Addison s disease

Endocrine diseases autoimmune thyreoiditis, primary myxedema, Addison s disease, type 1 diabetes mellitus (IDDM)... 

Historically the only melanocortin peptide to be used clinically is the parent hormone from which all these peptides are derived from namely ACTH (see above). It has also been used in the treatment infantile spasms for epilepsy, where it is administered as an intramuscular injection only over a 2-12 weeks period. Obvious side effects include weight gain, puffy face, high blood pressure and an increased risk of infection and should never be administered to patients with diabetics, renal or heart failure. ACTH is also used as a stimulation test to measure adrenal cortex activity, i.e. production of cortisol and is used to ascertain whether someone has Addison s disease. 

No effect on ACTH release in normal subjects, but suppresses elevated levels in Addison s disease and in ACTH producing tumours... 

Acyl-CoA Synthetase Adaptive Immunity Adaptor Proteins Addiction Addison s Disease Additive Interaction Adenosine Adenosine Receptors Adenoviruses Adenylate Cyclase Adenylyl Cyclases ADH ADHD... 

Other causes of shock include anaphylaxis, hypoglycemia, hypothyroidism, or Addison s disease. 

Fludrocortisone is contraindicated in patients with hypersensitivity to fludrocortisone and those with systemic fungal infections. Fludrocortisone is used cautiously in patients with Addison s disease infection, and during pregnancy (Pregnancy Category C) and lactation. Fludrocortisone decreases the effects of the barbiturates, hydantoins, and rifampin. There is a decrease in serum levels of the salicylates when those agents are administered with fludrocortisone... 

These drugs are used cautiously in patients with Addison s disease and during lactation. The thyroid hormones are classified as Pregnancy Category A and are considered safe to use during pregnancy. 

Potassium is contraindicated in patients who are at risk for experiencing hyperkalemia, such as those with renal failure, oliguria, or azotemia (file presence of nitrogen-containing compounds in the blood), anuria, severe hemolytic reactions, untreated Addison s disease (see Chap. 50), acute dehydration, heat cramps, and any form of hyperkalemia Potassium is used cautiously in patients with renal impairment or adrenal insufficiency, heart disease, metabolic acidosis, or prolonged or severe diarrhea. Concurrent use of potassium with... 

Addison s disease, pheochromocytoma, hyperadrenocorticism, hyponatremia, hyperkalemia, vitamin B12 deficiency... 

Lifelong glucocorticoid replacement therapy may be necessary for patients with adrenal insufficiency, and mineralocor-ticoid replacement therapy usually is required for those with Addison s disease. 

Secondary adrenal insufficiency occurs as a result of a pituitary gland dysfunction whereby decreased production and secretion of ACTH leads to a decrease in cortisol synthesis. Tertiary adrenal insufficiency is a disorder of the hypothalamus that results in decreased production and release of CRH, which, in turn, decreases pituitary ACTH production and release. In contrast to Addison s disease (i.e., primary adrenal insufficiency), aldosterone production is unaffected in the secondary and tertiary forms of the disease. Chronic adrenal insufficiency often has a good prognosis if diagnosed early and treated appropriately. 

After appropriate laboratory and diagnostic tests are performed, AB is diagnosed with Addison s disease. 

Adrenal gland hypofimction is associated with primary (Addison s disease) or secondary adrenal insufficiency. Adrenal insufficiency occurs when the adrenal glands do not produce enough cortisol and, in some cases, aldosterone. 

Primary adrenal insufficiency (Addison s disease) most often involves the destruction of all regions of the adrenal cortex. There are deficiencies of cortisol, aldosterone, and the various androgens. Medications that inhibit cortisol synthesis (e.g., ketoconazole) or accelerate cortisol metabolism (e.g., phenytoin, rifampin, phenobarbital) can also cause primary adrenal insufficiency. 

Weight loss, dehydration, hyponatremia, hyperkalemia, and elevated blood urea nitrogen are common in Addison s disease. 

Hyperpigmentation is common in Addison s disease and may involve exposed and nonexposed parts of the body. Hyperpigmentation is usually not seen in secondary adrenal insufficiency because of low amounts of melanocyte-stimulating hormone. 

Patients with Addison s disease have an abnormal response to the short cosyntropin-stimulation test. Plasma ACTH levels are usually 400 to 2,000 pg/mL in primary insufficiency versus normal to low (0 to 50 pg/mL) in secondary insufficiency. A normal cosyntropin-stimulation test does not rule out secondary adrenal insufficiency. 

Endocrine or hormonal dysregulation (Addison s disease, Cushing s disease, hyper- or hypothyroidism, menstrual-related or pregnancy-related or perimenopausal mood disorders)... 

Other causes include magnesium-containing antacids in patients with renal insufficiency, enteral or parenteral nutrition in patients with multiorgan system failure, magnesium for treatment of eclampsia, lithium therapy, hypothyroidism, and Addison s disease. 

Most importantly, the determination of cortisol levels is considered useful in the diagnosis and treatment of various ailments, namely Addison s Disease i.e., pernicious anaemia—a condition whereby the maturation of the red cells may not proceed beyond the stage of megaloblasts Cushing s Syndrome. 

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