Addisons Disease - Medical Malpractice LawyersLEGAL HELPLINE: ☎ 855 804 7125
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Addisons Disease - Medical Malpractice
Addison's disease is a hormonal, endocrine disease that involves a reduction or lack of production of cortisol and sometimes aldosterone in the adrenal gland. All ages of individuals can be affected by the disease and it has no sex predilection. The main symptoms are weakness, tiredness, weight loss and low blood pressure. The skin sometimes becomes hyperpigmented as though the person is tanned all over their body. The disease is often referred to as adrenal hypocortisolism or adrenal insufficiency.
Cortisol is produced primarily by the adrenal glands, which are small glands located above the kidneys. It has effects on every cell of the body and has hundreds of different effects on the body. It's most important effect is to aid the body in responding to stress but it also helps increase blood pressure, improve heart function, decrease immune over-responsiveness, maintain arousal, and regulate protein metabolism, fat metabolism and carbohydrate metabolism.
Cortisol is regulated by the hormone ACTH, which is secreted by the pituitary gland. Without ACTH, there is no cortisol production. Cortisol completes the cycle by signaling the pituitary gland to shut off ACTH production.
Aldosterone can also be affected by Addison's disease. Aldosterone regulates the salt and water balance in the body and acts directly on the kidneys. Without aldosterone, the kidneys lose too much water and the blood pressure begins to drop.
Addison's disease can be primary and is the direct result of damage or problems in the adrenal gland. It can also be secondary and can be the result of a pituitary gland failing to produce ACTH.
Addison's disease occurs in approximately 1 out of 100,000 individuals. By far and away, most causes of the disease are due to a gradual destruction of the cortex of the adrenal gland. About 70 percent are the direct result of an autoimmune disease. You don't begin to get symptoms until about 90 percent of the adrenal gland is involved in the destruction. Most often, both cortisol and aldosterone production are involved in the disease and Addison's disease can be a part of a bigger endocrine problem.
There are two types of larger endocrine problems associated with Addison's disease. These polyendocrine deficiency syndromes are referred to as type I and type II. Type I disease happens in kids and involves a host of other endocrine problems as well. Type II disease is called Schmidt's disease and is an affliction of young people. Low thyroid, poor sexual development, vitiligo, diabetes and other skin problems can occur with this disease. These polyendocrine deficiency syndromes are believed to be hereditary conditions that run in families.
Other causes of Addison's disease include tuberculosis, chronic infections, cancer and amyloidosis. Secondary adrenal insufficiency is less commonly associated with Addison's disease and involves damage to the pituitary gland that won't make ACTH. There can be tumours of the pituitary gland that make ACTH which need to be removed. Once removed, secondary Addison's disease develops.
The signs and symptoms of Addison's disease include fatigue that worsens over time, muscle weakness, weight loss, loss of appetite, nausea and vomiting, diarrhoea, low blood pressure, dizziness, fainting and hyperpigmentation. People with Addison's disease can become very depressed and can crave salty foods. Low blood sugar is a complication of Addison's disease in children especially.
The diagnosis of Addison's disease comes from doing an ACTH stimulation test to see if the adrenal gland responds appropriately to ACTH. A CRH stimulation test checks for secondary adrenal insufficiency.
Treatment of Addison's disease involves replacing the missing hormones. This means you take hydrocortisone tablets and Florinef, which replaces the aldosterone missing in the system.LEGAL HELPLINE: ☎ 855 804 7125
The author of the substantive medical writing on this website is Dr. Christine Traxler MD whose biography can be read here