Hypoadrenocorticism Flashcards

1
Q

What is the other name use for hypoadrenocorticism?

A

Addisons disease

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2
Q

What is the cause of hypoadrenocorticism?

A

Lack of mineralocorticoid and/or glucocorticoid secretion by the adrenal cortex

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3
Q

Describe primary hypoadrenocorticism

A

Caused by destruction of more than 95% of the adrenal cortex leading to a deficiency of mineralocorticoid and glucocorticoid secretion.
It is termed Addisons disease

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4
Q

Describe secondary hypoadrenocorticism

A

Deficiency in ACTH secretion by the pituitary gland leading to atrophy of the adrenal cortices and decreased/absent glucocorticoid secretion. Mineralocorticoid secretion remains sufficient.

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5
Q

Describe the predispositions for hypoadrenocorticism

A
  • Uncommon - best not to miss
  • Middle aged female
  • Standard Poodle, Beardies, Gt Dane, Portugese Water Dog, WHWT, St B, Wheaten T, Rottie Leonberger
  • Nova Scotia Duck-Tolling Retriever 10x more common, affects siblings
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6
Q

List the clinical signs of acute hypoadrenocorticism

A
  • Severe depression/collapse
  • Hypovolaemic
  • Weak pulses
  • Pale mm
  • Bradycardic
  • Dehydration
  • Hypothermic
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7
Q

List the clinical signs of chronic hypoadrenocorticism

A
  • Intermittent malaise
  • Vomiting
  • Diarrhoea
  • Lethargy
  • Weight loss
  • Intermittent collapse
  • Vague and intermittent
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8
Q

What is the cause of bradycardia in hypoadrenocorticism?

A

High potassium levels.
- Dehydration would normally cause tachycardia so the bradycardia suggests potassium levels have increased

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9
Q

Describe the haematology changes seen in hypoadrenocorticism

A
  • Mild non- regenerative anaemia: due to chronic disease or recent haemorrhage
  • Mild hypercalcaemia: due to shift in electrolyte balances and reduced excretion by the kidneys
  • Pre-renal azotaemia: chronic dehydration -> decreased GFR -> raised urea and creatinine
  • Lymphocytosis +/- eosinophilia = Inverse stress leukogram due to lack of glucocorticoids
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10
Q

Describe the sodium and potassium changes seen in hypoadrenocorticism

A

Animals with Addisons are deficient in mineralocorticoids (aldosterone) and therefore have
increased loss of sodium and chloride in the urine and reduced excretion of potassium

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11
Q

Describe the main features of atypical Addisons

A

Cortisol deficiency
Normal Mineralocorticoids
Usually progress to mineralocorticoid deficiency
May have abnormal aldosterone stimulation

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12
Q

List the DDx for high potassium and low sodium levels

A

Gastrointestinal disease
Renal failure (acute or chronic)
Parasitic infection (whipworms)
Urinary obstruction
Chronic effusion with repeated drainage
Pregnancy
Congestive heart failure
Diabetes mellitus
Chronic blood loss

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13
Q

Describe the changes seen on the ECG of patients with Addisons

A

Bradycardia
Tall, narrow T waves
Prolonged QRS interval
Decreased P wave amplitude
Prolonged P-R interval
Absent P wave
Complete heart block
Ventricular arrhythmias

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14
Q

How can Addisons be detected on radiography?

A

Hypovolaemia signs: microcardia, reduced vascular pattern and a small vena cava

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15
Q

Which test can be used to rule out Addisons

A

Basal cortisol using a single ACTH stimulation test

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16
Q

Describe the results of the ACTH stimulation test in Addisons

A

Dogs with Addisons have a low resting cortisol level and have a subnormal or negligible response to ACTH (few dogs with a basal cortisol > 50nmol/l turn out to have Addison’s).
The same result will be obtained in an animal that has been on steroids, so make sure that you rule this out before making a diagnosis.

17
Q

Describe fluid therapy for dogs with Addisons

A
  • IV fluids at 3-4 times maintenace.
    Use fluids that are low in potassium and preferably 0.9% NaCl.
  • Glucose can be added to the drip if necessary to make a 5% solution, as this will cause insulin release and reduce hyperkalaemia
18
Q

Describe steroid treatment for acute Addisons patients

A

An ACTH stimulation test should be performed before starting glucocorticoid therapy.
If the animal is extremely sick and treatment has to be initiated straight away, dexamethasone is the glucocorticoid that least interferes with the test.
As soon as the ACTH stimulation test has been performed, the animal should be treated with dexamethasone

19
Q

Describe steroid therapy for stabilised Addisons patients

A

Oral prednisolone
Fludrocortisone

20
Q

What are the side effects of Addisons treatment?

A

Acute renal disease
Myelinosis
- Depression, weakness, ataxia, tetraparesis, and decreased sensory perception
- Signs occur days later and are often irreversible

21
Q

Describe the prognosis of Addisons

A

Lifelong therapy
Add glucocorticoid when stressed
Normal life expectancy when treated and monitored correctly

22
Q

What is the cause of hyperaldosteronism?

A

Adrenal tumour producing aldosterone
Not reported in dogs

23
Q

What are the clinical signs of hyperaldosteronism?

A

PUPD
Weakness
Neck ventroflexion (hypokalaemia)
Hypertension (sodium retention)

24
Q

How is hyperaldosteronism treated?

A

Restrict sodium and supplement potassium
Surgical excision
Spironolactone (aldosterone antagonist)

25
Q

Name the tumour of the adrenal medulla secreting catecholamines

A

Pheochromocytoma

26
Q

List the clinical signs of a Pheochromocytoma

A

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

27
Q

How is a Pheochromocytoma diagnosed?

A

Radiography or ultrasound

28
Q

How is a Pheochromocytoma treated?

A

Radical excision (high risk), antihypertensive medication
Frequently metastasise