Addison's disease pathophysiology: Difference between revisions

Jump to navigation Jump to search
 
(3 intermediate revisions by 2 users not shown)
Line 11: Line 11:
{{CMG}} ; {{AE}} {{ADG}}
{{CMG}} ; {{AE}} {{ADG}}
==Overview==
==Overview==
The [[hypothalamus]] releases [[corticotropin-releasing hormone]] ([[CRH]]), which stimulates the [[pituitary gland]] to release [[Adrenocorticotropic hormone|corticotropin]] ([[ACTH]]). [[Adrenocorticotropic hormone|ACTH]] travels via the [[blood]] to the [[adrenal gland]], where it stimulates the release of [[cortisol]]. [[Cortisol]] is secreted by the [[Adrenal cortex|cortex]] of the [[adrenal gland]] from a region called the [[zona fasciculata]] in response to [[Adrenocorticotropic hormone|ACTH]]. Elevated levels of [[cortisol]] exert [[negative feedback]] on the [[Pituitary gland|pituitary]], which decreases the amount of [[Adrenocorticotropic hormone|ACTH]] released from the [[pituitary gland]]. Addison's disease results when the [[Adrenal gland|adrenal glands]] do not produce enough [[cortisol]] and [[aldosterone]].
The [[hypothalamus]] releases [[corticotropin-releasing hormone]] ([[CRH]]), which stimulates the [[pituitary gland]] to release [[corticotropin]] ([[ACTH]]). [[ACTH]] travels via the blood to the [[adrenal gland]], where it stimulates the release of [[cortisol]]. [[Cortisol]] is secreted by the cortex of the [[adrenal gland]] from a region called the [[zona fasciculata]] in response to [[ACTH]]. Elevated levels of cortisol exert [[negative feedback]] on the [[pituitary]], which decreases the amount of [[ACTH]] released from the [[pituitary gland]]. When the [[adrenal glands]] do not produce enough [[cortisol]] and [[aldosterone]], it results in Addison's disease.


==Normal Physiology of Adrenal Glands==
==Normal Physiology of Adrenal Glands==
Line 85: Line 85:
**Familial [[glucocorticoid]] insufficiency (associated with a recessive gene pattern)
**Familial [[glucocorticoid]] insufficiency (associated with a recessive gene pattern)
**[[Adrenomyeloneuropathy]] is known to be [[X-linked]]
**[[Adrenomyeloneuropathy]] is known to be [[X-linked]]
*Addison disease is associated with a variety of [[autoimmune]] conditions that have been linked to [[genetic]] factors
*Addison disease is associated with a variety of [[autoimmune]] conditions that have been linked to [[genetic]] factors.
*Patients with [[Autoimmune polyendocrine syndrome|autoimmune polyglandular failure]] might develop [[diabetes mellitus]], [[pernicious anemia]], and [[hypothyroidism]] secondary to [[antibodies]] which develop against the [[adrenal glands]]
*Patients with [[Autoimmune polyendocrine syndrome|autoimmune polyglandular failure]] might develop [[diabetes mellitus]], [[pernicious anemia]], and [[hypothyroidism]] secondary to [[antibodies]] which develop against the [[adrenal glands]].
[[Image:Renin-angiotensin-aldosterone system.png|center|frame|Source: By A. Rad (me) (Own work) [GFDL (<nowiki>http://www.gnu.org/copyleft/fdl.html</nowiki>) or CC-BY-SA-3.0 (<nowiki>http://creativecommons.org/licenses/by-sa/3.0/</nowiki>)], via Wikimedia Commons]]
[[Image:Renin-angiotensin-aldosterone system.png|center|frame|Source: By A. Rad (me) (Own work) [GFDL (<nowiki>http://www.gnu.org/copyleft/fdl.html</nowiki>) or CC-BY-SA-3.0 (<nowiki>http://creativecommons.org/licenses/by-sa/3.0/</nowiki>)], via Wikimedia Commons]]


==Associated conditions==
==Associated conditions==
Addison's disease is commonly seen associated with conditions such as:<ref name="pmid7734032">{{cite journal |vauthors=Zelissen PM, Bast EJ, Croughs RJ |title=Associated autoimmunity in Addison's disease |journal=J. Autoimmun. |volume=8 |issue=1 |pages=121–30 |year=1995 |pmid=7734032 |doi=10.1006/jaut.1995.0009 |url=}}</ref>
Addison's disease is commonly seen associated with conditions such as:<ref name="pmid7734032">{{cite journal |vauthors=Zelissen PM, Bast EJ, Croughs RJ |title=Associated autoimmunity in Addison's disease |journal=J. Autoimmun. |volume=8 |issue=1 |pages=121–30 |year=1995 |pmid=7734032 |doi=10.1006/jaut.1995.0009 |url=}}</ref>
*[[Autoimmune polyendocrine syndrome]]
*[[Autoimmune]] [[hypoparathyroidism]] resulting in [[hypocalcemia]]
*[[Autoimmune]] [[hypoparathyroidism]] resulting in [[hypocalcemia]]
*[[Vitiligo]]
*[[Vitiligo]]

Latest revision as of 20:05, 11 October 2017

Title
https://https://www.youtube.com/watch?v=V6XcBp8EV7Q%7C350}}

Addison's disease Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Addison's disease from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X Ray

CT

MRI

Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Addison's disease pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Addison's disease pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Addison's disease pathophysiology

CDC on Addison's disease pathophysiology

Addison's disease pathophysiology in the news

Blogs on Addison's disease pathophysiology

Directions to Hospitals Treating Addison's disease

Risk calculators and risk factors for Addison's disease pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Overview

The hypothalamus releases corticotropin-releasing hormone (CRH), which stimulates the pituitary gland to release corticotropin (ACTH). ACTH travels via the blood to the adrenal gland, where it stimulates the release of cortisol. Cortisol is secreted by the cortex of the adrenal gland from a region called the zona fasciculata in response to ACTH. Elevated levels of cortisol exert negative feedback on the pituitary, which decreases the amount of ACTH released from the pituitary gland. When the adrenal glands do not produce enough cortisol and aldosterone, it results in Addison's disease.

Normal Physiology of Adrenal Glands

Hypothalamic–pituitary–adrenal axis

Source: By BrianMSweis (Own work) [CC BY-SA 3.0 (http://creativecommons.org/licenses/by-sa/3.0)], via Wikimedia Commons

Cortisol

Harmone Type of class Function
Cortisol Glucocorticoids
Aldosterone Mineralocorticoids

Pathophysiology

Addison's disease occurs when the adrenal glands do not produce enough cortisol and, in some cases, aldosterone. Adrenal insufficiency may arise due to insufficient release of cortisol from the adrenal glands. Insufficient cortisol secretion may be due to adrenal dysgenesis (the gland does not form adequately during development), impaired steroidogenesis (the gland is present but is biochemically unable to produce cortisol) or adrenal destruction (disease processes leading to the gland being damaged).[1][2][3]

Mechanism of adrenal insufficiency Definition Pathophysiology
Adrenal dysgenesis Gland does not form adequately during development
Impaired steroidogenesis
Adrenal destruction
  • Disease processes leading to the gland being damaged

Genetics

Source: By A. Rad (me) (Own work) [GFDL (http://www.gnu.org/copyleft/fdl.html) or CC-BY-SA-3.0 (http://creativecommons.org/licenses/by-sa/3.0/)], via Wikimedia Commons

Associated conditions

Addison's disease is commonly seen associated with conditions such as:[6]

References

  1. Sarkar SB, Sarkar S, Ghosh S, Bandyopadhyay S (2012). "Addison's disease". Contemp Clin Dent. 3 (4): 484–6. doi:10.4103/0976-237X.107450. PMC 3636818. PMID 23633816.
  2. Nieman LK, Chanco Turner ML (2006). "Addison's disease". Clin. Dermatol. 24 (4): 276–80. doi:10.1016/j.clindermatol.2006.04.006. PMID 16828409.
  3. SMART GA (1953). "Addison's disease". Postgrad Med J. 29 (330): 200–7. PMC 2500363. PMID 13055541.
  4. Honour JW (2009). "Diagnosis of diseases of steroid hormone production, metabolism and action". J Clin Res Pediatr Endocrinol. 1 (5): 209–26. doi:10.4274/jcrpe.v1i5.209. PMC 3005746. PMID 21274298.
  5. Michels AW, Eisenbarth GS (2010). "Immunologic endocrine disorders". J. Allergy Clin. Immunol. 125 (2 Suppl 2): S226–37. doi:10.1016/j.jaci.2009.09.053. PMC 2835296. PMID 20176260.
  6. Zelissen PM, Bast EJ, Croughs RJ (1995). "Associated autoimmunity in Addison's disease". J. Autoimmun. 8 (1): 121–30. doi:10.1006/jaut.1995.0009. PMID 7734032.

Template:WH Template:WS