Low plasma renin that fails to increase w/ volume depletionģ. Plasma Aldo (PA)/plasma renin activity (PRA) > 25Ģ. hypokalemia Diagnosis of Primary Aldosteronism, Three criteria 1. Hyperaldosteronism Isolated hypoaldosteronism Caused by adrenal gland destruction, chronic heparin therapy, unilateral adrenalectomy, & G-layer enzyme deficiencies-most often occurs in patients with mild renal insufficiency Hyperaldosteronism Can lead toģ. Aldo acts on kidney to increase blood pressure.ĥ. G-cells convert cholesterol to pregnenolone, & then into Aldo.ģ. An inherited family of enzyme disorders causing decreased cortisol & aldosterone (Aldo) productionĢ. Evaluation of adrenal function requires measuring relevant adrenal hormones, metabolites, & regulatory secretagogues Metabolic alkalosis Increased biocarbonate (HCO3)-caused by prolonged vomiting diuretic use, hypokalemia ** Aldosterone acts on the tubules of the kidneys to increase sodium retention and water retention = increased blood pressure Congenital Adrenal Hyperplasia 1. Secretagogues a substance that promotes secretion Decreased activity of any enzymes required for biosynthesis can occur as an acquired or inherited trait.

Rate limiting step is the process which determines the reaction rate. Conversion of cholesterol to pregnenolone is a rate-limiting* step in steroid biosynthesis. Evaluation of adrenal function requires measuring relevant adrenal hormones, metabolites, & regulatory secretagogues**.

Decreased activity of any enzymes required for biosynthesis can occur as an acquired or inherited trait.ĥ. Conversion of cholesterol to pregnenolone is a rate-limiting* step in steroid biosynthesis.Ĥ. Only free cholesterol can enter steroidogenic pathways in response to ACTH.ģ. All adrenal steroids are derived by sequential enzymatic conversion of a common substrate, cholesterol.Ģ. Sulfate DHEA to DHEA-S Cortex Steroidogenesis 1. Zona Reticularis, R-Zone (Adrenal gland) Cells (inner 10%)

Adrenal gland function ppt