Aortitis pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
===Inflammatory Aortitis=== | ===Inflammatory Aortitis=== | ||
====Gross Pathology==== | |||
On gross pathology, characteristic findings of aortitis include:<ref>{{Cite web | title =Aortitis | url =http://librepathology.org/wiki/index.php/Vasculitides#Aortitis }}</ref> | |||
*A tree-bark appearance | |||
*Scarring of the aortic media and destruction of the elastic lamina | |||
====Microscopic Pathology==== | ====Microscopic Pathology==== | ||
Extensive intimal and adventitial [[fibrosis]] and [[scarring]] with resultant luminal narrowing are characteristic findings of aortitis due to [[Takayasu arteritis]]. Extensive medial [[inflammation]] and [[necrosis]] are characteristic findings of aortitis due to [[giant cell arteritis]].<ref name="pmid18541754">{{cite journal| author=Gornik HL, Creager MA| title=Aortitis. | journal=Circulation | year= 2008 | volume= 117 | issue= 23 | pages= 3039-51 | pmid=18541754 | doi=10.1161/CIRCULATIONAHA.107.760686 | pmc=PMC2759760 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18541754 }} </ref> | Extensive intimal and adventitial [[fibrosis]] and [[scarring]] with resultant luminal narrowing are characteristic findings of aortitis due to [[Takayasu arteritis]]. Extensive medial [[inflammation]] and [[necrosis]] are characteristic findings of aortitis due to [[giant cell arteritis]].<ref name="pmid18541754">{{cite journal| author=Gornik HL, Creager MA| title=Aortitis. | journal=Circulation | year= 2008 | volume= 117 | issue= 23 | pages= 3039-51 | pmid=18541754 | doi=10.1161/CIRCULATIONAHA.107.760686 | pmc=PMC2759760 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18541754 }} </ref> | ||
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*Inflammatory cellular infiltrate of the aortic media, adventitia, and vasa vasorum | *Inflammatory cellular infiltrate of the aortic media, adventitia, and vasa vasorum | ||
*[[Granuloma]] formation and [[multinucleated giant cells]] | *[[Granuloma]] formation and [[multinucleated giant cells]] | ||
===Infectious Aortitis=== | ===Infectious Aortitis=== | ||
The majority of cases of infectious aortitis are due to [[bacteria]] seeding through a segment of the aortic wall with existing pathology via the vasa vasorum. [[Tuberculous]] aortitis occurs due to miliary spread or as a result of direct seeding of the [[thoracic aorta]] from adjacent infected tissues. Syphilitic aortitis most commonly involves the [[ascending aorta]]. Inflammatory involvement of tertiary syphilis begins at the adventitia of the [[aortic arch]] which progressively causes | The majority of cases of infectious aortitis are due to [[bacteria]] seeding through a segment of the aortic wall with existing pathology via the vasa vasorum. [[Tuberculous]] aortitis occurs due to miliary spread or as a result of direct seeding of the [[thoracic aorta]] from adjacent infected tissues. Syphilitic aortitis most commonly involves the [[ascending aorta]]. Inflammatory involvement of tertiary syphilis begins at the adventitia of the [[aortic arch]] which progressively causes obliterative endarteritis of the vasa vasorum. This leads to narrowing of the lumen of the vasa vasorum, causing ischemic injury of the medial [[aortic arch]] and then finally loss of elastic support and dilation of the vessel.<ref>{{Cite web | title =Syphilitic aortitis | url = https://en.wikipedia.org/wiki/Syphilitic_aortitis}}</ref> | ||
==References== | ==References== |
Revision as of 18:37, 16 September 2015
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2] Associate Editor(s)-in-Chief: Maliha Shakil, M.D. [3]
Overview
Aortitis is inflammation or infection of the aortic wall.[1] On microscopic histopathological analysis, extensive intimal and adventitial fibrosis and scarring with resultant luminal narrowing are characteristic findings of aortitis due to Takayasu arteritis. Extensive medial inflammation and necrosis are characteristic findings on microscopic histopathological analysis of aortitis due to giant cell arteritis.[1] The majority of cases of infectious aortitis are due to bacteria seeding through a segment of the aortic wall with existing pathology via the vasa vasorum.
Pathophysiology
Inflammatory Aortitis
Gross Pathology
On gross pathology, characteristic findings of aortitis include:[2]
- A tree-bark appearance
- Scarring of the aortic media and destruction of the elastic lamina
Microscopic Pathology
Extensive intimal and adventitial fibrosis and scarring with resultant luminal narrowing are characteristic findings of aortitis due to Takayasu arteritis. Extensive medial inflammation and necrosis are characteristic findings of aortitis due to giant cell arteritis.[1] Histopathological findings associated with aortitis due to either giant cell arteritis or Takayasu arteritis include:[1]
- Inflammatory cellular infiltrate of the aortic media, adventitia, and vasa vasorum
- Granuloma formation and multinucleated giant cells
Infectious Aortitis
The majority of cases of infectious aortitis are due to bacteria seeding through a segment of the aortic wall with existing pathology via the vasa vasorum. Tuberculous aortitis occurs due to miliary spread or as a result of direct seeding of the thoracic aorta from adjacent infected tissues. Syphilitic aortitis most commonly involves the ascending aorta. Inflammatory involvement of tertiary syphilis begins at the adventitia of the aortic arch which progressively causes obliterative endarteritis of the vasa vasorum. This leads to narrowing of the lumen of the vasa vasorum, causing ischemic injury of the medial aortic arch and then finally loss of elastic support and dilation of the vessel.[3]
References
- ↑ 1.0 1.1 1.2 1.3 Gornik HL, Creager MA (2008). "Aortitis". Circulation. 117 (23): 3039–51. doi:10.1161/CIRCULATIONAHA.107.760686. PMC 2759760. PMID 18541754.
- ↑ "Aortitis".
- ↑ "Syphilitic aortitis".