Hemostasis is a balance between procoagulant, anticoagulant and fibrinolytic processes in the blood vessel. Damage to a blood vessel initiates a cascade of events involving endothelial cells, platelets and proteins. The result is the formation of a platelet-fibrin clot. Meanwhile, anticoagulant and fibrinolytic processes are started to inhibit the formation of unwanted clots (thrombosis). The following events can be distinguished in hemostasis:

  1. Platelet adhesion and aggregation (primary hemostasis): after vessel wall damage, there is reflex vasoconstriction, and the formation of a platelet thrombus on the damaged subendothelium. Disorders: thrombocytopenia, thrombocytopathy, Von Willebrand disease.
  2. Coagulation (secondary hemostasis): after contact with tissue factor coagulation is activated, precursor pro-enzymes are converted to activated clotting factors which is accelerated by cofactors, finally resulting in fibrin formation by thrombin (the endpoint in the coagulation cascade). Disorders: coagulation factor deficiencies – hemophilia A (FVIII deficiency), hemophilia B (FIX deficiency).
  3. Anticoagulation: coagulation is inhibited by the inhibition of clotting factors and inactivation of cofactors.
  4. Fibrinolysis: lysis of fibrin to soluble fragments by plasmin and the repair of the vessel wall.

Platelet adhesion occurs as the result of


What is true about platelets?