Aortitis pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
===Inflammatory Aortitis=== | ===Inflammatory Aortitis=== | ||
Giant cell arteritis and Takayasu arteritis are associated with inflammatory cellular infiltrate of the aortic media, adventitia, and vasa vasorum. Eventually scarring of the aortic media and destruction of the elastic lamina may occur. On microscopic histopathological analysis, granuloma formation, a tree-bark appearance, and multinucleated giant cells may be seen in either Takayasu arteritis or | [[Giant cell arteritis]] and [[Takayasu arteritis]] are associated with inflammatory cellular infiltrate of the aortic media, adventitia, and vasa vasorum. Eventually scarring of the aortic media and destruction of the elastic lamina may occur. On microscopic histopathological analysis, [[granuloma]] formation, a tree-bark appearance, and [[multinucleated giant cells]] may be seen in either [[Takayasu arteritis]] or [[giant cell arteritis]]. 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]].<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> | ||
===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. | 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 17:25, 10 September 2015
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]
Overview
Aortitis is inflammation 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 is a characteristic finding 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. The classic histopathological finding in syphilitic aneursym is a “tree barking” appearance of the aortic intima.[1]
Pathophysiology
Inflammatory Aortitis
Giant cell arteritis and Takayasu arteritis are associated with inflammatory cellular infiltrate of the aortic media, adventitia, and vasa vasorum. Eventually scarring of the aortic media and destruction of the elastic lamina may occur. On microscopic histopathological analysis, granuloma formation, a tree-bark appearance, and multinucleated giant cells may be seen in either Takayasu arteritis or giant cell arteritis. 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]
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.[2]
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.
- ↑ "Syphilitic aortitis".