Co mep bruising COMEP
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The document discusses bruising and bleeding conditions. It provides learning objectives about physiological hemostasis, recognizing normal and pathological bruising patterns, taking a bleeding history, investigating causes of acquired and congenital bleeding disorders, common acquired bleeding disorders, and features of common congenital bleeding disorders. It also outlines coagulation pathways, current and new anticoagulant agents, key aspects of bleeding history taking, and treatment of coagulation factor deficiencies.
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Co mep bruising COMEP
- 1. Bruising (and bleeding conditions) CoMEP 14 th & 27 th April 2010
- 4. What physiological mechanisms come into play when a blood vessel is damaged?
- 6. von Willebrand factor in Primary Haemostasis
- 12. Senile Purpura
- 13. Bleeding Disorder Symptoms Immediate bleeding Delayed bleeding controlled by pressure not controlled by pressure Purpura & petechiae Muscle & joint bleeds Mucosal bleeding Large ecchymoses Epistaxis, menorrhagia Haematuria Bleed after venepuncture Bleed after im injection Post-traumatic bleeds Post-traumatic bleeds GI & CNS bleeds GI & CNS bleeds Platelet / Vascular Defects Clotting Factor Defects
- 14. Fibrin Fibrinogen Extrinsic Activation Intrinsic Activation Xa IIa TF/VIIa X IX IXa VIIIa Va II XIa XIIa XI XII Collagen, HMWK, PK Common Pathway Coagulation Pathways
- 15. Fibrin Fibrinogen Extrinsic Activation Intrinsic Activation Xa IIa TF/VIIa X IX IXa VIIIa Va II XIa XIIa XI XII Collagen, HMWK, PK Common Pathway Coagulation Pathways
- 16. Fibrin Fibrinogen Extrinsic Activation Intrinsic Activation Xa IIa TF/VIIa X IX IXa VIIIa Va II XIa XIIa XI XII Collagen, HMWK, PK Common Pathway Coagulation Pathways – lab assays APTT TCT PT Ca 2+ and phospholipid also required
- 17. Current & New Anticoagulant Agents Adapted from Weitz JI et al. J Thromb Haemost. 2005;3:1843-1853. Fibrin Fibrinogen Indirect Xa inhibitors Fondaparinux Danaparoid LMWH, UFH Xa Inhibitors : Rivaroxaban Apixaban IIa Inhibitors Ximelagatran Dabigatran ORAL PARENTERAL Xa IIa TF/ VIIa X IX IXa VIIIa Va II Antithrombin Indirect IIa inhibitors UFH, [LMWH] Warfarin FDPs, D-dimer Antithrombin Plasmin
- 18. Bleeding Disorder Symptoms Immediate bleeding Delayed bleeding controlled by pressure not controlled by pressure Purpura & petechiae Muscle & joint bleeds Mucosal bleeding Large ecchymoses Epistaxis, menorrhagia Haematuria Bleed after venepuncture Bleed after im injection Post-traumatic bleeds Post-traumatic bleeds GI & CNS bleeds GI & CNS bleeds Platelet / Vascular Defects Clotting Factor Defects
- 21. Fibrin Fibrinogen Extrinsic Activation Intrinsic Activation Xa IIa TF/VIIa X IX IXa VIIIa Va II XIa XIIa XI XII Collagen, HMWK, PK Common Pathway Coagulation Pathways – Haemophilia APTT TCT PT Isolated deficiency of Factors VIII, IX, XI or XII [intrinsic pathway] causes prolonged APTT with normal PT
- 27. Case 2
- 29. Disseminated Intravascular Coagulation Systemic activation of coagulation Intravascular deposition of fibrin Depletion of platelets and coagulation factors Thrombosis of small and midsize vessels and organ failure Bleeding
- 37. Decline of INR after warfarin cessation when INR >6 Days % INR > 4 Hylek et al. 2000
- 41. Case 4 – 64y male 4 days after commencing warfarin for PE
Editor's Notes
- 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.