What is the impact of unable to cleave factor Va due to the Factor V Leiden mutation?

The Factor V Leiden mutation results in a single nucleotide change in the gene coding for factor V, which leads to a resistance to cleavage by activated protein C (APC). Normally, the cleavage of factor Va by APC is an essential regulatory mechanism that serves to limit thrombosis by promoting the degradation of pro-coagulant factors.

As a result of the inability to cleave factor Va effectively, its presence remains prolonged in the circulation, which leads to increased production of thrombin. Thrombin is a potent pro-coagulant enzyme that activates platelets and converts fibrinogen to fibrin, ultimately driving the clotting process. Therefore, individuals with the Factor V Leiden mutation have a higher risk of thromboembolic events due to the uncontrolled activation of coagulation pathways, resulting in increased thrombin production.

In contrast, other choices do not accurately reflect the consequences of the mutation. For instance, degradation of thrombin is actually decreased because its production is enhanced due to persistent factor Va activity. Similarly, inhibition of coagulation would not occur; rather, coagulation is hyperactive. Additionally, the mutation does not directly relate to the breakdown of platelets, as its primary effects are on the clotting factors rather than on platelet turnover.