Addisons Disease Made Simple - Primary Adrenal Faliure 

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Addisons Disease Made Simple
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Addison’s disease, also known as primary adrenal insufficiency, is a long-term endocrine disorder in which the adrenal glands do not produce enough steroid hormones.[1] Symptoms generally come on slowly and may include abdominal pain, weakness, and weight loss. Darkening of the skin in certain areas may also occur. Under certain circumstances, an adrenal crisis may occur with low blood pressure, vomiting, lower back pain, and loss of consciousness. An adrenal crisis can be triggered by stress, such as from an injury, surgery, or infection.[1]
Addison's disease arises from problems with the adrenal gland such that not enough of the steroid hormone cortisol and possibly aldosterone are produced,[1] most often due to damage by the body's own immune system in the developed world and tuberculosis in the developing world.[2] Other causes include certain medications, sepsis, and bleeding into both adrenal glands.[1][2] Secondary adrenal insufficiency is caused by not enough adrenocorticotropic hormone (ACTH) (produced by the pituitary gland) or CRH (produced by the hypothalamus). Despite this distinction, adrenal crises can happen in all forms of adrenal insufficiency. Addison's disease is generally diagnosed by blood tests, urine tests, and medical imaging.[1]
Treatment involves replacing the absent hormones.[1] This involves taking a corticosteroid such as hydrocortisone and fludrocortisone.[1][3] These medications are usually taken by mouth.[1] Lifelong, continuous steroid replacement therapy is required, with regular follow-up treatment and monitoring for other health problems.[4] A high-salt diet may also be useful in some people. If symptoms worsen, an injection of corticosteroid is recommended and people should carry a dose with them. Often, large amounts of intravenous fluids with the sugar dextrose are also required. Without treatment, an adrenal crisis can result in death
The signs and symptoms include fatigue; lightheadedness upon standing or difficulty standing, muscle weakness, fever, weight loss, anxiety, nausea, vomiting, diarrhea, headache, sweating, changes in mood or personality, and joint and muscle pains. Some patients have cravings for salt or salty foods due to the loss of sodium through their urine.[8] Hyperpigmentation of the skin may be seen, particularly when the patient lives in a sunny area, as well as darkening of the palmar crease, sites of friction, recent scars, the vermilion border of the lips, and genital skin.[9] These skin changes are not encountered in secondary and tertiary hypoadrenalism.[10]
On physical examination, these clinical signs may be noticed:[8]
Low blood pressure with or without orthostatic hypotension (blood pressure that decreases with standing)
Darkening (hyperpigmentation) of the skin, including areas not exposed to the sun. Characteristic sites of darkening are skin creases (e.g. of the hands), nipple, and the inside of the cheek (buccal mucosa); also, old scars may darken. This occurs because melanocyte-stimulating hormone (MSH) and ACTH share the same precursor molecule, pro-opiomelanocortin (POMC). After production in the anterior pituitary gland, POMC gets cleaved into gamma-MSH, ACTH, and beta-lipotropin. The subunit ACTH undergoes further cleavage to produce alpha-MSH, the most important MSH for skin pigmentation. In secondary and tertiary forms of adrenal insufficiency, skin darkening does not occur, as ACTH is not overproduced.
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