Which factor deficiency will likely impact platelet aggregation?

Fibrinogen Deficiency Will Impact Platelet Aggregation

Fibrinogen (Factor I) deficiency will most significantly impact platelet aggregation when it becomes deficient. Among the factors listed in the question, fibrinogen is the only one that plays a direct and critical role in platelet aggregation by binding to activated GPIIb/IIIa receptors on platelets.

Mechanism of Platelet Aggregation and the Role of Fibrinogen

Platelet aggregation involves several key steps:

1. Initial platelet adhesion: Platelets adhere to exposed subendothelial collagen
2. Platelet activation: This leads to conformational changes in platelet surface receptors
3. Fibrinogen binding: Activated GPIIb/IIIa receptors on platelets bind fibrinogen
4. Cross-linking: Fibrinogen forms bridges between platelets, enabling aggregation

Fibrinogen serves as the primary bridging molecule between activated platelets. When fibrinogen is deficient, platelet aggregation is severely impaired despite normal platelet function 1.

Analysis of Each Factor Listed in the Question

B. Fibrinogen (Factor I)

• Fibrinogen is essential for platelet aggregation by binding to activated GPIIb/IIIa receptors
• Deficiency directly impairs platelet-platelet interactions
• Has a long half-life of 96-150 hours 1
• Afibrinogenemia has a prevalence of 1/500,000 and can cause significant bleeding 1

A. Factor XIII

• Functions primarily in clot stabilization by cross-linking fibrin
• Acts after initial platelet aggregation has occurred
• Does not directly participate in platelet-platelet binding
• Has a long half-life of 144-300 hours 1

C. Factor VIII

• Functions as a cofactor in the tenase complex for thrombin generation
• While Factor VIII can enhance platelet function when platelets are co-stimulated with TRAP-6 2, it does not directly mediate platelet-platelet binding
• Factor VIII deficiency (hemophilia A) primarily affects secondary hemostasis rather than primary platelet aggregation

D. Stuart-Prower Factor (Factor X)

• Functions in the common pathway of coagulation
• Primarily involved in thrombin generation
• Does not directly participate in platelet-platelet binding

Clinical Implications

Fibrinogen deficiency presents with:

• Prolonged bleeding time
• Poor clot formation
• Impaired platelet aggregation in laboratory testing
• Risk of spontaneous bleeding

The diagnosis of afibrinogenemia shows:

• Prolonged PT and aPTT
• Abnormal thrombin time
• Defective platelet aggregation responses 1

Conclusion

Among the factors listed, fibrinogen is the only one that serves as a direct bridging molecule between platelets during aggregation. Its deficiency directly impairs platelet aggregation even when platelet function is otherwise normal, making it the correct answer to this question.