Endocarditis pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
The pathogenesis of infective endocarditis includes valvular damage, altered and turbulent flow, bacteremia, and lack of blood supply to the | The pathogenesis of infective endocarditis includes valvular damage, altered and turbulent flow, bacteremia, and lack of blood supply to the [[valve]]s.<ref name=abc> Infective endocarditis. Wikipedia (2015). URL=https://en.wikipedia.org/wiki/Infective_endocarditis#Pathogenesis Accessed on September 21, 2015</ref><ref name=endo> Endocarditis. Wikipedia (2015). URL= https://en.wikipedia.org/wiki/Endocarditis Accessed on September 21, 2015</ref> Damaged endothelium becomes a site for attachment of infectious agents in infectious endocarditis. Nonbacterial thrombotic endocarditis is related to hypercoaguable states such as [[pregnancy]] or systemic bacterial [[infection]]. The characteristic lesion of endocarditis is a vegetation.<ref name="pmid11794152">{{cite journal| author=Mylonakis E, Calderwood SB| title=Infective endocarditis in adults. | journal=N Engl J Med | year= 2001 | volume= 345 | issue= 18 | pages= 1318-30 | pmid=11794152 | doi=10.1056/NEJMra010082 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11794152 }} </ref> Vegetations are composed of [[fibrin]], inflammatory cells, [[platelets]], and microorganisms.<ref name="pmid11794152">{{cite journal| author=Mylonakis E, Calderwood SB| title=Infective endocarditis in adults. | journal=N Engl J Med | year= 2001 | volume= 345 | issue= 18 | pages= 1318-30 | pmid=11794152 | doi=10.1056/NEJMra010082 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11794152 }}</ref> | ||
==Pathophysiology== | ==Pathophysiology== | ||
Revision as of 15:18, 28 September 2015
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Maliha Shakil, M.D. [2]
Overview
The pathogenesis of infective endocarditis includes valvular damage, altered and turbulent flow, bacteremia, and lack of blood supply to the valves.[1][2] Damaged endothelium becomes a site for attachment of infectious agents in infectious endocarditis. Nonbacterial thrombotic endocarditis is related to hypercoaguable states such as pregnancy or systemic bacterial infection. The characteristic lesion of endocarditis is a vegetation.[3] Vegetations are composed of fibrin, inflammatory cells, platelets, and microorganisms.[3]
Pathophysiology
Pathogenesis
Infective Endocarditis
The pathogenesis of infective endocarditis includes:[1][2]
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Nonbacterial thrombotic endocarditis
Nonbacterial thrombotic endocarditis (NBTE), also called marantic endocarditis is most commonly found on previously undamaged valves.[2] As opposed to infective endocarditis, the vegetations in NBTE are small, sterile, and tend to aggregate along the edges of the valve or the cusps.[2] Also unlike infective endocarditis, NBTE does not cause an inflammation response from the body.[2] NBTE usually occurs due to hypercoaguable states such as systemic bacterial infection or pregnancy.[2] NBTE may also occur in patients with cancer, particularly mucinous adenocarcinoma.[2] Libman-Sacks endocarditis is another form of sterile endocarditis; this form occurs more often in patients with lupus erythematosus and is thought to be due to the deposition of immune complexes. Libman-Sacks endocarditis involves small vegetations, while infective endocarditis is composed of large vegetations.[2] These immune complexes precipitate an inflammatory reaction, which helps to differentiate it from NBTE.[2] Also unlike NBTE, Libman-Sacks endocarditis does not seem to have a preferred location of deposition and may form on the undersurfaces of the valves or even on the endocardium.[2]
Gross and Microscopic Pathology
The characteristic lesion of endocarditis is a vegetation.[3] Vegetations are composed of fibrin, inflammatory cells, platelets, and microorganisms.[3] Characteristic features of endocarditis on gross pathology and histopathological analysis include:[4]
| Endocarditis Subtype | Features on Gross Pathology | Features on Histopathological Microscopic Analysis |
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| Nonbacterial Thrombotic Endocarditis |
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Pathology
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Heart; Breast intraductal papilloma metastasis. Thrombotic Nonbacterial Endocarditis (Infected): Gross mitral valve natural color vegetations well illustrated these were secondarily infected with staphylococcus case of 8 year survival breast intraductal papillary adenocarcinoma with extensive metastases. Aortic valve also involved
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Thrombotic Nonbacterial Endocarditis Infected: Micro low mag H&E fibrin vegetation with masses of staphylococci and inflammatory cells in valve secondarily infected case 8 year survival breast papillary intraductal adenocarcinoma with extensive metastases gross is aortic valve lesions.
Videos
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References
- ↑ 1.0 1.1 Infective endocarditis. Wikipedia (2015). URL=https://en.wikipedia.org/wiki/Infective_endocarditis#Pathogenesis Accessed on September 21, 2015
- ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 2.8 2.9 Endocarditis. Wikipedia (2015). URL= https://en.wikipedia.org/wiki/Endocarditis Accessed on September 21, 2015
- ↑ 3.0 3.1 3.2 3.3 Mylonakis E, Calderwood SB (2001). "Infective endocarditis in adults". N Engl J Med. 345 (18): 1318–30. doi:10.1056/NEJMra010082. PMID 11794152.
- ↑ Infective Endocarditis. Libre Pathology (2015). URL=http://librepathology.org/wiki/index.php/Infective_endocarditis Accessed on September 21, 2015