Editing Adrenal: Hyperaldosteronism (section)

=== Primary ===

* '''<span style="color:#ff0000">Aldosterone secretion is independent of the RAAS'''
** '''<span style="color:#ff0000">Renin levels are suppressed'''
* '''<span style="color:#ff0000">Can lead hypokalemia, hypomagnesemia, alkalosis, fluid depletion or retention, refractory hypertension, cardiac dysfunction and arrhythmias'''
** '''Hypernatremia does not occur because sodium reabsorption is accompanied by water uptake, thereby maintaining isotonicity.'''
** '''<span style="color:#ff0000">Most patients are normokalemic'''
*** Although hypokalemia has been classically described as a common finding in primary aldosteronism, '''only 9-37% of newly diagnosed patients are hypokalemic'''
** Hypertension secondary to hyperaldosteronism is associated with an increased risk of end-organ damage compared with essential hypertension
* '''<span style="color:#ff0000">Causes (8):'''
*# '''Bilateral hyperplasia (60%), also referred to as idiopathic hyperplasia''';
*#* Clinically, patients with bilateral adrenal hyperplasia have less severe hypertension and are less likely to be hypokalemic compared with patients with aldosterone-producing adenomas
*# '''Aldosterone-producing adrenal adenoma (35%)'''
*# '''Unilateral adrenal hyperplasia (2%)'''
*# '''Aldosterone-producing adrenal cortical carcinoma  (<1%)'''
*# '''Ectopic aldosterone-producing tumour (<1%)'''
*# '''Familial hyperaldosteronism I (<1%)'''
*#* '''Aldosterone production is mediated by ACTH in familial hyperaldosteronism type I'''
*# '''Familial hyperaldosteronism II (<1%)'''
*# '''Familial hyperaldosteronism III (<1%)'''