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BLOODCOUAGULATION

BLOODCOUAGULATION. 1. Very, very short definition of hemostasis 2 . Not so short, but still short description of the general mechanism 3 . The cascade - initation , proceeding, control 5 . Diseases,deficiencies – and (shortly) about treatments . HEMOSTASIS = PREVENTION OF BLOODLOSS.

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BLOODCOUAGULATION

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  1. BLOODCOUAGULATION 1. Very, very short definition of hemostasis 2. Not so short, but still short description of the general mechanism 3. The cascade - initation, proceeding, control 5. Diseases,deficiencies – and (shortly) about treatments

  2. HEMOSTASIS = PREVENTION OF BLOODLOSS Achieved by four phases/mechanisms Vascular phase – damaged vessel contracts Platelet phase – formation of the platelet Coagulation phase – formation of the blood clot Tissue repair

  3. GENERAL MECHANISM OF BLOODCOAGULATION • Balance between anticouagulants/procoagulants • Damageon vessel – cascacade – prothrombinactivator • Prothrombin – thrombin • Fibrinogen – fibrin

  4. Platelets: • adheres to broken vesselwall - prothrombin attach to prothtrombinreceptors on platalets • release fibrin stabilizing factor (FXIII)- covalent crosslinks between the fibrin molecules • activate own contractile elemen = broken wall of vessel is pulled together

  5. THE CASCADE • formation of prothrombin activator • extrinsic pathway • intrinsic pathway • common pathway = epw and ipw ending the same way...

  6. EXTRINSIC PW 1. Initiated by traumatized tissue – releases complex of tissue factors 2. TFs = phospholipids from membranes of tissue + lipoproteincomplex 3. TF+ FVII = complex 4. Complex + Ca2+ act on FX = FXa (activated) 5. FXa+ phospholipids + FV – act on prothrombrin in presense of Ca2+ - prothrombin split – thrombin Thrombinconvertfibrinogen to fibrin

  7. INTRINSIC PW 1 Damaged vessels wall expose collagenfibers– FXII – FXIIa. Platelets - attach to collagen – release platelet factor 3(lipoprotein) 2 FXIIa – FXI – FXIa. * HMWkininogen * Prekallikrein(Fletcher factor) 3 FXIa – FIX – FIXa 4 FIXa + FVIII + phospholipids (from platelets) + platelet factor 3 (from platelets) – FX – FXa 5 FXa + FV + phopspholipids (from platelets or tissue) = prothrombin activator – prothrombin – thrombin – fibrinogen – fibrin

  8. COMMON PW=5 • EXTRINSIC PW • explosive • initiated by tissue factors • clotting within 15 sec if severe trauma • INTRINSIC PW • slower • initiated when FXII + platelets contact with collagen • 1 – 6 minutes to cause clotting • CA2+ • promotes/ accelerates the bloodclotting reactions

  9. WHEN CLOT IS FORMED – it contracts • contractile elements of platelets • serum (fluid without fibrinogen and clotting factors) is expressed from clot – within 20 – 60 minutes

  10. CONTROL OF CASCADE • To prevent excessive clotting (which might lead to thromobosis – more about that later): Fibrinolysis • Plasminogen is activated = converted into plasminby: • plasma kallikrein • t-PA = tissue plasminogen activator • urikinase • Plasmin: re-dissolves the soluble fibrins – fibrinopeptides • inhibits thrombinformation = polymerization of fibrin is halted

  11. DISEASES, DEFICIENSIES Vitamin K: needed for synthesis of • prothrombin • FVII • FIX • FX • protein c HEMOPHILIA • HA = FVIII (85%) • HB = FIX (15 %) • von Willebrand´sTHROMBOEMBOLIC CONDITIONS THROMBOEMBOLIC CONDITIONS • Thrombus – an abnormal clot in vessel • Emboli – thrombus sailing with blood stream - NOT GOOD.  

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