| Summary: | The liver plays a central role in the control of haemostasis being the site of synthesis of most of the coagulation factors and natural anticoagulants, as well as fibrinolytic factors except the main activators of the fibrinolytic system (t-PA and u-PA). The liver also clears many of the activated clotting and fibrinolytic factors, as well as haemostatic activation complexes (TAT and PAP) and end product of fibrin degradation, FDP. Therefore, liver disease results in a complex and multifactorial pattern of defects in haemostatic function in the form of: (i) decreased synthesis of coagulation factors (ii) Abnormal protein synthesis e.g. dysfibrinogen (iii) Deficiency of natural anticoagulants (iv) Enhanced fibrinolytic activity (v) Quantitative and qualitative platelet defects (vi) Consumptive coagulopathy as in advanced liver disease. These abnormalities of haemostasis, which often occurs in the form of multiple defects, underlie the haemorrhagic diathesis, which often complicates liver disease. In the same manner, measurement of various haemostatic factors can be employed to reflect the degree of liver damage
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