Thrombotic thrombocytopenic purpura pathophysiology: Difference between revisions
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==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 | |||
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. | |||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
Revision as of 18:06, 7 August 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 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.