insulin dose
  • If female, when last in season
  • Is patient prone to GI signs or usually resistant?
  • Any change to routine (diet, insulin, exercise)
100
Q

What findings would be expected on biochem in diabetic ketoacidosis?

A
  • Hyponatremia
  • Hypokalaemia
  • Low CO2
  • Hyperglycaemia
  • High BUN
  • Elevated liver enzymes

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