Adrenocorticosteroids glucocorticoids

The adrenocorticosteroids have several important physiologic and pharmacologic functions. The glucocorticoids (cortisol, corticosterone) are primarily involved in the control of glucose metabolism and the body s ability to deal with stress. Glucocorticoids have other attributes, such as their ability to decrease inflammation and suppress the immune system. Mineralocorticoids, such as aldosterone, are involved in maintaining fluid and electrolyte balance in the body. 

Adrenocorticosteroids The group of steroid hormones produced by the adrenal cortex. These drugs include the glucocorticoids (cortisol, cortisone), min-eralocorticoids (aldosterone), and sex hormones (androgens, estrogens, progestins). 

The toxicity of therapeutic doses of ACTH resembles that of the glucocorticoids (see Chapter 39 Adrenocorticosteroids Adrenocortical Antagonists), with the added adverse effect of hyperandrogenism in women. The occasional development of antibodies to animal ACTH or to depot cosyntropin (a preparation not currently available in the USA) has produced anaphylactic reactions or refractoriness to ACTH therapy in a few individuals. Painful swelling occurs at the injection site more often with the zinc hydroxide depot preparation than with the gelatin preparation. Contraindications are similar to those of glucocorticoids. When immediate effects are desired, glucocorticoids are preferable. 

The toxicity of high-dose, long-term glucocorticoid therapy can be severe and is discussed in Chapter 39 Adrenocorticosteroids Adrenocortical Antagonists. 

Side effects of glucocorticoids are reviewed in Chapter 39 Adrenocorticosteroids Adrenocortical Antagonists. 

Several relatively common disorders result in aldosterone secretion abnormalities and aberrations of electrolyte status. In Addison s disease, the adrenal cortex is often destroyed through autoimmune processes. One of the effects is a lack of aldosterone secretion and decreased Na+ retention by the patient. In a typical Addison s disease patient, serum [Na+] and [CL] are 128 and 96 meq/L, respectively (see Table 16.2 for normal values). Potassium levels are elevated, 6 meq/L or higher, because the Na+ reabsorption system of the kidney, which is under aldosterone control, moves K+ into the urine just as it moves Na+ back into plasma. Thus, if more Na+ is excreted, more K+ is reabsorbed. Bicarbonate remains relatively normal. The opposite situation prevails in Cushing s disease, however, in which an overproduction of adrenocorticosteroids, especially cortisol, is present. Glucocorticoids have mild mineralocorticoid activities, but ACTH also increases aldosterone secretion. This may be caused by an oversecretion of ACTH by a tumor or by adrenal hyperplasia or tumors. Serum sodium in Cushing s disease is slightly elevated, [K+] is below normal (hypokalemia), and metabolic alkalosis is present. The patient is usually hypertensive. A more severe electrolyte abnormality is seen in Conn s syndrome or primary aldosteronism, usually caused by an adrenal tumor. Increased blood aldosterone levels result in the urinary loss of K+ and H+, retention of Na+ (hypernatremia), alkalosis, and profound hypertension. 

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