A 43-year-old female presents to the clinic with a chief complaint of fever, chills, nausea and vomiting and weakness. She has been unable to keep any food, liquids or medications down. The symptoms began 3 days ago and have not responded to ibuprofen, acetaminophen, or Nyquil when she tried to take them. The temperature has reached as high as 102˚F. Allergies: none known to drugs or food or environmental Medications-20 mg prednisone po qd, omeprazole 10 po qam PMH-significant for 20-year history of steroid dependent rheumatoid arthritis (RA). GERD. No other significant illnesses or surgeries. Social-denies alcohol, illicit drugs, vaping, tobacco use Physical exam Thin, ill appearing woman who is sitting in exam room chair as she said she was too weak to climb on the exam table. VS Temp 101.2˚F, BP 98/64, pulse 110, Resp 16, PaO2 96% on room air. ROS negative other than GI symptoms. Based on the patient’s clinical presentation, the APRN diagnoses the patient as

An adrenal insufficiency requires some type of trigger or stressor such as surgery, trauma, infection or acute withdrawal of glucocorticoids. The patient had several factors contributing to her present situation. She had RA x 20 years that necessitated oral prednisone. Increased levels of both glucocorticoids (primarily cortisol) and mineralocorticoids (primarily aldosterone) are needed for the body to adapt to the stress Corticotropin-releasing hormone (CRH) from the hypothalamus eventually prompts release of ACTH from the anterior pituitary gland. ACTH then stimulates release and 3 synthesis of cortisol from the adrenal cortex. Cortisol mobilizes amino acids from skeletal muscle and generally enhances the liver’s capacity for gluconeogenesis as well as enhances normal immune activity and maintenance of cardiovascular integrity. It also influences fat, carbohydrate and protein. Catecholamines cause vasoconstriction, which in the kidney, probably initiates release of renin, stimulating the rennin-angiotensionaldosterone-system (RAAS). Antidiuretic hormone (ADH, also called vasopressin), is released from the hypothalamus and posterior pituitary during periods of stress. Both aldosterone and ADH attempt to conserve water and electrolytes to sustain a sufficient vascular volume.