Primary and secondary hyperaldosteronism
Terms in this set (17)
mineralcorticoid produced in zona glomerulosa of the adrenal cortex.
Secreted in response to ↑potassium and ↓sodium levels.
regulated by angiotensin II (āng,renin)
what is the effect of aldosterone?
↑pottassium urinary excretion
↑BP and Na levels
describe primary hyperaldosteronism
characterized by ↑aldosterone without ↑renin secretion.
leads to ↑sodium and water retention and ↑potassium excretion (HTN and alkalosis)
is one of the leading cause of secondary HTN
more common in women.
the ↑ volume leads to ↓renin secretion (and angiotensin II)→helpful in diagnosis
etiology of primary hyperaldosteronism
bilateral adrenal hyperplasia:70%.main cause
Conn syndrome (adrenal adenoma producing aldosterone (30%)
unilateral adrenal hyperplasia 2% cases
how can primary hyperaldosteronism lead to metabolic alkalosis?
when the K+ is sufficiently depleted due to aldosterone,the H+/Na+ pump in the distal nephron become active.
there is a ↑H+ excretion and Na retention.
the H+ is generated mainly from carbonic anhydrase in the renal tubule leading to ↑ bicarbonate production.
the ↑in H excretion and ↑bicarbonate production leads to metabolic alkalosis.
high pH levels also leads to hypocalcemia.
clinical feature of primary hyperaldosteronism?
complications of HTN?
is the edema in primary hyperaldosteronism?
it is not typically associated with edema. (even though it is volume expansoion)
-this is due to spontanous natriuresis and diuresis (aldosterone escape)
-appears to be ANP mediated
-if present,either wrong diagnosis or associated with other complications
inviestigations of primary hyperaldosteronism?lab
beta-blockers,ACEi,spironolactone may interfere with testing;should be stopped up to 6 weeks before.
-24 h urine collection; Na,P,18-hydroxycortisol
-Aldosterone to renin ration
-captopril supression test (if aldo.levels remain unchanges after captoril adm. diagnosis can be made)
-biochemistry: *hypokalemia *hypernatremia * ↑bicarbonate
aldosterone to renin ration
if ratio is <10 ; then investigate causes for secondary hyperaldosteronism
if ratio >20 ; the primary h.ald. is likely
Imaging of primary hyperaldosteronsism?
Abdominal CT; localisation of the tumour if present
Adrenal vein catheterisation ; with measurement of aldosterone (unilateral or bilateral disease)
treatment of primary hyperaldosteronism?
spironolactone ; treat hypokalemia and HTN
amiloride ; blocks Na/K pump
surgery; adrenalectomy is now rarely indicated. surgical removal of tumour if present.
describe secondary hyperaldosteronism
characterised by ↑RAS activation leading to ↑aldosterone secretion
etiology of sec.hyperaldosteronism?
*accelerated HTN and renal stenosis are common
*normotensive causes incl: congestive heart failure, cirrhosis and nephrotic syndrome
*diuretic and laxative use are also causes
*rare: juxtaglomerular tumour and Bartter syndrome
clinical feature of sec.hyperaldosteronism?
-(same as primary)
investiagtions of sec.hyperaldosteronism?
↑renin and ↑aldosterone
aldosterone to renin ration <10
treatment of sec.hy?
focused on treating the underlying cause