Hemostasis and Clot Formation

The process of stopping bleeding while maintaining normal blood flow.

Plasma proteins, platelets, and blood vessels.

Fibrinogen (coagulating protein), thrombin (initiator), and platelets (facilitators).

Vasoconstriction → primary hemostasis → secondary hemostasis → fibrinolysis.

Reduce blood flow and blood loss at the injury site.

Platelets adhere, activate, and aggregate to form an initial platelet plug.

Coagulation factors generate fibrin to stabilize the platelet plug.

Fibrinolysis, the controlled breakdown of fibrin clots.

Procoagulation, antifibrinolysis
Less coagulation: fibrinolysis, anticoagulation

To form clots where needed while preventing excessive clotting or bleeding.

Convert soluble fibrinogen into insoluble fibrin.

The liver.

Inactive proenzymes (zymogens) that become activated through proteolysis.

Calcium (Ca²⁺) and phospholipids.

Factors 10 and 13a.

Factor I (fibrinogen) and factor III (tissue factor).

Factors 2, 7, 9, 10 and the anticoagulant proteins C and S.
2+7=9 add a 1 and it’s a 10

It enables post-translational carboxylation needed for functional coagulation proteins.

Factor 7

Each activated factor activates multiple downstream molecules, rapidly increasing thrombin and fibrin production.

It explains laboratory coagulation testing but does not fully represent coagulation in living tissues.

On exposed subendothelial tissues and fibroblasts after vessel injury.

They provide surfaces and signals that control where and when coagulation occurs.

Blood contacts tissue factor-bearing cells, generating a small amount of thrombin.

Thrombin activates nearby platelets, causing shape changes, degranulation, and increased procoagulant surface.

It flips to the outer platelet membrane, providing a negatively charged surface for coagulation complexes.

Coagulation complexes assemble on activated platelets, generating a large burst of thrombin.

They provide phospholipid surfaces where coagulation factors assemble and activate.

Thrombin generates fibrin, which polymerizes and is cross-linked by factor 13a.

Within developing clots where plasminogen and its activators bind fibrin.

Plasminogen activators, especially tissue plasminogen activator (tPA).

Degrade fibrin into fibrin degradation products.

Inhibit plasminogen activators to limit fibrinolysis.

Inhibit plasmin to prevent excessive fibrin breakdown.

Antithrombin, protein C/protein S, and tissue factor pathway inhibitor (TFPI).

A liver-produced plasma protease inhibitor that inactivates thrombin, 9a, and 10a.

It enhances antithrombin activity, increasing inhibition of coagulation factors.

Thrombin binds endothelial thrombomodulin and activates protein C.

Inactivates factors 5a and 8a to reduce coagulation.

Factirs 2,7,9,10 complex.

Through nitric oxide (NO), prostacyclin (PGI₂), and adenosine diphosphatase activity.

The liver (hepatocytes) clears activated factors and degradation products; blood flow removes activated factors from the injury site.

Activates factors 5, 8, 11, 13 and platelets, promoting aggregation and thromboxane A₂ production.

It activates protein C, promotes NO/PGI₂ and tPA release, activates leukocytes, and increases endothelial integrin expression.