Addison's Disease: Difference between revisions
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== Associated Co-morbidities == | == Associated Co-morbidities == | ||
Addison's disease can occur alone, or it can occur along with other autoimmune disorders, leading to polyendocrine syndrome<ref name="Winqvist" /><ref name="NIDDK">http://endocrine.niddk.nih.gov/pubs/addison/addison.htm</ref>.<br> | Addison's disease can occur alone, or it can occur along with other autoimmune disorders, leading to polyendocrine syndrome<ref name="Winqvist" /><ref name="NIDDK">Loechner K. Adrenal Insufficiency and Addison's Disease. http://endocrine.niddk.nih.gov/pubs/addison/addison.htm</ref>.<br> | ||
*Type I Diabetes Mellitus | *Type I Diabetes Mellitus | ||
*Hypoparathyroidism | *Hypoparathyroidism | ||
*Thyroiditis | *Thyroiditis | ||
*Pernicious Anemia | *Pernicious Anemia | ||
*Vitiligo (a loss of pigment on areas of the skin) | *Vitiligo (a loss of pigment on areas of the skin) | ||
*Chronic Active Hepatitis | *Chronic Active Hepatitis | ||
Revision as of 02:29, 12 April 2010
Original Editors - Elizabeth Bohnert from Bellarmine University's Pathophysiology of Complex Patient Problems project.
Lead Editors - Your name will be added here if you are a lead editor on this page. Read more.
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]
[Image courtesy of Britannica.com. Available at http://www.britannica.com/EBchecked/topic/6405/adrenal-gland]
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 (especially of the mouth and scars), 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
[Image courtesy of University of South Carolina School of Medicine. Available at http://pathmicro.med.sc.edu/ghaffar/tolerance2000.htm]
Associated Co-morbidities[edit | edit source]
Addison's disease can occur alone, or it can occur along with other autoimmune disorders, leading to polyendocrine syndrome[4][5].
- Type I Diabetes Mellitus
- Hypoparathyroidism
- Thyroiditis
- Pernicious Anemia
- Vitiligo (a loss of pigment on areas of the skin)
- Chronic Active Hepatitis
Medications[4][edit | edit source]
Acute Therapy:
• 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:
• 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]
Test Results That Suggest Addison's Disease[6]
| Test | Result |
| Blood Chemistry | |
| Serum Na | < 135 mEq/L |
| Serum K | > 5 mEq/L |
| Ratio of Serum Na:K | <30:1 |
| Plasma Glucose, fasting | < 50 mg/dL |
| Plasma HCO3 | < 15-20 mEq/L |
| BUN | > 20 mg/dL |
| Hematology | |
| Hct | Elevated |
| WBC Count | Low |
| Lymphocytes | Relative lymphocytes |
| Eosinophils | Increased |
| Imaging | |
|
Evidence of calcification in adrenal areas Renal TB Pulmonary TB |
[Chart courtesy of Merck.com. Available at http://merck.com/mmpe/sec12/ch153/ch153b.html]
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]
add text here
Medical Management (current best evidence)[edit | edit source]
Refer to Medications
Physical Therapy Management (current best evidence)[edit | edit source]
add text here
Alternative/Holistic Management[7] (current best evidence)[edit | edit source]
• A combination of Barago officinalis (Borage), Eleutherococcus senticosis (Siberian Ginseng), and Astragalus membranaceous (Huang Qi) help support the function of the adrenal glands and assist the body in 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]
add text here
Case Reports[edit | edit source]
Addison’s disease presenting with idiopathic intracranial hypertension in 24-year-old woman: a case report[8] [view article at Journal of Medical Case Reports]
Premature Mortality in Patients with Addison’s Disease: A Population-Based Study [9] [view article at The Journal of Clinical Endocrinology & Metabolism]
Resources
[edit | edit source]
National Adrenal Diseases Foundation: www.nadf.us
Mayo Clinic: www.mayoclinic.com
The Canadian Addison Society: www.addisonsociety.ca
National Endocrine and Metabolic Diseases Information Service: www.endocrine.niddk.nih.gov
Recent Related Research (from Pubmed)[edit | edit source]
<div class="researchbox"><rss>http://eutils.ncbi.nlm.nih.gov/entrez/eutils/erss.cgi?rss_guid=12kswG5SFWVBwde5m7P41jWIM34qOEGxEb5FCX2J9zhajC3sAA%7Ccharset=UTF-8%7Cshort%7Cmax=10</rss></div>
References
[edit | edit source]
- ↑ 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.
- ↑ Loechner K. Adrenal Insufficiency and Addison's Disease. http://endocrine.niddk.nih.gov/pubs/addison/addison.htm
- ↑ http://merck.com/mmpe/sec12/ch153/ch153b.html
- ↑ http://www.nativeremedies.com/ailment/what-is-addisons-disease.html
- ↑ Sharma D, Mukherjee1 R, Moore P, Cuthbertson DJ. Addison’s disease presenting with idiopathic intracranial hypertension in 24-year-old woman: a case report. Journal of Medical Case Reports. 2010; 4(60).
- ↑ Bergthorsdottir R, Leonsson-Zachrisson M, Oden A, Johannsson G. Premature Mortality in Patients with Addison’s Disease: A Population-Based Study. The Journal of Clinical Endocrinology & Metabolism. 2006; 91(12): 4849-4853.
