Tissue activation/activator pathway.
Trauma to the vessel wall.
Conformational change occurs, leading to the release of granule contents and thromboxane A2 formation.
They help assess the functionality of the coagulation system and identify disorders.
12 seconds.
Factors outside the vascular system.
Promotes vasodilation and inhibits platelet activation and clotting.
Vascular constriction, formation of platelet plug, formation of blood clot, growth of fibrous tissue.
The smooth muscle in the vessel wall contracts near the injury point, reducing blood loss.
It acts as a vasoconstrictor and activates more platelets.
They amplify the platelet activation response and promote aggregation.
It helps to prevent platelet adhesion to damaged surfaces.
It is an integral membrane protein that serves as a receptor for factor VII.
Tissue injury, which releases tissue factor (factor III).
It is essential for the synthesis of factors II, VII, IX, X, and Protein C.
Factor XIII.
It acts as a cofactor, helping anchor Factor XII to the surface.
It is an essential cofactor for the formation of several clotting factors.
It is the first mechanism that occurs to prevent blood loss.
Kallikrein, which acts as a protease.
A higher chance of having a clot.
vWF released by activated platelets binds to platelet receptor GPIb/Ia, activating more platelets.
Factor Xa + Phospholipid + Factor V.
It converts fibrinogen into fibrin monomers.
150,000 to 300,000 per microliter (μl).
A condition characterized by low blood platelet count.
1 to 6 minutes.
A blood vessel is severed, causing blood and components to leak out.
The process where platelets aggregate at the site of injury to stop bleeding.
The concentration of prothrombin in the blood and the time required for coagulation.
Anticoagulants oppose or limit coagulation to restore the clot-free condition of the blood.
A high risk of bleeding.
They prevent platelets from adhering to endothelium under normal conditions and facilitate adhesion to injured vessels.
Inhibits platelet adhesion and aggregation.
Thrombin.
Factor VIII (Antihemophilic Factor) deficiency.
In 15 to 20 seconds.
Prevention of blood loss or hemorrhage.
By chemicals released from the injury site and contact with underlying collagen.
They help maintain blood flow by preventing excessive clotting.
Integrins platelet receptor and von Willebrand Factor (vWF).
It enhances the conversion of Factor XII into XIIa through positive feedback.
Various conditions that affect normal blood clotting and bleeding.
Primary hemostasis and Secondary hemostasis.
Binds to and inhibits Factor Xa and thrombin.
Factors XII, XI, VIII, Prekallikrein, HMW kininogen, Ca²⁺, and phosphatidylserine.
Vitamin K.
It stops the coagulation cascade as the clot is ready to be degraded.
It indicates a lack of platelets or issues with platelet function.
Extrinsic pathway, intrinsic pathway, and common pathway.
Clotting factors specific to each pathway (extrinsic and intrinsic).
Factor X or Stuart factor.
The process of breaking down fibrin in blood clots.
Factors III, VII, and X.
Factor IXa, Factor VIIIa, Ca²⁺, and negatively charged phospholipids.
Factor X is converted into its activated form, FXa.
Factor IX together with factor VIII and Ca2+ generates intrinsic tenase.
Contact with negatively charged surfaces.
Thrombocytopenia is low platelet count, while thrombocytosis is elevated platelet count, which can increase clotting risk.
In the liver.
Fibrin, which forms a mesh trapping more platelets and erythrocytes to produce a clot.
High-molecular-weight kininogen (HMWK).
To assess the total function of the coagulation cascade and measure the time it takes for fibrin strands to form after an injury.
Factor XIa.
It is quicker responding and more direct.
Factor Xa.
It converts prothrombin to thrombin.
Thrombin converts fibrinogen to fibrin, stabilizing the platelet plug.
A condition characterized by a very low platelet count.
It breaks down fibrin, fibrinogen, and various coagulation factors.
It dissolves the clot by breaking down fibrin and fibrinogen.
6 to 10 minutes.
ADP, ATP, serotonin, vWF, clotting factor V, and fibrinogen.
Factor XIa combined with Ca²⁺.
Smoothness of the endothelial cell surface and the presence of thrombomodulin and thrombin complex.
The formation of prothrombin activator.
Fibrin fibers.
Agents that inhibit platelet activation; examples include Aspirin and Clopidogrel.
Aggregates of platelets and erythrocytes trapped within a mass of fibrin strands.
1. Formation of Prothrombin Activator; 2. Conversion of Prothrombin to Thrombin; 3. Conversion of Fibrinogen to Fibrin.
It allows GPIIb/IIIa to bind fibrinogen, forming bridges between platelets.
The conversion of plasminogen to plasmin.
Tissue plasminogen activator or urokinase-type plasminogen activator.
It is converted into its active form, XIIa.
A condition where large amounts of tissue factor are released, leading to numerous small clots and bleeding tendencies.
<p>Calcium</p>
