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Co mep bruising april10f3

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  • The limitations of heparin and warfarin have prompted the development of new anticoagulant drugs for prevention and treatment of venous and arterial thromboembolism. The coagulation system, as illustrated in a simplified manner on this slide, is triggered by the tissue factor (TF)/factor VIIa complex, which activates FIX and FX. Activated FIX converts small amounts of prothrombin to thrombin, which is sufficient to amplify coagulation by activating factors V and VIII, platelets, and platelet-bound factor XI. Coagulation is propagated when FIXa binds to FVIIIa on the surface of activated platelets, forming intrinsic tenase, which, in turn, activates FX. Activated FX binds to activated factor V to form prothrombinase, which converts prothorombin (Factor II) to thrombin (Factor IIa). In the final step, thrombin converts fibrinogen to fibrin. New anticoagulants on the near- and intermediate-term horizon affect the propagation and fibrin formation stages of the coagulation pathway. This segment will review the most imminent new agents. Reference Weitz JI, Bates SM. New anticoagulants. J Thromb Haemost. 2005;3:1843-1853.
  • The limitations of heparin and warfarin have prompted the development of new anticoagulant drugs for prevention and treatment of venous and arterial thromboembolism. The coagulation system, as illustrated in a simplified manner on this slide, is triggered by the tissue factor (TF)/factor VIIa complex, which activates FIX and FX. Activated FIX converts small amounts of prothrombin to thrombin, which is sufficient to amplify coagulation by activating factors V and VIII, platelets, and platelet-bound factor XI. Coagulation is propagated when FIXa binds to FVIIIa on the surface of activated platelets, forming intrinsic tenase, which, in turn, activates FX. Activated FX binds to activated factor V to form prothrombinase, which converts prothorombin (Factor II) to thrombin (Factor IIa). In the final step, thrombin converts fibrinogen to fibrin. New anticoagulants on the near- and intermediate-term horizon affect the propagation and fibrin formation stages of the coagulation pathway. This segment will review the most imminent new agents. Reference Weitz JI, Bates SM. New anticoagulants. J Thromb Haemost. 2005;3:1843-1853.
  • The limitations of heparin and warfarin have prompted the development of new anticoagulant drugs for prevention and treatment of venous and arterial thromboembolism. The coagulation system, as illustrated in a simplified manner on this slide, is triggered by the tissue factor (TF)/factor VIIa complex, which activates FIX and FX. Activated FIX converts small amounts of prothrombin to thrombin, which is sufficient to amplify coagulation by activating factors V and VIII, platelets, and platelet-bound factor XI. Coagulation is propagated when FIXa binds to FVIIIa on the surface of activated platelets, forming intrinsic tenase, which, in turn, activates FX. Activated FX binds to activated factor V to form prothrombinase, which converts prothorombin (Factor II) to thrombin (Factor IIa). In the final step, thrombin converts fibrinogen to fibrin. New anticoagulants on the near- and intermediate-term horizon affect the propagation and fibrin formation stages of the coagulation pathway. This segment will review the most imminent new agents. Reference Weitz JI, Bates SM. New anticoagulants. J Thromb Haemost. 2005;3:1843-1853.
  • The limitations of heparin and warfarin have prompted the development of new anticoagulant drugs for prevention and treatment of venous and arterial thromboembolism. The coagulation system, as illustrated in a simplified manner on this slide, is triggered by the tissue factor (TF)/factor VIIa complex, which activates FIX and FX. Activated FIX converts small amounts of prothrombin to thrombin, which is sufficient to amplify coagulation by activating factors V and VIII, platelets, and platelet-bound factor XI. Coagulation is propagated when FIXa binds to FVIIIa on the surface of activated platelets, forming intrinsic tenase, which, in turn, activates FX. Activated FX binds to activated factor V to form prothrombinase, which converts prothorombin (Factor II) to thrombin (Factor IIa). In the final step, thrombin converts fibrinogen to fibrin. New anticoagulants on the near- and intermediate-term horizon affect the propagation and fibrin formation stages of the coagulation pathway. This segment will review the most imminent new agents. Reference Weitz JI, Bates SM. New anticoagulants. J Thromb Haemost. 2005;3:1843-1853.
  • Type of bruise – lumpy or flat, immediate or delayed, bruises, purpura or petechiae Location – soft tissue – subcut or muscle haematoma legs & arms, trunk, back etc
  • The limitations of heparin and warfarin have prompted the development of new anticoagulant drugs for prevention and treatment of venous and arterial thromboembolism. The coagulation system, as illustrated in a simplified manner on this slide, is triggered by the tissue factor (TF)/factor VIIa complex, which activates FIX and FX. Activated FIX converts small amounts of prothrombin to thrombin, which is sufficient to amplify coagulation by activating factors V and VIII, platelets, and platelet-bound factor XI. Coagulation is propagated when FIXa binds to FVIIIa on the surface of activated platelets, forming intrinsic tenase, which, in turn, activates FX. Activated FX binds to activated factor V to form prothrombinase, which converts prothorombin (Factor II) to thrombin (Factor IIa). In the final step, thrombin converts fibrinogen to fibrin. New anticoagulants on the near- and intermediate-term horizon affect the propagation and fibrin formation stages of the coagulation pathway. This segment will review the most imminent new agents. Reference Weitz JI, Bates SM. New anticoagulants. J Thromb Haemost. 2005;3:1843-1853.
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