Addison's disease

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Addison's Disease



Addison's disease is a disorder involving disrupted functioning of the part of the adrenal gland called the cortex. This results in decreased production of two important chemicals (hormones) normally released by the adrenal cortex: cortisol and aldosterone.


The adrenals are two glands, each perched on the upper part of the two kidneys. The outer part of the gland is known as the cortex; the inner part is known as the medulla. Each of these parts of the adrenal gland is responsible for producing different types of hormones.
Cortisol is a very potent hormone produced by the adrenal cortex. It is involved in regulating the functioning of nearly every type of organ and tissue throughout the body, and is considered to be one of the few hormones absolutely necessary for life. Cortisol is involved in:
  • the very complex processing and utilization of many nutrients, including sugars (carbohydrates), fats, and proteins
  • the normal functioning of the circulatory system and the heart
  • the functioning of muscles
  • normal kidney function
  • production of blood cells
  • the normal processes involved in maintaining the skeletal system
  • proper functioning of the brain and nerves
  • the normal responses of the immune system
Aldosterone, also produced by the adrenal cortex, plays a central role in maintaining the appropriate proportions of water and salts in the body. When this balance is upset, the volume of blood circulating throughout the body will fall dangerously low, accompanied by a drop in blood pressure.
Addison's disease is also called primary adrenocortical insufficiency. In other words, some process interferes directly with the ability of the adrenal cortex to produce its hormones. Levels of both cortisol and aldosterone drop, and numerous functions throughout the body are disrupted.
Addison's disease occurs in about four in every 100,000 people. It strikes both men and women of all ages.

Causes and symptoms

The most common cause of Addison's disease is the destruction and/or shrinking (atrophy) of the adrenal cortex. In about 70% of all cases, this atrophy is believed to occur due to an autoimmune disorder. In an autoimmune disorder, the immune system of the body, responsible for identifying foreign invaders such as viruses or bacteria and killing them, accidentally begins to identify the cells of the adrenal cortex as foreign, and destroy them. In about 20% of all cases, destruction of the adrenal cortex is caused by tuberculosis. The remaining cases of Addison's disease may be caused by fungal infections, such as histoplasmosis, coccidiomycosis, and cryptococcosis, which affect the adrenal gland by producing destructive, tumor-like masses called granulomas; a disease called amyloidosis, in which a starchy substance called amyloid is deposited in abnormal places throughout the body, interfering with the function of whatever structure it is present within; or invasion of the adrenal glands by cancer.
In about 75% of all patients, Addison's disease tends to be a very gradual, slowly developing disease. Significant symptoms are not noted until about 90% of the adrenal cortex has been destroyed. The most common symptoms include fatigue and loss of energy, decreased appetite, nausea, vomiting, diarrhea, abdominal pain, weight loss, muscle weakness, dizziness when standing, dehydration, unusual areas of darkened (pigmented) skin, and dark freckling. As the disease progresses, the patient may appear to have very tanned, or bronzed skin, with darkening of the lining of the mouth, vagina, and rectum, and dark pigmentation of the area around the nipples (aereola). As dehydration becomes more severe, the blood pressure will continue to drop and the patient will feel increasingly weak and light-headed. Some patients have psychiatric symptoms, including depression and irritability. Women lose pubic and underarm hair, and stop having normal menstrual periods.
When a patient becomes ill with an infection, or stressed by an injury, the disease may suddenly and rapidly progress, becoming life-threatening. Symptoms of this "Addisonian crisis" include abnormal heart rhythms, severe pain in the back and abdomen, uncontrollable nausea and vomiting, a drastic drop in blood pressure, kidney failure, and unconsciousness. About 25% of all Addison's disease patients are identified due to the development of Addisonian crisis.

Key terms

Gland — A collection of cells whose function is to release certain chemicals, or hormones, which are important to the functioning of other, sometimes distantly located, organs or body systems.
Hormone — A chemical produced in one part of the body, which travels to another part of the body in order to exert its effect.


Many patients do not recognize the slow progression of symptoms and the disease is ultimately identified when a physician notices the areas of increased pigmentation of the skin. Once suspected, a number of blood tests can lead to the diagnosis of Addison's disease. It is not sufficient to demonstrate low blood cortisol levels, as normal levels of cortisol vary quite widely. Instead, patients are given a testing dose of another hormone called corticotropin (ACTH). ACTH is produced in the body by the pituitary gland, and normally acts by promoting growth within the adrenal cortex and stimulating the production and release of cortisol. In Addison's disease, even a dose of synthetic ACTH does not increase cortisol levels.
To distinguish between primary adrenocortical insufficiency (Addison's disease) and secondary adrenocortical insufficiency (caused by failure of the pituitary to produce enough ACTH), levels of ACTH in the blood are examined. Normal or high levels of ACTH indicate that the pituitary is working properly, but the adrenal cortex is not responding normally to the presence of ACTH. This confirms the diagnosis of Addison's disease.


Treatment of Addison's disease involves replacing the missing or low levels of cortisol. In the case of Addisonian crisis, this will be achieved by injecting a potent form of steroid preparation through a needle placed in a vein (intravenous or IV). Dehydration and salt loss will also be treated by administering carefully balanced solutions through the IV. Dangerously low blood pressure may require special medications to safely elevate it until the steroids take effect.
Patients with Addison's disease will need to take a steroid preparation (hydrocortisone) and a replacement for aldosterone (fludrocortisone) by mouth for the rest of their lives. When a patient has an illness which causes nausea and vomiting (such that they cannot hold down their medications), he or she will need to enter a medical facility where IV medications can be administered. When a patient has any kind of infection or injury, the normal dose of hydrocortisone will need to be doubled.


Prognosis for patients appropriately treated with hydrocortisone and aldosterone is excellent. These patients can expect to enjoy a normal lifespan. Without treatment, or with substandard treatment, patients are always at risk of developing Addisonian crisis.



Williams, Gordon H., and Robert G. Dluhy. "Hypofunction of the Adrenal Cortex." In Harrison's Principles of Internal Medicine, edited by Anthony S.Fauci, et al. New York: McGraw-Hill, 1997.


National Adrenal Disease Foundation. 505 Northern Boulevard, Suite 200, Great Neck, NY 11021. (516) 487-4992.

Addison's disease

a rare syndrome resulting from chronic adrenocortical insufficiency. If there is normal function of the testes and ovaries, the physiologic effects from decreased production of the adrenal sex hormones are minor. The disease may occur as either a primary or a secondary deficit in hormone production. Primary insufficiency is thought to be due to autoimmune disease involving the adrenal glands. Causes include tubercular infection, fungal infections, amyloidosis, and nonsecreting tumors of the adrenal cortex. Secondary causes are related to deficient production of adrenocorticotropic hormone (ACTH), the hormone that triggers the release of hormones from the adrenal cortex, which itself is secreted by the pituitary gland. Underfunctioning of the pituitary, its surgical removal, and certain pituitary tumors can eventually result in a decrease or total absence of ACTH.

Serious and potentially life-threatening problems associated with Addison's disease are fluid and electrolyte imbalance and profound hypoglycemia. Deficiency of mineralocorticoids leads to depletion of sodium (hyponatremia), resulting in depletion of extracellular fluid and potassium retention (hyperkalemia). The patient experiences generalized malaise and muscular weakness, muscle pain, orthostatic hypotension, and vulnerability to cardiac arrhythmias.

Deficiency of cortisol adversely affects blood sugar levels, causing hypoglycemic reactions. Anorexia, nausea, vomiting, flatulence, and diarrhea can also occur. These symptoms, as well as anxiety, mental depression, and loss of mental acuity, are believed to be related to absence of the cyclic peaks of cortisol output that normally occur every 24 hours. Hyperpigmentation of certain areas of the skin occurs only in primary adrenal insufficiency. An insufficient supply of cortisol signals the pituitary gland to secrete more ACTH, which has the effect of increasing the coloration of scars, skin folds, pressure areas, and the areolae of the nipples. Diagnosis of Addison's disease also includes synthetic ACTH stimulation testing.
PatientCare. Treatment of Addison's disease is focused on replacement of the deficient hormones; that is, on administration of exogenous glucocorticoids and mineralocorticoids. Replacement therapy usually brings about a rapid recovery.

Acute nursing care is concerned with intensive support of the patient should there be an addisonian crisis, prevention of problems related to hypoglycemia and orthostatic hypotension, alleviation of gastrointestinal problems, and instruction of the patient in self-care. It includes providing regular feedings throughout the day and providing for adequate rest. When fasting is required for diagnostic studies or surgery, the patient probably will need intravenous feedings of glucose to avoid profound hypoglycemia. Maintenance doses of exogenous glucocorticoids are especially important during fasting. Gastrointestinal problems require attention to adequate nutrition and avoidance of foods that are irritating to the gastrointestinal mucosa and difficult to digest.

The patient's intake and output are measured regularly, and postural blood pressure is checked periodically. The apical-radial pulse is taken along with other vital signs to identify early symptoms of hyperkalemia. Cardiac monitoring may be indicated if cardiac arrhythmias develop. Safety measures must be taken to prevent falls during spells of weakness and fainting that may occur.

Stress, even relatively mild physical and emotional stress, can quickly bring on an addisonian crisis. When this occurs, the physiologic defense provided by cortisol is no longer operating, and the patient suffers from hypotension and eventual circulatory collapse. Absence of mineralocorticoids compounds the problem by depletion of extracellular fluids and impairment of cardiac function. Treatment should be immediately initiated if addisonian crisis is suspected.

A person with Addison's disease usually can lead a fairly normal life with exogenous hormone therapy. Patient education includes instruction in the signs and symptoms of inadequate or excess steroid replacement (which require return to the health care provider or clinic), in the importance of avoiding stressful situations whenever possible, and in the ideal regimen of diet and rest to avoid hypoglycemic reactions. The patient should carry an injectable form of cortisol when traveling for emergency treatment. Anyone with Addison's disease should wear a medical identification tag stating that he or she has the condition and is receiving steroid therapy.

Addison's disease

A disease caused by partial or total failure of adrenocortical function, which is characterized by a darkening of the skin and mucous membranes, anemia, weakness, and low blood pressure.

Addison's disease

Etymology: Thomas Addison
a life-threatening condition caused by partial or complete failure of adrenocortical function, often resulting from autoimmune processes, infection (especially tubercular or fungal), neoplasm, or hemorrhage in the gland. All three general functions of the adrenal cortex (glucocorticoid, mineralocorticoid, and androgenic) are lost. Also called Addison's syndrome, adrenocortical insufficiency. See also adrenal crisis.
observations The disease is characterized by increased bronze pigmentation of the skin and mucous membranes; weakness; decreased endurance; anorexia; dehydration; weight loss; GI disturbances; salt cravings; anxiety, depression, and other emotional distress; and decreased tolerance to physical and emotional stress. The person's requirements for glucocorticoid, mineralocorticoid, and salt are increased by stress, as in infection, trauma, and surgical procedures. The onset is usually gradual, over a period of weeks or months. Laboratory tests reveal abnormally low blood concentrations of sodium and glucose, a greater than normal level of serum potassium, and a decreased urinary output of certain steroids. The diagnosis is established if the amount of cortisol in the plasma and steroid in the urine does not increase after stimulation with adrenocorticotropic hormone.
interventions Treatment includes replacement therapy with glucocorticoid and mineralocorticoid drugs, an adequate fluid intake, control of sodium and potassium balance, and a diet high in complex carbohydrates and protein. Follow-up care includes continued administration of glucocorticoid drugs.
nursing considerations Complications include high fever, confused behavior, and adrenal crisis. With careful management, the patient's resistance to infection, capacity for work, and general well-being can be maintained. Nursing care includes administering corticosteroids and other drugs, observing the patient for signs of abnormal sodium and potassium levels, monitoring body weight and fluid intake and output, and encouraging adequate intake of nutrients. The patient also needs protection against stress while in the hospital and instruction in the importance of avoiding stress at home. The significance of emotional distress, the value of wearing a Medic Alert bracelet or tag, the signs of impending crisis, the use of a prepared kit for emergencies, and the importance of scrupulous attention to drug and diet regimens are emphasized before discharge. Discharge teaching also emphasizes the need to take cortisone after meals or with milk to prevent gastric irritation and the development of ulcers.

Addison's disease

Chronic adrenal insufficiency Endocrinology A endocrinopathy characterized by ↓ production of aldosterone and cortisol Etiology Trauma, hemorrhage, TB of adrenal gland, pituitary gland destruction Clinical Weakness, hypotension, easy fatigability, weight loss, N&V, abdominal pain, muscle and joint pain, amenorrhea, bronzing of the skin and hyperpigmentation-especially at skin folds Lab Anemia, neutropenia, eosinophilia, lymphocytosis, hypoglycemia, ↓ Na+, ↓ cortisol, ↑ Ca2+, ↑ K+, ↑ BUN Management Hydrocortisone, fludrocortisone Warning Pts should wear medical alert bracelet. See Polyglandular autoimmune syndrome.

Addison's disease

A disorder of the adrenal glands leading to a deficient output of cortisol and aldosterone. There is weakness, tiredness, pigmentation of the skin, low blood pressure, intestinal disorders and inability to cope with injury or surgical stress. Treatment is by steroid replacement, usually with hydrocortisone. (Thomas Addison, 1793–1860, English physician).

Addison's disease

a disease caused by a deficiency of adrenocorticosteroid hormones (e.g. CORTISONE, ALDOSTERONE) produced by cells of the ADRENAL GLAND cortex, and named after Thomas Addison (1793–1860), the English physician who first described it. The major symptoms of the disease are lowered blood pressure, lowered blood-sugar levels, reduced kidney function, loss of weight, extreme muscular weakness, and a brownish pigmentation of the skin and mucous membranes.
Addison's disease; primary hypoadrenalism adrenal cortex insufficiency due to loss of adrenocortical function, secondary to autoimmune disease or tuberculosis; characterized by weakness, tiredness, weight loss, vomiting and anorexia, epidermal pigmentation (of mucosa, face, recent scars and skin creases), postural hypotension, loss of body hair and cessation of menses

Addison's disease

see primary hypoadrenocorticism.
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