Apparent mineralocoicoid excess is d/t

D i.e. 11 13 hydroxysteroid dehydrogenase Apparent mineralocoicoid excess is d/t inhibition or absence of /V hydroxysteroid dehydrogenase type 2Q AME syndrome & 11 HSD type 2 Invitro (in lab), the mineralocoicoid receptor has much higher affinity for glucocoicoids than the glucocoicoid receptor does, & glucocoicoids are present in large amount in body (vivo). But binding of glucocoicoids to mineralocoicoid receptor (& so production of mineralcoicoid effects by glucocoicoids) is prevented by presence of 11 3 hydroxyl steroid dehydrogenase tye 2 enzyme in mineralocoicoid sensitive tissues. This enzyme leaves aldosterone untouched, but conves coisol to coisone & coicosterone to its 11 oxy derivatives. These 11 oxy derivatives do not bind to receptor. If 11 hydroxysteroid dehydrogenase type 2 is congenitally absent or inhibited by prolonged ingestion of licorice (containing glycyrrhetinic), coisol has marked mineralocoicoid effects resulting in apparent mineralocoicoid excess (AME syndrome. Patient with AME have clinical picture of hyper aldosteronism because coisol is acting on their mineralo coicoid receptors, & their plasma aldosterone levels and plasma rennin activity is low.