Addison's Disease

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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]


[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, 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[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[5]

 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]

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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[6] (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]

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Case Reports[edit | edit source]

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Resources
[edit | edit source]

National Adrenal Diseases Foundation

The Mayo Clinic

Recent Related Research (from Pubmed)[edit | edit source]

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References
[edit | edit source]

  1. 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. 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. 3.0 3.1 3.2 Goodman CC, Snyder TE. Differential Diagnosis for Physical Therapists: Screening for Referral. St. Louis: Elsevier; 2007.
  4. Winqvist O, Rorsman F, Kampe O. Autoimmune Adrenal Insufficiency: Recognition and Management. BioDrugs. 2000; 13(2): 107-114.
  5. http://merck.com/mmpe/sec12/ch153/ch153b.html
  6. http://www.nativeremedies.com/ailment/what-is-addisons-disease.html