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  • image 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 To ensure the proper treatment of Cushing’s syndrome, diagnostic procedures should (a) establish the presence of hypercortisolism and (b) discover the underlying etiology of the disease.
  • image The rationale for treating Cushing’s syndrome is to reduce the morbidity and mortality resulting from disorders such as diabetes mellitus, cardiovascular disease, and electrolyte abnormalities.
  • image The treatment of choice for both ACTH-dependent and ACTH-independent Cushing’s syndrome is surgery, whereas pharmacologic agents are reserved for adjunctive therapy, refractory cases, or inoperable disease.
  • image Pharmacologic agents that may be used to manage the patient with Cushing’s syndrome include steroidogenesis inhibitors, adrenolytic agents, neuromodulators of ACTH release, and glucocorticoid-receptor blocking agents.
  • imageSpironolactone, a competitive aldosterone receptor antagonist, is the drug of choice in bilateral adrenal hyperplasia (BAH)–dependent hyperaldosteronism.
  • image Addison’s 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 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 Virilism results from the excessive secretion of androgens from the adrenal gland and often manifests as hirsutism in females.

On completion of this chapter, the reader will be able to:

  1. Describe the roles of the various zones of the adrenal cortex in hormone synthesis.

  2. Explain the regulation of glucocorticoid, adrenal androgen, and mineralocorticoid secretion.

  3. Describe and differentiate the various etiologies of Cushing’s syndrome.

  4. Interpret the results of lab tests used to diagnose Cushing’s syndrome.

  5. Compare and contrast therapeutic regimens for treatment of Cushing’s syndrome, based on the etiology of the disease in a particular patient.

  6. Discuss the methods of, and rationale behind, steroid replacement in the treatment of adrenal adenoma.

  7. Explain the difference between primary and secondary aldosteronism.

  8. Interpret the results of lab tests used to diagnose primary aldosteronism.

  9. Recommend a therapeutic regimen for treatment of primary aldosteronism, based on the etiology of the disease in a particular patient.

  10. Compare and contrast the symptoms and presentation of patients with primary and secondary adrenal insufficiency.

  11. Construct a treatment plan for a patient with acute adrenal insufficiency.

  12. Describe how specific enzyme deficiencies lead to congenital adrenal hyperplasia.

  13. List several options for the treatment of hirsutism.

  14. Discuss some of the potential side effects of systemic glucocorticoid use, and how the risk of developing these side effects may be minimized.

  15. Recommend appropriate counseling points for a patient initiating long-term glucocorticoid therapy.

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 ...

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