Addison's Disease: Difference between revisions
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<div class="noeditbox">Welcome to [[Pathophysiology of Complex Patient Problems|PT 635 Pathophysiology of Complex Patient Problems]] This is a wiki created by and for the students in the School of Physical Therapy at Bellarmine University in Louisville KY. Please do not edit unless you are involved in this project, but please come back in the near future to check out new information!!</div> <div class="editorbox"> | |||
'''Original Editors '''- [[Pathophysiology of Complex Patient Problems|Students from Bellarmine University's Pathophysiology of Complex Patient Problems project.]] | '''Original Editors '''- [[Pathophysiology of Complex Patient Problems|Students from Bellarmine University's Pathophysiology of Complex Patient Problems project.]] | ||
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== Definition/Description == | == Definition/Description == | ||
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.<ref name="Goodman, Fuller">Goodman CC, Fuller KS. Pathology: Implications for the Physical Therapist. St. Louis: Elsevier; 2009.</ref><ref name="Kumar, Abbas">Kumar V, Abbas AK, Fausto N. Pathologic Basis of Disease. Philadelphia: Elsevier; 2005.</ref> 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.<ref name="Goodman, Fuller" /> | 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.<ref name="Goodman, Fuller">Goodman CC, Fuller KS. Pathology: Implications for the Physical Therapist. St. Louis: Elsevier; 2009.</ref><ref name="Kumar, Abbas">Kumar V, Abbas AK, Fausto N. Pathologic Basis of Disease. Philadelphia: Elsevier; 2005.</ref> 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.<ref name="Goodman, Fuller" /> | ||
== Prevalence == | == Prevalence == | ||
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. | 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 == | == Characteristics/Clinical Presentation == | ||
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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.”<ref name="Kumar, Abbas" /> Some of the clinical signs and symptoms of Addison’s disease include: | 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.”<ref name="Kumar, Abbas" /> Some of the clinical signs and symptoms of Addison’s disease include: | ||
•<span class="Apple-tab-span" style="white-space:pre"> </span>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<ref name="Goodman, Fuller" /><ref name="Kumar, Abbas" /> | •<span class="Apple-tab-span" style="white-space:pre"> </span>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<ref name="Goodman, Fuller" /><ref name="Kumar, Abbas" /> | ||
•<span class="Apple-tab-span" style="white-space:pre"> </span>Slowly developing weakness and fatigue<ref name="Kumar, Abbas" /><ref name="Goodman, Snyder">Goodman CC, Snyder TE. Differential Diagnosis for Physical Therapists: Screening for Referral. St. Louis: Elsevier; 2007.</ref> | •<span class="Apple-tab-span" style="white-space:pre"> </span>Slowly developing weakness and fatigue<ref name="Kumar, Abbas" /><ref name="Goodman, Snyder">Goodman CC, Snyder TE. Differential Diagnosis for Physical Therapists: Screening for Referral. St. Louis: Elsevier; 2007.</ref> | ||
•<span class="Apple-tab-span" style="white-space:pre"> </span>Hypotension due to increased sodium excretion from decreased aldosterone secretion<ref name="Goodman, Fuller" /><ref name="Kumar, Abbas" /><ref name="Goodman, Snyder" /> | •<span class="Apple-tab-span" style="white-space:pre"> </span>Hypotension due to increased sodium excretion from decreased aldosterone secretion<ref name="Goodman, Fuller" /><ref name="Kumar, Abbas" /><ref name="Goodman, Snyder" /> | ||
•<span class="Apple-tab-span" style="white-space:pre"> </span>Severe abdominal, low back, or leg pain<ref name="Goodman, Fuller" /> | •<span class="Apple-tab-span" style="white-space:pre"> </span>Severe abdominal, low back, or leg pain<ref name="Goodman, Fuller" /> | ||
•<span class="Apple-tab-span" style="white-space:pre"> </span>Gastrointestinal disturbances such as nausea, vomiting, anorexia, weight loss, and diarrhea<ref name="Kumar, Abbas" /><ref name="Goodman, Snyder" /> | •<span class="Apple-tab-span" style="white-space:pre"> </span>Gastrointestinal disturbances such as nausea, vomiting, anorexia, weight loss, and diarrhea<ref name="Kumar, Abbas" /><ref name="Goodman, Snyder" /> | ||
•<span class="Apple-tab-span" style="white-space:pre"> </span>Hypoglycemia due to decreased glucocorticoids causing decreased gluconeogenesis<ref name="Goodman, Fuller" /><ref name="Kumar, Abbas" /> | •<span class="Apple-tab-span" style="white-space:pre"> </span>Hypoglycemia due to decreased glucocorticoids causing decreased gluconeogenesis<ref name="Goodman, Fuller" /><ref name="Kumar, Abbas" /> | ||
•<span class="Apple-tab-span" style="white-space:pre"> </span>Decreased stress tolerance (infections, trauma, surgery, etc.)<ref name="Goodman, Fuller" /><ref name="Kumar, Abbas" /> | •<span class="Apple-tab-span" style="white-space:pre"> </span>Decreased stress tolerance (infections, trauma, surgery, etc.)<ref name="Goodman, Fuller" /><ref name="Kumar, Abbas" /> | ||
•<span class="Apple-tab-span" style="white-space:pre"> </span>Salt craving | •<span class="Apple-tab-span" style="white-space:pre"> </span>Salt craving<br> | ||
== Associated Co-morbidities == | == Associated Co-morbidities == | ||
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•<span class="Apple-tab-span" style="white-space:pre"> </span>Intravenously administered hydrocortisone (100 mg), repeated every 6 hours for the first 24 hours | •<span class="Apple-tab-span" style="white-space:pre"> </span>Intravenously administered hydrocortisone (100 mg), repeated every 6 hours for the first 24 hours | ||
•<span class="Apple-tab-span" style="white-space:pre"> </span>Intravenously administered rapid infusion of saline (2-4L) during the first 12 hours | •<span class="Apple-tab-span" style="white-space:pre"> </span>Intravenously administered rapid infusion of saline (2-4L) during the first 12 hours<br> | ||
Maintenance Therapy<ref name="Winqvist" />: | Maintenance Therapy<ref name="Winqvist" />: | ||
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•<span class="Apple-tab-span" style="white-space:pre"> </span>Glucocorticoid Replacement: 15-20 mg of hydrocortisone daily, divided into 3 or 4 doses to simulate normal adrenal secretions | •<span class="Apple-tab-span" style="white-space:pre"> </span>Glucocorticoid Replacement: 15-20 mg of hydrocortisone daily, divided into 3 or 4 doses to simulate normal adrenal secretions | ||
•<span class="Apple-tab-span" style="white-space:pre"> </span>Mineralocorticoid Replacement: 0.05-0.1 mg of fludrocortisones daily | •<span class="Apple-tab-span" style="white-space:pre"> </span>Mineralocorticoid Replacement: 0.05-0.1 mg of fludrocortisones daily<br> | ||
== Diagnostic Tests/Lab Tests/Lab Values == | == Diagnostic Tests/Lab Tests/Lab Values == | ||
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== Causes == | == Causes == | ||
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 [[HIV/AIDS|acquired immune deficiency syndrome (AIDS)]], or metastatic cancers.”<ref name="Kumar, Abbas" /> The primary sites of the metastases to the adrenal glands usually arise from carcinomas of the lungs or [[Breast Cancer|breasts]].<ref name="Kumar, Abbas" /> | 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 [[HIV/AIDS|acquired immune deficiency syndrome (AIDS)]], or metastatic cancers.”<ref name="Kumar, Abbas" /> The primary sites of the metastases to the adrenal glands usually arise from carcinomas of the lungs or [[Breast Cancer|breasts]].<ref name="Kumar, Abbas" /> | ||
== Systemic Involvement == | == Systemic Involvement == | ||
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== Medical Management (current best evidence) == | == Medical Management (current best evidence) == | ||
Refer to | Refer to Medications | ||
== Physical Therapy Management (current best evidence) == | == Physical Therapy Management (current best evidence) == | ||
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add text here | add text here | ||
== Alternative/Holistic Management (current best evidence) == | == Alternative/Holistic Management<ref name="Native Remedies">http://www.nativeremedies.com/ailment/what-is-addisons-disease.html</ref> (current best evidence) == | ||
•<span class="Apple-tab-span" style="white-space:pre"> </span>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 | |||
•<span class="Apple-tab-span" style="white-space:pre"> </span>Ginger works as an anti-nausea medication and helps to decrease physicial and emotional stress | |||
•<span class="Apple-tab-span" style="white-space:pre"> </span>Liquorice improves the activity of mineralocorticoids<br> | |||
== Differential Diagnosis == | == Differential Diagnosis == | ||
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[http://www.nadf.us/diseases/addisons.htm National Adrenal Diseases Foundation] | [http://www.nadf.us/diseases/addisons.htm National Adrenal Diseases Foundation] | ||
[http://www.mayoclinic.com/health/addisons-disease/DS00361/DSECTION=tests%2Dand%2Ddiagnosis The Mayo Clinic]<br> | [http://www.mayoclinic.com/health/addisons-disease/DS00361/DSECTION=tests%2Dand%2Ddiagnosis The Mayo Clinic]<br> | ||
== Recent Related Research (from [http://www.ncbi.nlm.nih.gov/pubmed/ Pubmed]) == | == Recent Related Research (from [http://www.ncbi.nlm.nih.gov/pubmed/ Pubmed]) == | ||
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see [[Adding References|adding references tutorial]]. | see [[Adding References|adding references tutorial]]. | ||
<references /> | <references /> | ||
[[Category:Bellarmine_Student_Project]] | |||
Revision as of 04:57, 8 March 2010
Original Editors - Students 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]
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]
add text here
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]
add text here
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[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]
add text here
Case Reports[edit | edit source]
add links to case studies here (case studies should be added on new pages using the case study template)
Resources
[edit | edit source]
National Adrenal Diseases Foundation
Recent Related Research (from Pubmed)[edit | edit source]
see tutorial on Adding PubMed Feed
Extension:RSS -- Error: Not a valid URL: Feed goes here!!|charset=UTF-8|short|max=10
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
