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Hemostasis: the spontaneous arrest of bleeding from ruptured blood vessels Mechanisms:

Blood Physiology Professor A.M.A Abdel Gader MD, PhD, FRCP (Lond., Edin), FRSH (London) Professor of Physiology , College of Medicine & King Khalid University Hospital King Saud University Riyadh. Hemostasis: the spontaneous arrest of bleeding from ruptured blood vessels Mechanisms:

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Hemostasis: the spontaneous arrest of bleeding from ruptured blood vessels Mechanisms:

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  1. Blood PhysiologyProfessor A.M.A Abdel GaderMD, PhD, FRCP (Lond., Edin), FRSH (London)Professor of Physiology, College of Medicine &King Khalid University HospitalKing Saud UniversityRiyadh

  2. Hemostasis: • the spontaneous arrest of bleeding • from ruptured blood vessels • Mechanisms: • Vessel wall • Platelet • Blood coagulation • Fibrinolytic system

  3. Memostatic Mechanisms: • Mechanisms: • Vessel wall • Platelet • Blood coagulation • Fibrinolytic system

  4. Memostatic Mechanisms- cont • Vessel wall • Immediately After injury a localized Vasoconstriction • Mechanism -Hurmoral factors: • local release of thromboxane A2 & 5HT by platelets • Systemic release of adrenaline • Nervous factors

  5. Platelet haemostatic plug formation

  6. Platelets – cont. Site of formation: Bone marrow Steps: Stem cell Megakaryoblast Megakaryocyte Platelets

  7. Megakayocyte andplatelet formation

  8. Platelets Thrombocytes are • Fragments of megakaryocytes in bone marrow

  9. Platelets Formation (Thrombopoiesis) Regulation of thrombopoiesis by Thrombombopoietin

  10. Platelet Functions Begins with Platelet activation

  11. Platelet Activation • Adhesion • Shape change • Aggregation • Release • Clot Retraction

  12. Platelet Adhesion • Platelets stick to exposed collagen underlying damaged endothelial cells in vessel wall

  13. Platelet Release Reaction • Platelets activated by adhesion • Extend projections to make contact with each other • Release thromboxane A2, serotonin & ADP activating other platelets • Serotonin & thromboxane A2 are vasoconstrictors decreasing blood flow through the injured vessel. ADP causes stickiness & aggregation

  14. Platelet Aggregation • Activated platelets stick together and activate new platelets to form a mass called a platelet plug • Plug reinforced by fibrin threads formed during clotting process

  15. Platelet shape change and Aggregation

  16. Platelet Activation • Adhesion • Shape change • Aggregation • Release • Clot Retraction

  17. Platelet • Adhesion Endothelium 2. Shape change • 3. Aggregation

  18. Platelet Aggregation

  19. Platelet plug formation

  20. Platelet Plug Aggregation of platelets at the site of injury to stop bleeding • Exposed collagen attracts platelets • Activated platelets release of platelet ADP & TXA2the stickiness of platelets Platelets aggregation  plugging of the cut vessel • Intact endothelium secret prostacyclin inhibit aggregation

  21. Activated Platelets Secrets: • 5HT  vasoconstriction • Platelet phospholipid (PF3)  clot formation • Thromboxane A2 (TXA2) is a prostaglandin formed from arachidonic acid Function of TXA2: • vasoconstriction • Platelet aggregation (TXA2 inhibited by aspirin)

  22. Clotting Factors

  23. Extrinsic pathway Intrinsic Pathway Tissue factor FXII FXIIa Factor VII & Ca ++ FXI FXIa FIX FIXa FVIII X Xa FV+ Ca+P Prothrombin Thrombin Fibrinogen Fibrin The Coagulation Cascade

  24. The “Cascade”, “Waterfall” model Main feature: Depicts the coagulation process as: a series of proteolytic reactions >> each protease cleaves and activates the subsequent protease

  25. Activation Blood Coagulation • Intrinsic Pathway: all clotting factors present in the blood • Extrinsic Pathway: triggered by tissue factor • Common Pathway

  26. Fibrinolysis Plasminogen activators Plasminogen Plasmin Anti-activators Anti-plasmin Coagulation Fibrin FDP The fibrinolytic System

  27. ANTICOAGULANTS Anticoagulants: Substances that prevent blood coagulation

  28. Anticoagulants-cont. Types: • Substances that remove Ca++ from the blood: Citrate, oxalate, EDTA (Sequestrene) Ethylene Diamine Tetra chloro-Acetate

  29. Anti-coagulants-cont. 2. Heparin • Action: • inhibit the conversion of prothrombin to thrombin • inactivate thrombin (anti-thrombin III) • Uses: • Open heart surgery, Post-operative to prevent deep vein thrombosis • Collection of blood samples in labs.

  30. Anticoagulants-cont. 3. Warfarin • Inhibits the synthesis of Vit-K dependent clotting Factors (II, VII, IX & X) by the liver • Widely used in medicine as a oral anticoagulant

  31. Anticoagulants-cont. 4.Naturally occurring anticoagulants: • Control intravascular clotting • Antithrombin III inhibit thrombin, X, VIII, IX, XII • Protein C inhibit factor VIII, V

  32. Bleeding Disorders

  33. Bleeding Disorders Diseases characterized by excessive bleeding: • Vascular defects • Congenital • Acquired • Platelet defects • Low platelet count  Thrombocytopenia 3. Coagulation defects • Congenital • Acquired

  34. Petechiae, Purpura

  35. 3. Coagulation defects • Congenital: • Haemophilia A(deficient factor VIII), • Haemophilia B (deficient factor IX, Chrismas Disease) Treatment: • Replacing the missing factor • Transfusing: fresh frozen plasma, clotting factor concentrate

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