Pericarditis pathophysiology: Difference between revisions

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{{Pericarditis}}
{{Pericarditis}}


{{CMG}}; '''Associate Editor(s)-In-Chief:''' [[Varun Kumar, M.B.B.S.]], {{CZ}}, [[User:Rim Halaby|Rim Halaby]]
{{CMG}}; '''Associate Editor(s)-In-Chief:''' [[Varun Kumar, M.B.B.S.]], {{CZ}}, [[User:Rim Halaby|Rim Halaby]]{{Homa}}


==Overview==
==Overview==
Pericarditis is [[inflammation]] of the [[pericardium]], which is the double-walled sac that contains the [[heart]] and the roots of the [[great vessels]]. There can be an accompanying accumulation of fluid that can be either [[serous]] (free flowing fluid) or [[fibrinous]] (an [[exudate]], which is a thick fluid composed of proteins, [[fibrin]] strands, inflammatory cells, cell breakdown products, and sometimes [[bacteria]]). Vascular congestion of the [[pericardium]] is also present. The underlying [[myocardium]] may or may not be inflamed as well. If the [[myocardium]] is involved in the [[inflammatory process]], it is called myopericarditis, and [[CK]] and [[troponin]] levels may be elevated.
Pericarditis is [[inflammation]] of the [[pericardium]], which is the double-walled sac that contains the [[heart]] and the roots of the [[great vessels]]. There can be an accompanying accumulation of [[fluid]] that can be either [[serous]] (free flowing [[fluid]]) or [[fibrinous]] (an [[exudate]], which is a thick [[fluid]] composed of [[proteins]], [[fibrin]] strands, [[inflammatory cells]], [[cell]] breakdown products, and sometimes [[bacteria]]). [[Vascular congestion]] of the [[pericardium]] is also present. The underlying [[myocardium]] may or may not be [[inflamed]] as well. If the [[myocardium]] is involved in the [[inflammatory process]], it is called [[myopericarditis]], and [[CK]] and [[troponin]] levels may be elevated. [[Cardio|Cardiotropic]] [[viruses]] usually spread to the [[myocardium]] and [[pericardium]] [[Hematogen|hematogenously]] and cause [[acute]] [[inflammation]] with [[Infiltration (medical)|infiltration]] of [[Polymorphonuclear cells|polymorphonuclear]] ([[PMN]]) [[leukocytes]] and [[pericardial]] vascularization. Most [[patients]] with [[viral]] pericarditis recover completely with few developing recurrences. Some [[patients]] develop [[constrictive pericarditis]] which could be disabling. [[Bacterial]] pericarditis results from [[contiguous]] spread of [[infection]] within the [[chest]], either [[de novo]] or after [[surgery]] or [[trauma]], spread from [[infective endocarditis]], [[Hematogen|hematogenous]], or direct [[inoculation]] as a result of [[Penetrating trauma|penetrating injury]] or [[cardiothoracic surgery]].


==Pathophysiology==
==Pathophysiology==
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====Layers of the Pericardium====
====Layers of the Pericardium====
*The [[pericardium]] is made up of two layers:
*The [[pericardium]] is made up of two layers:<ref =="" “kishore”="">Kishore, K. (2003). The Heart of Structural Development: The Functional Basis of the Location and Morphology of the Human Vascular Pump. J Postgrad Med, 49:282-4.</ref><ref =="" "moore"="">Moore, K. L., Agur, A. M., & Dalley, A. F. (2011). Essential Clinical Anatomy - Fourth Edition. Lippincott Williams & Wilkins.</ref><ref =="" "tank"="">Tank, P. W. (2009). Grant's Dissector - Fourteenth Edition. Lippincott Williams & Wilkins.</ref>
**Fibrous pericardium
**[[Fibrous]] [[pericardium]]:
***Hard protective external layer
***Hard protective external layer
***Attached to [[sternum]] anteriorly by sterno-pericardial ligaments and fused with the central tendon of the [[diaphragm]] and great vessels to allow mobility of the pericardial sac against sudden cardiac overfilling
***Attached to [[sternum]] anteriorly by [[Sternum|sterno]]-[[pericardial]] [[ligaments]] and fused with the [[central tendon]] of the [[diaphragm]] and [[great vessels]] to allow [[mobility]] of the [[pericardial sac]] against sudden [[cardiac]] overfilling
**Serous pericardium
**[[Serous pericardium]]:
***Smooth internal layer made up of 2 components:
***Smooth [[internal]] layer made up of 2 components:
****Parietal: reflects onto fibrous pericardium
****[[Parietal]]: reflects onto [[fibrous pericardium]]
****Visceral: reflects onto [[heart]] and great vessels and forms the epicardium, the external layer of the heart wall
****[[Visceral]]: reflects onto [[heart]] and [[great vessels]] and forms the [[epicardium]], the external layer of the [[heart]] wall
*Pericardial cavity: Potential space between parietal and visceral layers. It contains a serous fluid film that occupies the cavity and functions as lubricant against friction by all chest movements.<ref =="" “kishore”="">Kishore, K. (2003). The Heart of Structural Development: The Functional Basis of the Location and Morphology of the Human Vascular Pump. J Postgrad Med, 49:282-4.</ref><ref =="" "moore"="">Moore, K. L., Agur, A. M., & Dalley, A. F. (2011). Essential Clinical Anatomy - Fourth Edition. Lippincott Williams & Wilkins.</ref><ref =="" "tank"="">Tank, P. W. (2009). Grant's Dissector - Fourteenth Edition. Lippincott Williams & Wilkins.</ref>
*[[Pericardial cavity]]: Potential space between [[parietal]] and [[visceral]] layers. It contains a [[serous fluid]] film that occupies the [[cavity]] and functions as [[lubricant]] against [[friction]] by all [[chest]] movements.


====Pericardial Sinuses====
====Pericardial Sinuses====


*There are two small chambers or sinuses located where the visceral and parietal pericardia are continuous with one another within the pericardial cavity.
*There are two small chambers or [[Sinuse|sinuses]] located where the [[visceral]] and [[parietal]] [[pericardium]] are [[continuous]] with one another within the [[pericardial cavity]].<ref =="" “kishore”="">Kishore, K. (2003). The Heart of Structural Development: The Functional Basis of the Location and Morphology of the Human Vascular Pump. J Postgrad Med, 49:282-4.</ref><ref =="" "moore"="">Moore, K. L., Agur, A. M., & Dalley, A. F. (2011). Essential Clinical Anatomy - Fourth Edition. Lippincott Williams & Wilkins.</ref><ref =="" "tank"="">Tank, P. W. (2009). Grant's Dissector - Fourteenth Edition. Lippincott Williams & Wilkins.</ref>
*Transverse sinus:
*[[Transverse sinus]]:
**Located posterior to the [[pulmonary trunk]] and [[ascending aorta]] at the level between the [[superior vena cava]] and [[aortic arch]]
**Located [[posterior]] to the [[pulmonary trunk]] and [[ascending aorta]] at the level between the [[superior vena cava]] and [[aortic arch]]
**Formed after dorsal mesocardium rupture embryonically
**Formed after [[dorsal]] [[myocardium]] ruptured [[Embryonic|embryonically]]
**Functional role is to allow the unhindered expansion of great arteries posteriorly during cardiac [[systole]]
**Functional role is to allow the unhindered expansion of [[great arteries]] [[Posterior|posteriorly]] during [[cardiac]] [[systole]]
**Utilized surgically to pass surgical clamps or place ligatures around great arteries.
**Utilized [[Surgery|surgically]] to pass surgical [[Clamp connection|clamps]] or place [[Ligature|ligatures]] around [[great arteries]].
*Oblique sinus:
*[[Oblique sinus]]:
**A blind recess (cul-de-sac) posterior to the [[left atrium]] between [[superior vena cava]], right and left [[pulmonary vein]]s inferior to the transverse sinus
**A blind recess (cul-de-sac) [[posterior]] to the [[left atrium]] between [[superior vena cava]], right and left [[pulmonary vein]]s inferior to the [[Transverse sinuses|transverse sinus]]
**Formed embryonically by the incorporation of the [[pulmonary vein]] tributaries into the [[left atrium]]
**Formed [[Embryonic|embryonically]] by the incorporation of the [[pulmonary vein]] [[tributaries]] into the [[left atrium]]
**Functional role believed to be the expansion of the left atrium upon normal collapse of the thorax<ref =="" “kishore”="">Kishore, K. (2003). The Heart of Structural Development: The Functional Basis of the Location and Morphology of the Human Vascular Pump. J Postgrad Med, 49:282-4.</ref><ref =="" "moore"="">Moore, K. L., Agur, A. M., & Dalley, A. F. (2011). Essential Clinical Anatomy - Fourth Edition. Lippincott Williams & Wilkins.</ref><ref =="" "tank"="">Tank, P. W. (2009). Grant's Dissector - Fourteenth Edition. Lippincott Williams & Wilkins.</ref>
**Functional role believed to be the expansion of the [[left atrium]] upon normal [[collapse]] of the [[thorax]]


<div align="center">
<div align="center"><gallery heights="125" widths="125">
<gallery heights="125" widths="125">
Image:Pericardium.JPG
Image:Pericardium.JPG
Image:Pericardial sinuses.JPG
Image:Pericardial sinuses.JPG
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<br />
====Diseases of the Pericardium====
====Diseases of the Pericardium====


* [[Pericarditis]] is an inflammatory condition of the pericardium.
* [[Pericarditis]] is an [[inflammatory]] condition of the [[pericardium]].
* [[Pericardial effusion]] is fluid accumulation in the pericardial sac.
* [[Pericardial effusion]] is [[fluid]] accumulation in the [[pericardial sac]].
* [[Constrictive pericarditis]] occurs when there is a scar encasing, the heart that chronically constricts the filling of the heart.
* [[Constrictive pericarditis]] occurs when there is a [[scar]] encasing, the [[heart]] that [[Chronic (medicine)|chronically]] constricts the filling of the [[heart]].
* [[Cardiac tamponade]] is a medical emergency in which fluid in the pericardial sac acutely restricts the filling of the heart. This requires surgical drainage or [[pericardiocentesis]].
* [[Cardiac tamponade]] is a [[medical emergency]] in which [[fluid]] in the [[pericardial sac]] [[Acute (medicine)|acutely]] restricts the filling of the [[heart]]. This requires [[Surgery|surgical]] drainage or [[pericardiocentesis]].
 
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==== Additional Images ====
 
 


===Additional Images===
<br /><gallery>
<gallery>
  Image:Gray806.png|The phrenic nerve and its relations with the vagus nerve.
  Image:Gray806.png|The phrenic nerve and its relations with the vagus nerve.
  Image:Gray846.png|Thoracic portion of the sympathetic trunk.
  Image:Gray846.png|Thoracic portion of the sympathetic trunk.
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  Image:Gray1178.png|The thymus of a full-time fetus, exposed in situ.
  Image:Gray1178.png|The thymus of a full-time fetus, exposed in situ.
</gallery>
</gallery>


===Pathogenesis===
===Pathogenesis===
*Cardiotropic viruses usually spread to the [[myocardium]] and [[pericardium]] hematogenously and cause acute [[inflammation]] with infiltration of polymorphonuclear ([[PMN]]) [[leukocytes]] and pericardial vascularization. This may cause [[pericardial effusion]] and [[fibrinous]] change of the pericardium. The pericardium may also develop a [[serous]] or hemorrhagic effusion. Most patients with viral pericarditis recover completely with few developing recurrences.<ref name="pmid1920818">{{cite journal| author=Ilan Y, Oren R, Ben-Chetrit E| title=Acute pericarditis: etiology, treatment and prognosis. A study of 115 patients. | journal=Jpn Heart J | year= 1991 | volume= 32 | issue= 3 | pages= 315-21 | pmid=1920818 | doi= | pmc= | url= }} </ref><ref name="pmid2249218">{{cite journal| author=Shabetai R| title=Acute pericarditis. | journal=Cardiol Clin | year= 1990 | volume= 8 | issue= 4 | pages= 639-44 | pmid=2249218 | doi= | pmc= | url= }} </ref> Some patients develop [[constrictive pericarditis]] which could be disabling.<ref name="pmid5489188">{{cite journal| author=Matthews JD, Cameron SJ, George M| title=Constrictive pericarditis following Coxsackie virus infection. | journal=Thorax | year= 1970 | volume= 25 | issue= 5 | pages= 624-6 | pmid=5489188 | doi= | pmc=PMC472200 | url= }} </ref>
*Cardiotropic [[viruses]] usually spread to the [[myocardium]] and [[pericardium]] [[Hematogen|hematogenously]] and cause [[acute]] [[inflammation]] with [[Infiltration (medical)|infiltration]] of [[Polymorphonuclear cells|polymorphonuclear]] ([[PMN]]) [[leukocytes]] and [[pericardial]] vascularization. This may cause [[pericardial effusion]] and [[fibrinous]] change of the [[pericardium]]. The [[pericardium]] may also develop a [[serous]] or [[hemorrhagic]] effusion. Most [[patients]] with [[viral]] pericarditis recover completely with few developing recurrences. Some [[patients]] develop [[constrictive pericarditis]] which could be disabling.<ref name="pmid5489188">{{cite journal| author=Matthews JD, Cameron SJ, George M| title=Constrictive pericarditis following Coxsackie virus infection. | journal=Thorax | year= 1970 | volume= 25 | issue= 5 | pages= 624-6 | pmid=5489188 | doi= | pmc=PMC472200 | url= }} </ref><ref name="pmid1920818">{{cite journal| author=Ilan Y, Oren R, Ben-Chetrit E| title=Acute pericarditis: etiology, treatment and prognosis. A study of 115 patients. | journal=Jpn Heart J | year= 1991 | volume= 32 | issue= 3 | pages= 315-21 | pmid=1920818 | doi= | pmc= | url= }} </ref><ref name="pmid2249218">{{cite journal| author=Shabetai R| title=Acute pericarditis. | journal=Cardiol Clin | year= 1990 | volume= 8 | issue= 4 | pages= 639-44 | pmid=2249218 | doi= | pmc= | url= }} </ref>
 
*[[Bacterial]] pericarditis results from:<ref name="pmid930941">{{cite journal| author=Klacsmann PG, Bulkley BH, Hutchins GM| title=The changed spectrum of purulent pericarditis: an 86 year autopsy experience in 200 patients. | journal=Am J Med | year= 1977 | volume= 63 | issue= 5 | pages= 666-73 | pmid=930941 | doi= | pmc= | url= }} </ref><ref name="pmid4200204">{{cite journal| author=Kauffman CA, Watanakunakorn C, Phair JP| title=Purulent pneumococcal pericarditis. A continuing problem in the antibiotic era. | journal=Am J Med | year= 1973 | volume= 54 | issue= 6 | pages= 743-50 | pmid=4200204 | doi= | pmc= | url= }} </ref><ref name="pmid1138554">{{cite journal| author=Rubin RH, Moellering RC| title=Clinical, microbiologic and therapeutic aspects of purulent pericarditis. | journal=Am J Med | year= 1975 | volume= 59 | issue= 1 | pages= 68-78 | pmid=1138554 | doi= | pmc= | url= }} </ref><ref name="pmid4076207">{{cite journal| author=Ribeiro P, Shapiro L, Nihoyannopoulos P, Gonzalez A, Oakley CM| title=Pericarditis in infective endocarditis. | journal=Eur Heart J | year= 1985 | volume= 6 | issue= 11 | pages= 975-8 | pmid=4076207 | doi= | pmc= | url= }} </ref><ref name="pmid4402567">{{cite journal| author=Roberts WC, Buchbinder NA| title=Right-sided valvular infective endocarditis. A clinicopathologic study of twelve necropsy patients. | journal=Am J Med | year= 1972 | volume= 53 | issue= 1 | pages= 7-19 | pmid=4402567 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4402567  }} </ref>
#[[Contiguous]] spread of [[infection]] within the [[chest]], either [[de novo]] or after [[surgery]] or [[trauma]].
#Spread from [[infective endocarditis]]
#[[Hematogen|Hematogenous]] spread of [[infection]]
#Direct [[inoculation]] as a result of [[Penetrating trauma|penetrating injury]] or [[cardiothoracic surgery]]


*Bacterial pericarditis results from:
*[[Tuberculous]] pericarditis develops from [[lymphatic]] spread of peritracheal, peribronchial or [[mediastinal]] [[lymph nodes]] or by [[contiguous]] spread from a focus of [[infection]] in the [[lung]] or [[pleura]]. There are four pathologic stages observed:<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>
#Contiguous spread of [[infection]] within the chest,<ref name="pmid930941">{{cite journal| author=Klacsmann PG, Bulkley BH, Hutchins GM| title=The changed spectrum of purulent pericarditis: an 86 year autopsy experience in 200 patients. | journal=Am J Med | year= 1977 | volume= 63 | issue= 5 | pages= 666-73 | pmid=930941 | doi= | pmc= | url= }} </ref><ref name="pmid4200204">{{cite journal| author=Kauffman CA, Watanakunakorn C, Phair JP| title=Purulent pneumococcal pericarditis. A continuing problem in the antibiotic era. | journal=Am J Med | year= 1973 | volume= 54 | issue= 6 | pages= 743-50 | pmid=4200204 | doi= | pmc= | url= }} </ref> either de novo or after surgery or trauma.<ref name="pmid1138554">{{cite journal| author=Rubin RH, Moellering RC| title=Clinical, microbiologic and therapeutic aspects of purulent pericarditis. | journal=Am J Med | year= 1975 | volume= 59 | issue= 1 | pages= 68-78 | pmid=1138554 | doi= | pmc= | url= }} </ref>
#Spread from [[infective endocarditis]]<ref name="pmid4076207">{{cite journal| author=Ribeiro P, Shapiro L, Nihoyannopoulos P, Gonzalez A, Oakley CM| title=Pericarditis in infective endocarditis. | journal=Eur Heart J | year= 1985 | volume= 6 | issue= 11 | pages= 975-8 | pmid=4076207 | doi= | pmc= | url= }} </ref><ref name="pmid4402567">{{cite journal| author=Roberts WC, Buchbinder NA| title=Right-sided valvular infective endocarditis. A clinicopathologic study of twelve necropsy patients. | journal=Am J Med | year= 1972 | volume= 53 | issue= 1 | pages= 7-19 | pmid=4402567 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4402567 }} </ref>
#Hematogenous spread of [[infection]]
#Direct inoculation as a result of penetrating injury or [[cardiothoracic surgery]]


*Tuberculous pericarditis develops from lymphatic spread of peritracheal, peribronchial or mediastinal lymph nodes or by contiguous spread from a focus of [[infection]] in the [[lung]] or [[pleura]]. There are four pathologic stages observed:<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 (chemistry)|deposition]], [[granuloma]]s and abundant [[mycobacterium]].
:*Stage 1: Presence of diffuse [[fibrin]] deposition, [[granuloma]]s and abundant [[mycobacterium]].


:*Stage 2: Development of [[serous]] or serosanguineous [[pericardial effusion]] with a predominantly lymphocytic exudate with [[monocyte]]s and foam cells.
:*Stage 2: Development of [[serous]] or [[Serosanguineous discharge|serosanguineous]] [[pericardial effusion]] with a predominantly [[lymphocytic]] [[exudate]] with [[monocyte]]s and [[foam cells]].


:*Stage 3: Absorption of effusion with organization of granulomatous caseation and thickening of pericardium secondary to deposition of [[fibrin]] and [[collagen]].
:*Stage 3: [[Absorption]] of effusion with the organization of [[granulomatous]] caseation and thickening of [[pericardium]] [[secondary]] to [[Deposition (chemistry)|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 [[granuloma]]s by fibrous tissue.
:*Stage 4: [[Development]] of [[constrictive pericarditis]]. The [[pericardial space]] is obliterated by [[dense]] [[adhesions]] with marked thickening of the parietal layer and replacement of [[granuloma]]s by [[fibrous]] [[tissue]].


:These types of [[granulomatous]] pericarditis also occur with [[fungal infection]]s, [[rheumatoid arthritis]] (RA), and [[sarcoidosis]].
:These types of [[granulomatous]] pericarditis also occur with [[fungal infection]]s, [[rheumatoid arthritis]] ([[RA]]), and [[sarcoidosis]].


*Pericarditis in [[renal failure]] is thought to result from [[inflammation]] of the visceral and parietal layers of the pericardium by metabolic toxins such as [[urea]], [[creatinine]], [[uric acid]], methylguanidine, [[guanidinoacetate]], [[parathyroid hormone]], [[Beta-2 microglobulin|beta2-microglobulin]], and others. It may be associated with hemorrhagic or [[serous]] effusion.
*Pericarditis in [[renal failure]] is thought to result from [[inflammation]] of the [[visceral]] and [[parietal]] layers of the [[pericardium]] by [[metabolic]] [[toxins]] such as [[urea]], [[creatinine]], [[uric acid]], methylguanidine, [[guanidinoacetate]], [[parathyroid hormone]], [[Beta-2 microglobulin|beta2-microglobulin]], and others. It may be associated with [[hemorrhagic]] or [[serous]] effusion.


==Gross Pathology Images==
==Gross Pathology Images==
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==References==
==References==
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{{Reflist|2}}
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Latest revision as of 23:39, 29 July 2020

Pericarditis Microchapters

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Varun Kumar, M.B.B.S., Cafer Zorkun, M.D., Ph.D. [2], Rim Halaby Homa Najafi, M.D.[3]

Overview

Pericarditis is inflammation of the pericardium, which is the double-walled sac that contains the heart and the roots of the great vessels. There can be an accompanying accumulation of fluid that can be either serous (free flowing fluid) or fibrinous (an exudate, which is a thick fluid composed of proteins, fibrin strands, inflammatory cells, cell breakdown products, and sometimes bacteria). Vascular congestion of the pericardium is also present. The underlying myocardium may or may not be inflamed as well. If the myocardium is involved in the inflammatory process, it is called myopericarditis, and CK and troponin levels may be elevated. Cardiotropic viruses usually spread to the myocardium and pericardium hematogenously and cause acute inflammation with infiltration of polymorphonuclear (PMN) leukocytes and pericardial vascularization. Most patients with viral pericarditis recover completely with few developing recurrences. Some patients develop constrictive pericarditis which could be disabling. Bacterial pericarditis results from contiguous spread of infection within the chest, either de novo or after surgery or trauma, spread from infective endocarditis, hematogenous, or direct inoculation as a result of penetrating injury or cardiothoracic surgery.

Pathophysiology

Anatomy and Physiology of Pericardium

Layers of the Pericardium

Pericardial Sinuses





Diseases of the Pericardium


Additional Images




Pathogenesis

  1. Contiguous spread of infection within the chest, either de novo or after surgery or trauma.
  2. Spread from infective endocarditis
  3. Hematogenous spread of infection
  4. Direct inoculation as a result of penetrating injury or cardiothoracic surgery
These types of granulomatous pericarditis also occur with fungal infections, rheumatoid arthritis (RA), and sarcoidosis.

Gross Pathology Images

Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology









Microscopic Pathology Images

Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology



Videos

AKS7kSl4x5k}} Acute Fibrinous Pericarditis

{{#ev:youtube|5fz_W1YxbC8}}

References

  1. Kishore, K. (2003). The Heart of Structural Development: The Functional Basis of the Location and Morphology of the Human Vascular Pump. J Postgrad Med, 49:282-4.
  2. Moore, K. L., Agur, A. M., & Dalley, A. F. (2011). Essential Clinical Anatomy - Fourth Edition. Lippincott Williams & Wilkins.
  3. Tank, P. W. (2009). Grant's Dissector - Fourteenth Edition. Lippincott Williams & Wilkins.
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