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Warfarin: directly inhibits thrombin
4%
17/422
Heparin: activates antithrombin 3
60%
252/422
Aspirin: reversibly inhibits COX-1
8%
33/422
Clopidogrel: antagonizes ADP receptors on endothelial cells
25%
107/422
Prasugrel: reduced risk of bleeding compared to other drugs in its class
2%
10/422
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Heparin activates antithrombin 3 and heparin cofactor 2 and is monitored using aPTT. Unfractionated heparin is a heterogeneous group of anionic, sulfated glycosaminoglycans. Heparin provides immediate-onset anticoagulation and is indicated for prophylaxis and treatment of peripheral arterial embolism. Heparin should be started immediately in patients with evidence of arterial emboli or thrombosis, as suggested by this man's painful, pulseless foot, to prevent thrombotic propagation. As reviewed by Sontheimer, anticoagulants such as heparin and warfarin have not been shown to provide any benefit in treating patients with intermittent claudication. However, heparin is beneficial in reducing morbidity and mortality in patients with acute limb ischemia while they are being evaluated for further treatment. Hirsh et al. discuss the mechanism of action of heparin. The heparin-AT complex inactivates a number of coagulation enzymes, including thrombin factor (IIa) and factors Xa, IXa, XIa, and XIIa. Of these inactivated factors, thrombin and factor Xa are the most responsive to inhibition. For inhibition of thrombin, heparin must bind to both the coagulation enzyme and AT, but binding to the enzyme is less important for inhibition of activated factor X. Illustration A depicts heparin bound to the thrombin-antithrombin III complex. Incorrect Answers: Answer 1: Warfarin inhibits the vitamin K-dependent synthesis of clotting factors II, VII, IX and X, as well as regulatory factors proteins C and S. Answer 3: Aspirin irreversibly inhibits COX-1 and COX-2. Answers 4 & 5: Clopidogrel and prasugrel antagonize ADP receptors on platelets. Prasugrel has increased risk of bleeding compared to clopidogrel.
3.1
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