Thrombotic thrombocytopenic purpura pathophysiology: Difference between revisions
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== Pathophysiology == | == Pathophysiology == | ||
* The exact pathogenesis of TTP is not completely understood. | * The exact pathogenesis of TTP is not completely understood. | ||
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 | * It is understood that TTP is caused by either deficiency of a plasma metalloprotease, ADAMTS13. | ||
aggregation and thrombosis in small vessels.<ref name="pmid20058209">{{cite journal |vauthors=Tsai HM |title=Pathophysiology of thrombotic thrombocytopenic purpura |journal=Int. J. Hematol. |volume=91 |issue=1 |pages=1–19 |date=January 2010 |pmid=20058209 |pmc=3159000 |doi=10.1007/s12185-009-0476-1 |url=}}</ref> | 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.<ref name="pmid20058209">{{cite journal |vauthors=Tsai HM |title=Pathophysiology of thrombotic thrombocytopenic purpura |journal=Int. J. Hematol. |volume=91 |issue=1 |pages=1–19 |date=January 2010 |pmid=20058209 |pmc=3159000 |doi=10.1007/s12185-009-0476-1 |url=}}</ref> | ||
* | * VWF and platelets are decumbneted | ||
==References== | ==References== | ||
Revision as of 13:42, 13 September 2018
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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
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.