Outline Anti-coagulant and anti-thrombotic drugs Haemostasis and Thrombosis Year 3 Dentistry
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1 Outline Anti-coagulant and anti-thrombotic drugs Year 3 Dentistry Professor Yotis Senis Cellular Haemostasis y.senis@bham.ac.uk I. Haemostasis and II. Coagulation and anti-coagulants III. Platelets and anti-thrombotics IV. Fibrinolysis and clot busters Definitions Haemostasis (Greek) haemo- blood, -stasis stand still the stopping of bleeding Thrombus (Greek) thrombos lump, clot a blood clot (Greek) thrombos lump, clot formation of a thrombus Embolus (Greek) embolos stopper a detached blood clot Anti-thrombotic therapies Anti-coagulant a drug that prevents blood from clotting Anti-thrombotic a drug that prevents thrombus formation Thrombolytic (clot buster) a drug that dissolves blood clots Coagulation (Latin) coagulare to make curdle the process by which blood turns to a solid I ain t got time to bleed! Good Bad tourniquet haemostatics injectable foam Jessie The Body Ventura, Predator, 1987 saline blood Stops bleeding transient non-occlusive Blocks blood supply chronic occlusive embolize 1
2 Factors contributing to thrombosis Haemostasis and Blood flow immobile atrial fibrillation Coagulation clot Platelets haemostatic plug thrombus blood clot Endothelial Injury trauma atherosclerosis Virchow s Triad Hypercoagulation inherited pregnancy medication mortar s bricks Distinct patterns of thrombosis Arterial high shear system s critical white thrombi predominantly s anti- drugs (aspirin, ) Venous low shear system coagulation critical red thrombi predominantly red blood cells anti-coagulants (heparin, warfarin) Arterial thrombosis endothelial cells PGI 2 NO PECAM-1 CD39 TF leukocyte thrombus blood TF shell flow s TF TF, TF TF TF core VWF smooth muscle cells TF TF TF Venous thrombosis Coagulation endothelial cells blood flow valve turbulence thrombus amplification s clot 2
3 I Coagulation initiation and amplification (polyanions) Intrinsic pathway I Positive feedback Common pathway IX IXa (VIIIa, PS, Ca 2+ ) X Xa TF:VIIa Extrinsic pathway X (Va, PS, Ca 2+ ) II pro (II) (IIa) IIa VIII IX IXa TF:VIIa VIIIa, PS, Ca 2+ X Xa X V Va, PS, Ca 2+ pro VII II IIa (I) (Ia) clot clot surface contact I Negative feedback Haemostatic functions of regulates coagulation APC IX IXa TF:VIIa VIIIa, PS, Ca 2+ X Xa X APC Va, PS, Ca 2+ pro : thrombomodulin activation vasoconstriction clot APC Activated Protein C (physiological anti-coagulant) thrombomodulin receptor on endothelial cells (physiological anti-coagulant) Anti-coagulant drugs Anti III physiological suicide inhibitor Heparin Warfarin (Coumadin) Thrombin inhibitor Dabigatran Factor Xa inhibitor Rivaroxaban heparin (glycosaminoglycan) + anti (serpin) + active site co-factor suicide inhibitor enzyme : complex (inactive) 07/10/2015 serine protease : anti III serpin: serine protease inhibitor 3
4 Anti III inhibits coagulation Warfarin structure I Warfarin Vitamin K analogue IX IXa TF:VIIa VII VIII VIIIa, PS, Ca 2+ X Xa X V Va, PS, Ca 2+ II pro IIa : anti III clot Vitamin K Inactive II, VII, IX, X Warfarin mechanism of action Active II, VII, IX, X Factor Commonly used anti-coagulant drugs Unfractionated heparin LMW heparin Warfarin Xa IIa inhibitors inhibitors Liver Vitamin K recycling Xa IXa VIIIa VIIa Va Warfarin Warfarin Platelets highly reactive blood cells activated resting agonist Platelet receptors and agonists R PAR-1 P2Y 12 Gq Gq Gi PGI 2 R Gs activation PGI 2 GPVI GPIb-IX-V a2b1 VWF : Src family kinases 4
5 Platelet activation and inhibition Secretion and positive feedback resting Activators VWF Inhibitors PGI 2 nitric oxide ITIM receptors CD39 dense granules calcium serotonin a-granules coagulation factors chemo-attractants anti-bacterial factors angiogenic factors paracrine agonist Platelet Anti-thrombosis resting activated autocrine Platelet activation and aggregation integrin Integrin activation and binding integrin low affinity high affinity PAR-1 coagulation resting factors discoid shape granular integrins inactive activated s shape change degranulation integrin activation aggregation adhesion spreading procoagulant Gq inside-out signalling outside-in signalling Prothrombotic activity of s Anti-thrombotic drugs: old and new vorapaxar polymers R PAR-1 P2Y 12 inactive zymogen pro active serine protease COX ticagrelor abciximab integrilin aspirin Proase complex PS Xa Ca 2+ Va enzyme co-factor surface GPVI antagonist a2b1 GPIb-IX-V VWF GPIb-IX-V antagonist PS: phosphatidylserine blue old / established green new / under development 5
6 antagonists Excellent anti-thrombotic drugs Abciximab monoclonal antibody TP P2Y 12 Integrilin snake venom peptide analogue restricted to acute hospital care, e.g. unstable angina COX risk of excessive bleeding aspirin oral blockers trials stopped due to lack of efficacy and increased mortality Combined global sales: $7 billion Sir John Vane Nobel Prize 1982 Aspirin and inhibit the action of and positive feedback mediators P2Y 12 antagonists cyclooxygenase inhibitor (aspirin) P2Y 12 antagonist (, ticagrelor) The thienopyridine is metabolised to its active metabolite via two cytochrome P450 enzymes aspirin irreversible blockade of P2Y 12 receptor AA PLC PI 3kinase Ticagrelor is a new, non-competitive antagonist with increased therapeutic benefit and less bleeding Thrombolytics clot busters The olytic system Fibrinolysis the degradation of a clot endothelial cells plasminogen (zymogen) tpa (endothelial cells) upa (kidney) plasmin (serine protease) degradation tpa: tissue plasminogen activator upa: urokinase-type plasminogen activator stable thrombus blood clot 6
7 Commonly used clot busters The Holy Grail of anti-thrombotic therapy recombinant tpa (alteplase, reteplase, tenecteplase) urokinase (abbokinase, kinlytic) streptokinase (secreted by streptococci) Prevent thrombosis No bleeding side-effects All three classes of clot busters active plasminogen Monty Python, The Holy Grail, 1975 Haemostasis vs haemorrhaging Coagulation Platelet Activation Haemorrhaging Haemostasis Anti-coagulation Platelet Inhibition Fibrinolysis 7
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