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Year 4 > SA Endocrine > Flashcards

SA Endocrine Flashcards

1
Q

Briefy describe the hypothalamus-pituitary-thyroid axis

A

Hypothalamus releases TRH (thyroid releasing hormone)

  • > Pituitary gland releases TSH (thyroid stimulating hormone)
  • > Thyroid gland releases T4 and T3
  • > These have a negative feedback effect on the pituitary gland and hypothalamus
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2
Q

Of T3 and T4, which is more numerous in peripheral tissues?

A

T4

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3
Q

Which is more potent, T3 or T4?

A

T3

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4
Q

How are thyroid hormones bound in the blood?

A

To plasma proteins

Only unbound thyroid hormones are active

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5
Q

What are the functions of the thyroid hormones?

A
  • Increase metabolic rate and 02 consumption of most tissues
  • Positive inotropic and chronotropic effects on heart (increase HR and contractility)
  • Cause hypertension (increase number and affinity of beta-adrenergic receptors)
  • Metabolic effects of muscle and adipose tissue (weight loss)
  • Stimulate erythropoiesis and regulate cholesterol synthesis and degradation
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6
Q

Which kinds of dogs are affected by hypothyroidism?

A

Middle aged to older

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7
Q

What are the 2 main forms of hypothyroidism in dogs?

A

Congenital and acquired (may be primary or secondary)

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8
Q

How may canine hypothyroidism occur?

A
  • Result of thyroid hypoplasia/aplasia/dyshormonogenesis (thyroid anatomically normal but can’t synthesise normal thyroid hormones)
  • Disproportionate dwarfism
  • Autosomal recessive in Fox and Rat terriers
  • Panhypopituitarism in GSD (deficiency in all pituitary hormones)
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9
Q

Give some primary causes of acquired hypothyroidism in dogs

A
  • Lymphocytic thyroiditis and/or idiopathic atrophy

- Aggressive thyroid neoplasia and treatment with potentiated sulphonamides

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10
Q

Give some clinical signs of canine hypothyroidism

A
  • Obesity with a normal appetite
  • Lethargy
  • Exercise intolerance
  • Cold intolerance (always looking for warmth)
  • Hair thinning/alopecia (oily trunk and tail)
  • Skin hyperpigmentation
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11
Q

What would you see on a haematology of a dog with hypothyroidism?

A

Mild normocytic, normochromic, non-regenerative anaemia (32-44% of cases)

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12
Q

What would you see on a biochemistry of a dog with hypothyroidism?

A
  • Hypercholesterolaemia
  • Hypertriglyceridaemia
  • Mild elevations in creatinine kinase, ALP and ALT
  • Elevation of circulating fructosamine
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13
Q

How can you measure thyroid hormones?

A
  • Total T4 (tT4)
  • Free T4 (fT4)
  • Total T3 (tT3)
  • TSH
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14
Q

Why may you get false positive results when doing a total T4 test to diagnose canine hypothyroidism?

A

Total T4 can be reduced by non-thyroid illness and drug therapy (eg sulphonamides)

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15
Q

Which dog breeds have lower-than-normal values for total T4?

A

Greyhounds and other sighthounds and sled dogs

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16
Q

What is the best way to diagnose canine hypothryoidism?

A

TSH combined with tT4

Will have low tT4 and high TSH due to lack of negative feedback

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17
Q

How do you treat canine hypothyroidism?

A

Levothyroxine

  • Start at 0.01-.02mg/kg q 12hrs (lower dose for cardiac patients)
  • Metabolic signs should resolve in a few weeks, but dermatological changes may take months to resolve
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18
Q

What are the only 3 instances that a dog may develop hyperthyroidism?

A
  • Over-supplementation in hypothyroid dogs
  • Neoplasia affecting thyroid gland
  • Raw food diet containing neck meat and thyroid tissue (not in UK)
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19
Q

Which cat breed is predisposed to diabetes?

A

Burmese

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20
Q

Which kinds of cats are more affected by hyperthyroidism?

A
  • Older cats 13-14 years old

- (Himalayan and Siamese are less at risk)

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21
Q

How does feline hyperthyroidism typically occur?

A
  • Nodular adenomatous hyperplasia of thyroid gland (usually both lobes)
  • Occasionally due to functional malignant tumours (1-3% of cases)
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22
Q

Give the clincial signs of feline hyperthyroidism

A
  • Weight loss with increased appetite
  • PUPD
  • Hyperactivity/behaviour change eg nervous/aggressive
  • GI signs (vomiting/diarrhoea)
  • Tachycardia, heart murmur, cardiac failure
  • Systemic hypertension
  • Skin and hair coat changes
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23
Q

What is a ‘thyroid storm’?

A

Hyperthyroid cats:

-Stress eg vets -> increased hypertension -> tachycardia (due to excess T4) -> could have sudden death

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24
Q

What may you see on a haematology and biochemistry of a cat with hyperthyroidism?

A
  • Mild to moderate erythrocytosis and macrocytosis
  • Increased Heinz bodies
  • Leukocytosis
  • Increased mean platelet size
  • Increased ALP, ALT, AST, LDH
  • Azotaemia
  • Reduced fructosamine
  • Hypokalaemia
  • Hyperphostpahtaemia
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25
Q

What may you see on a urinalysis of a cat with hyperthyroidism?

A

May see low SG due to polyuria (+/- renal failure)

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26
Q

How do you usually diagnose feline hyperthyroidism?

A

Clincial signs and tT4

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27
Q

How else could you diagnose feline hyperthyroidism?

A
  • T3 suppression tests (for borderline/early cases)
  • Radionucleotide uptake and imaging (scintigraphy; differentiates between bilateral and unilateral disease)
  • Both rarely used
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28
Q

What are the main treatment options for feline hyperthyroidism?

A
  • Medical
  • Surgery
  • Radioiodine
  • Low-iodine diet
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29
Q

How can you medically manage hyperthyroidism in cats?

A
  • Thiamazole (previously called methimazole; Felimazole): 2.5mg/cat q 12 hrs initially, or available in cream form- ear pinnae
  • Carimazole (Vidalta; metabolised to thiamazole): 15mg once daily (as less bioavailable)
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30
Q

How often should you measure tT4 after starting medical tx for feline hyperthyroidism?

A

After 2 weeks then, once stable, every 3 months

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31
Q

Why may you give beta blockers to a cat with hyperthyroidism?

A
  • Used to stabilise cats prior to surgery
  • Decrease the neuromuscular and cardiovascular effects of hyperthyroidism (eg hyperexcitablity, hypertension, cardiac hypertrophy)
  • Don’t use in cats with congestive heart failure or asthma
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32
Q

Why may you give potassium iodate to a cat with hyperthyroidism?

A
  • Used to stabilise cats prior to surgery

- Source of stable iodine, which may temporarily decrease the rate of thyroid hormone systhesis

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33
Q

Give some pros and cons of surgical removal of the thyroid gland to tx feline hyperthyroidism

A

Pros:

  • Curative
  • Generally available

Cons:

  • Greater anaesthetic risks due to CV, hepatic and GI dysfunction
  • Possible complications eg larygneal paralysis, Horners, hypocalcaemia, recurrence of hyperthyroidism
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34
Q

Give some pros of radioactive iodine treatment to treat feline hyperthyroidism

A
  • Only targets affected thyroid tissue

- Treats any hyperfunctioning ectopic tissue

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35
Q

Give some cons of radioactive iodine treatment to treat feline hyperthyroidism

A
  • Cat must be isolated for up to 3 weeks as will be radioactive (as are faeces-need proper disposal)
  • Expensive
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36
Q

Give some side effects of medical treatment of feline hyperthyroidism

A
  • Anorexia, vomiting, lethargy
  • Facial/cervial excoriations
  • Bleeding diatheses (epistaxis and oral bleeding)
  • Hepatopathy, may have icterus
  • Eosinophilia, lymphocytosis, leukopenia
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37
Q

Why may azotaemia become evident after medical management of feline hyperthyroidism has begun?

A

-Hyperthryoidism increases GFR, so may have been masking underlying renal failure

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38
Q

What are the 4 surgical techniques for thyroid removal?

A
  • Extracapsular
  • Intracapsular
  • Modified extracapsular
  • Modified intracapsular
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39
Q

Describe an extracapsular thyroidectomy

A
  • Ligate cranial and caudal thyroid arteries
  • Intact thyroid is removed with its capsule with no attempt to preserve the external parathyroid gland
  • High rate of post-op hypocalcaemia
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40
Q

Describe an intracapsular thyroidectomy

A
  • Incise thyroid capsule
  • Bluntly dissect thyroid gland from capsule
  • Capsule left in situ to preserve the cranial parathyroid gland
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41
Q

Describe a modified extracapsular thyroidectomy

A
  • Incise the thyroid capsule around the cranial parathyroid gland and separate it from the thyroid gland
  • The parathyroid branch of the cranial thyroid artery is preserved
  • Remove remaining thyroid gland with capsule, leaving an intact cranial parathyroid gland
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42
Q

Describe a modified intracapsular thyroidectomy

A
  • Incise the ventral capsule of thyroid gland
  • Bluntly dissect away the thyroid parenchyma from the capsule
  • Cranial PT gland and blood vessels are preserved
  • Most of the capsule is removed apart from a small cuff surrounding the parathyroid gland
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43
Q

Which technique is recommended for surgical thyroidectomy?

A

Either modified intracapsular or modified extracapsular

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44
Q

What should you do if you accidentally damage the blood supply to the parathyroid gland when removing the thyroid gland?

A

Transplantation of parathyroid gland:

  • Cut into 1mm cubes
  • Insert into sternohyoideus/thyroideus
  • Should be functional within 1-3 weeks
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45
Q

Why may hypocalcaemia occur after thyroid gland removal?

A

-Damage to parathyroid blood supply, or inadvertent parathyroidectomy

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46
Q

What is secreted by functional adrenal adenomas and carcinomas?

A

Cortisol

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47
Q

What is secreted by a phaeochromocytoma?

A

Catecholamines eg adrenaline

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48
Q

Give some complications of adrenalectomy

A
  • Haemorrhage (very vascular)
  • Pulmonary thromboembolsim
  • Hypoadrenocorticism
  • Surges of catecholamine release when handling phaeochromocytomas -> hypertension, vetricular tachycardia, arrhythmias
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49
Q

Cortisol is produced where? Under the control of what?

A

Adrenal glands (zona fasiculata) under the control of ACTH

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50
Q

Give some functions of cortisol

A

Homeostasis during stress:

  • Gluconeogenesis
  • Glycoen synthesis
  • Immune/inflammation suppression
  • Delayed wound healing
  • Catabolism (fat and protein deradation)
  • Inhibition of DNA/protein synthesis
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51
Q

What is the key function of aldosterone?

A

Retention of sodium and excretion of potassium by the kidney

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52
Q

What kinds of dogs are affected by hyperadrenocortism (cushings)?

A

Middle aged to older dogs

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53
Q

Give some common clinical signs of hyperadrenoacorticism (Cushings)

A
  • PUPD
  • Polyphagia
  • Panting
  • Abdominal distension (pot belly)
  • Endocrine alopecia
  • Hepatomegaly
  • Muscle weakness
  • Systemic hypertension
  • Bruising, coat changes
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54
Q

What haem and biochem results would you see in a dog with hyperadrenocorticism (Cushings)?

A
  • Increased ALKP and ALT
  • Hypercholesterolaemia
  • Eosinopenia
  • Thrombocytosis
  • Lymphopenia
  • Hyperglycaemia
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55
Q

What may you see on a urinalysis in a dog with hyperadrenocorticism (Cushings)?

A
  • Low specific gravity (<1.018-1.020)
  • Proteinuria
  • UTI
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56
Q

What is the difference between pituitary-dependent and adrenal-dependent hyperadrenocorticism?

A
  • Pituitary-dependent: excessive secretion of ACTH by a pituitary tumour -> adrenal hyperplasia -> increased cortisol secretion
  • Adrenal-dependent: caused by an adrenal tumour which secretes excessive amounts of cortisol
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57
Q

What is the cause of iatrogenic hyperadrenocorticism?

A

Excessive glucocorticoid administration

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58
Q

Which dog breeds are predisposed to hyperadrenocorticism (cushings)?

A

Labradors, poodles, beagles, daschunds, terriers

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59
Q

How do you test for hyperadrenocorticism (cushings)?

A
  • ACTH stimulation test
  • Low-dose dexamethasone suppression test
  • Urine cortisol creatinine ratio (good for proving animal does not have cushings)
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60
Q

Describe the ACTH stimulation test

A
  • Give 5ug/kg ACTH
  • Measure cortisol levels at 0 and 1 hours
  • Avoid feeding during test
  • A normal healthy animal should have post ACTH concentrations that are 2-3 times higher than the basal values of cortisol
  • An affected, hypertrophied gland will produce even more cortisol
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61
Q

Describe the low dose dexamethasone suppression test

A
  • 0.01mg/kg dexamethasone iv
  • Blood sample at 0, 3 and 8 hours
  • Avoid feeding during test
  • A healthy animal will suppress cortisol to <50% of the basal level after 3 hours and to <40 nmol/l after 8 hours
  • An animal with adrenal dependent HAC will fail to suppress at 3 and 8 hours
  • An animal with pituitary dependent HAC will suppress at 3 hours and escape suppression at 8 hours.
62
Q

How would the adrenals appear on an US if affected by adrenal-dependent and pituitary-dependent hyperadrenocorticism?

A

Adrenal-dependent: one adrenal bigger than the other

Pituitary-dependent: both glands are stimulated so both are big

63
Q

What is the most effective test for diagnosing hyperadrenocorticism?

A

Low dose dexamethasone suppression test

64
Q

How do you treat hyperadrenocorticism (cushings)?

A
  • Trilostane (inhibits glucocorticoid synthesis)
  • Starting dose= 2.5mg/kg sid
  • Lifelong tx
65
Q

Which test allows you to differentiate between adrenal- and pituitary-dependent hyperadrenocorticism?

A

Low dose dexamethasone suppression test
-A healthy animal will suppress cortisol to <50% of the
basal level after 3 hours and to <40 nmol/l after 8 hours
-An animal with adrenal dependent HAC will fail to
suppress at 3 and 8 hours
-An animal with pituitary dependent HAC will suppress at 3 hours and escape suppression at 8 hours
Can also do ACTH assay: normal= 20-100pg/ml, PDH= >45, ADH= <20

66
Q

Give some side effects of Trilostane (tx for hyperadrenocorticism)

A
  • Adrenal necrosis
  • Hypoadrenocorticism
  • Lack of efficacy
  • Vomiting and diarrhoea
67
Q

How should you monitor hyperadrenocorticism (cushings) once medical treatment has started?

A

Do ACTH stimulation tests every 3 months for the first year then every 6 months

68
Q

Give a clinical sign of a pituitary macroadenoma

A

Dullness

Adenoma >10mm

69
Q

What causes primary hypoadrenocorticism (Addisons)?

A

Destruction of >90% of adrenal cortex -> reduced glucocorticoid secretion

70
Q

What causes secondary hypoadrenocorticism (Addisons)?

A

Deficiency in ACTH secretion by the pituitary gland (eg trauma, tumour) -> atrophy of adrenal cortex-> reduced glucocorticoid secretion`

71
Q

Which dog breeds are predisposed to hypoadrenocorticism (Addisons)?

A

Standard Poodle, Beardies, Great Dane, Portugese Water Dog, WHWT, St Bernard, Wheaten Terrier, Rottweiler, Leonberger

72
Q

Which kinds of dogs are more affected by hypoadrenocorticism (Addisons)?

A

Middle aged females

73
Q

Give some clinical signs of hypoadrenocorticism (Addisons)

A
  • Vague malaise
  • Vomiting (+/- blood) and diarrhoea/melaena
  • Lethargy, weakness
  • PUPD
  • Abdominal pain
  • Hypovolaemic collapse
74
Q

What would you find on a physical examination of a dog with hypoadrenocorticism (Addisons)?

A
  • Weak pulses
  • Increased CRT (sign of poor perfusion)
  • Dehydration
  • Bradycardia
  • Abdominal pain
  • Collapse/syncope
75
Q

What might you find on a haem and biochem of a dog with hypoadrenocorticism (Addisons)?

A
  • Mild non-regenerative anaemia
  • Mild hypercalcaemia
  • Pre-renal azotaemia
  • Lymphpcytosis +/- eosinophilia
  • Acidosis
  • Na:K <27:1 (high potassium, low sodium)
  • Isosthenuric to hypersthenuric urine
76
Q

How do you treat acute hypoadrenocorticism (Addisonian crisis)?

A
  • IV fluids (0.9% NaCl) to correct hypovolaemia (3-4x maintenance)
  • Glucose can be added to cause insulin release and reduce hyperkalaemia
  • ACTH stimulation test
  • Dexamethasone sodium phosphate 0.1-0.2mg/kg iv q 24hrs
  • Or constant infusion of hydrocortisone at a rate of 0.625mg/kg/h
  • Once eating: oral prednisolone (can usually be discontinued once animal is stable) and fludrocortisone q 24hrs. DOCP q 25 days
77
Q

Give some adverse outcomes of treatment for hypoadrenocorticism (Addisons)

A
  • Acute renal failure

- Myelinosis (depression, weakness, ataxia, tetraparesis)

78
Q

What is a phaechromocytoma?

A

Tumour of the adrenal medulla secreting catecholamines (eg adrenaline)

79
Q

Give some clinical signs of a phaeochromocytoma

A

Signs usually episodic:

  • Anxiety
  • Tachycardia
  • Tachypnoea
  • Vomiting
  • Diarrhoea
  • Weight loss
  • Hypertension (retinal detachment)
80
Q

How do you diagnose a phaeochromocytoma?

A

Radiography or US

81
Q

How do you treat a phaeochromocytoma?

A

Radical excision of adrenal gland, antihypertensive medication

82
Q

What causes hyperaldosteronism?

A

Adrenal tumour producing aldsterone

83
Q

Give some clinical signs of hyperaldosteronism

A
  • PUPD
  • Weakness
  • Neck ventroflexion (hypokalaemia)
  • Hypertension (sodium retention -> water retention -> increases BP)
84
Q

How do you treat hyperaldosteronism?

A
  • Restrict sodium and supplement potassium
  • Surgical excision
  • Spironolactone (aldosterone antagonist)
85
Q

Give the 5 major differential diagnoses for PUPD

A
  • Diabetes insipidus
  • Osmotic diuresis
  • Iatrogenic (eg glucocorticoids)
  • Renal medullary washout
  • Primary polydipsia (problem of thirst centre in brain)
86
Q

Define polydipsia

A

Drinking >100ml/kg/day

87
Q

What tests should you run when investigating PUPD?

A
  • Haem and biochem
  • Bile acids (liver disease?)
  • T4 (hyperthyroidism)
  • Urinalysis (diabetes)
88
Q

When should you do a water deprivation test?

What does it allow you to differentiate?

A
  • After all other dynamic testing (eg bloods, bile acids, T4, urinalysis, HAC has been ruled out)
  • Allows you to differentiate central diabetes insipidus, primary nephrogenic diabetes insipidus, and primary PD
89
Q

What is DDAVP?

A

ADH analogue

90
Q

What is the recommended starting dose for insulin in diabetic dogs?
What about cats?

A
  • Start with an intermediate insulin at a dose of 0.25-0.5 units/kg BID
  • 1 to 2 units BID for cats
91
Q

Give some endocrine causes of poor growth

A
  • GH deficiency
  • Hypothyroidism
  • Hypoadrenocorticism
  • Hyperadrenocorticism
  • Diabetes mellitus
  • Pituitary dwarfism (rare)
92
Q

Pituitary dwarfism affects primarily which breed of dog?

A

GSD

93
Q

How does pituitary dwarfism occur?

A
  • Rare congenital lesion (developmental defect in pituitary gland)
  • Failure of GH secretion
  • May be combined with deficiencies in FSH, LS, TSH
94
Q

Give some features of pituitary dwarfism

A
  • Proportionate dwarfism
  • Failure to develop adult coat
  • Delayed dental eruption
  • Delayed dental eruption
  • Delayed growth plate closure
  • Thin, fragile, hyperpigmented skin
  • Pyoderma
  • Immature gonads
95
Q

How can you treat pituitary dwarfism?

A
  • Progestagens (induces GH secretion from mammary tissue)

- GH (results usually disappointing)

96
Q

What is acromegally?

A

Excess GH

97
Q

When does acromegally occur in dogs and cats?

A
  • Cats: pituitary tumour in older males (often diabetic)
  • Dogs: mammary tissue in response to progestagens/progesterone in intact females (luteal phase) or females receiving progestagens
98
Q

Describe the pathogenesis of acromegally

A

Chronic excess GH -> insulin antagonism -> diabetes mellitus

-> also anabolic effects on organs, bone, cartilage

99
Q

Give some clinical features of acromegally

A
  • Insulin-resistant diabetes mellitus
  • Excessive growth of extremities
  • Prognathism, wide interdental spaces
  • Soft tissue proliferation
100
Q

How would you diagnose acromegally?

A
  • Clinical signs inc diabetes mellitus
  • Increased liver enzymes
  • Elevated IGF-1
  • MRI/CT
101
Q

How would you treat acromegally?

A

Bitch: spay/stop progestagens. Bony changes are irreversible
Cat: control diabetes mellitus. Surgery (hypophysectomy-pituitary gland removal). Radiation of pituitary mass

102
Q

What are the functions of PTH?

A
  • Reabsorption of calcium and phosphate from bone
  • Stimulates absorption of calcium and phosphate from gut via synthesis of calcitriol
  • Increased urinary excretion of PO4 and retention of Ca2+
  • Overall effects= increase blood Ca2+ and decrease blood PO4
103
Q

What causes primary hyperpararthyroidism?

A
  • Excess of PTH
  • Most cases are due to a functional adenoma (rarely carcinoma)
  • Results in hypercalcamia
104
Q

Give some clinical signs of hypercalcaemia

A
  • Muscle weakness, lethargy, anorexia, vomiting, gut stasis
  • PUPD
  • Dystrophic calcification
  • Calcium oxalate crystals may cause cystitis
  • Acute renal failure
105
Q

How do you treat hyperparathyroidism?

A 
Restore normal calcium level:
-Fluids (0.9% NaCl)
-Frusemide
-Prednisolone
-Calcitonin
-Bisphosphonates
Surgical removal of parathyroid tumour once stabilised
106
Q

What causes secondary hyperparathyroidism?

A
  • Nutritional secondary hyperpaathyroidism (rare; unbalanced homemade diets)
  • Renal secondary hyperpaathyroidism (rubber jaw; secondary to chronic renal failure)
107
Q

What is pseudo-hyperparathyroidism?

A

Caused by a PTH-like protein secreted by malignant apocrine tumours eg anal sac tumours, multiple myelomas, lymphomas

108
Q

What causes hypoparathyroidism?

A
  • Lack of PTH: can be primary or secondary
  • Primary: immune-mediated destruction of parathyroid glands
  • Secondary: damage to glands by thyroid surgery (cats), local disease etc
  • Results in hypocalcaemia and hyperphosphataemia
109
Q

Give some clinical signs of hypocalcaemia

A
  • Muscle twitching, spasm, tetany
  • Anxiety
  • Weakness, ataxia
  • Seizures
  • Tachycardia, weak pulses
110
Q

How do you treat hypocalcaemia?

A
  • Emergency: iv fluids, iv calcium borogluconate

- Maintenance: oral calcium, oral vitamin D

111
Q

Give some factors that cause diabetes in dogs

A 
Insulin deficiency 
Loss of islets: 
-Infection
-Pancreatitis
-Immune-mediated disease
-Hormonal/drug antagonism (eg long-term steroids)

Predisposing:

  • Obesity
  • Endocrinopathy
  • Hyperlipaemia
112
Q

Give some factors that cause diabetes in cats

A

Insulin resistance +/- relative insuin deficiency caused by:

  • Obesity
  • GH (may also have acromegaly)
  • Corticosteroid use
  • Amyloid deposition
  • Pancreatitis
  • Neoplasia
113
Q

Give the functons of insulin

A
  • Stimulates uptake of glucose by muscles and other cells

- Inhibits lipolysis

114
Q

Give some clinical signs of diabetes mellitus

A
  • PUPD
  • Polyphagia
  • Weight loss
  • White cataract formation in dogs (rare in cats)
115
Q

How do you diagnose diabetes mellitus?

A

-History (eg sudden onset PUPD)
-Clinical signs
-Haem/biochem
-Urinalysis (low SG, glycosuria, ketonuria, active sediment)
-Glycosylated Hb and fructosamine
-Persistent fasting hyperglycemia (fasting blood
glucose greater than 11mmol/l)

116
Q

How do you treat diabetes mellitus?

A
  • Lifelong in dogs: insulin, diet, routine

- Cats: insulin; may go in and out of remission

117
Q

What are the 3 types of insulin?

A
  • Short-acting (regular or crystalline; primarily used for ketoacidosis)
  • Intermiediate-acting (Caninsulin)
  • Long-acting (eg Ultralente)
118
Q

How often should you give insulin to diabetic dogs?

A
  • Twice daily with food

- Starting dose: 0.25-0.5iu/kg

119
Q

What kind of diet would you recommend to a diabetic dog?

A

A diet low in fat and high in fibe

120
Q

How often should you give insulin to diabetic cats?

A
  • Twice daily

- Caninulin (intermiediate-acting) or Prozinc (long-acting)

121
Q

What kind of diet would you recommend to a diabetic cat?

A

High protein/low carbohydrate diet

122
Q

What are oral hypoglycaemic agents?

A
  • Alternative to insulin therapy
  • Sulfonylureas (cause stimulation of insulin release and increase insulin sensitivity. Require some residual beta cell function so are only suitable in cats, not dogs)
123
Q

How should you treat a diabetic pet experiencing a hypoglycaemic episode?

A
  • Give a sugary substance under the tongue
  • Feed ASAP
  • Avoid insulin dose if imminent
124
Q

What should you do if a diabetic pet is not eating?

A

Reduce insulin dose by 50% (don’t stop insulin as body will generate its own glucose)

125
Q

How can you monitor a diabetic pet?

A

Blood glucose curves (sample every 2 hours)

126
Q

On a blood glucose curve, when will blood glucose be lowest?

What value should it be?

A

6-8 hours after insulin is given

Should be between 4.5-9mmol/L

127
Q

How can you distinguish between diabetes mellitus and stress-induced hyperglycemia in cats?

A

Test fructosamine (diagnoses diabetes)

128
Q

Give some chronic complications of diabetes mellitus

A
  • Lens-induced uveitis
  • Ketoacidosis
  • Infections
  • Diabetic neuropathy
  • Cataracts
  • Diabetic retinopathy
129
Q

What would be your thoughts if you were treating a diabetic pet whose blood glucose wasn’t decreasing and it was on an insuin dose of >2iu/kg?

A

Insulin resistance?

  • UTI?
  • Concurrent diseases?
  • Insulin abtibodies?
130
Q

Give some causes of ketoacidosis

A
  • Insulin deficiency
  • Insulin resistance
  • Increasing circulating levels of diabetogenic hormones
131
Q

Give some negative effects that ketoacidosis has on the body

A
  • Metabolic acidosis
  • Fat oxidation
  • Spillage of ketones into urine -> osmotic diuresis -> loss of H2O and electrolytes -> reduced perfusion to kidneys ->azotaemia
  • Cellular dehydration
132
Q

Give some clinical signs of ketoacidosis

A
  • Vomiting
  • Depression
  • Dehydration
  • Weakness
  • Tachypnoea
133
Q

How do you treat ketoacidosis?

A
  • Provide adequate amounts of insulin (intramuscular insulin therapy/constant low-dose infusion)
  • Restore water and electrolyte losses (supplement K+, phohsphate, bicarb, give fluids-isotonic crystalloids with K+ in)
  • Correct acidosis (usually happens anyway as you correct other things)
  • Identify any concurrent illness
  • Provide CHO substrate
134
Q

What is the target range for blood glucose when treating diabetes mellitus?

A

5-10 mmol/l

135
Q

What is an insulinoma?

A
  • Rare

- Functional tumour of pancreatic beta cells -> high insulin levels -> hypoglycaemia

136
Q

Give some clinical signs of an insulinoma

A

-Often episodic
-Weakness, trembling, ataxia, seizures
+/- other neuro signs
-May have weight gain

137
Q

How do you diagnose an insulinoma?

A
  • Fast until animal becomes hypoglycaemic
  • Measure insulin: normal/high -> insulinoma
  • May see a small pancreatic mass on US
  • Will also have persistent hypoglycaemia
138
Q

How do you treat an insulinoma?

A
  • IV glucose if needed
  • Avoid excess stimulation of insulin: frequent small meals, diet high in complex carbohydrates and protein
  • Prednisolone
139
Q

What is a gastrinoma?

A
  • Pancreatic gastrin-producing tumour

- Stimulates parietal cells to produce lots of acid, risk of ulceration

140
Q

Where are the parathyroid glands located?

A 
2 associated with each thyroid gland:
1 cranial and external
1 internal (caudal half of thyroid)
141
Q

Give some clinical signs of hypocalcaemia post-operatively after thyroidectomy

A 
Restlessness
Facial/generalised muscle twitching
Weakness
Lethargy
Anorexia 
Seizures
142
Q

How do you treat acute hypocalcaemia following thyroidectomy?

A

10% calcium gluconate iv slowly over 10-20 mins
Once stable: CRI of calcium gluconate at 5-15mg/kg/hr iv
Monitor for bradycardia and arrhythmias
Once stable, give oral vit D and calcium

143
Q

Most parathyroid nodules in dogs are what?

A

Adenoma

144
Q

Is pituitary-dependent hyperadrenocorticism more common in small or large breed dogs?
What about adrenal-dependent?

A

PDH: small breeds
ADH: large breeds

145
Q

How do you treat hyperkalaemia seen with hypoadrenocorticism (Addisons)?

A

Dextrose saline and insulin

146
Q

How do you treat hypoadrenocorticism (Addisons)?

A 
Dexamethasone sodium phosphate (best)
Prednisolone 
Hydrocortisone
Fludrocortisone
For life
147
Q

Give a blood glucose range for a stable diabetic dog

A

5-12mmol/L over 24 hours

148
Q

How do you diagnose diabetic ketoacidosis?

A

Diabetes plus ketonuria

149
Q

What are the 2 main types of diabetes insipidus?

A

Central (neurogenic): lack of vasopressin -> reduced water retention
Nephrogenic: primary (ADH deficiency) or secondary (eg renal failure, Cushings, Addisons)

150
Q

Which hormones does the pituitary gland secrete?

A 
FLAT PEG
FSH
LH
ACTH
Prolactin
Endorphins
GH
151
Q

How do you diagnose pituitary dwarfism?

A

Decreased IGF-1

Year 4 (51 decks)

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