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Small animal endocrinopathies Flashcards

Canine hypoadrenocorticism, diabetes

1
Q

What are the 3 zones of the adrenal cortex and what does each produce?

A
  • Glomerulosa: mineralocorticoids (aldosterone)
  • Fasciculata: glucocorticoids
  • Reticularis: Androgens
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2
Q

What is a potential, but less common, pathological process of adrenal insufficiency?

A

Mineralocorticoids abnormal first, and then progress to glucocorticoid deficient i.e. moving inwards starting at the glomerulosa

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3
Q

What stimulates the release of aldosterone?

A
  • RAAS
  • Decreased BP detected by baroreceptors in macula densa in distal tubule, also cardiac and arterial baroreceptors
  • Renin released from kidneys -> angiotensin release -> aldosterone release
  • Also increased potassium concentratione
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4
Q

What are the functions of aldosterone?

A
  • Acts on distal tubule cells, and CD to increase reabsorption of Na and Cl and therefore water
  • Stimulates K+ secretion into tubular lumen
  • Stimulates secretion of H+ in exchange for k+ in collecting tubules and so regulates acid/base
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5
Q

What are the different types of hypoadrenocorticism?

A
  • Primary/Addison’s
  • Secondary
  • Iatrogenic
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6
Q

What are the potential causes of primary hypoadrenocorticism?

A
  • Idiopathic atrophy (immune mediated, associated with other endocrinopathies)
  • Iatrogenic (e.g. drugs, mitotane, trilostane), or surgery )bilateral adrenalectomy)
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7
Q

Describe the pathophysiology of primary hypoadrenocorticism

A
  • Deficiency of glucocorticoids and mineralocorticoids
  • Occurs with loss of 85-90% of adrenal cortex
  • CRH and ACTH increase due to loss of negative feedback
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8
Q

Describe the pathophysiology of secondary hypoadrenocorticism

A
  • Deficiency of ACTH
  • Only cortisol deficiency, electrolytes normal
  • Rare
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9
Q

Describe the pathophysiology of iatrogenic hypoadrenocorticism

A
  • Exogenous steroids lead to adrenal atrophy
  • Cortisol deficiency only
  • Patient may have signs of Cushing’s syndrome
  • Patient may develop signs of Addison’s if steroids abruptly discontinued
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10
Q

Outline the signalment of canine hypoadrenocorticism

A
  • Young-middle aged dogs (4-6yrs)
  • 70% females
  • Standard poodles, bearded collies, Great Dane, Rottweiler, WHWT, soft coated wheaten terrier (but any breed possible)
  • Some inheritance
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11
Q

In relation to hypoadrenocorticism, what should be considered inthe Nova Scotian Duck tolling retriever?

A

Juvenile Addison’s at 5mo-1yr old, immune mediated disease

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12
Q

What are the pathophysiological effects of aldosterone deficiency?

A
  • Loss of Na+, Cl- and H20
  • Retention of K+ and H+
  • Pre-renal azotaemia
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13
Q

What are the pathophysiological effects of glucocorticoid deficiency

A
  • Decreased stress tolerance
  • GI signs, e.g. haemorrhagic gastroenteritis
  • Weakness
  • Appetite loss
  • Anaemia
  • Impaired gluconeogenesis
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14
Q

Describe the common clinical history of a dog with hypoadrenocorticism

A

Waxing and waning with non-specific signs worsened by stress

  • Anorexia, V/D, lethargy, depression, weakness
  • Shivering, weight loss, PUPD, abdominal pain
  • Should consider hypoA in any animal with waxing and waning signs esp GI
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15
Q

What are the signs of acute hypoadrenocorticism?

A
  • Marked hypovolaemia and azotaemia
  • Paradoxical relative bradycardia (hyperkalaemia)
  • Collapse, extreme weakness, hypothermia, recent history of V/D
  • Abdo pain, melena (dark black tarry faeces) may feature,
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16
Q

What oher condition might signs of an Addisonian crisis resemble?

A

Pancreatitis

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17
Q

What are the common biochemical features of hypoadrenocorticism?

A
  • Hyperkalaemia
  • Hyponatraemia
  • Hypocholridaemia
  • Na:K ratio <23
  • Hypercalcaemia
  • Electrolyte changes may lag behind clinical signs and history - if normal but still suspicious repeat biochem in a few months
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18
Q

What features of a complete blood count are common in hypoadrenocorticism?

A
  • Lack of stress leukogram (no neutrophilia, eosinopaenia and lymphopaenia)
  • Anaemia
  • Lymphocytosis
  • Eosinophilia
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19
Q

What features of biochemistry and urinalysis are common in hypoadrenocorticism?

A
  • Azotaemia
  • Decreased USG
  • Hypercalcaemia
  • Hypoglycaemia
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20
Q

What features may be seen on thoracic radiographs in hypoadrenocorticism?

A

Megoesophagus (but <1%)

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21
Q

Explain megaoesophagus in hypoadrenocorticism

A
  • May be muscle weakness, decreased Na and K = decreased membrane potential, decreased cortisol also associated with muscle weakness, reversible with treatment
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22
Q

What features may be seen on an electrocardiogram in hypoadrenocorticism?

A
  • Bradycardia
  • Peaked T waves
  • Widened QRS complexes
  • Decreased P wave amplitude/complete disappearance
  • Ventricular asystole
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23
Q

What are the definitive diagnostic tests for hypoadrenocorticism?

A
  • ACTH stim test

- Basal cortisol

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24
Q

What results would be expected in an Addisonian dog on an ACTH stim?

A

Flatline cortisol following ACTH administration i.e. no increase in cortisol production

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25
Q

How is basal cortisol used in the diagnosis of Addison’s?

A
  • Depends on levels of cortisol
  • > 55nmol/L - rule out Addison’s, bit below 55nmol/L may have false negatives
  • Resting cortisol <28nmol/L higher specificity vs 55nmol/L basal, can rule IN Addison’s if below 28nmol/L
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26
Q

What are the main treatment aims in hypoadrenocorticism?

A
  • Restore intravascular volume (treat shock)
  • Reverse hyperK
  • Replace lost mineralocorticoids and glucocorticoids
  • Correct life threatening arrhythmias
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27
Q

Describe the restoration of intravascular volume in an Addisonian crisis

A
  • 0.9% saline or Hartmann’s at 20-90ml/kg/hr
  • Assess every 10-15mins until improvement
  • Once restored reduce to maintenance (2ml/kg/hr), compensate for ongoing losses
  • Continue unil hydration status, urine output, serum electrolytes and azotaemia are corrected
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28
Q

What is the importance of correcting electrolytes in an Addisonian crisis?

A

If sodium abnormal will continue to lose fluids

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29
Q

How is hyperkalaemia treated in an Addisonian crisis?

A
  • Fluid therapy (normalise kidney outflow)
  • 10% calcium gluconate (0.5-1ml/kg IV slow over 20 mins)
  • IV dextrose/glucose (1ml/kg 50% dilute with saline, ideally via central line)
  • IV soluble insulin (0.25-0.5IU/kg IV) with glucose at 2-3g/unit insulin
  • Sodium bicarbonate 1-2mmol/kg
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30
Q

How are the mineralocorticoids and glucocorticoids dealt with in an Addisonian crisis?

A
  • Dexamethaseon single dose 0.1-0.2mg/kg IV (glucocorticoids only)
  • Hydrocortisone (initial 5mg/kg bolus over 5 min, then 1mg/kg IV q6h, balanced mineralocorticoid and glucocorticoid, short acting - frequent dose or CRI)
  • Methylprednisolone sodium (1-2mg/kg IV), rare in practce
  • Prednisolone oral (some mineralocorticoid activity)
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31
Q

What drugs are using in the long term treatment of hypoadrenocorticism

A
  • Desocycortone pivalate

- Fludrocortisone

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32
Q

Which drug is licensed in the long term treatment of hypoadrenocorticism?

A

Desoxycortone pivalate

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33
Q

Outline the use of desoxycortone pivalate in the treatment of hypoadrenocorticism

A
  • Mineralocorticoid replacement only, use with pred
  • IM inj. q20-30days
  • Reassess and adjust dose/frequency regularly
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34
Q

Outline the testing required when using desoxycortone pivalate

A
  • 10 day electrolyte test to show peak effect and assessment of adequacy of dose, use after each dose adjustment
  • 25 days = pre-injection sample, assess adequacy of dosing interval
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35
Q

Outline the use of fludrocortisone in the ongoing treatment of hypoadrenocorticism

A
  • Unlicensed
  • Mineralo and glucocorticoid replacement
  • Oral
  • Prohibitively expensive for most
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36
Q

How is therapy for hypoadrenocorticism monitored?

A
  • NOT ACTH stim test

- Clinical signs (shakey, weak, anorexia, V/D), electrolytes

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37
Q

What is a potential risk of correcting sodium in a hypoadrenocorticism too quickly?

A
  • Brain hyperosmolar, draws in water
  • Add too many salts, blood hyperosmolar relative to brain, water out of brain = brain shrinks
  • Myelin and axons strip away = seizuring and death
  • CNS needs time to equilibrate
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38
Q

What is atypical hypoadrenocorticism?

A

Primary hypoadrenocorticism where glucocorticoid disturbance precedes mineralocorticoid, so no electrolyte imbalance, may go on to develop mineralocorticoid imbalance

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39
Q

What metabolic products may also be raised in hyperadrenocorticism?

A

Progesterone, androstendione, 17-alpha hydroxy progesterone etc.

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40
Q

Outline the physiological activity of the HPA axis

A
  • Released by paraventricular nuclei in hypothalamus
  • Into pars distalis, leads to ACTH release
  • ACTH activates CYP450 enzymes and cholesterol metabolism produces cortisol + other metabolites
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41
Q

What are the potential causes of pituitary dependent hyperadrenocorticism?

A
  • Microadenomas (<10mm diameter, 80% of cases)
  • Macroadenomas (>10mm diameter, slow growing, not always neuro signs)
  • 70% pars distalis, 30% pars intermedia
42
Q

What are the potential causes of adrenal dependent hyperadrenocorticism?

A
  • 50% are carcinomas, 50% adenomas

- Mostly unilateral, can be bilateral

43
Q

Describe the signalment of adrenal dependent hyperadrenocorticism

A
  • Older dogs (11-12yrs) ADH
  • Larger breeds more at risk of ADH
  • Females more at risk vs males
44
Q

Describe the signalment of pituitary dependent hyperadrenocorticism

A
  • Middle ages dogs (7-9yrs)
  • Small breeds: poodles, dachsunds, small terriers
  • No sex predisposition
45
Q

Give the most common clinical signs of Cushings

A
  • Insidious onset, may initially be intermittent
  • PUPD
  • Abdo enlargement, polyphagia
  • Hepatomegaly, muscle wasting/weakness, lethargy/exercise intolerance/panting, skin changes (alopecia tenting, visible vessels, comedones)
  • alopecia
  • Repro changes
  • Calcinosis cutis
46
Q

What less common signs may also be associated with Cushing’s?

A
  • V/D
  • Pruritus
  • Improvement of chroic pruritus/atopy (endogenous steroid increase = anti itch)
47
Q

What is required for the diagnosis of Cushing’s?

A
  • High index of suspicion, thorough history and clin exam,
  • Blood biochem and CBC
  • Urinalysis
  • imaging
  • Diagnostic tests
48
Q

What would these biochemistry findings indicate?

  • Elevated ALP, ALT, cholesterol, bile acids, fasting glucose
  • Reduced BUN
A

Cushing’s

49
Q

What findings would be expected on CBC in a Cushingoid dog?

A
  • Lymphopaenia
  • Eosinopaenia
  • Neutrophilia
  • Monocytosis
  • Erythrocytosis
    (Stress leukogram)
50
Q

What findings would be expected on urinalysis in a Cushingoid dog?

A
  • USG <1.015, but be <1.008 (hyposthenuric)
  • UP:UC >1.0 (50% of dogs)
  • Evidence of UTI
51
Q

What findings may be seen on an abdominal radiograph of a Cushingoid dog?

A

Good contrast, hepatomegaly, pot-bellied appearance, calcinosis cutis, distended bladder

52
Q

What types of diagnostic test are required to make a definitive diagnosis of Cushing’s?

A

A screening test and a differentiation test

53
Q

What screening tests are used for Cushing’s?

A
  • Cortisol:creatinine ratio
  • ACTH stim test
  • Low dose dexamethasone suppression test
  • 17-alpha-OH progesterone
54
Q

Outline how screening tests are used in the diagnosis of Cushing’s

A
  • Low suspicion: rule out with urine cortisol:creatinine ratio
  • If use ACTH stim and clear positive + clinical findings that fit = treat
  • If ACTH negative but high index of suspicion, perfrom LDDS
  • If positive = treat, if negative, consider other ddx
  • With equivocal results consider re-testing later
55
Q

Outline how the urinary cortisol:creatinine ratio is carried out

A
  • Easy
  • Owner collects urine sample in morning at home (remove influence of stress)
  • Low ratio = extremely unlikely
  • High ratio = possible, but high number of false positives (but >100 strongly suggetive)
  • Good to rule OUT
56
Q

Describe the sensitivity and specificity of urinary cortisol:creatinine ratio for the diagnosis of Cushing’s

A
  • High sensitivity (~100%)

- Low specificity

57
Q

Describe the sensitivity and specificity of the ACTH stim test for the diagnosis of Cushing’s

A
  • Fairly high sensitivty, ~85% of PDH, >50% of ADH
  • Best specificity (few false positives)
  • Rule IN
58
Q

Describe how the ACTH stim test for Cushing’s diagnosis is carried out

A
  • Starve overnight, collect heparin sample at T0
  • Inject ACTH analogue IV
  • Collect second sample 30-60min later in heparin tube
59
Q

Compare the normal and positive result for Cushing’s on an ACTH stim test

A
  • Normal: pre-stim <200nmol/L, post stim <600nmol/L

- Positive: post-stim >600nmol/L

60
Q

What may lead to a false positive on an ACTH stim test?

A

Animals with infections, fracture, sepsis, renal failure, acute kidney injury etc as will have been under significant stress

61
Q

Describe the sensitivity and specificity of the low dose dexamethasone suppression test for the diagnosis of Cushing’s

A
  • High sensitivity (90-95% PDH, most ADH)
  • Low specificity, more false positives
  • Good for ruling OUT
62
Q

Describe the protocol for the low dose dexamethasone suppression test for Cushing’s

A
  • Starve overnight, collect baseline heparin sample
  • Inject 0.01mg/kg dex IV
  • Collect heparine samples at 3hr and 8hr
63
Q

Compare the normal result and positive results on a low dose dexamethasone test for Cushing’s

A
  • Normal: suppress to 50% basal by 3hrs and remain suppressed
  • Positive: cortisol >50nmol/L at 8hrs
64
Q

How might the low dose dexamethasone test be used as a differentiation test for Cushing’s?

A
  • Limited use

- Adrenals autonomous, no suppression in ADH even when suppress ACTH release further BUT not always

65
Q

Outline the use of 17-alpha-OH progesterone when screening for Cushing’s

A
  • Extended adrenal package gives 5 additional hormones
  • Interpret with caution
  • Most non-cortisol Cushing dogs have increase in progesterone and 17-a-OH- progesterone due to cross-reactivity at receptors
66
Q

What tests may be used have been identified as differentiation tests in Cushing’s?

A
  • Endogenous ACTH concentration
  • Abdominal ultrasound
  • (High dose dexamethasone suppression test)
67
Q

Compare the prognosis for ADH and PHD

A

PDH better, more susceptible to medical management (NB if PDH, macroadenoma may cause neuro signs at some point)

68
Q

Briefly outline endogenous ACTH concentration in Cushing’s differentiation

A
  • Labile hormone, test difficult in general practice, false negatives common
  • Higher in PDH
69
Q

Briefly outline the use of abdominal ultrasound for differentiation of hyperadrenocorticism

A
  • Measure dimensions of adrenal glands
  • PDH both same size +/- hypertrophy
  • ADH one enlarged, the other atrophied
70
Q

Outline the use of high dose dexamethasone suppression test in the differentiation of hyperadrenocorticism

A
  • In PDH, high dose dex should inhibit pit ACTH secretion through -ve feedback so suppress cortisol
  • AD autonomous = no cortisol suppression
71
Q

What is the main disadvantage of the HDDS test for the differentiation of Cushing’s?

A

25-30% of PDH cases fail to suppress with HDDS, no longer a recommended test

72
Q

What other conditions does Cushing’s predispose to?

A
  • UTI
  • Glomerulonephropathies
  • Hypertension
  • Thromboembolic disease
  • Diabetes mellitus
73
Q

What is the prognosis for Cushing’s?

A

Well treated and monitored dogs ~5yrs

74
Q

What management options are available for Cushing’s?

A
  • Medical (trilostane, mitotane)

- Surgical (adrenalectomy)

75
Q

Compare the drugs that can be used to treat Cushing’s

A

Trilostane licensed, mitotane unlicensed

76
Q

Describe the mechanism of action of trilostane

A
  • Competitively inhibits 3-betahydroxysteroid dehydrogenase
  • Decreases steroid production
  • Reversible
  • Low risk of side effects as duration of activity not prolonged
77
Q

Describe the mechanism of action and key side effect of mitotane

A
  • Cytotoxic

- Can lead to Addisons

78
Q

Outline the use of surgery in the treatment of Cushing’s

A
  • Choice of treatment for ADH
  • Advanced imaging used prior to identify local invasion/metastatic disease
  • Complication rate can be high
  • Consider referral
79
Q

What is a significant risk during adrenalectomy for the treatment of ADH?

A

If malignant tumour can end up with adrenal storms in surgery and lose patient under GA

80
Q

How should a canine hyperadrenocorticism case be monitored?

A
  • History, clinical exam and ACTH stim test
  • Regular monitoring following administration of trilostane in order to titrate dose
  • Recheck 10-14 days after initiating/changing treatment
  • Perform ACTH stim 4-6 hours post medication
81
Q

What are potential complications of trilostane treatment?

A
  • Signs of hypoadrenocorticism with over doses
  • Steroid withdrawal
  • Necrosis of adrenal glands when start on trilostane, but minimal side effects
82
Q

What is the prognosis for a case of hyperadrenocorticism?

A
  • If well managed, several years
83
Q

Outline the cost implication to the owner associated with canine HAC

A
  • Drugs add up quickly

- Surgery (is possible) is a one off cost (£3-5k) as animal will be cured after

84
Q

Which cat breed is predisposed to diabetes mellitus?

A

Burmese cats

85
Q

Compare the pathogenesis of diabetes mellitus in cats and dogs

A
  • Cats due to insulin resistance

- Dogs due to reduced insulin production

86
Q

What does NIDDM mean?

A

Non insulin dependent diabetes mellitus, produce some insulin but no response peripherally leading to hyperglycaemia

87
Q

How does failure of glycaemic control lead to further insulin resistance?

A
  • Chronic hyperglycaemia impairs insulin secretion
  • if over 2 weeks, leads to glycogen deposition and cell death as a result
  • Termed glucose toxicity
88
Q

What is the role of glucose and lipid in type II diabetes?

A

Glucose and lipid toxicity occur with chronic high circulating levels of lipid/glucose which impair insulin secretion

89
Q

What are potential underlying causes of impaired insulin secretion in the cat leading to a diabetic state (type II) and how will these lead to diabetes?

A
  • Pancreatitis
  • Pancreatic neoplasia
  • Acromegaly
  • Hyperadrenocorticism
  • Lead to reduced secretion of insulin, or reduced insulin sensitivity (acromegaly, HAC)
90
Q

What are potential causes of peripheral insensitivity to insulin in cats?

A
  • Obesity

- Stress (multicat household, comorbidities, chronic disease)

91
Q

Briefly describe type I diabetes in cats

A
  • Rare in cats

- Usually due to immune mediated destruction

92
Q

What is the result of amyloid deposition in the pancreas of a cat?

A

Diabetes, end stage, no recovery

93
Q

Describe the pathophysiology of diabetes mellitus in the cat

A
  • Decreased tissue utilisation of glucose, amino acids, FFAs
  • Increased gluconeogenesis, glycogenolysis, tissue catabolism
  • Osmotic diuresis and secondary PD
  • Polyphagia
  • Cataracts due to osmotic effects
  • Ketoanaemia, ketoacidosis
94
Q

Why does polyphagia occur with diabetes mellitus?

A

Insulin required in satiety centre of brain

95
Q

Outline a diagnostic plan for cats with suspected diabetes mellitus

A
  • Clinical history

- Confirmatory tests: urine glucose, fructosamine, rule out other possible causes

96
Q

What condition would this clinical history be suggestive of in a cat?

  • 13yo MN
  • PUPD
  • Weight loss, polyphagia
  • Plantigrade stance, peripheral neuropathy
A
  • Diabetes mellitus
  • (Hyperthyroidism)
  • Typically DM: middle aged-older cats, neutered males over represented
97
Q

Why is a simple blood test not good for diagnosis of diabetes mellitus in the cat?

A

Stress hyperglycaemia can be significant

98
Q

What are the advantages and disadvantages of a fructosamine test in a cat for diabetes mellitus?

A
  • Shows long term picture of hyperglycaemia, better indicator of glucose metabolism over last 2-3 weeks
  • Volatile parameter affected by concurrent disease (e.g. reduced albumin, common in older of hyperthyroid cats)
99
Q

What value on a fructosamine result would indicate diabetes mellitus in a cat?

A

> 400umol/l

100
Q

What condition commonly occurs with diabetes mellitus in cats and dogs and what is the importance of this?

A

An active UTI, impacts on ability to stabilise patient

ENI2 (10 decks)

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