Heparin-induced thrombocytopenia pathophysiology: Difference between revisions
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{{Heparin-induced thrombocytopenia}} | {{Heparin-induced thrombocytopenia}} | ||
{{CMG}}; '''Associate Editor(s)-In-Chief:''' [[Priyamvada Singh|Priyamvada Singh, M.B.B.S.]] [mailto: | {{CMG}}; '''Associate Editor(s)-In-Chief:''' [[Priyamvada Singh|Priyamvada Singh, M.B.B.S.]] [mailto:psingh13579@gmail.com] | ||
==Overview== | ==Overview== | ||
[[Heparin-induced thrombocytopenia]] is diagnosed when the [[platelet]] count falls by > 50% typically after 5-10 days of [[heparin]] therapy. It is caused by antibodies to complexes between [[heparin]] and [[platelet factor 4]] (PF4). These antibody complexes stimulates the procoagulant pathways due to activation of [[platelet]] and [[endothelium]]. | [[Heparin-induced thrombocytopenia]] is diagnosed when the [[platelet]] count falls by > 50% typically after 5-10 days of [[heparin]] therapy. It is caused by antibodies to complexes between [[heparin]] and [[platelet factor 4]] (PF4). These antibody complexes stimulates the procoagulant pathways due to activation of [[platelet]] and [[endothelium]]. | ||
Revision as of 14:58, 2 November 2012
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Heparin-induced thrombocytopenia |
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Differentiating Heparin-induced thrombocytopenia from other Diseases |
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Diagnosis |
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Treatment |
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Case Studies |
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Heparin-induced thrombocytopenia pathophysiology On the Web |
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American Roentgen Ray Society Images of Heparin-induced thrombocytopenia pathophysiology |
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Heparin-induced thrombocytopenia pathophysiology in the news |
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Directions to Hospitals Treating Heparin-induced thrombocytopenia |
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Risk calculators and risk factors for Heparin-induced thrombocytopenia pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Priyamvada Singh, M.B.B.S. [2]
Overview
Heparin-induced thrombocytopenia is diagnosed when the platelet count falls by > 50% typically after 5-10 days of heparin therapy. It is caused by antibodies to complexes between heparin and platelet factor 4 (PF4). These antibody complexes stimulates the procoagulant pathways due to activation of platelet and endothelium.
Pathophysiology
- It is caused by antibodies to complexes between heparin and platelet factor 4 (PF4).
- More than 90% patients have these anti–PF4-heparin antibodies in their plasma.
- These antibodies bind to the platelet's surface and induce their activation by cross-linking Fc IIA receptors and bind to the surface of the endothelium, inducing procoagulant activity.
- Platelets activated with these antibodies, increase their release of platelet factor 4 (PF4). Thus, a viscous cycle continues.