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Addison’s Disease

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Addison’s disease is named after Dr. Thomas Addison (1793-1860) and is caused by a lack of aldosterone and cortisol production due to primary adrenocortical insufficiency. Aldosterone is a steroid hormone of the adrenal cortex that functions in the regulation of blood pressure and the salt and water balance of the body. Cortisol helps the body respond to stress, maintains blood pressure and cardiovascular function, regulates energy and metabolism of proteins, carbohydrates, and fats, maintains arousal and a sense of well being, and modulates neuronal and immune-cell function. The symptoms of Addison’s disease include fatigue, nausea, abdominal pain, weight loss, low blood pressure, darkening of the skin, and salt craving. Addison’s disease is actually a clinical syndrome by which its signs and symptoms characterize primary adrenal failure. Addison’s disease can occur after tuberculoses or by any malignant disease which causes damage to the adrenal glands and inhibits their ability to produce cortisol. Inadequate secretion of adrenocorticotropic hormone (ACTH) by the pituitary gland will also cause a cortisol deficiency. Addison’s disease can prove tricky for doctors to diagnose. Aside from a pattern of symptoms in a patient’s medical history and the telltale dark tanning of the skin, Addison’s disease is primarily diagnosed through a series of biochemical lab tests. These tests include the measuring of blood pressure, serum sodium and potassium, cortisol, ACTH, serum aldosterone, serum thyroid stimulating hormone (TSH), and total thyroxine (T4). X-ray exams of the pituitary and adrenal glands are also performed to check for abnormalities. To treat Addison’s disease, one must substitute adequate doses of the hormones that the adrenal glands are failing to produce. Cortisol is replaced with 15-25 mg of hydrocortisone (a synthetic glucocorticoid)

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