Addison's disease overview
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Addison disease develops as a result of bilateral adrenal cortex destruction. Both cortisol and aldosterone production are reduced. Autoimmune destruction of the adrenal glands is the most common cause in the western world, but infections such as tuberculosis, hemorrhage, adrenal vein thrombosis, and carcinoma are also known to significant causes. Tuberculosis remains the most common cause worldwide of Addison disease. The onset of Addison disease is often gradual, and symptoms of the disease can be difficult to recognize. It may go undetected until an illness or other stress precipitates adrenal crisis. Treatment should not be withheld to confirm diagnosis. Treatment should be the priority, as the disease is fatal if it remains untreated. Diagnosis is made with rapid, high-dose adrenocorticotropic hormone (ACTH) stimulation testing. If the patient is hypovolemic, dexamethasone and intravenous normal saline should be given before stimulation testing is performed. The main stay of therapy is with a combination of glucocorticoids and mineralocorticoids. Glucocorticoid doses needs to be doubled when patients have an episode of minor fever, infection, minor trauma, or minor physical stress. Intravenous stress-dose corticosteroids are needed for surgery requiring general anesthesia and for major trauma.
Historical Perspective
Addison's disease is named after Dr.Thomas Addison, the British physician who first described the condition in his paper On the Constitutional and Local Effects of Disease of the Suprarenal Capsules in 1855.
Classification
Adrenal insufficiency disorders may be classified into two categories depending on the duration of symptoms and depending on the etiology into acute or chronic forms, and primary or secondary adrenal insufficiency.
Pathophysiology
The hypothalamus releases corticotropin-releasing hormone (CRH), which stimulates the pituitary gland to release corticotropin (ACTH). ACTH travels via the blood to the adrenal gland, where it stimulates the release of cortisol. Cortisol is secreted by the cortex of the adrenal gland from a region called the zona fasciculata in response to ACTH. Elevated levels of cortisol exert negative feedback on the pituitary, which decreases the amount of ACTH released from the pituitary gland. When the adrenal glands do not produce enough of the hormone cortisol and aldosterone it results in Addison's disease.
Causes
Common causes of Addison's disease include autoimmune, tuberculosis AIDS, CMV, hemorrhage, infarction, sarcoidosis, infections.
Differentiating Addisons disease from other diseases
Addison's disease must be differentiated from other diseases that cause hypotension, skin pigmentation, and abdominal pain such as myopathies, celiac disease, Peutz-Jeghers syndrome ,anorexia nervosa, syndrome of inappropriate anti-diuretic hormone (SIADH), neurofibromatosis, porphyria cutanea tarda, salt-depletion nephritis and bronchogenic carcinoma.
Diagnosis
Ultrasound
Abdominal ultrasound is typically normal in Addison's disease except for the small size of adrenal glands.
Treatment
Surgery
Surgeries may require significant adjustments to medication regimens prior to, during, and following any surgical procedure. The best preparation for any surgery, regardless of how minor or routine it may be, is to speak to one's primary care physician about the procedure and medication implications well in advance of the surgery.