Non-bacterial thrombotic endocarditis pathophysiology
non-bacterial thrombotic endocarditis |
Differentiating non-bacterial thrombotic endocarditis from other Diseases |
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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
- The exact pathogenesis of non-bacterial thrombotic endocarditis is not completely understood, however, several factors have been implicated.
- The factors thought to be involved in instigating NBTE include[1]; Immune complexes[2], hypoxia [3][4], hypercoagulability[5], and carcinomatosis[6].
- It is understood that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
- [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
- Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
- [Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
- The progression to [disease name] usually involves the [molecular pathway].
- The pathophysiology of [disease/malignancy] depends on the histological subtype.
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
- ↑ 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)
- ↑ Bedikian A., Valdiviesco M., Luna M., Bodey G.P.. Nonbacterial thrombotic endocarditis in cancer patients with or without concomitant disseminated intravascular coagulation, Med Pediatr Oncol, 1978, vol. 4 (pg. 149-157)