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.