Anticoagulants mechanism of action

Hirsh J, Dalen JE, Anderson DR et al (2001) Oral anticoagulants mechanism of action, clinical effectiveness, and optimal therapeutic range. Chest 119 (Suppl.) 8S-21S... 

Gomez-Lechon MJ, Donato MT, Castell JV, Jover R (2003) Human hepatocytes as a tool for studying toxicity and drug metabolism. Curr Drug Metab 4 292-312 Hirsch J, Dahlen J, Anderson DR, Poller L, Bussey H, Ansell J, Deykin D (2001) Oral anticoagulants mechanism of action, clinical effectiveness, and optimal therapeutic range. Chest 119(Suppl) 8S-21S... 

McNeely T, Griffith M. The anticoagulant mechanism of action of heparin in contact-activated plasma inhibition of factor X activation. Blood 1985 65 1226-31. 

Compare and contrast the mechanisms of action of drugs used for ventricular rate control, conversion to sinus rhythm and maintenance of sinus rhythm in patients with AF, and explain the importance of anticoagulation for patients with AF. 

Walker, C. and Royston, D. 2002. Thrombin generation and its inhibition a review of the scientific basis and mechanism of action of anticoagulant therapies. British Journal of anaesthesia 88(6), 848-863. 

Mechanism of Action A direct thrombin inhibitor that reversibly binds to thrombin-active sites. Inhibits thrombin-catalyzed or thrombin-induced reactions, including fibrin formation, activation of coagulant factors V, VIII, and XIII also inhibits protein C formation, and platelet aggregation. Therapeutic Effect Produces anticoagulation. Pharmacokinetics Following IV administration, distributed primarily in extracellular fluid. Protein binding 54%. Metabolized in the liver. Primarily excreted in the feces, presumably through biliary secretion. Half-life 39-51 min. 

Mechanism of Action An anticoagulant that specifically and reversibly inhibits thrombin by binding to its receptor sites. Therapeutic Effect Decreases acute ischemic complications in patients with unstable angina pectoris. 

Mechanism of Action An antithrombin that inhibits factor Xa and thrombin in the presence of low-molecular-weight heparin. Only slightly influences platelet aggregation, PT, and aPTT. Therapeutic Effect Produces anticoagulation. 

Mechanism of Action An anticoagulant that binds specifically and directly to thrombin, inhibiting free circulating and clot-bound ihmmhinT herapeuticEffect Prolongs the clotting time of human plasma. 

Mechanism of Action An anticoagulant that inhibits thrombogenic action of thrombin (independent of anf ithrombin II and nof inhibif ed by platelet factor 4). One molecule of lepirudin binds to one molecule of fhrombin. Therapeutic Effect Produces dose-dependent increases in aPTT. 

Mechanism of Action A protein that complexes with heparin to form a stable salt. Therapeutic Effect Reduces anticoagulant activity of heparin. 

Mechanism of Action A low-molecular-weight heparinthat inhibits factor Xa. Causes less inactivation of thrombin, inhibition of platelets, and bleedingthan standard heparin. Does not significantlyinfluence bleeding time, PT, aPTT. Therapeutic Effect Produces anticoagulation. 

Mayer, A. M. S., Rodriguez, A. D., Berlinck, R. G. S., and Hamann, M. T. (2009). Marine pharmacology in 2005-6 Marine compounds with anthelmintic, antibacterial, anticoagulant, antifungal, antiinflammatory, antimalarial, antiprotozoal, antituberculosis, and antiviral activities affecting the cardiovascular, immune and nervous systems, and other miscellaneous mechanisms of action. Biochim. Biophys. Acta 5, 283-308. 

Mayer AMS, Hamann MT (2004) Marine Pharmacology in 2000 Marine Compounds with Antibacterial, Anticoagulant, Antifungal, Anti-Inflammatory, Antimalarial, Antiplatelet, Antituberculosis, and Antiviral Activities Affecting the Cardiovascular, Immune, and Nervous Systems and Other Miscellaneous Mechanisms of Action. Mar Biotechnol 6 37... 

In the same way, the mechanism of action of drugs and coagulant and anticoagulant medication takes place through the variation of surface charge in the blood vessels. 

Inactive factors 1. Mechanism of action Heparin acts indirectly by binding to antithrombin III to cause a rapid anticoagulant effect. Maximal anticoagulation occurs within minutes after intravenous heparin injection (unlike vitamin K antagonist anticoagulants, such as war-... 

There are very few agents like the anticoagulant warfarin whose toxicity and therapeutic effects are produced by the same mechanism. In most cases beneficial and harmful effects recruit different mechanisms of action. As far as CO is concerned not only does its mechanism of toxic and physiological actions differ, but the source from where it is derived matters too. So the mechanisms of action of inhaled-and heme-generated CO also seem to differ. Since the focus of this chapter is CO toxicity, we will attempt to elaborate the mechanism of its toxicity more than the mechanism of its physiologic actions. 

De ite differmces in their mechanisms of action and in vitro activities, pentasaccharide, DX-9065a and TAP have been shown to be effective antithrombotic agents in experimental models of venous thrombosis, coronary artery occlusion, arterial thrombolysis and acute reocclusion, restenosis after angioplasty, dialysis, and DIG. Pentasaccharide has also demonstrated measurable antithrombotic effects in human trials. Both TAP and DX-9065a produce measurable in vitro anticoagulant effects. In contrast, pentasaccharide does not produce an anticoagulant effect by the typical clot based assays. Thus, with fector Xa inhibitors there is not necessarily a correlation between current lab assays and antithrombotic efficacy as there is with heparin. 

Marlar RA, Kleiss AJ, Griffin JH. Mechanism of action of human activated protein C, a thrombin-dependent anticoagulant enzyme. Blood 1982 59(5) 1067-72. 

No case reports of toxicity have been directly attributed to bromadiolone. However, based on its mechanism of action as an anticoagulant, it is expected that excessive human exposure of bromadiolone is likely to produce epistaxis, bleeding of gums, pallor, and sometimes petechial hemorrhage leading to hematomas around the joints and on the buttocks. 

The use of OEP with antiplatelets, thrombolytics, low-molecular-weight heparins, or anticoagulants may result in a delayed but increased risk of bleeding, and concomitant use is not advised (54,59). The mechanism of action is theorized to be decreased thromboxane B2 synthesis and increased prostacyclin production caused by y-linolenic acid, resulting in inhibition of platelet aggregation and prolonged bleeding time (42). 

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