Hyperaldosteronism, Pheochromocytoma Flashcards
(23 cards)
when and from where is renin released?
released from the juxtaglomerular cells when decreases in blood pressure are sensed in the glomerulus
what are the respective functions of renin and ACE?
renin catalyzes angiotensinogen –> angiotensin I
ACE catalyzes angiotensin I –> angiotensin II
how does angiotensin II increase blood pressure? (2)
- vasoconstriction
2. increase aldosterone release from adrenal cortex
function of aldosterone (2) and where it works
- sodium and water reabsorption
- potassium and H+ secretion (loss)
works in distal convoluted tubule
2 major symptoms of hyperaldosteronism
hypertension and hypokalemia
first test after suspicion of primary hyperaldosteronism
plasma aldosterone:renin activity ratio (should be greater than 20)
major difference between primary and secondary hyperaldosteronism
in primary hyperaldosteronism, renin is suppressed, whereas in secondary hyperaldosteronism, renin levels are increased
treatment for hyperaldosteronism caused by bilateral adrenal gland tumors
aldosterone receptor antagonist: spironolactone, eplerenone
Type I AME: pathogenesis
impaired activity of 11beta-HSD2, which usually inactivates cortisol to cortisone –> cortisol accumulates in the kidney and binds to mineralocorticoid receptors and creates a physiological picture similar to hyperaldosteronism
Type I AME: ____tension, ____kalemia, metabolic ____osis, _____ renin activity, _____ aldosterone, and _____ plasma cortisol levels
hypertension; hypokalemia, metabolic alkalosis, low renin activity, low aldosterone, normal plasma cortisol levels
Type I AME: treatment
mineralocorticoid receptor antagonists: spironolactone, eplerenone
Liddle syndrome: pathogenesis
mutations in epithelial sodium channel –> enhanced activity of the sodium channel causing increased sodium reabsorption, potassium wasting, hypertension, and hypokalemia
Liddle syndrome: ____tension, ____kalemia, _____ renin activity, _____ aldosterone, and _____ plasma cortisol levels
hypertension, hypokalemia, low renin activity, low aldosterone, normal plasma cortisol levels
Liddle syndrome: treatment
potassium-sparing diuretics: amiloride and triamterene
- dx: high renin, high aldosterone
2. dx: low renin, high aldosterone
- secondary hyperaldosteronism
2. primary hyperaldosteronism
block the effects of aldosterone at the receptor level (2)
spironolactone and eplerenone
pathogenesis of pheochromocytoma vs. paraganglioma
pheochromocytoma: tumor of chromaffin cells of adrenal medulla
paraganglioma: tumor that arises from extra-adrenal ganglia of the sympathetic nervous system
what are adrenal medullary (chromaffin cells) made of?
modified postganglionic sympathetic nerves that lack axons and secrete their neurotransmitter (mainly epinephrine) directly into the blood
what do pheochromocytomas and paragangliomas respectively secrete? what is responsible for this difference?
pheochromocytomas: epinephrine and norepinephrine
paragangliomas: norepinephrine
cortisol bathes the adrenal medulla and cortisol induces expression of PNMT, which converts norepinephrine into epinephrine
dx: hypertension, sweating, headaches, palpitations
pheochromocytoma
2 diagnostic tests for pheochromocytoma
plasma free metanephrines and urinary catecholamines
best way to image a pheochromocytoma
CT abdomen/adrenal glands
treatment of pheochromocytoma
alpha blockade (phrnoxybenzamine) followed by beta-blockers (prior to tumor resection
