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Coagulation cascade
- 1. BLOOD COAGULATION Extrinsic and Intrinsic Pathway
- 2. Hemostasis: • The term hemostasis means maintenance of normal blood flow and prevention of blood loss. • Hemostasis is the process of forming clots in the walls of damaged blood vessels and preventing blood loss, while maintaining blood in a fluid state within the vascular system. • Hemostasis involves 4 main steps: 1. Vascular spasm 2. Platelets reaction 3. Formation of platelet plug 3. Blood coagulation
- 3. • A set of reactions in which blood is transformed from a liquid to a gel, forming a clot. • The general mechanism of coagulation are: • Formation of Prothrombin activator • Conversion of Prothrombin into thrombin • Catalytic conversion of fibrinogen into a fibrin by thrombin that ultimately enmeshes platelets, blood cells and plasma to form the clot. • Coagulation follows intrinsic and extrinsic pathways Coagulation:
- 4. Clotting Factors: Clotting Factors Synonyms Factor I Fibrinogen Factor II Prothrombin Factor III Tissue factor/Tissue thromboplastin Factor IV Calcium Factor V Proaccelerin/Labile factor/Ac-globulin Factor VI Factor VII Stable factor/Proconvertin Factor VIII Anti-hemophilic factor/Anti-hemophilic factor A/Anti-hemophilic globulin Factor IX Christmas factor/Anti-hemophilic factor B/Plasma thromboplastin component Factor X Stuart factor/Stuart power factor Factor XI Plasma thromboplastin antecedent/Anti-hemophilic factor C Factor XII Hageman factor Factor XIII Fibrin stabilizing factor
- 5. Coagulation in detail: Common Pathway
- 6. Extrinsic Pathway Intrinsic pathway Fibrinogen Fibrin Thrombin Prothrombin Xa Va VIIa TF IXa VIIIa XIa XIIa XIIIa Soft clot Cross-linked Fibrin Hard clot V VIII
- 7. Extrinsic Pathway: Begins with a traumatized vessel wall or traumatized extra-vascular tissue that come in contact with blood. Tissue Trauma Tissue Factor VII VIIa X Xa Ca++ Prothrombin Activator Prothrombin Thrombin Ca++ V Platelet phospholipid Ca++
- 8. Intrinsic Pathway: Begins with trauma to blood or exposure of the blood to collagen from a traumatized blood vessel wall. XII XIIa XIaXI IX IXa VIIIa VIII HMW Kininogen, prekallikrein X Xa Prothrombin Activator Prothrombin Thrombin Ca++ V Platelet phospholipid Platelet phospholipid, Ca++ Ca++ Ca++
- 9. Summary: I. Coagulation means blood converts into a gel like form by the involvement of many clotting factors strong enough to prevent further blood loss from the area of injury. II. Coagulation Occurs by two pathways EXTRINSIC and INTRINSIC but occurs simultaneously. III.Tissue injury initiates EXTRINSIC PATHWAY while injury to blood itself or its contact with collagen initiates INTRINSIC PATHWAY. IV.Both pathways involves the formation of PROTHROMBIN ACTIVATOR that activates Prothrombin to Thrombin which helps in formation of Fibrin that polymerizes and cross-links into a mesh and trapping platelets, blood cells and plasma; forms the clot, thus maintaining HEMOSTASIS.
- 10. Reference: •Guyton and Hall Textbook of Medical Physiology, A South Asian Edition •Internet
- 11. Created by: Niraj Phoju Student KIST Medical College, Lalitpur, Nepal
Notas do Editor
- Homeostasis means maintenance of normal blood flow and volume. It is the process of forming clots in the wall of injured vessels to prevent further blood loss and maintain the blood in fluid state in the vessel. Following any injury hemostasis is maintained by 4 main steps: 1. Constriction of the injured vessel to limit the blood flow 2. Platelet aggregation 3. formation of platelet plug that seals the wound 4. And finally blood clotting or in other words blood coagulation.
- Coagulation refers to the set of reactions in which blood is transformed from a liquid to a gel, forming a clot and resulting in homeostasis by ceasing further loss of blood from the damaged vessel, followed by repair. Generally clotting occurs in 3 essential steps: Complex cascade of chemical reactions involving about a dozen of clotting factors, occur in response to trauma to the vessel wall or blood itself, resulting in the formation a complex of activated substance called prothrombin activator. Prothrombin activator catalyses the conversion of prothrombin to thrombin. Thrombin acts as enzyme to convert fibrinogen to fibrin fibres that entraps platelet, blood cells and plama, thus forming clot.
- As said earlier the process of coagulation involves about a dozen of clotting or coagulation factors. Each factor is designated a Roman number. To indicate the activated form, a small letter ‘a’ is added after the Roman number. Factor 6 is absent as it was earlier considered what we now call activated factor 5.
- This is the overall skeleton of the coagulation cascade. It is seen that both the Extrinsic and Intrinsic pathway goes on to activate Factor X and forming Prothrombin activator which convert Prothrombin to thrombin which subsequently catalyzes the conversion of fibrinogen to fibrin fibers. The fibrin fibers upon the action of fibrin stabilizing factor i.e. Factor XIII cross-links forming a mesh which enmeshes the platelets, blood cells and plasma to form the clot. And this is the common pathway that both extrinsic and intrinsic pathway ultimately reach.
- Again the same thing. The inactive factor I i.e. fibrinogen is activated by thrombin which is formed from Prothrombin by the action of Prothrombin activator. And both the pathways activate factor X which is an important component to form the Prothrombin activator. Finally the activated fibrinogen i.e. Fibrin which are actually the monomers formed after the removal of LMW peptide bonds from fibrinogen, have the automatic ability to polymerise with other fibrin monomers to form fibrin fibers. These fibers are not cross linked thus weak forming soft clot. Soon thrombin also activates the Factor XIII (Fibrin Stabilizing Factor) that causes stronger covalent bonding and cross-linking between the fibers making them stronger called Hard clot.
- Now talking about each pathway separately, EXTRINSIC PATHWAY begins with any factor that causes tissue trauma, that may be vascular wall trauma or extra vascular tissue trauma. The traumatized tissue release a complex of several factors called TISSUE FACTOR or TISSUE THROMBOPLASTIN that function mainly as proteolytc enzyme. The tissue factor activates Factor VII with which it complexes in the presence of calcium to activate Factor X. Now the common pathway starts. Activated Factor X complexes with the factor V and in the presence of calcium forms PROTHROMBIN ACTIVATOR which in presence of calcium and platelet phospholipid converts PROTHROMBIN to THROMBIN. Then the process proceeds as discussed earlier. Here actually the Factor V of the activator complex is initially inactive which is activated by the formed thrombin once the clotting begins.
- Now coming to INTRINSIC PATHWAY, it begins with any factors that causes trauma to blood cells or the introduction of the blood cells to collagen. Initially the blood trauma causes activation of Factor XII and release of the platelet phospholipids due to damage to platelets. Then the activated Factor XII enzymatically activates Factor XI in the presence of HIGH MOLECULAR WEIGHT KININOGEN and PREKALLIKREIN. Similarly activated Factor XI activates Factor IX in the presence of calcium. Now the activated Factor IX along with Factor VIII, activated by thrombin; platelet phospholipids and calcium activates Factor X and once again starts the common pathway forming Prothrombin activator that converts Prothrombin to Thrombin and leading to the formation of the fibrin mesh and finally clot as described earlier.
- Now we have probably come to the end of this presentation, so summarizing the presentation……..