Lecture 22 - Steroid Abnormalities Flashcards
Low glucose?
hypoglycaemia, glucocorticoid deficiency (cortisol)
High potassium?
hyperkalaemia, mineralcorticoid deficiency (aldosterone)
Mechanisms of glucocorticoid (cortisol) deficiency?
hyponatraemia (loss of cortisol driven ADH inhibition), hypoglycaemia (loss of gluconeogensis), hypotension (loss of cortisol effect on vascular tone)
Mechanisms of mineralcorticoid (aldosterone) deficiency?
hyponatraemia (urine Na+ loss with intravascular volume contraction), hyperkalaemia (reduced K excretion), metabolic acidosis (reduced renal H+ excretion)
Aldosterone homeostasis?
Angiotensin II + ACTH + K stimulate aldosterone production by adrenal cortex to increase sodium, water and therefore intravascular volumeq
Types of adrenal failure?
primary (adrenal gland) and secondary (hypothalamus/pituitary)
Identifying primary adrenal failure?
increased ACTH due to lack of cortisol for negative feedback
Primary Adrenal Failure/A good tan?
lack of cortisol inhibition leads to increased POMC leading to increased ACTH and MSH (ATCH contains alpha-MSH also), increase of these products leads to pigmentation
Simple obesity?
signs around 3-4yr, taller as kids but reverted to normal height in puberty due to glucocorticoid excess
Other signs of glucocorticoid excess?
moon face, thinning skin, myopathy, androgen excess, hypertension, glucose intolerance
Cortisol and receptor affinity?
equalt to glucocorticoid and mineralcorticoid, no mineralcorticoid effects due to rapid metabolism, effects occur in excess cortisol
Partial loss of function of glucocorticoid receptor?
Glucocorticoid resistance - high cortisol, hypokalaemia, hypotension, hyperandrogenism, fatigue
Loss of function of mineralcorticoid receptor?
Pseudohypoaldosteronism - high aldosterone and renin, high K and low Na, depleted ECF
ACTH receptor loss of function mutation?
severe cortisol deficiency from birth - hypotension, low Na, hypoglycaemia
XX karyotype leading to male phenotype?
defect in 21 hydroxylase -> lowered cortisol synthesis -> high ACTH -> high adrenal precursors and hyperplasia