ADRENAL GLAND

also called Suprarenal Gland, either of two small and virtually identical triangular endocrine glands, one at the upper end of each kidney. The adrenal glands show considerable species variation in size, shape, and nerve supply. In humans each gland averages a weight of about 4.5 g (0.16 ounce) and measures about 25 mm (1 inch) wide, 50 mm (2 inches) long, and 5 mm (0.2 inch) thick. Each gland consists of two parts: an inner medulla, which produces epinephrine and norepinephrine (q.v.), and an outer cortex, which secretes steroid hormones. The two parts are completely different in embryological origin, structure, and function. In almost all other vertebrates, the cells of the two parts are to varying degrees interspersed. In the adult human the outer cortex comprises about 90 percent of the gland. The cortex is made up of three structurally different concentric zones. From the outermost inward, they are zona glomerulosa, zona fasciculata, and zona reticularis. The zona glomerulosa is principally responsible for the secretion of aldosterone. Aldosterone maintains the concentration of sodium, potassium, and chloride in the blood within the narrow limits essential for life. The inner two zones-fasciculata and reticularis-operate almost as a physiological unit and are controlled by the adrenocorticotropic hormone, secreted by the pituitary gland (q.v.). Their principal function is the secretion of cortisol and of some adrenal androgens, or male hormones. Cortisol has two primary roles: (1) gluconeogenesis-i.e., the breakdown of protein to form glucose-and (2) an anti-inflammatory action. It also exerts a potent antiallergic action. Thus cortisol can reduce disease manifestations without having any direct effect on the causative agent. The medulla of the adrenal gland is made up of columnar cells that secrete epinephrine and norepinephrine. These hormones belong to a class of chemicals called catecholamines, which are darkened when oxidized by potassium dichromate. The medulla, therefore, is frequently referred to as chromaffin tissue. Diseases of the adrenal glands may be divided into those of the cortex and those of the medulla. The only known disease of the medulla is a tumour (pheochromocytoma; q.v.) that results in secretion of excessive quantities of epinephrine and norepinephrine. Symptoms are periodic episodes of high blood pressure, palpitation of the heart, sweats, pounding headaches, anxiety, nausea, and vomiting. The symptoms can be successfully treated with medication. Diseases of the cortex may be manifested as hyperfunction (excessive secretion of adrenocortical hormones) or hypofunction (insufficient secretion of such hormones). The latter is known as Addison's disease (q.v.). Adrenocortical hyperactivity may be congenital or acquired; the former always is due to hypertrophy, or enlargement, of both adrenal glands, the latter to either tumour or hypertrophy. Congenital adrenal hypertrophy in the female infant results in masculinization with pseudohermaphroditism; in the male, virilism or sexual precocity occurs. Acquired adrenocortical hyperfunction is manifested by Cushing's syndrome or the adrenogenital syndrome (qq.v.), or both. Cushing's syndrome is characterized by obesity, rounding of the face, amenorrhea, high blood pressure, diabetes, osteoporosis, thinning and easy bruising of the skin, weakness, and often mental disturbances. The adrenogenital syndrome consists of virilizing manifestations in the female and sexual precocity in the preadolescent male. The treatment for adrenal tumour is surgical removal of the affected adrenal gland. The forms of therapy available for acquired nontumorous adrenal hyperfunction with Cushing's syndrome are: (1) irradiation of the pituitary, (2) pituitary irradiation and removal of one adrenal gland, (3) removal of most of the adrenals, (4) total removal of the adrenals, and (5) removal of the pituitary. If both adrenals are removed, the patient must thereafter be maintained on controlled dosages of synthetic cortisol-like and related adrenal steroids. Primary aldosteronism (i.e., the production of excess aldosterone) is a selective form of adrenocortical hyperfunction, usually due to a tumour. The syndrome is characterized by (1) hypertension, (2) reduction in the serum potassium level, (3) an increase in the carbon dioxide content of the blood, (4) evidence of renal damage, (5) an increase in the urinary excretion of potassium, and (6) a considerable increase in the urinary excretion of aldosterone. The clinical manifestations often include tetany, muscle weakness, and passage of large amounts of urine. Successful removal of the adrenal tumour generally results in a reversal of the symptoms. See also endocrine system.