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:
- 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.
- 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).
- Anticoagulation: coagulation is inhibited by the inhibition of clotting factors and inactivation of cofactors.
- Fibrinolysis: lysis of fibrin to soluble fragments by plasmin and the repair of the vessel wall.
Platelet adhesion occurs as the result of
Extra info: Reflex vasoconstriction and the formation of a thrombus occur as the result of platelet aggregation, not visa-versa. An increase in blood volume causes a dilution of platelets and thus they are less likely to adhere to each other.
What is true about platelets?
Extra info: They are formed in the bone marrow from megakaryocytes. Their life span is about 7 days. Endothelium produces prostacyclin that inhibits aggregation of platelets.