Addison's Disease: Difference between revisions
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== Physical Therapy Management (current best evidence) == | == Physical Therapy Management (current best evidence) == |
Revision as of 04:16, 9 March 2010
Original Editors - Students from Bellarmine University's Pathophysiology of Complex Patient Problems project.
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Definition/Description[edit | edit source]
Addison’s disease is another name for primary chronic adrenal insufficiency. It is a condition where the adrenal cortex (the outer layer of the adrenal gland that produces mineralocorticoids, glucocorticoids, and androgens) is progressively destroyed, resulting in decreased secretions of the hormones.[1][2] Cortisol, a glucocorticoid, and aldosterone, a mineralcorticoid, are the primary hormones that are decreased with this disease, causing body wide metabolic disorders and fluid imbalances.[1]
Prevalence[edit | edit source]
Addison’s disease occurs in about 4 out of 100,000 Americans each year. Even though it is seen throughout the lifespan in both genders, it most commonly occurs in middle-aged white females.
Characteristics/Clinical Presentation[edit | edit source]
Addison’s disease will develop insidiously, with the signs of the disease not developing “until at least 90% of both glands is destroyed and the levels of circulating glucocorticoids and mineralocorticoids are significantly decreased.”[2] Some of the clinical signs and symptoms of Addison’s disease include:
• Darkened pigmentation of the skin, due to increased secretion of melanin-secreting hormone (MSH) corresponding with increased secretion of ACTH, which is released to try to stimulate the work of the adrenal glands[1][2]
• Slowly developing weakness and fatigue[2][3]
• Hypotension due to increased sodium excretion from decreased aldosterone secretion[1][2][3]
• Severe abdominal, low back, or leg pain[1]
• Gastrointestinal disturbances such as nausea, vomiting, anorexia, weight loss, and diarrhea[2][3]
• Hypoglycemia due to decreased glucocorticoids causing decreased gluconeogenesis[1][2]
• Decreased stress tolerance (infections, trauma, surgery, etc.)[1][2]
• Salt craving
Associated Co-morbidities[edit | edit source]
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Medications[edit | edit source]
Acute Therapy[4]:
• Intravenously administered hydrocortisone (100 mg), repeated every 6 hours for the first 24 hours
• Intravenously administered rapid infusion of saline (2-4L) during the first 12 hours
Maintenance Therapy[4]:
• Glucocorticoid Replacement: 15-20 mg of hydrocortisone daily, divided into 3 or 4 doses to simulate normal adrenal secretions
• Mineralocorticoid Replacement: 0.05-0.1 mg of fludrocortisones daily
Diagnostic Tests/Lab Tests/Lab Values[edit | edit source]
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Causes[edit | edit source]
There are a number of causes for Addison’s disease, however “90% of all cases are attributable to one of four diseases: autoimmune adrenalitis, tuberculosis, the acquired immune deficiency syndrome (AIDS), or metastatic cancers.”[2] The primary sites of the metastases to the adrenal glands usually arise from carcinomas of the lungs or breasts.[2]
Systemic Involvement[edit | edit source]
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Medical Management (current best evidence)[edit | edit source]
Refer to Medications
Physical Therapy Management (current best evidence)[edit | edit source]
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Alternative/Holistic Management[5] (current best evidence)[edit | edit source]
• Barago officinalis (Borage), Eleutherococcus senticosis (Siberian Ginseng), and Astragalus membranaceous (Huang Qi) help support the function of the adrenal glands and assist the body dealing with normal stressors
• Ginger works as an anti-nausea medication and helps to decrease physicial and emotional stress
• Liquorice improves the activity of mineralocorticoids
Differential Diagnosis[edit | edit source]
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Case Reports[edit | edit source]
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Resources
[edit | edit source]
National Adrenal Diseases Foundation
Recent Related Research (from Pubmed)[edit | edit source]
<div class="researchbox"><rss>http://eutils.ncbi.nlm.nih.gov/entrez/eutils/erss.cgi?rss_guid=1FmSTaOY8T61qUiDbtWB8DKbABydbT1nBbdS3jbUhlKogjrQuO%7Ccharset=UTF-8%7Cshort%7Cmax=10</rss></div>
References[edit | edit source]
see adding references tutorial.
- ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 Goodman CC, Fuller KS. Pathology: Implications for the Physical Therapist. St. Louis: Elsevier; 2009.
- ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 2.8 2.9 Kumar V, Abbas AK, Fausto N. Pathologic Basis of Disease. Philadelphia: Elsevier; 2005.
- ↑ 3.0 3.1 3.2 Goodman CC, Snyder TE. Differential Diagnosis for Physical Therapists: Screening for Referral. St. Louis: Elsevier; 2007.
- ↑ 4.0 4.1 Winqvist O, Rorsman F, Kampe O. Autoimmune Adrenal Insufficiency: Recognition and Management. BioDrugs. 2000; 13(2): 107-114.
- ↑ http://www.nativeremedies.com/ailment/what-is-addisons-disease.html