Endocarditis pathophysiology: Difference between revisions
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** Initiating phase | ** Initiating phase | ||
*** Immune complexes | *** Immune complexes | ||
****circulating immune complexes and complement deposition can initiate the process. | ****circulating immune complexes and complement deposition can initiate the process.<ref>{{cite book | last = Williams | first = Ralph | title = Immune complexes in clinical and experimental medicine | publisher = Harvard University Press | location = Cambridge, Mass | year = 1980 | isbn = 978-0674444386 }}</ref> | ||
****The example for this initiating factor in libman sacks endocarditis in lupus patients.<ref name="pmid3135393">{{cite journal |vauthors=Ford PM, Ford SE, Lillicrap DP |title=Association of lupus anticoagulant with severe valvular heart disease in systemic lupus erythematosus |journal=J. Rheumatol. |volume=15 |issue=4 |pages=597–600 |date=April 1988 |pmid=3135393 |doi= |url=}}</ref> | ****The example for this initiating factor in libman sacks endocarditis in lupus patients.<ref name="pmid3135393">{{cite journal |vauthors=Ford PM, Ford SE, Lillicrap DP |title=Association of lupus anticoagulant with severe valvular heart disease in systemic lupus erythematosus |journal=J. Rheumatol. |volume=15 |issue=4 |pages=597–600 |date=April 1988 |pmid=3135393 |doi= |url=}}</ref> | ||
*** Hypoxia | *** Hypoxia |
Revision as of 16:12, 2 January 2020
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Endocarditis Microchapters |
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Endocarditis pathophysiology On the Web |
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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. 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. Vegetations are composed of fibrin, inflammatory cells, platelets, and microorganisms.
Pathophysiology
Pathogenesis
Infective Endocarditis
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Nonbacterial Thrombotic Endocarditis
- The exact pathogenesis of nonbacterial thrombotic endocarditis is not completely understood.
- We can divide the pathogenesis pathway of nonbacterial endocarditis into to phase:
- Nonbacterial thrombotic endocarditis (NBTE), also called marantic endocarditis is most commonly found on previously undamaged valves.
- The vegetations in NBTE are small, sterile, and tend to aggregate along the edges of the valve or the cusps.
- Unlike infective endocarditis, NBTE does not cause an inflammation response from the body.
- NBTE usually occurs due to hypercoaguable states such as systemic bacterial infection or pregnancy.
- NBTE may also occur in patients with cancer, particularly mucinous adenocarcinoma.
- 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.
- These immune complexes precipitate an inflammatory reaction, which helps to differentiate it from NBTE.
- 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]
Genetics
Associated Conditions
Gross Pathology
Microscopic Pathology
Gross and Microscopic Pathology
The characteristic lesion of endocarditis is a vegetation. Vegetations are composed of fibrin, inflammatory cells, platelets, and microorganisms.[5] Characteristic features of endocarditis on gross pathology and histopathological analysis include:[6]
Endocarditis Subtype | Features on Gross Pathology | Features on Histopathological Microscopic Analysis |
Infective Endocarditis |
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Nonbacterial Thrombotic Endocarditis |
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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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Nonbacterial Thrombotic 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
- ↑ Infective endocarditis. Wikipedia (2015). https://en.wikipedia.org/wiki/Infective_endocarditis#Pathogenesis Accessed on September 21, 2015
- ↑ 2.0 2.1 Endocarditis. Wikipedia (2015). https://en.wikipedia.org/wiki/Endocarditis Accessed on September 21, 2015
- ↑ Williams, Ralph (1980). Immune complexes in clinical and experimental medicine. Cambridge, Mass: Harvard University Press. ISBN 978-0674444386.
- ↑ Ford PM, Ford SE, Lillicrap DP (April 1988). "Association of lupus anticoagulant with severe valvular heart disease in systemic lupus erythematosus". J. Rheumatol. 15 (4): 597–600. PMID 3135393.
- ↑ 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