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CVSOH BVSc4 > Endocrine - medicine > Flashcards

Endocrine - medicine Flashcards

1
Q

What are the roles of thyroid hormones on the body?

A

Increase metabolism
Increase heart rate/contractility
Increase activity levels - responsiveness to catecholamines
Regulate other hormones

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2
Q

What make up thyroid hormones?

A

Iodine containing amino acids (require dietary iodide for production)

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3
Q

Where is the thyroid gland located?

A

Two lobes either side of the trachea

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4
Q

What are the fractions of thyroid hormone?

A

Mostly in protein bound state - reservoir
Metabolically active free portion - T3 and T4

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5
Q

What are the names of T3 and T4?

A

T4 - total thyroxine
T3 - Triiodothyronine

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6
Q

What is the difference between T4 and T3?

A

T4 - major secretory product of the thyroid gland
T3 - converted to this in periphery, better uptake into cells so mroe rapid action

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7
Q

What is the regulatory axis of thyroid hormones?

A

The hypothalamic-pituitary-thyroid axis
TRH - thyrotropin releasing hormone
TSH - thyroid stimulating hormone (thyrotropin)

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8
Q

What is non-thyroidal illness/euthyroid sick syndrome?

A

Disease elsewhere in the body suppresses T4 production

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9
Q

What animal tends to get hypothyroidism and why?

A

DOgs - canine hypothyroidism is the most commonly acquired disease of adult dogs
Immune mediated lymphocytic infiltrate causes thyroiditis and progresses to idiopathic atrophy

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10
Q

What are the most common clinical sign of canine hypothyroidism?

A

Dermatological changes - alopecia, hyperpigmentation, skin thickening

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11
Q

Other the dermatological changes, what other clinical signs does hypothyroidism cause?

A

Lethargy, weight gain
Bradycardia
Neuromuscular weakness

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12
Q

When do you test for hypothyroidism?

A

Only test for hypothyroidism in presence of CLINICAL SUSPICION - non-thyroidal illness/euthyroid sick syndrome

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13
Q

What can be seen on biochem/haematology to support clinical suspicion to diagnose hypothyroidism?

A

Haematology - mild non-regenerative anaemia
Biochem - hyperlipaemia (hypercholesterolaemia and/or hypertriglyceridaemia) after fasting

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14
Q

What is tested for on a thyroid panel?

A

Total T4
TSH

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15
Q

What is seen on a thyroid panel to suggest hypothyroidism?

A

Low total T4 and high TSH

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16
Q

What does it mean if TSH is high but T4 is normal on a thyroid panel?

A

Recovering from a non-thyroidal illness
May be early hypothyroidism - retest in 1-3 months

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17
Q

What does it mean if T4 is low but TSH is normal?

A

Non-thyroidal illness
Possibly hypothyroid - retest in 1-3 months

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18
Q

What other tests for hypothyroidism can you get from the lab other than a tyroid panel?

A

Utility of free T4
Thyroglobulin antibody assay

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19
Q

When and why would you use a test for utility of free T4 when suspect hypothyroidism?

A

Free T4 less affected by non-thyroidal illness so more accurately reflect thyroid function
Use if suspicious of hypothyroidism but thyroid panel inconclusive

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20
Q

What does a thyroglobulin antibody assay tell you?

A

Tells you that antibodies that are released during lymphocytic thyroiditis are present - immune mediated destruction of thyroid gland
Antibodies = thyroiditis (not hypothyroidism)

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21
Q

What breed have naturally lower T4 than others?

A

Greyhounds

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22
Q

What drugs can reduce thyroid hormone levels?

A

Glucocorticoids
NSAIDS
Trimethoprim sulphonamide
Phenobarbitone

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23
Q

How do you treat hypothyroidism?

A

Lifelong twice daily supplementation with synthetic levothyroxine sodium
Ideally without food

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24
Q

How do you monitor levothyroxine replacement?

A

If twice daily = Peak T4/TSH - about 3hrs after administration
If once daily = trough T4/TSH - should be low normal

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25
Q

When do clinical signs of hypothyroidism resolve after treatment/

A

Can take weeks to months

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26
Q

What are some factors that cause treatment failure in hypothyroidism?

A

Incorrect diagnosis
Insufficient time
Expired drug
Inadequate dosing, not giving every day
Obesity
Concurrent disease

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27
Q

What is the name for a crisis and collapse due to hypothyroidism and concurrent disease?

A

Myxoedema coma

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28
Q

What is cretinism?

A

Congenital hypothyroidism

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29
Q

What does congenital hypothyroidism cause?

A

Disproportionate dwarfism
(growth hormone deficiency causes proportionate dwarfism)
Impaired mental development

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30
Q

What does canine thyroid neoplasia present as? What does it cause?

A

NON-secretory - not associated with hyperthyroidism
Usually unilateral
Usually malignant - carcinoma

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31
Q

How do you treat canine thyroid neoplasia?

A

Surgical resection +/- adjunctive radiation therapy
Histology of excisional biopsy

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32
Q

How does canine thyroid neoplasia differ from feline thyroid neoplasia?

A

Canine - non-secretory, malignant, rare
Feline - benign, cause hypERthyroidism, very common

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33
Q

What causes feline hypothyrodism?

A

Naturally occurring - very rare
Most commonly iatrogenic - secondary to treatment of hyperthyroidism

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34
Q

What is the most common feline endocrinopathy?

A

Hyperthyroidism

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35
Q

What are the two presentations of feline hyperthyroidism?

A

Multinodular adenomatous hyperplasia/adenomas - autonomously functioning follicles
Functional thyroid carcinoma - less common

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36
Q

What are the main risk factors for developing hyperthyroidism?

A

Increasing age
Female
Canned food - iodine deficiency/excess?
Indoor?
Litter tray use?
Exposure to chemical products - thyroid disruptors eg. flea/pest control, garden/household products

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37
Q

What are the most commonly seen clinical signs of hyperthyroidism in cats?

A

Weight loss
Polyphagia
Hyperactivity
(PUPD, V+/D+, CV, Resp signs)
May have palpable goitre
Poor coat condition

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38
Q

What is apathetic hyperthyroidism?

A

Weight loss
Inappetence/anorexia
Lethargy
But same diagnosis

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39
Q

What are the common differential diagnoses for polyphagia (increased appetite) with weight loss?

A

Hyperthyroidism
Diabetes mellitus
Exocrine pancreatic insufficiency
SI GI disease

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40
Q

What are the common differential diagnoses for PUPD with weight loss?

A

Hyperthyroidism
Diabetes mellitus
Chronic kidney disease

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41
Q

What are the common differential diagnoses for polyphagia (increased appetite) with PUPD?

A

Hyperthyroidism
Diabetes mellitus

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42
Q

What are the common differential diagnoses for vomiting, diarrhoea, inappetence with weight loss?

A

Hyperthyroidism
Chronic enteropathies

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43
Q

How many hyperthyroid cats get a palpable goitre?

A

70% of hyperthyroid cats
Anywhere from base of tongue to base of heart - can drop into thoracic inlet

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44
Q

How do you diagnose hyperthyroidism?

A

Increased total T4 - very straight forward as very high sensitivity and specificity

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45
Q

What adjunctive diagnostics can you use in hyperthyroidism?

A

BP and retinal exam - hypertension common
Haem/biochem
Urinalysis
Echocardiography - can cause hypertrophic cardiomyopathy and heart failure in cats

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46
Q

What is seen on haem/biochem in hyperthyroidism?

A

High haematocrit- T4 stimulates erythropoeitin
Increased liver enzymes - reactive hepatopathy
Hyperphosphataemia - increased bone turnover

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47
Q

What drug do you give to medically manage hyperthyroidism? What do they do?

A

Carbimazole (pro-drug) (Cats are like “carbs-in-ma-hole” cos they’re hungry heheh)
Methimazole
Have same effect - reversible inhibits thyroid hormone synthesis (if stop then will become hyperthyroid again)

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48
Q

What good effects on the body does hyperthyroid medical management have?

A

Rapid effective control of hyperthyroidism
Reverses adverse systemic effects
Improves patient morbidity and QOL
Unmasks concurrent renal disease - enable evaluation

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49
Q

How does medical management of hyperthyroidism unmask concurrent renal disease?

A

Hyperthyroidism causes increased glomerular filtration rate - increases blood flow to the kidneys which reduces the amount of creatinine in the blood
When reduce T4 then reduce GFR to normal which increases the creatinine in the cats
The drugs do not cause kidney disease, they just reduce the pathologically high GFR back to normal so can see previously hidden kidney disease in these cats
Need to continue the drug treatment - high GFR for a long time can speed up kidney disease so it makes it worse if you stop the drugs even though it looks like it is causing kidney disease

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50
Q

What is the aim of hyperthyroid medical therapy?

A

Total T4 in the LOWER HALF of the reference interval - regular monitoring in 3 week/3 month intervals (if stable)

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51
Q

What are the adverse clinical signs/side effects of medical management of hyperthyroidism?

A

Anorexia
Vomiting
Lethargy
Facial excoriation
Usually within first 1-2 months

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52
Q

What are 3 ways you can deal with the adverse clinical signs of medical management of hyperthyroidism?

A

Surgical management
Discontinue and restart at lower dose in a week
Give drugs transdermally rather that orally

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53
Q

What adverse lab findings can be found in medical management of hyperthyroidism? When should you discontinue treatment?

A

Thrombocytopaenia, neutropenia - discontinue treatment
Acute toxic hepatopathy - discontinue treatment
Azotemia - from unmasking CKD, continue treatment

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54
Q

What are the advantages of long term medical management of hyperthyroidism?

A

Usually effective
Reversible
No anaesthesia or hospitalisation needed
No lump sum cost - incremental yearly

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55
Q

What are the disadvantages of long term medical management of hyperthyroidism?

A

Non curative - dose escalation overtime, tumour worsens
Twice daily administration
Regular monitoring needed
Side effects

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56
Q

What are the two permanent treatments of hyperthyroidism?

A

Radioiodine - gold standard
Surgery - semicurative

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57
Q

How does radioiodine cure hyperthyroidism in cats?

A

Subcut administration of radioisotope of iodine I131
This concentrates in the thyroid glands and radiation causes follicular cell death

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58
Q

What are the advantages of radioactive iodine treatment of hyperthyroidism?

A

Curative - in 95% of cases
Dont need lifelong treatment/monitoring
No anaesthesia

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59
Q

What are the disadvantages of radioactive iodine treatment of hyperthyroidism?

A

Expensive - £3500
Limited availability - only certain centres do it
Period of isolation/handling restrictions
Irreversible - may cause hypothyroidism

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60
Q

What are the advantages of surgical management of hyperthyroidism?

A

Often curative
Readily available - offered in general practice
No ongoing treatment/monitoring

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61
Q

What are the disadvantages of surgical management of hyperthyroidism?

A

Short term expense (£1500-3400)
Anaesthesia/hospitalisation
Risk of surgical trauma
Risk of post-op hypoparathyroidism
Irreversible - risk of hypothyroidism

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62
Q

Why can surgical management of hyperthyroidism potentially cause hypoparathyroidism?

A

Parathyroid glands close to thyroid glands
PTH maintains serum calcium
Risk of surgical trauma/bruising

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63
Q

What are the principles of dietary management of hyperthyroidism?

A

Feed exclusively iodine restricted diet - limit thyroid hormone production

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64
Q

What are the pros and cons of dietary management of hyperthyroidism?

A

No pills, no surgery , no isolation
Affordable
But takes longer to respond to treatment, doesnt reduce T4 to lower half of reference range
Submaximal clinical improvement
Must feed diet exclusively

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65
Q

What can cause canine hyperthyroidism?

A

Naturally occurring hyperthyroidism - very rare
But increasing from raw-fed diets - particularly feeding cow goitres

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66
Q

Where is cortisol produced?

A

Adrenal glands - zona fasiculata

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67
Q

What regulates cortisol secretion?

A

Hypothalamic-pituitary-adrenal axis - CRH, ACTH

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68
Q

What are the most common causes of naturally occurring hyperadrenocorticism?

A

Pituitary dependent - most common 85% (usually smaller dogs)
Adrenal tumour - carcinoma (usually larger dogs)

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69
Q

What changes to the adrenal glands do pituitary dependent and adrenal dependent hyperadrenocorticism cause?

A

Pituitary dependent - bilateral hypertrophy
Adrenal dependent - contralateral adrenal atrophy (not needed)

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70
Q

What is an iatrogenic cause of hyperadrenocorticism?

A

Chronic glucocorticoid (steroid) use

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71
Q

What are the main clinical signs of hyperadrenocorticism (cushings)?

A

PUPD
Polyphagia
Dermatological signs - bilateral flank alopecia
Pot belly
Muscle wastage

72
Q

What is seen on haem/biochem in hyperadrenocorticism?

A

Increased haematocrit
Stress leukogram
High ALP/ALT
Hypercholesterolaemia
Hypertriglyceridaemia

73
Q

What is seen on urinalysis in hyperadrenocorticism?

A

Poorly concentrated urine
Proteinuria

74
Q

What tests do you do to support clinical suspicion of hyperadrenocorticism?

A

Urinary cortisol : creatinine ratio
If this is positive then ACTH stimulation test
And/or low dose dexamethasone suppression test

75
Q

What do urinary cortisol : creatinine ratio suggest?

A

Normal = excludes hyperadrenocorticism
High = may have hyperadrenocorticism but may not, poor specificity (many patients without cushings will have a high test result)

76
Q

What is the ACTH stimulation test a test for?

A

Adrenal reserve - how much capacity the adrenal gland has to produce cortisol
Gold standard test for adrenal hypofunction

77
Q

How does the ACTH stimulation test work?

A

Measures serum cortisol pre and 1hr post IV injection of synthetic ACTH

78
Q

What type of hyperadrenocorticism is the ACTH stimulation test most sensitive for?

A

Pituitary dependent - excessive response to ACTH because their pituitary gland can make more ACTH than a normal patient

79
Q

How does a low dose dexamethasone suppression test work?

A

Dexamethosone has a negative feedback effect on CRH and ACTH in a healthy patient, suppressing cortisol release
But in patients with hyperadrenocorticism it may not suppress cortisol

80
Q

What effect does the low dose dexamethasone suppression test have on adrenal dependent hyperadrenocorticism patients?

A

Cortisol wont be supressed at any point in the test - the autonomously functioning tumour isnt susceptible to regulation

81
Q

What effect does the low dose dexamethasone suppression test have on pituitary dependent hyperadrenocorticism patients?

A

Escape from suppression - dexamethosone has a transient inhibitory effect on ACTH but will break through suppression

82
Q

What is the gold standard treatment for adrenal dependent hyperadrenocorticism?

A

Adrenalectomy - surgery

83
Q

What is the medical therapy for hyperadrenocorticism?

A

Trilostane - synthetic steroid analogue that reversibly inhibits enzyme involved in steroid production

84
Q

What is the most common adverse event in hyperadrenocorticism treatment?

A

Iatrogenic hypoadrenocorticism

85
Q

How often do you give trilostane for hyperadrenocorticism?

A

Twice daily - drug duration of action is 8-10 hours

86
Q

When do you use medical management for hyperadrenocorticism (trilostane)?

A

pituitary dependent hyperadrenocorticism - cant do surgery on pituitary gland

87
Q

What is the cost of treating hyperadrenocorticism?

A

Trilostane - £1000-£3000 a year
Adrenalectomy - £6000-8000

88
Q

What are the differentials for an incidentaloma (adrenal mass that you werent expecting to find)?

A

Check it actually is an adrenal mass
Cortisol producing - hyperadrenocorticism
Aldosterone producing - hyperaldosteronism
Catecholamine producing - phaeochromocytoma
Other neoplasm

89
Q

What is Conn’s syndrome?

A

Hyperaldosteronism - high aldosterone
In cats

90
Q

What does Conn’s syndrome cause?

A

Hypertension and/or hypokalaemia - aldosterone is crucial in electrolyte and intravascular volume homeostasis
Hypokalaemic myopathy - neck ventroflexion, weakness, inappetence

91
Q

How do you diagnose Conn’s syndrome (hyperaldosteronism)?

A

Abdominal ultrasound - unilateral adrenal mass
Serum aldosterone concentration
Hypokalaemia
Hypertension

92
Q

How do you treat Conn’s syndrome (hyperaldosteronism)?

A

Adrenalectomy
Or medically with spironolactone, K+ supplementation and amlodipine for hypertension)

93
Q

What is a phaeochromocytoma?

A

Catecholamine producing tumour

94
Q

What does feline hyperadrenocorticism (cushings) syndrome present as? How common is it?

A

Presents as diabetes mellitus - the high steroid inhibits insulin
Extremely rare
Also get skin fragility

95
Q

What is addisons disease?

A

Hypoadrenocorticism

96
Q

What are the differentials for hyperkalaemia?

A

Aldosterone deficiency
Acute kidney injury
Urinary tract obstruction/rupture
Fluid shifts
(EDTA contamination of blood sample)

97
Q

What does an ECG look like from hyperkalaemia?

A

Flattened P wave
Wide QRS
Spiked T wave

98
Q

How do you diagnose hypoadrenocorticism?

A

ACTH stimulation test - evaluate cortisol before and after giving ACTH

99
Q

What result will you get on ACTH stimulation test in hypoadrenocorticism?

A

Failure of stimulation - cortisol not released

100
Q

What is hypoadrenocorticism?

A

Adrenocortical failure due to idiopathic immune mediated adrenalitis and atrophy

101
Q

What does mineralocorticoid (aldosterone) deficiency cause on haem/biochem?

A

Hyperkalaemia (high potassium) with hyponatremia (low sodium)
Azotemia

102
Q

Why does mineralocorticoid (aldosterone) deficiency in hypoadrenocorticism cause azotemia? What kind of azotemia is it

A

Because low sodium causes hypovolaemia from water loss so reduced glomerular perfusion
Pre renal but may lack concentrating ability because low sodium

103
Q

What are the presenting signs of mineralocorticoid (aldosterone) deficiency?

A

Hypovolaemic shock
Hyperkalaemia/hyponatremia
Inappropriate bradycardia for poor perfusion state

104
Q

What is the difference between ‘typical’ and ‘atypical’ hypoadrenocorticism?

A

Typical - mineralocorticoid (aldosterone) deficiency (may have both tho)
Atypical - exclusively glucocorticoid (cortisol) deficiency

105
Q

What are the haem/biochem signs of glucocorticoid (cortisol) deficiency in hypoadrenocorticism?

A

Lack of or a reverse stress leukogram
Anaemia of chronic disease

106
Q

What is a normal stress leukogram?

A

High neutrohils and monocytes
Low lymphocytes and low eosinophils
(LEMON)

107
Q

What is the reverse stress leukogram in glucocorticoid (cortisol) deficiency?

A

High lymphocytes and eosinophils
Low neutrophils and monocytes

108
Q

What is the initial management of an animal having an addisonian crisis/collapse?

A

Fluid therapy
Management of hyperkalaemia

109
Q

What lifelong management/treatment do dogs with hypoadrenocorticism need?

A

Glucocorticoid therapy - required lifelong in ALL hypoadrenocorticoid patients (typical and atypical)
Mineralocorticoid therapy - required lifelong in patients presenting with evidence of mineralocorticoid deficiency (typical)

110
Q

What drugs do you give for hypoadrenocorticism?

A

Prednisolone - at lowest effective daily dose
(hydrocortisone in acute setting)
Desoxycortone pivalate (DOCP) - subcut every 25 days

111
Q

What is the prognosis of hypoadrenocorticism?

A

Excellent if diagnosed and treated correctly
Life limiting if not treated
Will have persistant PUPD from glucocorticoids
Expensive treatment

112
Q

What electrolyte is linked to calcium due to hormonal regulation?

A

Phosphate

113
Q

Where is phosphate primarily stored?

A

In bone
And intracellularly

114
Q

What is the role of phosphate in the body?

A

Metabolic reactions
Cellular processes
Membrane structure - phospholipids

115
Q

What does low blood calcium stimulate?

A

PTH release

116
Q

What are the effects of PTH?

A

Increased calcium
Decreased phosphate

117
Q

What are the differentials for hypercalcaemia?

A

HARDIONSGG
Hyperparathyroidism
Addisons disease
Renal disease
High vitamin D
Idiopathic
Osteolytic
Neoplastic (PTHrp)
Spurious
Granulomatous (macrophage) inflammation
Growth

118
Q

What are the 3 diseases causing hypercalcaemia due to an increase in PTH/PTHrp?

A

Primary hyperparathyroidism
Renal disease (high phosphate)
Neoplastic (PTHrp)

119
Q

What are the 2 diseases causing hypercalcaemia due to an increase in vitamin D?

A

Hypervitaminosis D - excessive ingestion of vitamin D
Granulomatous inflammation - macrophages can produce vitamin D analogues

120
Q

How do you tell if it is pattern PTH/PTHrp mediated hypercalcaemia or pattern vitamin D mediated hypercalcaemia?

A

Pattern PTH/PTHrp mediated hypercalcaemia - concurrent low phosphate
pattern vitamin D mediated hypercalcaemia - concurrent hyperphosphataemia

121
Q

If you know that it is a PTH/PTHrp pattern mediated hypercalcaemia, how do you tell what caused it?

A

Clinically well dog - primary hyperparathyroidism most likely
Clinically unwell dog - neoplasia most likely

122
Q

If you know that it is vitamin D pattern mediated hypercalcaemia, how do you tell what caused it?

A

Enquire about vitamin D related intoxication - diet, supplements, houseplants
Look for cause of inflammation

123
Q

What is the most common cause of hypercalcaemia in cats? How do you diagnose it?

A

Idiopathic hypercalcaemia - diagnosis by exclusion through haem, biochem, imaging, PTH/vit D measurement

124
Q

How do you manage hypercalcaemia (with low phosphate)?

A

Identify/treat underlying disease
0.9% NaCl (NOT hartmanns) saline diuresis
Glucocorticoids - pred

125
Q

How do you manage hypercalcaemia and hyperphosphataemia?

A

Glucocorticoids/bisphosphonates
Salmon calcitonin
Bisphosphonates (osteoclast inhibitors)
Must treat as risk of tissue mineralisation in the kidneys - CKD

126
Q

How do you manage idiopathic hypercalcaemia in cats?

A

Often dont need drug therapy
Encourage water intake
Diet modification - renal diet, fibre supplements
Glucocorticoids/bisphosphonates if this fails

127
Q

What are the differentials for hypocalcaemia?

A

Pregnancy/lactation
EDTA contamination from test tube
Hypoalbuminaemia
Acute kidney injury
Pancreatitis
Sepsis
Dietary

128
Q

What are the clinical signs of hypocalcaemia?

A

Anorexia
Restlessness
Facial rubbing, lip licking
Twitching
Stiffness
Seizures

129
Q

How do you treat hypocalcaemia?

A

Emergency - calcium gluconate bolus IV
Chronic - oral vitamin D

130
Q

What are the signs of hyperglycaemia?

A

Polyuria/polydipsia - glucose in urine pulls water with it
Polyphagia - lack of intracellular glucose so always hungry
Weight loss
Diabetic cateracts

131
Q

What type of diabetes mellitus do dogs get?

A

Type 1 - insulin dependent diabetes
Absolute insulin deficiency due to irreversible loss of beta cell function
Treat with exogenous insulin

132
Q

What causes gestational diabetes mellitus?

A

Heavy progesterone dependent phase of cycle - progestogens are insulin inhibitors so become insulin resistant

133
Q

What is the renal threshold for glucose?

A

> 10-12mmol/l

134
Q

What is normal glucose level?

A

3-5mmol/l

135
Q

What is found on haem/biochem/urinalysis in diabetes mellitus?

A

Hyperglycaemia with glucosuria
High liver enzymes
Hyperlipaemia
Normal USG despite polyuria - glucose contributes
Ketonuria
Hypertension

136
Q

What insulin do you give dogs with diabetes mellitus?

A

Lente insulin - caninsulin
Use vet pen - 40iu/ml syringes
REFRIGERATE

137
Q

What is the starting dose for insulin for dogs?

A

0.25iu/kg

138
Q

What adjunctive management of canine diabetes mellitus can you do alongside insulin?

A

Diet modification - correct obesity, high fibre/complex carb diet
Consistent exercise
Neuter entire female bitches

139
Q

How do you review diabetes mellitus in dogs?

A

Glucose curves
(Fructosamine evaluation if cant do)

140
Q

How do you do a glucose curve?

A

Test glucose before giving insulin and every 2 hours after
Ear prick (dont squeeze)

141
Q

What are the optimal readings in a glucose curve?

A

Range between 4.5 and 17mmol/l
Nadir (lowest glucose) between 4.5-7.3mmol/l

142
Q

What are 3 findings on glucose curve that can indicate insulin not correct dose?

A

Too long/short action - nadir in <6hrs of injection or >12hrs after injection
Somogyi overswing
Resistance

143
Q

What is a somogyi overswing?

A

Physiologic response to impending hypoglycaemia - rebound of insulin resistant hyperglycaemia
Occurs if nadir is too low
Or there is a rapid drop in glucose

144
Q

How should you treat a somogyi overswing?

A

Reduce dose by 25-50% - usually due to starting on too much insulin or increasing dose too quickly

145
Q

How should you address glucose curves being too short or too long?

A

Consider changing insulin type or frequency

146
Q

What can cause lack of action/resistance to glucose?

A

Somogyi overswing
Insulin storage/bottle
Concurrent disease/drugs - chronic infections, inflammatory disease, endocrinopathies, neoplasia
Maybe insulin antibodies - uncommon

147
Q

What are the complications of diabetes mellitus management in dogs? How do you manage them?

A

Inappetence - if eat less than half of meal then give half dose of insulin
Vomiting, lethargy - investigate if persists
Hypoglycaemia - feed, glucogel

148
Q

What are the differentials of hypoglycaemia in dogs?

A

Inadequate synthesis of glucose - liver dysfunction, small dogs with small liver storage
Excessive consumption - sepsis
Excess hypoglycaemic agents - insulin from owner, insulinoma

149
Q

What type of diabetes mellitus do cats get? What causes it?

A

Type 2 - non-insulin dependent
Relative insulin insufficiency from beta cell dysfunction
And concurrent diseases causing insulin resistance

150
Q

What are some causes of insulin resistance in cats?

A

Exogenous glucocorticoids
Hyperthyroidism
Acromegaly - excess growth hormone
Stress induced

151
Q

How do you tell if a cat has stress induced hyperglycaemia or diabetes mellitus?

A

Evaluate for concurrent glucosuria and/or fructosamine - shows more long term

152
Q

What is the renal threshold for glucose in cats?

A

11-16mmol/l - higher than in dogs

153
Q

How do you treat diabetes mellitus in cats?

A

Protamine zinc insulin (prozinc)

154
Q

What is diabetic remission and when does it occur?

A

Diabetes mellitus resolves so insulin no longer required - in 25% of cats, usually in first 34 months of treatment
Especially if can remove cause of insulin resistance eg. glucocorticoids

155
Q

What are the complications of uncontrolled diabetes mellitus in cats and how do they differ from dogs?

A

Diabetic neuropathy - hind limbs affected
Rarely/dont really get diabetic cateracts

156
Q

What causes ketone bodies to form?

A

Fat breakdown releases Acetyl CoA
Cant enter krebs cycle due to no carbs
SO oxidation of Acetyl CoA into ketone bodies

157
Q

What is the clinical significance of ketone bodies?

A

Indicate lipolysis - krebs cycle failure
Diabetic ketoacidosis - emergency

158
Q

How do you identify the presence of ketones?

A

Dipstix - acetone, acetoacetate
Lab - betahydroxybutyrate

159
Q

How do you differentiate between diabetic ketosis (well patient) and diabetic ketoacidosis (sick patient)?

A

Blood gas analysis

160
Q

How do you treat diabetic ketoacidosis?

A

Fluid therapy
Neutral insulin therapy - short acting rapid onset insulin
Hourly IM injections or continuous infusion over 8 hours
Get down to 14mmol/l

161
Q

What are common complications of neutral insulin therapy to treat diabetic ketoacidosis?

A

Hypokalaemia and hypophosphataemia - intracellular translocation
Need to supplement fluids with KCl
Sodium - correct no faster than 0.5mmol/l/hr as can cause water fluxes in and out of brain

162
Q

What are the measurements for PUPD?

A

Polyuria - urine production mroe than 50ml/kg/day
Polydypsia - water intake more than 100ml/kg/day

163
Q

What tends to cause PUPD?

A

Polyuria with compensatory polydipsia - cant concentrate urine so have to drink more

164
Q

What is the other name for ADH?

A

Vasopressin

165
Q

What controls thirst?

A

Angiotensin II - directly stimulates thirst
From RAAS
Maintains plasma osmolality and blood volume

166
Q

What are the 7 mechanisms of PUPD, from the head to the kidney?

A

Central diabetes insipidus
Primary nephrogenic diabetes insipidus
Secondary nephrogenic diabetes insipidus
Intrinsic renal disease
Osmotic diuresis
Psychogenic polydipsia
Medullary washout

167
Q

What is central diabetes insipidus?

A

Lack of arginine vasopressin/ADH production

168
Q

What is primary nephrogenic diabetes insipidus?

A

Congenital inability of collecting duct to respond to ADH (very very rare)

169
Q

What is secondary nephrogenic diabetes insipidus?

A

Submaximal response of the kidney to ADH due to an interfering factor

170
Q

What interfering factors can cause secondary nephrogenic diabetes insipidus?

A

Electrolyte disturbances - hypercalcaemia, hypokalaemia
Endocrinopathies
Drugs - steroids, phenobarbitone
Endotoxins - pyometra
Hepatic disease

171
Q

How can renal disease cause PUPD?

A

Nephron loss - cant concentrate urine
Post obstructive diuresis

172
Q

What is osmotic diuresis?

A

Loss of osmotic substances in urine - eg. glucose in urine pulling water with it diluting the urine

173
Q

What is psychogenic polydipsia?

A

Bored dogs drinking more - makes them wee more
Only disease where polydipsia causes polyuria
Wont drink more in a different more interesting environment

174
Q

What is medullary washout?

A

Loss of medullary concentration gradient in the kidney - urea or sodium deficit
Caused by chronic PUPD, hypoadrenocorticism (hyponatremia)

175
Q

How do you investigate PUPD?

A

Quantify water intake
Look at concurrent signs
Urinalysis
Haem/biochem
Imaging

176
Q

What 3 diseases might be causing PUPD if they dont show up on normal investigation?

A

Central diabetes insipidus
Primary nephrogenic diabetes insipidus
Psychogenic polydipsia

177
Q

How do you diagnose/tell the difference between central diabetes insipidus and primary nephrogenic diabetes insipidus?

A

DDAVP trial - give synthetic ADH
dogs with central diabetes insipidus will have a notable improvement
Dogs with primary nephrogenic diabetes insipidus cannot respond

CVSOH BVSc4 (86 decks)

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