Thus, in primary adrenal insufficiency, the combined effects of glucocorticoid and mineralocorticoid deficiency lead to orthostatic hypotension, hyponatremia, hyperkalemia, and a mild metabolic acidosis. Mineralocorticoid deficiency is clinically manifested through isosmotic dehydration, leading to hyponatremia, hyperkalemia, and metabolic acidosis. 30 Thus, glucocorticoid deficiency is clinically manifested as ACTH-mediated hyperpigmentation (if the hypothalamo-pituitary unit is normal), hypotension characterized by tachycardia, reduced stroke volume, decreased peripheral vascular resistance, and (in some cases) hypoglycemia. 24,29 Mineralocorticoid modulates the renal handling of sodium, potassium, and hydrogen ions, in effect promoting sodium retention at the expense of potassium and hydrogen excretion. Glucocorticoid modulates ACTH secretion, 23,24 maintains cardiac contractility, 25-27 modulates vascular response to the β-adrenoceptor agonists, 28 and is involved in hepatic glucose metabolism.

The actions of each class of steroid that have a role in the clinical syndromes of adrenal insufficiency, however, are limited in number. The actions and mechanisms of action of glucocorticoids and mineralocorticoids are treated extensively elsewhere in this text. This difference underlies the relatively different clinical presentations of primary and secondary adrenal insufficiency. In secondary adrenal insufficiency, however, only cortisol is deficient, because the adrenal gland is normal in this condition, and aldosterone is regulated primarily by the renin-angiotensin system, which is independent of the hypothalamus and the pituitary. The two major adrenal steroids that play an important role in the syndromes of adrenal insufficiency are cortisol and aldosterone both are usually deficient in primary adrenal insufficiency. Secondary adrenal insufficiency is caused by disordered function of the hypothalamus and pituitary gland and is characterized by a low cortisol production rate and a normal or low plasma ACTH concentration. A low cortisol production rate and a high plasma ACTH concentration characterize the condition. Primary adrenal insufficiency (Addison’s disease) is caused by disordered adrenal function. Bornstein, in Endocrinology: Adult and Pediatric (Seventh Edition), 2016 PathogenesisĪdrenal insufficiency can be categorized into two types, depending on the locus of the pathologic lesion causing the disorder.

Hyper adrenaline disorder