>It would be helpful for some of us who are not well versed in this field if you could identify the places where the various agents work in this cascade, such as Plavix (if it can have a role in this cascade whatsoever), Aspirin, ATryn, Coumadin, and heparin<
Plavix and aspirin are antiplatelet drugs rather than anticoagulants (#msg-26739622, #msg-18197555); they work on a separate system from the one depicted in the clotting-cascade diagram in the prior post.
Coumadin (warfarin) inhibits Vitamin K, which is needed for the synthesis of various inactivated clotting factors (the blue items in the diagram). It thereby down-regulates the clotting cascade at various places in a dose-dependent (but highly unpredictable) manner.
Unfractionated heparin inhibits FIIa (thrombin) and FXa. Low-molecular-weight heparins (LMWH) such as Lovenox inhibit FIIa and FXa, but the inhibition of FIIa is less effective than it is for unfractionated heparin (#msg-26898084).
Antithrombin (a.k.a. ATIII) inhibits the clotting cascade at several places; it must be bound to heparin or LMWH for those substances to inhibit FIIa and FXa effectively (#msg-26898084).
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