In a patient with a history of angina pectoris experiencing worsening chest pain, what will the administration of a monoclonal antibody against platelet IIb/IIIa receptors prevent?

• A. Adenosine binding to platelets
• B. ADP binding to platelets
• C. Fibrinogen binding to platelets
• D. Thrombin binding to platelets

Answer: (C)

The administration of a monoclonal antibody against platelet IIb/IIIa receptors will prevent fibrinogen binding to platelets. This is because the IIb/IIIa receptor is a crucial component of the platelet activation process. When platelets are activated, they undergo a change that allows them to bind fibrinogen, forming a bridge between adjacent platelets, which is essential for platelet aggregation and the formation of a stable blood clot.

By targeting and inhibiting the IIb/IIIa receptor, the monoclonal antibody effectively blocks the ability of fibrinogen to bind to platelets. This action decreases platelet aggregation, which is particularly important in a patient with angina pectoris, where thrombus formation can worsen ischemia and lead to more severe chest pain or even myocardial infarction.

Understanding the context of how IIb/IIIa receptors function within the hemostatic process highlights the rationale for using such therapies in conditions characterized by excessive platelet activity.