Clinical Features

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The clinical manifestations of chronic adrenal insufficiency develop gradually with subtle signs and symptoms that provide a diagnostic challenge. The clinical presentation of Addison's disease can be explained on the basis of a deficiency of cortisol and aldosterone and a lack of feedback suppression of ACTH and MSH.

Cortisol deficiency manifests clinically with anorexia, nausea, vomiting, lethargy, hypoglycemia with fasting, and inability to withstand even minor stresses without shock. The ability to excrete a free water load is also impaired and can lead to water intoxication. Lack of aldosterone results in impaired ability to conserve sodium and excrete potassium. The patient with aldosterone deficiency presents with sodium depletion, dehydration, hypotension, postural syncope, and decreased cardiac size and output. Renal blood flow is decreased, and azotemia may develop. Hyperkalemia is commonly seen but rarely is severe. Lack of suppression of ACTH and MSH secretion occurs because of deficient cortisol levels and results in increased pigmentation.

The overall clinical picture of a patient with Addison's disease is that of one who is weak and lethargic, with loss of vigor, and fatigue on exertion. The patient may have a feeble tachycardic pulse. Postural hypotension and syncope are common. In spite of hypotension, the extremities usually remain warm. Heart sounds may be soft or almost inaudible on auscultation.

Gastrointestinal symptoms are a prominent feature of chronic adrenal insufficiency and include anorexia, nausea, vomiting, weight loss, abdominal pain, and sometimes diarrhea.

Cutaneous manifestations of Addison's disease include increased brownish pigmentation over exposed body areas such as the face, neck, arms, and dorsum of the hands, and over friction or pressure points such as the elbows, knees, fingers, toes, and nipples. Pigmentation of mucous membranes, darkening of nevi and hair, and longitudinal pigmented bands in the nails may be seen. Vitiligo, mucocutaneous candidiasis, and alopecia may occur with Addison's disease that has an autoimmune cause. Women with Addison's disease may exhibit decreased growth of axillary and pubic hair because of adrenal androgen deficiency. This is not seen in men because of adequate testicular androgen.

Mentally these patients vary from alert to confused. Unconsciousness is rare unless the condition is preterminal. The sensory modalities of taste, olfaction, and hearing may be increased. Hyperkalemic paralysis is a rare, emergent complication of adrenal insufficiency; the patient presents with a rapidly ascending muscular weakness which leads to flaccid quadriplegia. Treatment of this complication consists of the intravenous administration of glucose and insulin or bicarbonate.

LABORATORY The usual laboratory findings in patients with primary adrenal insufficiency include hyponatremia, hyperkalemia, hypoglycemia, and azotemia. Hyponatremia is usually mild to moderate, and severe hyponatremia (<120 mEq/L) is rare. Hyperkalemia is usually mild, and the potassium level rarely exceeds 7 mEq/L. Initial potassium levels may be normal or low if protracted vomiting has occurred. Rarely, hyperkalemia may be severe and cause cardiac dysrhythmia or paralysis.

Hypoglycemia is infrequent in adults with chronic adrenal insufficiency in the absence of infection, fever or alcohol ingestion. Moderate elevation of the blood urea nitrogen (BUN) level may occur because of dehydration secondary to aldosterone deficiency. Azotemia is usually reversible with rehydration.

Electrocardiographic changes include flat or inverted I waves, a prolonged QI interval, low voltage, a prolonged PR or QRS interval, and a depressed SI segment. Ihe ECG changes reflective of hyperkalemia may also be present. Ihe chest x-ray film may show a small, narrow cardiac silhouette due to decreased intravascular volume. A flat plate film of the abdomen may show adrenal calcification, which is most commonly due to tuberculosis but may occur with infection or hemorrhage.

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