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Anticoagulant therapy

Anticoagulant therapy. Background Cost Benefit Complication. External(F7)15s Internal(F12)1 to6minute Result> prothrombin activator prothrombin (F2)>thrombin>fibrinogen(F1)>fibrin. Clot formation: fibers+platlet+red cell+plasma

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Anticoagulant therapy

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  1. Anticoagulant therapy • Background • Cost • Benefit • Complication

  2. External(F7)15s • Internal(F12)1 to6minute • Result>prothrombin activatorprothrombin(F2)>thrombin>fibrinogen(F1)>fibrin

  3. Clot formation: fibers+platlet+redcell+plasma • Restrictive clot formation:antithrombin3+thrombin(12_20minute) • Clot retraction:30to60minute • Clot leases During 24hours TPA release injury endothelium and activated plasminogen>plasmin(fibrinolisin)>leases: Fibrinogen,prothrombin,F5,F7

  4. Anticoagulant drugs: 1__HEPARIN • UFH or LMWH ?

  5. Heparin(UFH) release from mast cell basophile around capillary and concentration lung and liver • UFH: heterogenus mixture glycosaminoglycant with MW3000 to30,000 only one third is active anticoagulant with bind antithrombin and increase activation 1000X for neutralize troponin and F9,F10,F11,F12

  6. Half life: dependent dose 25U/kg 30min • 100u/kg60min • 400u/kg150min • aPTT only sensetive heparin range1.0-0.1u/ml • More than 1.ou/ml withACT(hemotec parker-itcedisonmedtronic)350-375 secischemic complication at 7days are 34%lower than thy were ACT171-295 • Heparin doses70 to 100iu/kg and target act250-350seconds but with GP2b/3a inhibitor 40-70iu/kg target ACT 200to 250sec

  7. Low molecular weight hepaarins(LMWH) • Manifactured from UFH withchemical or enzymatic fragment s one third size • Binds less readily to plasma protein, more resistant to neutralization by platelet F4(half life4hours),less effect on platelet function • Relatively selective inactivation factor xa

  8. Complication: • Bleeding,predispose with increase risk was :age ,alcohol,aspirin, ,renal failure, serious concurrent illness. LMWH risk more increase in RF • Prothaminesulfat dose not comletly effective in reverse antifactorxa activity inLMWH

  9. Thrombocytopenia:tow type • Begins 4-14 days exceptions are in patient received heparin the past three month.50% drop in platelet count • Dose depended 15% benign and self limited • Immune form(HIT) paradoxically cause serious arterial and venous thrombosis(HITT) mechanism interaction antibody IgG with complex of heparin and platelet factor4 is released on activation

  10. Declininplatlet count in HIT is usually:50;000 to 60,000/mm3 • Immune –mediated HIT is not heparin dose dependent even heparin flushes • HIT no single definitive laboratory test(platlet activation assay, serotonin release assay) • When HIT is suspected heparin discotinude but HIT is associated with marked hypercoagulable state with 30to 50% thrombosis in 30 days after diagnosis

  11. Threatment HITT • No LMWH because strong cross reaction with HIT • No warfari • Tow direct Thrombin inhibitors :lepirudin and argatroban and pentasacaridefondaparinux(binding platlet factor4)

  12. 2-Warfarin(coumadin) • Vitamin K antagonist Vkh2 is cofactor forF2(prothrombin)F7,F9,F10 • Mean plasma half life` 40hours metabolism is affected allelic variant of P450,CYP2C9 homozygous for active alleles with low warfarin dose and high bleeding complication and polimorphism in VK epoxidreductase(VKOR)gene also influence anticoagulant respone • Drugs: propranolol,amiodaron,clofibrate,cimetidine……increase warfarin levels and cholestyraminerifampin …..decreas high VK in diet(nutritional supplement)

  13. Loading doses of warfarin should not be used • Because:VK dependent factors have different half life F7 shortest initial increase INR withsevere F& deficiency state while still failing to provide antithrombotic effect. • Reduction in plasma level protein C (VK dependent anticoagulant with shortest HL) Lead to transient paradoxical hypercoagulated state.

  14. Managing warfarin overdose

  15. Pitfallin anticoagulant therapy

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