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For the chapter in the Wells Handbook, please go to Chapter 18. Adrenal Gland Disorders.



  • Image not available. Glucocorticoid secretion from the adrenal cortex is stimulated by adrenocorticotropic hormone (ACTH) or corticotropin that is released from the anterior pituitary in response to the hypothalamic-mediated release of corticotropin-releasing hormone (CRH).

  • Image not available. To ensure the proper treatment of Cushing syndrome, diagnostic procedures should (a) establish the presence of hypercortisolism and (b) discover the underlying etiology of the disease.

  • Image not available. The rationale for treating Cushing syndrome is to reduce the morbidity and mortality resulting from disorders such as diabetes mellitus, cardiovascular disease, and electrolyte abnormalities.

  • Image not available. The treatment of choice for both ACTH-dependent and ACTH-independent Cushing syndrome is surgery, whereas pharmacologic agents are reserved for adjunctive therapy, refractory cases, or inoperable disease.

  • Image not available. Pharmacologic agents that may be used to manage the patient with Cushing syndrome include steroidogenesis inhibitors, adrenolytic agents, neuromodulators of ACTH release, and glucocorticoid-receptor blocking agents.

  • Image not available. Spironolactone, a competitive aldosterone-receptor antagonist, is the drug of choice in bilateral adrenal hyperplasia (BAH)–dependent hyperaldosteronism.

  • Image not available. Addison disease (primary adrenal insufficiency) is a deficiency in cortisol, aldosterone, and various androgens resulting from the loss of function of all regions of the adrenal cortex.

  • Image not available. Secondary adrenal insufficiency usually results from exogenous steroid use, leading to hypothalamic–pituitary–adrenal (HPA)–axis suppression followed by a decrease in ACTH release, and low levels of androgens and cortisol.

  • Image not available. Virilism results from the excessive secretion of androgens from the adrenal gland and often manifests as hirsutism in females.

The adrenal glands were first characterized by Eustachius in 1563. After Addison identified a case of adrenal insufficiency in humans, adrenal anatomy and physiology flourished. Most of the work done in the early and mid-1900s centered on the glucocorticoid cortisol. With the discovery of aldosterone by Simpson and Tait in 1952, adrenal pharmacology turned toward the mineralocorticoid. Conn1 followed with his classical description of primary aldosteronism (PA) in 1955, and numerous clinicians and investigators have continued to explore the variety of disease processes promoted through the adrenal gland.


The adrenal glands are located extraperitoneally to the upper poles of each kidney (Fig. 76-1). On average, each adrenal gland weighs 4 g and is 2 to 3 cm in width and 4 to 6 cm in length. The gland is fed by small arteries from the abdominal aorta and renal and phrenic arteries. Drainage of the adrenal gland occurs via the renal vein on the left and the inferior vena cava on the right.

The adrenal medulla occupies 10% of the total gland and is responsible for the secretion of catecholamines. The adrenal cortex accounts for the remaining 90% and is responsible for the secretion ...

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