Thrombotic thrombocytopenic purpura pathophysiology: Difference between revisions
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* VWF and platelets are decumbneted | * VWF and platelets are decumbneted | ||
== 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] | |||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
Revision as of 13:43, 13 September 2018
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Thrombotic thrombocytopenic purpura Microchapters |
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Differentiating Thrombotic thrombocytopenic purpura from other Diseases |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Saeedeh Kowsarnia M.D.[2]
Overview
Pathophysiology
- The exact pathogenesis of TTP is not completely understood.
- It is understood that TTP is caused by either deficiency of a plasma metalloprotease, ADAMTS13.
The von Willebrand factor (VWF) is produced by the endothelial cells as an ultra-high-molecular-weight multimers. Normally, VWF is sliced by a plasma metalloproteinase called ADAMTS13 into smaller multimers. When the activity or the amount of the protease is not enough, the ultra-high-molecular-weight multimers of VWF commence platelet aggregation and thrombosis in small vessels.[1]
- VWF and platelets are decumbneted
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]
References
- ↑ Tsai HM (January 2010). "Pathophysiology of thrombotic thrombocytopenic purpura". Int. J. Hematol. 91 (1): 1–19. doi:10.1007/s12185-009-0476-1. PMC 3159000. PMID 20058209.