Blood Coagulation Cascade
Coagulation converts primary platelet plug into clot.
It may start with intrinsic pathway and/or exterinsic pathway → both the pathways merge at the common pathway.
Activated when blood comes in contact with negative surface.
Takes place on the surface of activated platelet.
starts with factors that are intrinsic to the blood → called intrinsic pathway.
High Molecular Weight Kiniogen anchors factor XII to platelet surface
Activation of factor XII to XIIa
XIIa activates prekallikrein into kallikrein → kallikrein speeds up conversion of XII to XIIa
XIIa activates XI into XIa
γ Carboxy glutamic acid residue of factor IX attaches it to platelet surface via calcium → XIa activates IX into IXa
IXa associates with VIIIa, Calcium, and phospholipids → this complex is called Tenase
Tenase activates X into Xa.
Starts with factors outside the blood → called extrinsic pathway.
Under healthy conditions, endothelial cells prevent exposure of tissue factor to the blood.
Injury to endothelium
↓ Tissue factor is exposed to blood
↓ Factor VII binds to tissue factor → tissue factor activates factor VII into VIIa
Tissue factor and VIIa associate with calcium and form "Tissue factor + VIIa + Ca" complex
This complex activates X into Xa.
Factor Xa associates with factor Va, calcium, and phospholipids
This complex is called prothrombinase
It converts prothrombin into thrombin
Thrombin converts fibrinogen into fibrin monomer
Fibrin monomers polymerize to form fibrin polymers
↓ Fibrin polymers form loose mesh around platelets
Thrombin converts Factor XIII (Fibrin stabilizing factor) into XIIIa
XIIIa cause covalent cross-linking between fibrin polymers → formation of stable fibrin.
Along with platelets, RBCs and WBCs also get trapped in clot when it is being formed.
Arterial clots have high proportion of platelets.
Venous clots have high proportion of fibrin.