Tuberculous pericarditis pathophysiology: Difference between revisions
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{{Tuberculous pericarditis}} | {{Tuberculous pericarditis}} | ||
{{CMG}}; '''Associate Editor-In-Chief:''' [[Varun Kumar]], M.B.B.S.; [[Lakshmi Gopalakrishnan]], M.B.B.S. | {{CMG}}; '''Associate Editor-In-Chief:''' [[Varun Kumar]], M.B.B.S.; [[Lakshmi Gopalakrishnan]], M.B.B.S. | ||
==Pathophysiology== | == Pathophysiology == | ||
[[Tuberculous pericarditis]] develops as a result of lymphatic spread from peritracheal, peribronchial or [[mediastinal lymphnodes]] or by contiguous spread from a focus of infection in the lung or pleura. This causes acute inflammation of the [[pericardium]] with infiltration of polymorphonuclear ([[PMN]]) leukocytes and pericardial vascularization. This may lead to [[pericardial effusion]] and fibrinous changes of the pericardium. There are four pathologic stages of involvement:<ref name="pmid18610109">{{cite journal| author=Peel AA| title=TUBERCULOUS PERICARDITIS. | journal=Br Heart J | year= 1948 | volume= 10 | issue= 3 | pages= 195-207 | pmid=18610109 | doi= | pmc=PMC481044 | url= }} </ref><ref name="pmid4050698">{{cite journal| author=Permanyer-Miralda G, Sagristá-Sauleda J, Soler-Soler J| title=Primary acute pericardial disease: a prospective series of 231 consecutive patients. | journal=Am J Cardiol | year= 1985 | volume= 56 | issue= 10 | pages= 623-30 | pmid=4050698 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4050698 }} </ref><ref name="pmid16330703">{{cite journal| author=Mayosi BM, Burgess LJ, Doubell AF| title=Tuberculous pericarditis. | journal=Circulation | year= 2005 | volume= 112 | issue= 23 | pages= 3608-16 | pmid=16330703 | doi=10.1161/CIRCULATIONAHA.105.543066 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16330703 }} </ref> | [[Tuberculous pericarditis]] develops as a result of lymphatic spread from peritracheal, peribronchial or [[mediastinal lymphnodes]] or by contiguous spread from a focus of infection in the lung or pleura. This causes acute inflammation of the [[pericardium]] with infiltration of polymorphonuclear ([[PMN]]) leukocytes and pericardial vascularization. This may lead to [[pericardial effusion]] and fibrinous changes of the pericardium. There are four pathologic stages of involvement:<ref name="pmid18610109">{{cite journal| author=Peel AA| title=TUBERCULOUS PERICARDITIS. | journal=Br Heart J | year= 1948 | volume= 10 | issue= 3 | pages= 195-207 | pmid=18610109 | doi= | pmc=PMC481044 | url= }} </ref><ref name="pmid4050698">{{cite journal| author=Permanyer-Miralda G, Sagristá-Sauleda J, Soler-Soler J| title=Primary acute pericardial disease: a prospective series of 231 consecutive patients. | journal=Am J Cardiol | year= 1985 | volume= 56 | issue= 10 | pages= 623-30 | pmid=4050698 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4050698 }} </ref><ref name="pmid16330703">{{cite journal| author=Mayosi BM, Burgess LJ, Doubell AF| title=Tuberculous pericarditis. | journal=Circulation | year= 2005 | volume= 112 | issue= 23 | pages= 3608-16 | pmid=16330703 | doi=10.1161/CIRCULATIONAHA.105.543066 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16330703 }} </ref> | ||
:'''Stage 1:''' Presence of diffuse [[fibrin]] deposition, [[granulomas]] and abundant [[mycobacterium]] | : '''Stage 1:''' Presence of diffuse [[fibrin]] deposition, [[granulomas]] and abundant [[mycobacterium]] | ||
:'''Stage 2:''' Development of [[serous]] or serosanguineous pericardial effusion with a predominantly lymphocytic exudate with [[monocytes]] and [[foam cell]]s | : '''Stage 2:''' Development of [[serous]] or serosanguineous pericardial effusion with a predominantly lymphocytic exudate with [[monocytes]] and [[foam cell]]s | ||
:'''Stage 3:''' Absorption of the effusion with organization of granulomatous [[caseation]] and thickening of [[pericardium]] secondary to deposition of [[fibrin]] and [[collagen]]. | : '''Stage 3:''' Absorption of the effusion with organization of granulomatous [[caseation]] and thickening of [[pericardium]] secondary to deposition of [[fibrin]] and [[collagen]]. | ||
:'''Stage 4:''' Development of [[constrictive pericarditis]]. The pericardial space is obliterated by dense adhesions with marked thickening of [[parietal]] layer and replacement of [[granulomas]] by fibrous tissue. | : '''Stage 4:''' Development of [[constrictive pericarditis]]. The pericardial space is obliterated by dense adhesions with marked thickening of [[parietal]] layer and replacement of [[granulomas]] by fibrous tissue. | ||
[[Effusive constrictive pericarditis]]<ref name="pmid14749455">{{cite journal| author=Sagristà-Sauleda J, Angel J, Sánchez A, Permanyer-Miralda G, Soler-Soler J| title=Effusive-constrictive pericarditis. | journal=N Engl J Med | year= 2004 | volume= 350 | issue= 5 | pages= 469-75 | pmid=14749455 | doi=10.1056/NEJMoa035630 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14749455 }} </ref> may be seen in some patients. The visceral pericardium thickens with [[fibrin]] deposition (changes of [[constrictive pericarditis]]) and concomitantly there is presence of [[pericardial effusion]] which may present as [[cardiac tamponade]]. In this scenario, the [[diastolic pressure]] continues to be elevated after [[pericardiocentesis]] due to persistent pericardial constriction. | [[Effusive constrictive pericarditis]]<ref name="pmid14749455">{{cite journal| author=Sagristà-Sauleda J, Angel J, Sánchez A, Permanyer-Miralda G, Soler-Soler J| title=Effusive-constrictive pericarditis. | journal=N Engl J Med | year= 2004 | volume= 350 | issue= 5 | pages= 469-75 | pmid=14749455 | doi=10.1056/NEJMoa035630 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14749455 }} </ref> may be seen in some patients. The visceral pericardium thickens with [[fibrin]] deposition (changes of [[constrictive pericarditis]]) and concomitantly there is presence of [[pericardial effusion]] which may present as [[cardiac tamponade]]. In this scenario, the [[diastolic pressure]] continues to be elevated after [[pericardiocentesis]] due to persistent pericardial constriction. | ||
==References== | == References == | ||
{{reflist|2}} | {{reflist|2}} | ||
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[[Category:Up-To-Date]] | [[Category:Up-To-Date]] | ||
[[Category:Up-To-Date cardiology]] | [[Category:Up-To-Date cardiology]] | ||
[[Category:Needs overview]] | |||
Revision as of 23:03, 10 December 2012
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Varun Kumar, M.B.B.S.; Lakshmi Gopalakrishnan, M.B.B.S.
Pathophysiology
Tuberculous pericarditis develops as a result of lymphatic spread from peritracheal, peribronchial or mediastinal lymphnodes or by contiguous spread from a focus of infection in the lung or pleura. This causes acute inflammation of the pericardium with infiltration of polymorphonuclear (PMN) leukocytes and pericardial vascularization. This may lead to pericardial effusion and fibrinous changes of the pericardium. There are four pathologic stages of involvement:[1][2][3]
- Stage 1: Presence of diffuse fibrin deposition, granulomas and abundant mycobacterium
- Stage 2: Development of serous or serosanguineous pericardial effusion with a predominantly lymphocytic exudate with monocytes and foam cells
- Stage 3: Absorption of the effusion with organization of granulomatous caseation and thickening of pericardium secondary to deposition of fibrin and collagen.
- Stage 4: Development of constrictive pericarditis. The pericardial space is obliterated by dense adhesions with marked thickening of parietal layer and replacement of granulomas by fibrous tissue.
Effusive constrictive pericarditis[4] may be seen in some patients. The visceral pericardium thickens with fibrin deposition (changes of constrictive pericarditis) and concomitantly there is presence of pericardial effusion which may present as cardiac tamponade. In this scenario, the diastolic pressure continues to be elevated after pericardiocentesis due to persistent pericardial constriction.
References
- ↑ Peel AA (1948). "TUBERCULOUS PERICARDITIS". Br Heart J. 10 (3): 195–207. PMC 481044. PMID 18610109.
- ↑ Permanyer-Miralda G, Sagristá-Sauleda J, Soler-Soler J (1985). "Primary acute pericardial disease: a prospective series of 231 consecutive patients". Am J Cardiol. 56 (10): 623–30. PMID 4050698.
- ↑ Mayosi BM, Burgess LJ, Doubell AF (2005). "Tuberculous pericarditis". Circulation. 112 (23): 3608–16. doi:10.1161/CIRCULATIONAHA.105.543066. PMID 16330703.
- ↑ Sagristà-Sauleda J, Angel J, Sánchez A, Permanyer-Miralda G, Soler-Soler J (2004). "Effusive-constrictive pericarditis". N Engl J Med. 350 (5): 469–75. doi:10.1056/NEJMoa035630. PMID 14749455.