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MLAB 1227: Coagulation K eri Brophy-Martinez

MLAB 1227: Coagulation K eri Brophy-Martinez. Overview of Hemostasis: Part Two. Function of Platelets. Surveillance of blood vessel continuity Checks endothelial lining for gaps and breaks Fill-in small gaps caused by separation of endothelial cells Formation of primary hemostatic plug

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MLAB 1227: Coagulation K eri Brophy-Martinez

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  1. MLAB 1227: CoagulationKeri Brophy-Martinez Overview of Hemostasis: Part Two

  2. Function of Platelets • Surveillance of blood vessel continuity • Checks endothelial lining for gaps and breaks • Fill-in small gaps caused by separation of endothelial cells • Formation of primary hemostatic plug • Surface for coagulation factors to make secondary hemostatic plug • Aid in healing injured tissue

  3. Formation of Primary Hemostatic Plug • Once the platelets “normal” environment is changed, they become activated or adhesive • Stages of plug formation • Adhesion • Secretion • Aggregation • Stabilization

  4. Stage 1: Platelet Adhesion • Platelets attach to non-platelet surfaces, suchascollagen fibers in the subendothelium • Platelets move from the blood vessels and into the tissues. • Exposure to surfaces in the tissues causes them to bind to collagen with the presence of von Willebrand factor ( vWF) through the Glycoprotein Ib/IX receptor • Results in a bridge formation, which triggers a shape change in the platelets • Reversible • No energy required

  5. Platelet Activation • Platelets undergo a shape change from disc to spiny sphere with projections • Activation required for 1O hemostatic plug formation • Activation continues until Ca ++ threshold met • Platelets remain localized in injured area • http://tiny.cc/abmhmw

  6. Activation Platelet shape change after exposure to agonist. Agonists include: ADP, Serotonin, collagen, thrombin

  7. Stage 2: Platelet Secretion/ Platelet release reaction • Secretion • Requires ATP • Provides a positive feedback by releasing more agonists to stimulate more plt receptors • Release of Granule contents • Causing vasoconstriction • Release of ADP(agonist)= increased Ca+, plt release, increase in fibrinogen receptors • Trigger a secondary aggregation which is irreversible

  8. What’s in a Granule? • Granules consist mainly of: • Alpha granules: Factor V, vWF, Fibrinogen, platelet factor 4, β-thromboglobulin • Factor V: receptor on platelet surface for factor Xa & prothrombin • PF4: heparin neutralizing factor • Dense bodies: ATP, ADP, serotonin, Ca

  9. Side note • Heparin is used on patients who clot excessively. Endothelial cells make heparin-like molecules and expose them on their surface. PF4 binds these substances. Heparin can complex with bound PF4 and heparin will be neutralized.

  10. Stage 3: Platelet aggregation • Chemical changes cause platelets to aggregate and stick to one another • Newly arriving platelets become activated by agonists • Exposure of GPIIb/IIIa sites bind fibrinogen • Fibrinogen + activated platelets serves as a bridge between two platelets • Calcium must be present

  11. Adhesion & Aggregation • http://www.platelet-research.org

  12. Final Stage : Stabilization of Clot • AKA: primary hemostatic plug formation • Thrombus formation • Platelets release Factor V • Expose factor III (TF) • Accelerating coagulation cascade • Promote activation of clotting factors

  13. Stages of 1o plug formation

  14. Blood clot

  15. Coagulation System • Composed of 14 coagulation factors (serine proteases) which are interdependent (Factors I through XIII – there is no Factor VI – and PK and HMWK) • Inactive form of each is an enzyme precursor which is usually designated by a Roman numeral but also given a name – Ex. Factor I fibrinogen. Numbers correspond to order of discovery NOT order in cascade. • Active forms are usually designated by the letter “a” after the Roman numeral and may also have a different name – Ex. Ia Fibrin • Cofactors are needed for many reactions in the cascade – Ex. Calcium, platelet factor 3 (PF3) • Each molecule must be present in sufficient quantity as well as functioning normally • Final product is fibrin mesh or clot which completely stops bleeding • Secondary hemostasis • Slow contraction or retraction and lysis of the clot occurs

  16. Fibrinolytic System • Plasminogen is converted to plasmin • Plasmin enzymatically attacks the fibrin molecule producing fibrin degradation products (FDPs, sometimes called FSPs) that are cleared from the circulation by macrophages • Fibrin is a product formed during hemostasis, tissue repair or inflammation • Fibrin plays a temporary role • Once injury heals, the fibrin clot is lysed

  17. Coagulation Inhibition System • Provides balance and control of clotting mechanisms • Natural inhibitors and anticoagulants circulate in the plasma to: • Prevent clotting when it’s not needed • Limit or localize the clotting that is needed • Examples: Protein C and S, antithrombin III

  18. References • McKenzie, Shirlyn B., and J. Lynne. Williams. "Chapter 29." Clinical Laboratory Hematology. Boston: Pearson, 2010. Print. • Platelet Research Laboratories. Platelet Function. Retrieved from http://www.platelet-research.org/1/function_hemo.htm.

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