020215 hyperaldosteronism, pheochr

Question 1

aldosterone has what effects?

Answer 1

renal water and sodium retention

potassium and H+ excretion

Question 2

primary hyperaldosteronism

Answer 2

adrenal adenoma autonomously produces aldosterone

Question 3

what levels of hormones are observed with primary hyperaldosteronism?

Answer 3

increased aldosterone (causing increased BP and hypokalemia)
decreased renin

Question 4

when should you consider testing for primary hyperaldosteronism

Answer 4

HTN and hypokalemia
resistant HTN
adrenal incidentaloma and HTN
onset of HTN at young age
severe HTN
whenever considering secondary HTN

Question 5

how do you test for primary hyperaldosteronism

Answer 5

measure ratio of plasma aldosterone to plasma renin (renin activity or concentration)–the ratio should be increased, and there should be potassium depletion

Question 6

what ratio of plasma aldosterone concentration to plasma renin activity is suggestive of primary hyperaldosteronism?

Answer 6

over 20

Question 7

causes of primary hyperaldosteronism

Answer 7

aldosterone-secreting adrenocortical adenoma

bilateral hyperplasia of zona glomerulosa

Question 8

causes of secondary hyperaldosteronism

Answer 8

anything that decreases BP/volume

renal ischemia
decreased intravascular volume (CHF, diuretics, hypoproteinemic states), sodium wasting disorders (chronic renal failure)

Question 9

what should you do for the pt whom you suspect has primary hyperaldosteronism

Answer 9

biochem first-ratio of plasma aldosterone to plasma renin

then do a CT or MRI. if it’s a unilateral adrenal tumor, do adrenalectomy. if they are bilaterally abnormal or normal adrenals, do selective venous catheterization for aldosterone and cortisol-if unilaterally has increased aldosterone, do adrenalectomy. if both have hyperfxn or if fail to localize, then do medical management.

Question 10

tx for bilateral adrenal disease

Answer 10

mineralocroticoid receptor antagnosists (spironolactone and eplerenone)

Question 11

11beta HSD2

Answer 11

converts cortisol to cortisone so that kidney is protected from cortisol binding to mineralcorticoid receptor

Question 12

PNMT is expressed much more where?

Answer 12

in adrenal medulla than sympathetic nerves so that NE is primary product of SNS whereas epinephrine is primary product of adrenal medulla

Question 13

pheochromocytoma

Answer 13

tumor of chromaffin cells of adrenal medulla

Question 14

paragangliomas

Answer 14

tumors outside of the adrenal gland; arise from ganglia of the sympathetic nervous system

Question 15

what is secreted by pheocrhomocytomas

Answer 15

epinephrine and NE

Question 16

what is secreted by paragangliomas and metastases of pheochromocytomas

Answer 16

primary NE

Question 17

catechoalminae excess-clinical manifestations

Answer 17

–increased HR (palpitations)
–increased contractility (angina)
–arteriolar constriction, causing HTN
–venoconstriction, causing decreased plasma volume (dizziness, orthostatic hypotension, circulatory collapse)
–suppression of insulin release
–increased glucose output from liver
etc

Question 18

biochemical tests to determine whether pt has pheochromocytoma

Answer 18

24 hour urinary tests for catecholamines
or
plasma tests for free metanephrines (metabolites of NE and E)

Question 19

what tests should you do for suspected pheochromocytoma?

Answer 19

first, biochemical test

then imaging: CT or MRI
for CT (131 I-MIBG nuclear medicine test or somatostatin radionuclide)

Question 20

tx for pheochromocytoma

Answer 20

surgical:
first, alpha blockade (phenoxybenzamine)–treat to normal BP or orthostasis

second, beta adrenergic blockade to treat tachycardia

then appropriate hydration
then surgical adrenalectomy