Coagulation flow chart:

Vasoconstriction:
1.	Local contractile response: 60 second neurogenic spasm; 30-60 minute myogenic spasm = vasoconstriction and increased tissue pressure
2.	Humoural substance release: serotonin from dense granules of platelets and endothelin from injured epithelial cells also promote vasoconstriction
Platelet plug formation (primary hemostasis):
1.	Adhesion: Binding of membrane glycoproteins, integrins to exposed collagen and other subendothelial adhesion factors of damaged blood vessel to platelets. Van Willibrand factor quite important. Tissue thromboplastin generates only a small amount of thrombin from prothrombin at this point.
2.	Activation: Change of platelet changes from disc shaped to pseudopods, release of granule content (ADP and fibrinogen primarily responsible for platelet aggregation)
3.	Aggregation: ADP stimulates release of thromboxane A. Some thrombin promotes platelet adhesion and activation. Serotonin causes vasoconstriction. Platelet plug at this point = UNSTABLE hemostatic plug
4.	Other reactions: in adjacent intact endothelium, ADP promotes release of prostacyclin and nitric oxide, which inhibit platelet aggregation and cause vasodilation, respectively. This ensures efficient blood flow around injured site.
Blood coagulation
1.	Initiated by two factors: exposed subendothelial tissue and translocation of negatively charged phospholipids to the platelet cell membrane.
2.	Extrinsic and intrinsic pathways converge on formation of Xa.
3.	Common pathway results in large thrombin production and formation of fibrin mesh
4.	Clot retraction and fibrinolysis