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Understanding Blood Coagulation and Hemostasis: Mechanisms, Phases, and Disorders

This article provides an overview of blood coagulation and hemostasis, essential processes for preventing blood loss. It outlines the four primary phases: vascular contraction, platelet formation, coagulation, and tissue repair. The cascade mechanism is described in detail, including the extrinsic and intrinsic pathways leading to clot formation. Additionally, it discusses diseases like hemophilia and thromboembolic conditions, and highlights treatments associated with deficiencies and excess clotting. Understanding these complex mechanisms is crucial for improving clinical outcomes.

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Understanding Blood Coagulation and Hemostasis: Mechanisms, Phases, and Disorders

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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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