Adrenal gland disorders Flashcards
What are the three areas of the adrenal cortex? what do they secrete?
Zona glomerulosa:
-mineralocorticoids (aldosterone, causes reabsoprtion of sodium and excretion of potassium)
Zona fasciculata:
-glucocorticoids (cortisol)
Zona reticularis:
- glucocorticoids
- sex steroids
How is the adrenal medulla innervated? what does it secrets?
Central core of adrenal gland
- innervated by pre-synaptic fibres from SNS
- neuroendocrine (chromaffin) cells secrete catecholamines
What are the primary causes for adrenocortical insufficiency (low adrenal cortex hormones)? split into chronic and acute
Chronic:
- addisons (most common primary cause adrenal insufficiency)
- congenital adrenal hyperplasia
- adrenal TB
- Met.s
Acute:
- rapid withdrawal of steroids
- crisis in those with chronic adrenal insufficiency
- massive haemorrhage into adrenals
what are the secondary causes for adrenocortical insufficiency? (lack ACTH)
- Pituitary/hypothalamus disease
- exogenous steroid use
What are the primary causes of aldosteronism (high aldosterone levels)
Adrenal adenoma (conn's syndrome) Bilateral adrenal hyperplasia (commonest cause)
What are the secondary causes of aldosteronism (high aldosterone levels)
- increased renin
- decreased renal perfusion
- hypovolaemia
- pregnancy
What are the causes for adrenal cortex hormones to be high?
- cushings syndrome
- congenital adrenal hyperplasia (high androgens but low cortisol)
- acquired adrenocortical hyperplasia (endogenous ACTH prod.)
- adrenocortical carcinoma (rare, likely to be functional)
What tumours occur in the adrenal medulla?
- phaeochromocytoma
- neuroblastoma
What is addison’s disease? what is it assoc. with?
Autoimmune destruction of the adrenal cortex
-assoc. with other autoimmune disease
What are the clinical features of addisons disease?
¥ Anorexia, weight loss ¥ Fatigue/lethargy ¥ Dizziness and low BP ¥ Abdominal pain, vomiting, diarrhoea Skin pigmentation (as high ACTH levels)
How is adrenal insufficiency diagnosed?
‘Suspicious biochemistry’:
¥ Na low , high K
¥ hypoglycaemia
SHORT SYNACTHEN TEST:
¥ Measure plasma cortisol before and 30 minutes after iv ACTH injection
¥ Normal: baseline >250nmol/L, post ACTH >480
ACTH levels:
¥ Should be high (causes skin pigmentation)
There is no cortisol being produced so this acts on the anterior pituitary to stimulate ACTH production and it acts on the hypothalamus to stimulate CRH production. You give a synacthen test as this should stimulate cortisol production with normal adrenal glands. If cortisol does increase there could be a problem elsewhere
What is the management of primary adrenal insufficiency?
¥ Do not delay treatment to confirm diagnosis ¥ Hydrocortisone as cortisol replacement ¥ If unwell, give intravenously first ¥ Usually 15-30mg daily in divided doses ¥ Try to mimic diurnal rhythm ¥ Fludrocortisone as aldosterone replacement ¥ Careful monitoring of BP and K ¥ Need education ¥ ‘sick day rules’ ¥ Cannot stop suddenly ¥ Need to wear identification
What is the difference in clinical features of secondary adrenal insufficiency to primary? what is the management of secondary adrenal insufficiency?
clinical features are similar to addisons but
• Skin is pale as no increase in ACTH
• aldosterone production intact as is regulated by RAS pathway
Treatment:
• Hydrocortisone replacement (fludrocortisone is not necessary)
What is primary aldosteronism? what does this cause?
¥ Autonomous production of aldosterone independent of its regulators (angiotensin II/potassium)
¥ Commonest secondary cause of hypertension
What are the clinical features of aldosteronism?
¥ Significant hypertension
¥ Hypokalaemia (in around 30%)
¥ Alkalosis
