Hemophilia A (factor VIII deficiency) results in a prolonged aPTT with normal PT. This pattern is explained by the fact that factor VIII participates in:

• A The intrinsic (contact activation) pathway — factor VIII is a cofactor in the tenase complex that activates factor X ✓
• B The extrinsic pathway — tissue factor/factor VIIa complex activation
• C The final common pathway — factor VIII directly activates prothrombin
• D Fibrinogen cross-linking by factor XIII in clot stabilization

Explanation

Factor VIII is a cofactor in the intrinsic tenase complex (factor IXa/factor VIIIa complex) that activates factor X on phospholipid surfaces. The intrinsic pathway is assessed by aPTT. The PT (extrinsic pathway) is normal because factors VII, X, V, II, and fibrinogen (common pathway) are unaffected. Hemophilia B (factor IX deficiency) gives an identical coagulation profile.

Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.

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