Clinical Application

Disorders of the Adrenal Cortex

John F. Kennedy's beautiful bronze complexion may have resulted not from sunbathing, but from a disorder of the adrenal glands. When he ran for the presidency in 1960, Kennedy knew he had Addison disease, but his staff kept his secret, for fear it would affect his career. Kennedy had almost no adrenal tissue, but was able to function by receiving mineralocorti-coids and glucocorticoids, the standard treatment.

In Addison disease, the adrenal cortex does not secrete hormones sufficiently due to immune system attack (autoimmunity) or an infection such as tuberculosis. Signs and symptoms include decreased blood sodium, increased blood potassium, low blood glucose level (hypo-glycemia), dehydration, low blood pressure, frequent infections, fatigue, nausea and vomiting, loss of appetite, and increased skin pigmentation. Some sufferers experience salt cravings—one woman reported eating bowls and bowls of salty chicken noodle soup, with pickles and briny pickle juice added! Without treat ment, death comes within days from severe disturbances in electrolyte balance.

An adrenal tumor or oversecretion of ACTH by the anterior pituitary causes hypersecretion of glucocorticoids (primarily cortisol), resulting in Cushing syndrome. It may also result from taking corticosteroid drugs for many years, such as to treat asthma or rheumatoid arthritis. Tissue protein level plummets, due to muscle wasting and loss of bone tissue. Blood glucose level remains elevated, and excess sodium is retained. As a result, tissue fluid increases, blood pressure rises, and the skin appears puffy and thin and may bruise easily.

Adipose tissue deposited in the face and back produce a characteristic "moon face" and "buffalo hump." Increase in adrenal sex hormone secretion may masculinize a female, causing growth of facial hair and a deepening voice. Other symptoms include extreme fatigue, sleep disturbances, skin rashes, headache, and leg muscle cramps.

Treatment of Cushing syndrome attempts to reduce ACTH secretion. This may entail removing a tumor in the pituitary gland or partially or completely removing the adrenal glands.

Both Addison disease and Cushing syndrome are rare, and for this reason, they are often misdiag-nosed, or, in early stages, the patient's report of symptoms is not taken seriously. Addison disease affects thirty-nine to sixty people of every million, and Cushing syndrome affects five to twenty-five people per million. ■

(gluconeogenesis). Glucagon also stimulates breakdown of fats into fatty acids and glycerol.

In a negative feedback system, a low concentration of blood glucose stimulates release of glucagon from the alpha cells. When blood glucose concentration returns toward normal, glucagon secretion decreases. This mechanism prevents hypoglycemia from occurring at times when glucose concentration is relatively low, such as between meals, or when glucose is being used rapidly— during periods of exercise, for example.

The hormone insulin is also a protein, and its main effect is exactly opposite that of glucagon. Insulin stimulates the liver to form glycogen from glucose and inhibits conversion of noncarbohydrates into glucose. Insulin also has the special effect of promoting the facilitated diffusion (see chapter 3, p. 86) of glucose through the membranes of cells bearing insulin receptors. These cells include those of cardiac muscle, adipose tissues, and resting skeletal muscles (glucose uptake by exercising skeletal muscles is not dependent on insulin). Insulin ac tion decreases the concentration of blood glucose, promotes transport of amino acids into cells, and increases protein synthesis. It also stimulates adipose cells to synthesize and store fat.

An enzyme called glucokinase enables beta cells to "sense" glucose level, important information in determining rates of synthesis of glucagon and insulin. One form of a rare type of diabetes mellitus, maturity-onset diabetes of the young (MODY), is caused by a mutation in a gene encoding glucokinase—the beta cells cannot accurately assess when they must produce insulin. Other genetic mutations that cause MODY alter insulin's structure, secretion, or cell surface receptors, or the ability of liver cells to form glycogen in response to insulin. MODY is treated with drugs or dietary modification.

A negative feedback system sensitive to the concentration of blood glucose regulates insulin secretion.

Common bile duct

Common bile duct

Bile Duct Small Intestines

Small intestine

Islet of Langerhans

Hormone-secreting islet cells

Figure

Small intestine

Islet of Langerhans

Hormone-secreting islet cells

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