Pathology - ​Addison Disease 
Primary adrenocortical insufficiency (Addison disease) develops when there is diminished secretion of all the adrenal cortical hormones. Diagnostic testing includes a cosyntropin (synthetic ACTH) stimulation test, which fails to trigger cortisol release. Low levels of cortisol induce ACTH release, which is responsible for the increased skin pigmentation due to its structural similarities to melanocyte-stimulating hormone. Low cortisol also decreases the ability to maintain blood glucose and produces fasting hypoglycemia. Low aldosterone levels lead to urinary salt loss and volume depletion, causing hypotension and decreased heart size. A compensatory increase in ADH secretion due to hypovolemia induces water retention and hyponatremia. Lack of cortisol makes hypotension worse due to decrease of vasopressor reactivity of blood vessels. Low aldosterone levels also prevent proper potassium excretion and produces hyperkalemia. Loss of libido and pubic hair (especially in females) occur as a result of decreased circulating adrenal androgens. Addison disease is rare and most instances are caused to autoimmune destruction of the adrenal cortex. Secondary adrenal insufficiency, due to decrease of ACTH secretion, is not associated with any pigmentation changes. In this scenario, aldosterone synthesis is preserved by stimulation from the renin–angiotensin axis. Addison disease is treated with glucocorticoid and mineralocorticoid supplements.