Thrombophilia pathophysiology: Difference between revisions

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{{CMG}}
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==Overview==
==Overview==
==Pathophysiology==
The Virchow's triad has been described classically as the patho-physiologic mechanism responsible for any thrombosis, which includes 3 components:
* [[Endothelial dysfunction]]
* [[Venous stasis]]
* [[Hypercoaguability]]
The mechanism of thrombophilia involves affecting the pathway of thrombosis<ref name="pmid11309638">{{cite journal |author=Seligsohn U, Lubetsky A |title=Genetic susceptibility to venous thrombosis |journal=N. Engl. J. Med. |volume=344 |issue=16 |pages=1222–31 |year=2001 |month=April |pmid=11309638 |doi=10.1056/NEJM200104193441607 |url=}}</ref>:
[[Image: Figure_thrombophilia_mechanism.jpg‎]]
Adapted from: N Engl J Med. 2001 Apr 19;344(16):1222-31.
==References==
==References==
{{reflist|2}}
{{reflist|2}}

Revision as of 13:21, 21 September 2012


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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Pathophysiology

The Virchow's triad has been described classically as the patho-physiologic mechanism responsible for any thrombosis, which includes 3 components:

The mechanism of thrombophilia involves affecting the pathway of thrombosis[1]:

Adapted from: N Engl J Med. 2001 Apr 19;344(16):1222-31.

References

  1. Seligsohn U, Lubetsky A (2001). "Genetic susceptibility to venous thrombosis". N. Engl. J. Med. 344 (16): 1222–31. doi:10.1056/NEJM200104193441607. PMID 11309638. Unknown parameter |month= ignored (help)

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