Cascada de Coagulación
Hemostasis and Coagulation Mechanisms
Overview of Hemostasis
- Damage to blood vessels activates three basic mechanisms for hemostasis: vasoconstriction, platelet adhesion, and degranulation.
- Vasoconstriction occurs immediately to reduce blood loss; exposed collagen and von Willebrand factor facilitate platelet shape change and adhesion.
Platelet Activation
- Degranulation of platelets releases serotonin (a vasoconstrictor), ADP, and thromboxane A2.
- ADP attracts more platelets to the site, while thromboxane A2 promotes further platelet aggregation and vasoconstriction.
- This positive feedback loop strengthens the platelet plug at the injury site.
Coagulation Process
- The damaged tissue releases tissue factor (TF or thromboplastin), activating the extrinsic pathway of coagulation with calcium ions.
- Factor XII activates Factor XI, which in turn activates Factor IX along with cofactor VIII, initiating the intrinsic pathway leading to Factor X activation.
Formation of Fibrin Clot
- Activated Factor X interacts with Factors III, V, calcium ions, and thromboplastin to activate prothrombinase.
- Prothrombinase converts prothrombin into thrombin; thrombin then converts fibrinogen into fibrin.
- Fibrin forms a loose mass that stabilizes into a tight clot as red blood cells aggregate within it.
Inhibition of Platelet Aggregation
- Aspirin inhibits thromboxane A2 synthesis through irreversible acetylation of cyclooxygenase required for prostaglandins and thromboxane production.