Blood Homeostasis PDF

**Phase 1: Vascular Spasm** When a blood vessel is injured, the **vascular spasm** is the initial, reflexive narrowing (or vasoconstriction) of the blood vessel, reducing blood flow to the damaged area. This helps minimize blood loss temporarily. **Phase 2: Formation of the Platelet Plug** 1. **...

**Phase 1: Vascular Spasm** When a blood vessel is injured, the **vascular spasm** is the initial, reflexive narrowing (or vasoconstriction) of the blood vessel, reducing blood flow to the damaged area. This helps minimize blood loss temporarily. **Phase 2: Formation of the Platelet Plug** 1. **Platelet Adhesion**: Platelets are attracted to the exposed collagen fibers at the injury site. They adhere to these fibers with the help of **von Willebrand factor** (vWF), which acts like glue, securing the platelets to the damaged area. 2. **Platelet Activation and Aggregation**: Once adhered, platelets become activated, changing shape to better cover the injured area. They release chemical signals, such as **ADP** and **thromboxane A2**, which attract and activate more platelets to form a **platelet plug**. **Phase 3: Coagulation Cascade (Clot Formation)** This is the most complex part, involving two initial pathways---the intrinsic and extrinsic pathways---that converge into a **common pathway**. These steps involve a series of **clotting factors** (mostly enzymes and proteins) that activate each other in a cascade. 1. **Intrinsic Pathway**: Activated by trauma inside the blood vessel. It's slower but provides a more robust response. The intrinsic pathway involves several factors, including factors **XII, XI, IX, and VIII**. 2. **Extrinsic Pathway**: Activated by external trauma, such as tissue injury outside the blood vessel, and is faster. When tissue is damaged, **tissue factor** (Factor III) is released, which combines with Factor VII to activate Factor X. 3. **Common Pathway**: - **Activation of Factor X**: Both the intrinsic and extrinsic pathways ultimately activate **Factor X**. - **Prothrombin to Thrombin**: Activated Factor X, along with Factor V, forms the **prothrombinase complex**, which converts **prothrombin** (Factor II) into **thrombin**. - **Formation of Fibrin**: Thrombin then converts **fibrinogen** (a soluble plasma protein) into **fibrin** monomers. Thrombin also activates **Factor XIII**, which stabilizes the fibrin strands by cross-linking them, forming an insoluble **fibrin mesh**. This fibrin mesh, combined with the aggregated platelets, forms a **stable blood clot**. **Phase 4: Fibrinolysis (Clot Dissolution)** Once the vessel is healed, the clot is no longer needed and must be removed to restore normal blood flow. This happens through **fibrinolysis**, where: 1. **Plasminogen**, an inactive protein trapped within the clot, is activated to **plasmin** by tissue plasminogen activator (tPA) and urokinase. 2. **Plasmin** digests fibrin, breaking down the clot into fragments, which are removed by the body.