Thrombotic thrombocytopenic purpura pathophysiology: Difference between revisions
No edit summary |
|||
| Line 4: | Line 4: | ||
==Overview== | ==Overview== | ||
== Pathophysiology == | == Pathophysiology == | ||
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 | * The exact pathogenesis of TTP is not completely understood. | ||
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 | 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. | 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> | ||
* It is understood that TTP is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3]. | |||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
Revision as of 21:03, 12 September 2018
|
Thrombotic thrombocytopenic purpura Microchapters |
|
Differentiating Thrombotic thrombocytopenic purpura from other Diseases |
|---|
|
Diagnosis |
|
Treatment |
|
Case Studies |
|
Thrombotic thrombocytopenic purpura pathophysiology On the Web |
|
American Roentgen Ray Society Images of Thrombotic thrombocytopenic purpura pathophysiology |
|
Thrombotic thrombocytopenic purpura pathophysiology in the news |
|
Blogs on Thrombotic thrombocytopenic purpura pathophysiology |
|
Directions to Hospitals Treating Thrombotic thrombocytopenic purpura |
|
Risk calculators and risk factors for Thrombotic thrombocytopenic purpura pathophysiology |
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.
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]
- It is understood that TTP is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 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.