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platelets (hemostasis (1.vascular constriction (blood vessels ruptured or…

- - - - 1.platelet adhesion
        
        platelet swell
        
        -assume irregular forms with many irradiating psedopods
        -contractile proteins contract forcefully
        
        release of granules
        (contain multiple active factors
        
        -become sticky
        -platelet adhere to collagen in the tissues &
        to a protein- Von Willibrand factor(that anchor the platelet
        -also dependent on glycoproteins
        
        Normally, the endothelial cells express molecules that inhibit platelet adherence and activation while platelets circulate through the blood vessels.
        During an injury,
        subendothelial collagen from the extracellular matrix beneath the endothelial cells is exposed on the epithelium as the normal epithelial cells are damaged and removed,
        which releases von Willebrand Factor (VWF).
        VWF causes the platelets to change form
        with adhesive filaments (extensions) that adhere to the subendothelial collagen on the endothelial wall.
      - 2.platelet activation
        
        activated platelets exocites-ADP & throboxane A2
        activates other nearby platelets
        these additional platelets adhere to the
        original activated platelets
        
        After platelet adherence occurs,
        the subendothelial collagen binds to receptors on the platelet
        , which activates it.
        During platelet activation, the platelet releases a number of important cytokines and chemical mediators via degranulation.
        The released chemicals include
        ADP,
        VWF,
        thromboxane A2,
        platelet-derived growth factor (PDGF),
        vascular endothelial growth factor (VEGF),
        serotonin, and
        coagulation factors.
        The extra ADP and VWF is especially important because it causes nearby platelets to adhere and activate,
        as well as release more ADP, VWF, and other chemicals.
        Platelet plug formation is considered a positive feedback process because ADP and VWF levels are successively increased as more and more platelets activate to form the plug.
      - 3.platelet aggregation
        
        fibrinogen forms a bridge betw the surface
        receptors of different platelets
        increasing no of platelets form a platelet plug
        (loose plug that blocks bleeding if the vascular
        opening is small
        during the subsequent process of blood coagulation
        -fibrin threads form
        
        the final step of platelet plug formation is aggregation of the platelets into a barrier-like plug.
        Receptors on the platelet bind to VWF and fibrinogen molecules, which hold the platelets together.
        Platelets may also bind to subendothelial VWF to anchor them to the damaged endothelium.
        The completed plug will cover the damaged components of the endothelium and will stop blood from flowing out of it,
        but if the wound is large enough, blood will not coagulate until the fibrin mesh from the coagulation cascade is produced, which strengthens the platelet plug.
        If the wound is minor, the platelet plug may be enough to stop the bleeding without the coagulation cascade.