1 / 53

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:

egonzales
Download Presentation

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

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  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

More Related