Introduction Addison’s Disease is a rare and chronic disease that is characterized by adrenal insufficiency There is a decrease in hormones in the adrenal cortex such as glucocorticoids and mineralocorticoids (Margulies, 2011) cases diagnosed per 100,000 in the world per year. (Margulies, 2011) 1.4 million deaths per year around the world. (Margulies, 2011) Usually effects year-olds, but can be seen in all ages (Margulies, 2011)

History  First discovered by Thomas Addison in 1855 (Loechner,2009)  First described as an infection of the adrenal gland- most commonly TB. (Loechner,2009)  Now instead of infection, its most commonly characterized by an autoimmune destruction of the adrenal glands (Loechner,2009)

Causes of the Disease  Three different causes of the disease (Nieman,2010).  Adrenal Dysgenesis:  Genetic Causes  Imparied Steriodiogensis:  Congenital Adrenal Hyperplasia  Adrenal Destruction:  Autoimmune destruction

Causes of Disease  Adrenal Destruction:  Most common type in industrialized world (Nieman, et al.,2010).  Affects humoral and cell-mediated responses (Uibo, et al., 1994)  Immune reaction against enzyme 21-hydroxylase, a cytochrome P450 enzyme. (Uibo, et al., 1994)  Normal functioning 21-hydroxylase catalyzes the addition of an “-OH” on carbon 21 in steroids (Uibo, et al., 1994)  Addison’s Disease has an enormous amount of autoantibodies attack this enzyme and slowly kill off the adrenal cortex.  82.5% of autoantibodies are adrenal antibodies (Zelissen, et al., 1994).

Symptoms  Chronic fatigue  Muscle Weakness  Weight loss, Nausea, Diarrhea  Hyperpigmentation  Hypercalcemia, Hypoglycemia, Hypoatremia, and Hyperkalemia  Esinophilia and Lymphocytosis  Metabolic acidosis  Addisonian Crisis:  Severely low blood pressure and potential coma or death All information on this slide retrieved from: (Chakera, et al., 2010)

Diagnosis  Determined by low level of adrenal hormone after stimulation with synthetic ACTH hormone tetercosactide (Oelkers, et al.,1992 )  Short Test: (Oelkers, et al.,1992 )  Compares blood cortisol levels before and after  250 micrograms of tetracosactide  if abnormal go to long test  Long Test: (Oelkers, et al.,1992 )  1 mg of tetracosactide is administered and blood taken at 1, 4, 8, and 24 hours later

Current Treatment (Nieman, 2010)  Replacement corticoidsteroids or fludrocortisone acetate  Doses change according to lifestyle, i.e. stress, infection or injury  Have to carry emergency injection of hydrocortisone and card/bracelet indentifying their condition