ENI - Hypoadrenocorticism Flashcards
What are the physiological effects of glucocorticoids?
- Increase gluconeogenesis and glycogenolysis
- Stimulate proteolysis and lipolysis
- Fight or flight/stress
Describe the control of aldosterone release
- RAAS
- Renin release stimulated by baroreceptors in wall of afferent arteriole, macula densa cells stimulated by reduction of Cl delivery and cardiac and arterial baroreceptors
- Drop in BP stimulates renin secretion
- Renin released, converts angiotensinogen to angiotensin I and then to angiotensin II
- Angiotensin II potent vasoconstrictor and stimualtes release of aldosterone from adrenal cortex
Where is aldosterone released from?
Zona glomerularis of adrenal cortex
Describe aldosterone function
- Central role in BP regulation
- Increases reabsorption of Na, Cl and hence water and distal tubule and collecting duct
- Stimulates secretion of K+ into tubular lumen
- Stimulates secretion of H+ in exchange for K+ in collecting tubules (acid base balance)
- Some vasoconstrictor properties
What is the name given to primary hypoadrenocorticism?
Addison’s disease
Describe primary hypoadrenocorticism
- Deficiency of glucocorticoids and mineralocorticoids
- Loss of 85-90% of adrenal cortex
- May be immune mediated destruction of adrenal gland, likely autoimmune
- Destruction of glomerulosa and fasciculata, may spare reticularis
- Aggressive management as corticosteroids are essential for life
Give causes of primary hypoadrenocorticism in dogs
- Idiopathic: probably immune mediated destruction
- Iatrogenic: drugs (drugs used to manage Cushing’s) or surgery (bilateral adrenalectomy)
Describe secondary hypoadrenocorticism
- Deficiency of ACTH
- Only cortisol deficient (electrolytes normal)
- Rare
- Pituitary (sometimes hypothalamic lesion) leading to reduced/absent ACTH
- Only affects glucocorticoid production
- mineralocorticoid function preserved
What can be an effect of aldosterone deficiency?
Electrolyte imbalances
Outline iatrogenic hypoadrenocorticism
- Exogenous steroids leading to adrenal atrophy (neg feedback, loss of stimulation, sudden removal means unable to produce enoguh quickly)
- Cortisol deficiency only
- May have signs of Cushing’s syndrome
- Can be life threatening
Describe the signalment of canine hypoadrenocorticism
- Younger females (4-6 years, 70% females)
- Some breed predispositions: standard poodles, bearded collies, Portugese water dog, Leonberge, great Dane, Rottweiler, WHWT, soft coated wheaten terrier
- Extremely rare in cats
Describe the signs of aldosterone deficiency
- Loss of Na, Cl, H2O
- Retention of K+, H+
- Pre-renal renal failure
- Failure to retain water
- Electrolyte imbalances, dehydration, hypovolaemia
Describe the signs of glucocorticoid deficiency
- Decreased stress tolerance (no stress response of immune cells)
- Gastrointestinal signs
- Weakness
- Appetite loss
- Anaemia
- Impaired gluconeogenesis
Describe the clincal signs of chronic hypoadrenocorticism
- Waxing waning with non-specific signs
- Worsened by stress
- Anorexia, vomiting, diarrhoea, PUPD, weakness, lethargy, depression
- Often appear normal between bouts, esp after fluid therapy or steroids
- GI signs common
- Cannot cope with additional stress e.g. long walk,concurren disease, increased acitivty that day
- Chronically losing sodium so unable to concentrate tubular fluid
Describe the clinical signs of acute hypoadrenocorticism
- Crisis, marked hypovolaemia and azotaemia
- Collapsed, close to death, extremely weak
- Recent history of vomiting/diarrhoea, may be fresh or digested bloof present
- Hypovolaemic shock
- Paradox bradycardia
- Abdominal pain
