1. B. Warfarin does not produce an anticoagulant effect in vitro. It inhibits coagulation of blood only in vivo, because the effect depends upon warfarin's effect in the liver on the production of clotting factors. Warfarin does not require conversion into an active drug. It inhibits the post-ribosomal carboxy-lation of glutamic acid residues in the vitamin K-dependent clotting factors. Therefore, heparin rather than warfarin is used when blood is collected from donors and stored.
2. D. Warfarin is metabolized in the liver by P450 enzyme system and is appreciably metabolized before it is eliminated. Adverse drug reactions are seen in patients taking warfarin if a second drug displaces warfarin from its protein binding sites in the blood or induces or inhibits the hepatic P450 system. Warfarin can cross the placenta and exert anticoagulant and other effects in the fetus at normal doses given to the mother.
3. B. Thrombocytopenia is a frequent side effect association with heparin. This reduction in the level of circulating platelets increases bleeding. Purple toes are encountered during warfarin therapy. Heparin may be administered to pregnant mothers without risk to the fetus. Heparin requires antithrombin III for its anticoagulant action, but does not increase the level of this protein in the blood.
4. C. Aspirin inhibits platelet cyclooxygenase. Abciximab, a monoclonal antibody, binds to and inhibits the platelet glycoprotein IIb/IIIa receptor. Dipyridamole inhibits platelet cyclic AMP phosphodiesterase and raises cyclic AMP levels. Eptifibatide binds to the glycoprotein IIb/IIIa complex.
5. C. Reteplase binds to fibrin to cause a selective activation of fibrin-bound plasminogen. All fibri-nolytic drugs are administered IV. Streptokinase is antigenic, whereas reteplase is not. Thrombocytopenia is not normally caused by thrombolytic drugs.
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