Hemostasis in Pathology

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referred from Robbins, Basic pathology, *8th edition.

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Hemostasis in Pathology

  1. 1. What is normal hemostasis?<br />Normal hemostasis-<br /> process by which bleeding at any site arrested by the formation of a hemostatic plug.<br />1. Followed by removal of plug so that normal flow of blood through vessels is maintained.<br />
  2. 2. Components of hemostasis<br />Blood vessels- vasoconstriction<br />Platelets<br />Coagulation<br />Fibrinolytic system<br />Inhibitor of coagulation<br />
  3. 3. Blood vessels<br />Endothelial vessels activate<br />Coagulation cascade<br />Fibrinolytic systems<br />Protein C systems<br />vWF<br />
  4. 4. Properties of blood vessels<br />Prothrombotic prop.<br />vWF<br />Tissue factor –factor 3 + thromboplastin<br />Fibrinolysis inhibitor- PAIs<br />
  5. 5. Antithrombotic prop.<br />Antiplatelet effect- prostacyclins, nitric oxide<br />Anticoagulant effect –thrombomodulin<br />Thrombomodulin inactivates thrombin to make it an anticoagulant!<br />Fibrinolysis properties- t-PA<br />Clear fibrin deposits from endothelial surfaces.<br />
  6. 6. Role of platelets<br />Platelet adhere to exposed subendotheliat collagen<br />Adhered platelet undergo release reaction resulting in formation of aggregation.<br />1. adhesion-vWF- glycoprotein Ib assoc.<br />2. secretion/release- Ca2+ , ADP, thromboxane A2<br />3.aggregation-glycoprotein 2b- 3a receptors<br />Conformational changes of GP2b-3a allows platelet to bind fibrinogens.<br />
  7. 7. 2 pathways of coagulation<br />Intrinsic<br />Extrinsic<br />*final common pathway=<br />Prothrombin<br /> thrombin<br />
  8. 8. Assessment of the pathways<br />PT(prothrombin time)- extrinsic pathway<br />Factor 7, 10, 2, 5<br />PTT(partial thromboplastin time-intrinsic pathway<br />Factor 12, 11, 9, 8, 10, 5, 2 + fibrinogen<br />
  9. 9. Control of coagulation<br />Antithrombin<br />protein C and S<br />Fibrinolytic cascade<br />Plasminogenplasmin FSP (fibrin split products)<br />D-dimer is the most important FSP <br />
  10. 10. Summary of hemostasis<br />Primary hemostasis<br />BV constriction<br />Platelet plug formation<br />Secondary hemostasis<br />Activation of clotting cascade<br />Deposition &stabilisation of fibrin<br />
  11. 11. Tertiary hemostasis<br />Dissolution of fibrin clot<br />Removal of fibrin plug<br />
  12. 12. Bleeding disorders<br />Vascular abnormalities<br />Platelet disorders<br />CF (clotting factor) disorders<br />DIC (disseminated intravascular coagulation)<br />
  13. 13. Vascular abnormalities<br />Infection<br />Eg: meningococcemia,rickettsiosses, infective endocarditis<br />Drug reaction<br />Hereditary hemorrhagic telangiectesia<br />Autosomal dominant inheritance<br />Cushing syndrome<br />Heroch-scholeinpurpura<br />Systemic hypersensitivity disease of unknown cause<br />Polyarthralgia and acute glomerulonephritis<br />Palpable purpuric rash, coliclyabdomnal pain<br />=treated with steroids<br />
  14. 14. ITP<br />
  15. 15. ITP (idipathicthrombocutopenicpurpura)<br />Autoimmune disorder accelerated destruction of sensitized platelets by phagocytic cells in the RES.<br />*very2 important<br />
  16. 16. Clasification of ITP<br />Children / adult onset<br />Acute / chronic<br />Primary / secondary (idiopathic)<br />
  17. 17. Acute-children (post-infection)<br />Chronic-adult (&gt; female, 20-40 yrs. Old)<br />Autoimmune disorders<br />AntiplateletAb (IgG)<br />IgG coated platelets removed by spleen<br />&gt; megakaryocytes in bone marrow<br />*blood picture !!! Very important.<br />
  18. 18. Characteristic of ITP<br />Sudden onset of bruising / petechiae<br />Case history of infectious disease<br />Appear respiratory tract infection in about 3 weeks prior to onset of bleeding<br />Dangerous-intracerebellar hemorrhage<br />&lt;20,000 platelet count.<br />
  19. 19. ITP bone marrow aspirate<br />
  20. 20. Additional infos<br />t-PA most important plasminogen. plasminogen is activated by streptokinase.<br />To prevent excessive thrombi destruction, free plasminogen quickly bind to α2-antiplasmin.<br />
  21. 21. PAIs<br />Endothelial cells regulate anticoagulation balance by secreting PAIs. (plasminogen activation inhibitor)<br />PAI-block fibrinolysis, procoagulationefct.<br /> increased by certain cytokines.<br />role in I.V thrombosis accompanying severe inflammation.<br />

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