Polyarteritis nodosa pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
===Pathogenesis=== | ===Pathogenesis=== | ||
Polyarteritis nodosa is a disease of unknown cause that affects [[arteries]], the [[blood vessels]] that carry oxygenated [[blood]] to organs and [[tissues]]. It occurs when certain [[immune cells]] attack the affected [[arteries]].[[Inflammation]] starts in the vessel [[intima]] and results in [[fibrinoid necrosis]] by destroying the internal and external [[elastic]] [[lamina]]. [[Aneurysms]] and [[thrombi]] may develop at the site of [[lesions]]. One hypothesis is that this condition is caused by [[antibodies]] against HBV, via a [[Hypersensitivity#Type_3_-_immune_complex | type IIII hypersensitivity reaction]]. [[Hepatitis C]] associated polyarteritis nodosa is the most common type among the [[hepatitis C]] associated [[vasculitis]] and has a severe clinical presentation.<ref name="pmid20981809">{{cite journal |author=Saadoun D, Terrier B, Semoun O, ''et al.'' |title=Hepatitis C virus-associated polyarteritis nodosa |journal=Arthritis Care Res (Hoboken) |volume=63 |issue=3 |pages=427–35 |year=2011 |month=March |pmid=20981809 |doi=10.1002/acr.20381 |url=}}</ref> | * Polyarteritis nodosa is a disease of unknown cause that affects [[arteries]], the [[blood vessels]] that carry oxygenated [[blood]] to organs and [[tissues]]. | ||
* PAN affects the medium sized arterial vessels. | |||
** Most commonly occurs at the branching vessels and bifurcation points. | |||
* PAN does not affect:<ref name="pmid12350194">{{cite journal |vauthors=Stone JH |title=Polyarteritis nodosa |journal=JAMA |volume=288 |issue=13 |pages=1632–9 |date=October 2002 |pmid=12350194 |doi= |url=}}</ref> | |||
** Large vessels like aorta. | |||
** Capillaries | |||
** Small arterioles. | |||
** Venous system. | |||
* It occurs when certain [[immune cells]] attack the affected [[arteries]]. | |||
* [[Inflammation]] starts in the vessel [[intima]] and results in [[fibrinoid necrosis]] by destroying the internal and external [[elastic]] [[lamina]]. | |||
* [[Aneurysms]] and [[thrombi]] may develop at the site of [[lesions]]. | |||
* One hypothesis is that this condition is caused by [[antibodies]] against HBV, via a [[Hypersensitivity#Type_3_-_immune_complex | type IIII hypersensitivity reaction]]. | |||
* [[Hepatitis C]] associated polyarteritis nodosa is the most common type among the [[hepatitis C]] associated [[vasculitis]] and has a severe clinical presentation.<ref name="pmid20981809">{{cite journal |author=Saadoun D, Terrier B, Semoun O, ''et al.'' |title=Hepatitis C virus-associated polyarteritis nodosa |journal=Arthritis Care Res (Hoboken) |volume=63 |issue=3 |pages=427–35 |year=2011 |month=March |pmid=20981809 |doi=10.1002/acr.20381 |url=}}</ref> | |||
* Clinical responses to [[immunosuppressive]] therapy suggest that [[immunological]] mechanisms play an active pathogenic role. | |||
* Due to [[inflammation]] of the medium to small sized [[vessels]] in PAN and the presence of impaired [[endothelial]] function, there could be direct [[endothelial cell]] activation and damage resulting from proinflammatory [[cytokines]] or [[antibodies]] (anti-endothelial cells antibodies). | |||
** These anti-endothelial cells antibodies in turn stimulate greater production of cytokines and adhesion [[molecules]] potentiating the [[inflammation]] causing more damage to the vessels <ref name="pmid12525387">{{cite journal| author=Filer AD, Gardner-Medwin JM, Thambyrajah J, Raza K, Carruthers DM, Stevens RJ et al.| title=Diffuse endothelial dysfunction is common to ANCA associated systemic vasculitis and polyarteritis nodosa. | journal=Ann Rheum Dis | year= 2003 | volume= 62 | issue= 2 | pages= 162-7 | pmid=12525387 | doi= | pmc=1754444 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12525387 }} </ref>. | |||
* | |||
* Inflammation may start in the vessel intima and progress to include the entire arterial wall, destroying the internal and external elastic lamina, resulting in fibrinoid necrosis.<sup> [[null 6]] </sup>Aneurysms develop in the weakened vessel, carrying a subsequent risk for rupture and hemorrhage. Thrombi may develop at the site of the lesions. As lesions progress, proliferation of the intima or media may result in obstruction and subsequent tissue ischemia or infarction.<sup> [[null 9]]</sup> | |||
===Genetics=== | ===Genetics=== | ||
===Associated Conditions=== | ===Associated Conditions=== | ||
Revision as of 15:16, 9 May 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Ali Poyan Mehr, M.D. [2] Associate Editor(s)-in-Chief: Olufunmilola Olubukola M.D.[3]Cafer Zorkun, M.D., Ph.D. [4]; Haritha Machavarapu, M.B.B.S.
Overview
Pathophysiology
Pathogenesis
- Polyarteritis nodosa is a disease of unknown cause that affects arteries, the blood vessels that carry oxygenated blood to organs and tissues.
- PAN affects the medium sized arterial vessels.
- Most commonly occurs at the branching vessels and bifurcation points.
- PAN does not affect:[1]
- Large vessels like aorta.
- Capillaries
- Small arterioles.
- Venous system.
- It occurs when certain immune cells attack the affected arteries.
- Inflammation starts in the vessel intima and results in fibrinoid necrosis by destroying the internal and external elastic lamina.
- Aneurysms and thrombi may develop at the site of lesions.
- One hypothesis is that this condition is caused by antibodies against HBV, via a type IIII hypersensitivity reaction.
- Hepatitis C associated polyarteritis nodosa is the most common type among the hepatitis C associated vasculitis and has a severe clinical presentation.[2]
- Clinical responses to immunosuppressive therapy suggest that immunological mechanisms play an active pathogenic role.
- Due to inflammation of the medium to small sized vessels in PAN and the presence of impaired endothelial function, there could be direct endothelial cell activation and damage resulting from proinflammatory cytokines or antibodies (anti-endothelial cells antibodies).
- These anti-endothelial cells antibodies in turn stimulate greater production of cytokines and adhesion molecules potentiating the inflammation causing more damage to the vessels [3].
- Inflammation may start in the vessel intima and progress to include the entire arterial wall, destroying the internal and external elastic lamina, resulting in fibrinoid necrosis. null 6 Aneurysms develop in the weakened vessel, carrying a subsequent risk for rupture and hemorrhage. Thrombi may develop at the site of the lesions. As lesions progress, proliferation of the intima or media may result in obstruction and subsequent tissue ischemia or infarction. null 9
Genetics
Associated Conditions
The following conditions are associated with the development of polyarteritis nodosa:
- Hepatitis B infection
- Hepatitis C infection
References
- ↑ Stone JH (October 2002). "Polyarteritis nodosa". JAMA. 288 (13): 1632–9. PMID 12350194.
- ↑ Saadoun D, Terrier B, Semoun O; et al. (2011). "Hepatitis C virus-associated polyarteritis nodosa". Arthritis Care Res (Hoboken). 63 (3): 427–35. doi:10.1002/acr.20381. PMID 20981809. Unknown parameter
|month=ignored (help) - ↑ Filer AD, Gardner-Medwin JM, Thambyrajah J, Raza K, Carruthers DM, Stevens RJ; et al. (2003). "Diffuse endothelial dysfunction is common to ANCA associated systemic vasculitis and polyarteritis nodosa". Ann Rheum Dis. 62 (2): 162–7. PMC 1754444. PMID 12525387.