Addisons and Cushings Flashcards

1
Q

What are Addisons and Cushings and what is the difference?

A

Addisons = HYPOadrenocorticisom - Not enough cortisol and aldosterone produced.
Cushings = HYPERadrenocorticisom - Too much cortisol produced.

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2
Q

What are the possible causes of Cushings?

A

Ususally a pituitary tumour (85%) causing excess production of ACTH, which stimulates release of cortisol from the adrenal cortex.
Or an adrenal tumour (15%)

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3
Q

What are some actions of increased cortisol production seen with Cushings?

A

Cortisol promotes gluconeogenesis and catabolism of proteins and fat stores.

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4
Q

Cushings can lead to hyperglycaemia - why?

A

Cortisol promotes gluconeogenesis

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5
Q

Cushings is characterised by muscle weakness (pot belly, weakened resp muscles) - why?

A

Protein catabolism promoted by increased levels of cortisol.

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6
Q

PU/PD is seen with Cushings - why?

A

Increased cortisol causes inhibition of antidiuretic hormone (ADH)

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7
Q

Decreased hepatic function is seen with Cushings, what effects can this have?

A

Prolonged recoveries and hyper coagulation leading to possible pulmonary thromboembolism. Hepatomegaly also contributes to pot belly appearence.

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8
Q

What is the cause of hypercholesterolaemia in dogs with Cushings?

A

Lipid catabolism by increased production of cortisol

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9
Q

What are the treatments for Cushings?

A

Trilostane (aka Vetoryl) blocks adrenal synthesis of glucocorticoids (cortisol).

Hypophysectomy is surgical removal of the pituitary gland.

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10
Q

What are the general signs of Cushings in dogs?

A

Increased appetite (excess cortisol), weight gain, alopecia, thin skin, skin/UTIs (decr immune system - cortisol), muscle weakness (protein catabolism), panting (respiratory muscle weakness, hepatomegaly, stress), PU/PD (inhibition of ADH), hypertension (excess cortisol - SNS), anxiety, lethargy, facial nerve damage - facial drooping.

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11
Q

Prior to GA, should trilostane (Vetoryl) be administered in a patient with Cushings?

A

NO - Trilostane should be withheld the previous 24 hrs to avoid risk of HYPOcortisolaemia under GA leading to hypotension and the inability of the body to react to stressors under GA.

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12
Q

What are some anaesthetic considerations for dogs with Cushings?

A

Hypertension, hypoventilation (hypoxaemia/hypercapnia), thromboembolism, further SNS stimulation, prolonged recovery.

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13
Q

What are the anaesthesia drug considerations for dogs with Cushings?

A

Avoid long acting drugs such as ACP. Avoid SNS stimulating drugs such as ketamine, anticholinergics, alpha-2 agonists. Avoid heavily hepatically metabolised drugs such as diazepam (less so midazolam). Avoid NSAIDs. Avoid etomidate. Propofol is good for induction - less hepatic metabolism. Avoid etomidate as it may ‘go the other way’ and cause a significant drop in cortisol.

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14
Q

What causes Addisons?

A

Primarily due to immune destruction of adrenal cortex. Secondary hypoadrenocorticism is reduced production of ACTH from the pituitary - this effects cortisol production primarily.

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15
Q

Common signs of Addisons in dogs?

A

PU/PD, V+ & D+, anorexia, weight loss, impaired renal perfusion, anaemia, lethargy, muscle weakness, electrolyte imbalances (incr K+/decr Na+), hyperchloraemic acidosis.

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16
Q

What is the cause of PU/PD in dogs with Addisons?

A

Reduced aldosterone production leads to increased losses of Na+ and water.

17
Q

What are the causes of hypotension in dogs with Addisons?

A

Reduced production of both cortisol and aldosterone. Cortisol stimulates SNS - affecting blood vessels and heart function. Aldosterone regulates BP through retaining Na+ and water.

18
Q

What causes anaemia in dogs with Addisons?

A

If there is renal insufficiency due to reduced perfusion (hypovolaemia/hypotension) because kidneys produce erythropoietin which stimulates RBC production in the bone marrow.

19
Q

What is the cause of muscle weakness in dogs with Addisons?

A

Hyponatraemia (due to loss of Na+ with decreased aldosterone) because Na+ ions are involved in nerve impulse transmission, therefore muscle function.

20
Q

What electrolyte imbalances are seen with Addisons?

A

Hyperkalaemia due to increased retention of K+.
Hyponatraemia due to loss of Na+ in urine.
Hyperchloraemia due to balancing out loss of HCO3- in urine.

21
Q

What are the anaesthesia considerations with Addisons?

A

Hyperkalaemia (bradyarrhythmias, prolonged PQRS conduction).
Hypotension (hypovolaemia) affecting renal perfusion.
Hypoventilation (respiratory muscle weakness).
Hyperchloraemic metabolic acidosis.

22
Q

What is the zona glomerulosa?

A

Part of the adrenal cortex that produces aldosterone (mineral corticoid).

23
Q

How is aldosterone produced?

A

Stimulation by angiotensin 2 (part of RAAS) in response to low BP. Aldosterone then retains more Na+ which in turn retains more water due to osmotic pressure.

24
Q

What anaesthesia drug should absolutely not be used in patients with Addisons?

A

Etomidate because it blocks formation of cortisol for 2-6 hours post administration.

25
Q

What test is used to diagnose Addisons?

A

ACTH stimulation test - uses synthetic ACTH to stimulate adrenal cortex to see if cortisol is produced. Blood samples are taken before and after the injection and compared.

26
Q

What serum biochemistry results are often seen with Addisons?

A

Hyperkalaemia, hyponatraemia, hypoalbuminaemia, mild hypercalcaemia and in dehydrated patients, pre renal azotaemia.

27
Q

What is a stress leukogram?

A

A pattern of changes seen in the WBCs of dogs caused by cortisol. I.e changes seen in ill (physiologically stressed) patients.
It is characterised by an increase in mature neutrophils and monocytes (More M & N) and a decrease in lymphocytes and eosinophils (Less L & E).

28
Q

What might the absence of a stress leukogram in a sick dog indicate?

A

A dog with Addisons, as the stress leukogram is caused by cortisol which a dog with Addisons would be lacking. But sick animals would generally have a stress leukogram.

29
Q

What are the signs of an Addisonian crisis?

A

Dehydration, hypotension, bradyarrhythmias, azotaemia and collapse.

30
Q

What is the treatment for Addisonian crisis?

A

Fluid therapy with NACl (not Hartmanns - contains some K+) and monitor electrolytes.

31
Q

Hyperchloraemic metabolic acidosis (HMA) can be associated with dogs with Addisons - what is it?

A

HMA is caused by the loss of HCO3- ions in the urine (PU/PD - lack of aldosterone to retain Na+ & water) leading to more retention of Cl- ions to maintain electrical balance (buffering system). This causes an acidosis because HCO3- buffers H+ ions but Cl- is a bad pH buffer, thus causing an acidosis, termed hyperchloraemic acidosis.

32
Q

What acid-base blood results are typical with Addisons when there is a hyperchloraemic acidosis?

A

Low pH, no anion gap (because the acidosis is not due to an increase in unmeasured anions, but rather more Cl- anions), low bicarbonate.

33
Q

How does cortisol affect cardiac function?

A

By promoting number/responsiveness of beta receptors on the myocardium.

34
Q

Where is antidiuretic hormone (ADH) produced?

A

ADH is produced by the hypothalamus but is stored and released by the pituitary gland.