Addison disease

Oral Severe renal impairment with oliguria or azotemia untreated Addison disease hyperkalemia from any cause adynamia episodica hereditaria acute dehydration heat cramps patients receiving potassium-sparing diuretics or aldosterone-inhibiting agents. 

IV Diseases where high potassium levels may be encountered hyperkalemia renal failure and conditions in which potassium retention is present oliguria or azotemia anuria crush syndrome severe hemolytic reactions adrenocortical insufficiency (untreated Addison disease) adynamica episodica hereditaria acute dehydration heat cramps hyperkalemia from any cause early postoperative oliguria except during Gl drainage. 

Special risk Use with caution in the presence of cardiac disease, particularly in digitalized patients or in the presence of renal disease, metabolic acidosis, Addison disease, acute dehydration, prolonged or severe diarrhea, familial periodic paralysis, hypoadrenalism, hyperkalemia, hyponatremia, and myotonia congenita. 

Endocrine disorders Thyroid hormone therapy in patients with concomitant diabetes mellitus or insipidus or adrenal insufficiency (Addison disease) exacerbates the intensity of their symptoms. 

Zelissen PM, Croughs RJ, van Rijk PP, Raymakers JA. Effect of glucocorticoid replacement therapy on bone mineral density in patients with Addison disease. Ann Intern Med 1994 120(3) 207-10. 

Drugs with mineralocorticoidlike activity (aldosterone agonists) are frequently administered as replacement therapy whenever the natural production of mineralo-corticoids is impaired. Mineralocorticoid replacement is usually required in patients with chronic adrenocortical insufficiency (Addison disease), following adrenalectomy, and in other forms of adrenal cortex hypofunction. These conditions usually require both mineralocorticoid and glucocorticoid replacement. 

Addison disease only Asymptomatic Any Adrenocortical dysfunction with no neurological disease Biochemical defect with no symptoms... 

The adrenal cortex (AC) produces the glucocorticoid cortisol (hydrocortisone) in the zona fasciculata and the mineralocorticoid aldosterone in the zona glomerulosa. Both steroid hormones are vitally important in adaptation responses to stress situations, such as disease, trauma, or surgery. Cortisol secretion is stimulated by hypophyseal ACTH aldosterone secretion by angiotensin II in particular (p. 128). In AC failure (primary adrenocortical insuf ciency, Addison disease), both cortisol and aldosterone must be replaced when ACTH production is deficient (secondary adrenocortical insuf ciency), cortisol alone needs to be replaced. Cortisol is effective when given orally (30 mg/day, 2/3 a.m 1 /3 p.m.). In stress situations, the dose is raised 5- to 10-fold. Aldosterone is poorly effective via the oral route instead, the mineralocorticoid fludrocortisone (0.1 mg/day) is given. 

Cortisol. Cortisol, secreted by the adrenal cortex in response to adrenocorticotropic hormone (ACTH), stimulates gluconeogenesis and increases the breakdown of protein and fat. Patients with Cushing s syndrome have increased cortisol owing to a tumor or hyperplasia of the adrenal cortex and may become hyperglycemic. In contrast, people with Addisons disease have adrenocortical insufficiency because of destruction or atrophy of the adrenal cortex and may exhibit hypoglycemia. ... 

Addisons disease, results from progressive destruction or dysfunction of the adrenal glands by a local disease process or systemic disorder (Box 51-12), Worldwide, infectious diseases are the most common cause of primary adrenal insufficiency and include tuberculosis, fongal infections (histoplasmosis and cryptococcosis), and cytomegalovirus infections. Autoimmune adrenalitis accounts for more than 70% of cases reported in the Western world, with adrenal autoantibodies noted in more than 75% of cases,. The adrenal glands are atrophic, with loss of cortical cells but an intact medulla. Almost 50% of patients with autoimmune adrenalitis have an associated autoimmune disease with autoimmune thyroid disease the most common. 

Sizonenko PC, Paunier L. Hormonal changes in puberty III. Correlation of plasma dehy-droepiandrosterone, testosterone, FSH, and LH with stages of puberty and bone age in normal boys and girls and in patients with Addisons disease or hypogonadism or with premature or late adrenarche. J Clin Endocrinol Metab 1975 41 894-904. 

Most cases of Addison disease are a result of idiopathic atrophy of the adrenal cortex induced by autoimmune responses, although a number of other causes of adrenal cortex destruction have been described. Hypoadrenocorticism results in decreased production of cortisol and, in some... 

A. Hyperpigmentation is a feature of Addison disease, the diagnosis in this case. Decreased plasma cortisol because of adrenal insufficiency releases feedback inhibition of ACTH secretion by the pituitary, resulting in elevation of ACTH biosynthesis. The ACTH precursor peptide is cleaved to also yield melanocyte-stimulating hormone, the factor responsible for hyperpigmentation even in areas not exposed to sunlight. 

Most cases of Addison disease are because of idiopathic atrophy of the adrenal cortex induced by autoinunune responses. 

The glucocorticoids are used to treat Addison disease and adrenal insufficiency states, as a supplement in infantile respiratory distress syndrome, and in adrenal hyperplasia. 

The first type of autoimmune polyglandular syndrome, also referred to as APECED, is characterized by the presence of three major component diseases chronic candidiasis, hypoparathyroidism, and autoimmune Addison disease. It has primarily been seen, to... 

APGS type 2, also referred to as Schmidt syndrome, is characterized by Addison disease in association with autoimmune thyroid diseases and/or diabetes mellitus type 1. APGS type 2 may occur at any age and in both sexes (the female to male ratio is 2 1), but it is most common in middle-aged females and very rare in childhood. Several studies have revealed an association of this syndrome with various alleles within the HLA-DR3-canying haplotype. 

The least well characterized autoimmune polyglandular syndrome is the type 3 syndrome. This syndrome is defined by the presence of autoimmune thyroid disease with another autoimmune disease, such as diabetes mellitus type l, autoimmune gastritis, or myasthenia gravis, but in the absence of Addison disease. APGS type 3 primarily involves females (the female to male ratio is 7 1) who have HLA-DR3-associated autoimmune disease and is probably the most common of the autoimmune polyglandular syndrome disorders. Since different and multiple clinical combinations can be found, the classification of this type of autoimmune polyglandular syndrome is probably more complicated than originally anticipated. 

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