Coagulation

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Chapter: Essential pharmacology : Drugs Affecting Coagulation, Bleeding And Thrombosis

Haemostasis (arrest of blood loss) and blood coagulation involve complex interactions between the injured vessel wall, platelets and coagulation factors.


COAGULATION

 

Haemostasis (arrest of blood loss) and blood coagulation involve complex interactions between the injured vessel wall, platelets and coagulation factors. A cascading series of proteolytic reactions (Fig. 44.1) is started by:

 


 

i) Contact activation of Hageman factor: intrinsic system, in which all factors needed for coagulation are present in plasma. This is slow and takes several minutes to activate factor X.

 

ii) Tissue thromboplastin: extrinsic system, needs a tissue factor, but activates factor X in seconds.

 

The subsequent events are common in the two systems and result in polymerization of fibrinogen to form fibrin strands. Blood cells are trapped in the meshwork of fibrin strands producing clot.

 

Two in vitro tests ‘activated partial thromboplastin time’ (aPTT) and ‘prothrombin time’ (PT) are employed for testing integrity of the intrinsic, extrinsic and common pathways of the coagulation cascade. The results are interpreted as:

 


 

Most clotting factors are proteins present in plasma in the inactive (zymogen) form. By partial proteolysis they themselves become an active protease and activate the next factor. In addition to its critical role in cleaving and polymerizing fibrinogen, thrombin activates many upstream factors (especially f. XI, VIII and V) of the intrinsic and common pathways—amplifying its own generation and continuation of clot formation. It is also a potent activator of platelets.

 

On the other hand, factors like antithrombin, protein C, protein S, antithromboplastin and the fibrinolysin system tend to oppose coagulation and lyse formed clot. Thus, a check and balance system operates to maintain blood in a fluid state while in circulation and allows rapid haemostasis following injury.

 

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