Aortitis pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
===Inflammatory Aortitis=== | ===Inflammatory Aortitis=== | ||
Both GCA and Takayasu arteritis are associated with an inflammatory cellular infiltrate of the aortic media, adventitia, and vasa vasorum that contains a predominance of lymphocytes, macrophages, and multinucleated giant cells.2,3 Over time, scarring of the aortic media and destruction of the elastic lamina occur.2,3 Tree barking may be seen in both of these disorders, not just in syphilis-associated aortitis | Both GCA and Takayasu arteritis are associated with an inflammatory cellular infiltrate of the aortic media, adventitia, and vasa vasorum that contains a predominance of lymphocytes, macrophages, and multinucleated giant cells.2,3 Over time, scarring of the aortic media and destruction of the elastic lamina occur.2,3 Tree barking may be seen in both of these disorders, not just in syphilis-associated aortitis | ||
Granuloma formation and multinucleated giant cells may be seen in both GCA and Takayasu arteritis | Granuloma formation and multinucleated giant cells may be seen in both GCA and Takayasu arteritis | ||
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GCA has been associated with HLA-DR4, whereas Takayasu arteritis has been associated with HLA-BW52, HLA-DR2, and HLA-MB1 in Japanese patients and possibly with HLA-DR4 in non-Asian patients. | GCA has been associated with HLA-DR4, whereas Takayasu arteritis has been associated with HLA-BW52, HLA-DR2, and HLA-MB1 in Japanese patients and possibly with HLA-DR4 in non-Asian patients. | ||
aortitis has been reported in the HLA-B27–associated seronegative spondyloarthropathies Reiter syndrome and ankylosing spondylitis. | aortitis has been reported in the HLA-B27–associated seronegative spondyloarthropathies Reiter syndrome and ankylosing spondylitis. | ||
===Infectious Aortitis=== | |||
The majority of cases of bacterial 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 classic histopathological finding in syphilitic aneursym is a “tree barking” appearance of the aortic intima.<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> 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 16:16, 10 September 2015
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]
Overview
Aortitis is a term used to describe inflammation of the aortic wall.[1]
Pathophysiology
Inflammatory Aortitis
Both GCA and Takayasu arteritis are associated with an inflammatory cellular infiltrate of the aortic media, adventitia, and vasa vasorum that contains a predominance of lymphocytes, macrophages, and multinucleated giant cells.2,3 Over time, scarring of the aortic media and destruction of the elastic lamina occur.2,3 Tree barking may be seen in both of these disorders, not just in syphilis-associated aortitis Granuloma formation and multinucleated giant cells may be seen in both GCA and Takayasu arteritis Takayasu arteritis is more commonly associated with extensive intimal and adventitial fibrosis or scarring with resultant luminal narrowing.2,4,5 Aortic wall thickness generally is greater among patients with Takayasu aortitis than GCA.2,5 GCA is more commonly associated with extensive medial inflammation and necrosis and the formation of aortic aenurysms. GCA has been associated with HLA-DR4, whereas Takayasu arteritis has been associated with HLA-BW52, HLA-DR2, and HLA-MB1 in Japanese patients and possibly with HLA-DR4 in non-Asian patients. aortitis has been reported in the HLA-B27–associated seronegative spondyloarthropathies Reiter syndrome and ankylosing spondylitis.
Infectious Aortitis
The majority of cases of bacterial 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 classic histopathological finding in syphilitic aneursym is a “tree barking” appearance of the aortic intima.[1] 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 Gornik HL, Creager MA (2008). "Aortitis". Circulation. 117 (23): 3039–51. doi:10.1161/CIRCULATIONAHA.107.760686. PMC 2759760. PMID 18541754.
- ↑ "Syphilitic aortitis".