ok let's clarify...
HYPER-ALDOSTERONE:
1- An increase in Aldosterone stimuli in Collecting Tubule ;
a) Principal Cell:
--- increase Na+ and H20+ reabsorption--> leading to HYPERVOLEMIA and HYPERTENSION
--- increase K+ secretion --> leading to HYPOKALEMIA
B) INTERCALATED CELL:
--- increase H+ secretion --->leading to ALKALOSIS(METABOLIC ALKALOSIS), NOT metabolic acidosis.
2- DECREASE RENIN due to negative feedback inhibition or by ANP in Aldosterone Escape Phenomenon.
3- INCREASE IN CORTISOL
--- due to a compensatory mech to help with the blood pressure control or if low ACTH levels are present.
*** in Cushing Syndrome--> INCREASE CORTISOL leads to Adrenal Hyperplasia, shutting down ACTH by negative feedback. The Adrenal Hyperplasia/tumor/CA will eventually results in the Hyperaldosterone mech... BUT the primary cause is not really the oversecretion of Aldosterone but will acts very similar.
>>> in Pseudo-Hyper-Aldosteronism
same lab findings will be present just that Aldosterone could be normal b/c the problem is not really with Aldosterone oversecretion.
>>Example; Liddle's Syndrome -> the problem is in Na+ channels in the Collecting Tubules that cannot be controlled, thus elevated NA+ and H20+ reabsorption acting like over-Aldosterone stimuli.
Hope this can help, as Endocrine physio is a little tricky to be honest.
and BTW: feel free to debate, we are not machines, thus is impossible to know everything, but " 3 minds think better than just one"
