Hemostasis Quiz: Blood Clotting Mechanisms

Study Notes

Hemostasis refers to the process of blood clotting, which is essential to stop bleeding and maintain vascular integrity.
It involves a series of complex steps initiated by blood vessel injury.

Vasoconstriction (narrowing) of the blood vessel temporarily reduces blood flow to the injured area.
This vasoconstriction, or vascular spasm, is a reflex mechanism triggered by the injury.

Platelet Adhesion: Platelets adhere to exposed collagen fibers at the injury site with the help of von Willebrand factor (vWF), acting like glue.
Platelet Activation and Aggregation: Once adhered, platelets become activated, releasing chemical signals (ADP and thromboxane A2) that attract and activate more platelets, forming a platelet plug.

Intrinsic Pathway: Begins with trauma inside the blood vessel and involves factors XII, XI, IX, and VIII. It is slower than the extrinsic pathway but provides a more robust response.
Extrinsic Pathway: Activated by external trauma, involving tissue injury outside the blood vessel. Tissue damage releases tissue factor (Factor III), which combines with Factor VII to activate Factor X
Common Pathway: Both pathways converge at the activation of Factor X. Activated Factor X, along with Factor V, forms the prothrombinase complex, which converts prothrombin (Factor II) into thrombin. Thrombin converts fibrinogen (a soluble plasma protein) into fibrin monomers. This process also activates Factor XIII, which stabilizes the fibrin strands, forming an insoluble fibrin mesh that, together with the aggregated platelets, forms a stable blood clot.

The clot is dissolved through fibrinolysis after the vessel is healed.
Plasminogen, an inactive protein trapped within the clot, is activated to plasmin by tissue plasminogen activator (tPA) and urokinase.
Plasmin digests fibrin breaking down the clot into fragments removed by the body.