<unk> dison<unk>  develops as a result of bilateral<unk> renal cortex destruction or dysfunction leading to reduced cortisol and aldosterone production. Autoimmune destruction of the<unk> renal glands is the most common cause in the western world, but hemorrhage,<unk> renal vein thrombosis, carcinoma and infections such as tuberculosis are also known significant causes. Tuberculosis remains the most common cause worldwide of<unk> dison<unk> . The onset of<unk> dison<unk>  is often gradual, and symptoms of the<unk>  can be difficult to recognize. It may go undetected until an illness or other stress precipitates<unk> renal crisis. Treatment should not be withheld to confirm the diagnosis. Treatment should be the priority, as the<unk>  is fatal if it remains untreated. Diagnosis is made with rapid, high-dose<unk> renocorticotropic hormone (ACTH) stimulation testing. If the patient is hypovolemic, dexamethasone and intravenous normal saline should be given before stimulation testing is performed. The mainstay of therapy is a combination of glucocorticoids and mineralocorticoids. Glucocorticoid doses need 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 involving general anesthesia and for major trauma.
Addison's disease
Addison-gull syndrome
Addison-Gull syndrome
Sheehan's syndrome
Wilson's temperature syndrome
Zieve's syndrome
Fahr's syndrome
Graves' disease