Non-bacterial thrombotic endocarditis pathophysiology: Difference between revisions
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===Pathogenesis=== | ===Pathogenesis=== | ||
*Although the exact [[pathogenesis]] of [[non-bacterial thrombotic endocarditis]] is not completely understood<ref name="urlNon-bacterial Thrombotic Endocarditis | IntechOpen">{{cite web |url=https://www.intechopen.com/books/infective-endocarditis/non-bacterial-thrombotic-endocarditis |title=Non-bacterial Thrombotic Endocarditis | IntechOpen |format= |work= |accessdate=}}</ref>, [[Endothelial dysfunction|endothelial injury]] correlated with a [[hypercoagulable state]] has been implicated. | *Although the exact [[pathogenesis]] of [[non-bacterial thrombotic endocarditis]] is not completely understood<ref name="urlNon-bacterial Thrombotic Endocarditis | IntechOpen">{{cite web |url=https://www.intechopen.com/books/infective-endocarditis/non-bacterial-thrombotic-endocarditis |title=Non-bacterial Thrombotic Endocarditis | IntechOpen |format= |work= |accessdate=}}</ref>, [[Endothelial dysfunction|endothelial injury]] correlated with a [[hypercoagulable state]] has been implicated. | ||
*The main culprit that has been identified is damage to the [[endothelium]] and consequent exposure of sub[[endothelial]] [[connective tissue]] to [[Platelet|circulating platelets]]. | *The main culprit that has been identified is damage to the [[endothelium]] and consequent exposure of sub[[endothelial]] [[connective tissue]] to [[Platelet|circulating platelets]], platelet deposition and the formation of initial thrombi by the migration of inflammatory mononuclear cells<ref name="pmid27501336">{{cite journal |vauthors=Liu J, Frishman WH |title=Nonbacterial Thrombotic Endocarditis: Pathogenesis, Diagnosis, and Management |journal=Cardiol Rev |volume=24 |issue=5 |pages=244–7 |date=2016 |pmid=27501336 |doi=10.1097/CRD.0000000000000106 |url=}}</ref>. | ||
*Pathogenesis can be sub-sectioned into four factors thought to be involved in instigating NBTE. These include<ref name="pmid32">{{cite journal |vauthors=Beck ML, Freihaut B, Henry R, Pierce S, Bayer WL, Hendrickson WA, Ward KB, Wolf P, Feller K, Femmer K, Mohn GR |title=A serum haemagglutinating property dependent upon polycarboxyl groups |journal=Br. J. Haematol. |volume=29 |issue=1 |pages=149–56 |date=January 1975 |pmid=32 |doi=10.1111/j.1365-2141.1975.tb01808.x |url=}}</ref>; | *Pathogenesis can be sub-sectioned into four factors thought to be involved in instigating NBTE. These include<ref name="pmid32">{{cite journal |vauthors=Beck ML, Freihaut B, Henry R, Pierce S, Bayer WL, Hendrickson WA, Ward KB, Wolf P, Feller K, Femmer K, Mohn GR |title=A serum haemagglutinating property dependent upon polycarboxyl groups |journal=Br. J. Haematol. |volume=29 |issue=1 |pages=149–56 |date=January 1975 |pmid=32 |doi=10.1111/j.1365-2141.1975.tb01808.x |url=}}</ref>; | ||
#[[Immune complexes]]<ref>Williams R.C.Jr.. Immune complexes in clinical and experimental medicine, 19801st ed. p. 12</ref> | #[[Immune complexes]]<ref>Williams R.C.Jr.. Immune complexes in clinical and experimental medicine, 19801st ed. p. 12</ref> | ||
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*[[Tissue factor]] has been found to lead to a [[hypercoagulable state]], which may have predisposed the studied patient populations to [[Non-bacterial thrombotic endocarditis|NBTE]]<ref name="pmid16516597">{{cite journal |vauthors=Dutta T, Karas MG, Segal AZ, Kizer JR |title=Yield of transesophageal echocardiography for nonbacterial thrombotic endocarditis and other cardiac sources of embolism in cancer patients with cerebral ischemia |journal=Am. J. Cardiol. |volume=97 |issue=6 |pages=894–8 |date=March 2006 |pmid=16516597 |doi=10.1016/j.amjcard.2005.09.140 |url=}}</ref>. | *[[Tissue factor]] has been found to lead to a [[hypercoagulable state]], which may have predisposed the studied patient populations to [[Non-bacterial thrombotic endocarditis|NBTE]]<ref name="pmid16516597">{{cite journal |vauthors=Dutta T, Karas MG, Segal AZ, Kizer JR |title=Yield of transesophageal echocardiography for nonbacterial thrombotic endocarditis and other cardiac sources of embolism in cancer patients with cerebral ischemia |journal=Am. J. Cardiol. |volume=97 |issue=6 |pages=894–8 |date=March 2006 |pmid=16516597 |doi=10.1016/j.amjcard.2005.09.140 |url=}}</ref>. | ||
* | ====Hypercoagulability==== | ||
* | *The association between thrombosis and malignancy was first described by Trousseau in 1866<ref name="pmid30708967">{{cite journal |vauthors=Metharom P, Falasca M, Berndt MC |title=The History of Armand Trousseau and Cancer-Associated Thrombosis |journal=Cancers (Basel) |volume=11 |issue=2 |pages= |date=January 2019 |pmid=30708967 |pmc=6406548 |doi=10.3390/cancers11020158 |url=}}</ref>. | ||
*In 1956 Robbins and MacDonald<ref name="urlTHE SIGNIFICANCE OF NONBACTERIAL THROMBOTIC ENDOCARDITIS: AN AUTOPSY AND CLINICAL STUDY OF 78 CASES | Annals of Internal Medicine">{{cite web |url=https://doi.org/10.7326/0003-4819-46-2-255 |title=THE SIGNIFICANCE OF NONBACTERIAL THROMBOTIC ENDOCARDITIS: AN AUTOPSY AND CLINICAL STUDY OF 78 CASES | Annals of Internal Medicine |format= |work= |accessdate=}}</ref> hypothesized that valvular degeneration and hypercoagulable state played significant roles in the origin/formation of NBTE. | |||
==Genetics== | ==Genetics== | ||
Revision as of 11:23, 2 August 2020
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aisha Adigun, B.Sc., M.D.[2]
Overview
The exact pathogenesis of [disease name] is not fully understood.
OR
It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
OR
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
OR
Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
OR
[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
OR
The progression to [disease name] usually involves the [molecular pathway].
OR
The pathophysiology of [disease/malignancy] depends on the histological subtype.
Pathophysiology
Pathogenesis
- Although the exact pathogenesis of non-bacterial thrombotic endocarditis is not completely understood[1], endothelial injury correlated with a hypercoagulable state has been implicated.
- The main culprit that has been identified is damage to the endothelium and consequent exposure of subendothelial connective tissue to circulating platelets, platelet deposition and the formation of initial thrombi by the migration of inflammatory mononuclear cells[2].
- Pathogenesis can be sub-sectioned into four factors thought to be involved in instigating NBTE. These include[3];
Immune Complexes
- Circulating immune complexes were first identified in the formation of NBTE by Williams in 1980[9].
- Since that time, immunohistochemical techniques have been used to identify immunoglobulin and complement deposits within vessel walls in the zone of neovascularization of verrucose valvular lesions.[10]
- These findings are especially found in patients with systemic lupus erythematosus (SLE)[11].
Hypoxia
- Several studies have associated hypoxia with NBTE[12][13][14].
- These studies were conducted in both human[13][12] and animal[14] models and they found that, increased or persistent exposure to hypoxic insult can lead to an increase in circulating tissue factor.
- Tissue factor has been found to lead to a hypercoagulable state, which may have predisposed the studied patient populations to NBTE[12].
Hypercoagulability
- The association between thrombosis and malignancy was first described by Trousseau in 1866[15].
- In 1956 Robbins and MacDonald[16] hypothesized that valvular degeneration and hypercoagulable state played significant roles in the origin/formation of NBTE.
Genetics
[Disease name] is transmitted in [mode of genetic transmission] pattern.
OR
Genes involved in the pathogenesis of [disease name] include:
- [Gene1]
- [Gene2]
- [Gene3]
OR
The development of [disease name] is the result of multiple genetic mutations such as:
- [Mutation 1]
- [Mutation 2]
- [Mutation 3]
Associated Conditions
Conditions associated with [disease name] include:
- [Condition 1]
- [Condition 2]
- [Condition 3]
Gross Pathology
On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Microscopic Pathology
On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
References
- ↑ "Non-bacterial Thrombotic Endocarditis | IntechOpen".
- ↑ Liu J, Frishman WH (2016). "Nonbacterial Thrombotic Endocarditis: Pathogenesis, Diagnosis, and Management". Cardiol Rev. 24 (5): 244–7. doi:10.1097/CRD.0000000000000106. PMID 27501336.
- ↑ Beck ML, Freihaut B, Henry R, Pierce S, Bayer WL, Hendrickson WA, Ward KB, Wolf P, Feller K, Femmer K, Mohn GR (January 1975). "A serum haemagglutinating property dependent upon polycarboxyl groups". Br. J. Haematol. 29 (1): 149–56. doi:10.1111/j.1365-2141.1975.tb01808.x. PMID 32.
- ↑ Williams R.C.Jr.. Immune complexes in clinical and experimental medicine, 19801st ed. p. 12
- ↑ Nakanishi K., Tajima F., Nakata Y., Osada H., Ogata K., Kawai T., Torikata C., Suga T., Takishima K., Aurues T., Ikeda T.. Tissue factor is associated with the nonbacterial thrombotic endocarditis induced by a hypobaric hypoxic environment in rats, Virchows Arch, 1998, vol. 433 (pg. 375-379)
- ↑ Dutta T., Karas M.G., Segal A.Z., Kizer J.R.. Yield of transesophageal echocardiography for nonbacterial thrombotic endocarditis and other cardiac sources of embolism in cancer patients with cerebral ischemia, Am J Cardiol, 2006, vol. 97 6(pg. 894-898)
- ↑ MacDonald R.A., Robbins S.L.. The significance of nonbacterial thrombotic endocarditis: an autopsy and clinical study of 78 cases, Am Intern Med, 1957, vol. 46 (pg. 255-273)
- ↑ "Nonbacterial thrombotic endocarditis in cancer patients: Comparison of characteristics of patients with and without concomitant disseminated intravascular coagulation - Bedikian - 1978 - Medical and Pediatric Oncology - Wiley Online Library".
- ↑ Williams R.C.Jr.. Immune complexes in clinical and experimental medicine, 19801st ed. p. 12
- ↑ Shapiro RF, Gamble CN, Wiesner KB, Castles JJ, Wolf AW, Hurley EJ, Salel AF (December 1977). "Immunopathogenesis of Libman-Sacks endocarditis. Assessment by light and immunofluorescent microscopy in two patients". Ann. Rheum. Dis. 36 (6): 508–16. doi:10.1136/ard.36.6.508. PMC 1000155. PMID 339850.
- ↑ Nydegger UE, Lambert PH, Gerber H, Miescher PA (August 1974). "Circulating immune complexes in the serum in systemic lupus erythematosus and in carriers of hepatitis B antigen. Quantitation by binding to radiolabeled C1q". J. Clin. Invest. 54 (2): 297–309. doi:10.1172/JCI107765. PMC 301557. PMID 4847246.
- ↑ 12.0 12.1 12.2 Dutta T, Karas MG, Segal AZ, Kizer JR (March 2006). "Yield of transesophageal echocardiography for nonbacterial thrombotic endocarditis and other cardiac sources of embolism in cancer patients with cerebral ischemia". Am. J. Cardiol. 97 (6): 894–8. doi:10.1016/j.amjcard.2005.09.140. PMID 16516597.
- ↑ 13.0 13.1 Truskinovsky AM, Hutchins GM (April 2001). "Association between nonbacterial thrombotic endocarditis and hypoxigenic pulmonary diseases". Virchows Arch. 438 (4): 357–61. doi:10.1007/s004280000372. PMID 11355169.
- ↑ 14.0 14.1 Nakanishi K, Tajima F, Nakata Y, Osada H, Ogata K, Kawai T, Torikata C, Suga T, Takishima K, Aurues T, Ikeda T (October 1998). "Tissue factor is associated with the nonbacterial thrombotic endocarditis induced by a hypobaric hypoxic environment in rats". Virchows Arch. 433 (4): 375–9. doi:10.1007/s004280050262. PMID 9808440.
- ↑ Metharom P, Falasca M, Berndt MC (January 2019). "The History of Armand Trousseau and Cancer-Associated Thrombosis". Cancers (Basel). 11 (2). doi:10.3390/cancers11020158. PMC 6406548. PMID 30708967.
- ↑ "THE SIGNIFICANCE OF NONBACTERIAL THROMBOTIC ENDOCARDITIS: AN AUTOPSY AND CLINICAL STUDY OF 78 CASES | Annals of Internal Medicine".