What is a characteristic feature of Factor V Leiden mutation?

What is a characteristic feature of Factor V Leiden mutation?

• A. Increased clot breakdown
• B. Resistance to Protein C and S cleavage
• C. Enhanced fibrinolysis
• D. Accelerated healing process

Answer: (B)

Factor V Leiden is a genetic mutation that results in a variant form of factor V, a protein involved in the blood coagulation process. One of the most significant characteristics of the Factor V Leiden mutation is its resistance to the regulatory actions of activated protein C (APC). Normally, activated protein C functions to inactivate factor V and factor VIII, which helps to regulate blood clotting and reduce the risk of thrombosis. However, in individuals with the Factor V Leiden mutation, this regulatory mechanism is impaired. As a result, the mutated factor V is less effectively inactivated, leading to a prothrombotic state where the risk of abnormal blood clot formation in veins (venous thrombosis) is increased. This aspect of the mutation is essential for understanding the pathophysiology associated with Factor V Leiden and how it contributes to conditions such as deep vein thrombosis and pulmonary embolism. The other options do not accurately characterize the effect of the mutation; for instance, increased clot breakdown and enhanced fibrinolysis would suggest a reduction in clotting tendency, which is contrary to the effects observed in Factor V Leiden. Similarly, accelerated healing process does not relate to the mutation’s influence on coagulation and thrombosis. Thus, the resistance to protein

Factor V Leiden is a genetic mutation that results in a variant form of factor V, a protein involved in the blood coagulation process. One of the most significant characteristics of the Factor V Leiden mutation is its resistance to the regulatory actions of activated protein C (APC). Normally, activated protein C functions to inactivate factor V and factor VIII, which helps to regulate blood clotting and reduce the risk of thrombosis. However, in individuals with the Factor V Leiden mutation, this regulatory mechanism is impaired. As a result, the mutated factor V is less effectively inactivated, leading to a prothrombotic state where the risk of abnormal blood clot formation in veins (venous thrombosis) is increased.

This aspect of the mutation is essential for understanding the pathophysiology associated with Factor V Leiden and how it contributes to conditions such as deep vein thrombosis and pulmonary embolism. The other options do not accurately characterize the effect of the mutation; for instance, increased clot breakdown and enhanced fibrinolysis would suggest a reduction in clotting tendency, which is contrary to the effects observed in Factor V Leiden. Similarly, accelerated healing process does not relate to the mutation’s influence on coagulation and thrombosis. Thus, the resistance to protein