2. 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) 6-110 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 30-50 year-olds, but can be seen in all ages (Margulies, 2011)

3. 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)

4. 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

5. 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).

6. 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)

7. 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

8. 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