The intrinsic pathway of coagulation is initiated by factor XII (Hageman factor) contact activation on negatively charged surfaces. What is the physiological relevance of this pathway in vivo?

• A It amplifies coagulation via the XI → IX → X pathway but is NOT essential for haemostasis in vivo — patients with factor XII deficiency do NOT bleed abnormally ✓
• B It is the primary initiator of haemostasis, with TF/VIIa (extrinsic) pathway playing only a minor amplifying role
• C It is exclusively responsible for fibrin clot formation at sites of vascular injury via XI activation
• D Its primary role is fibrinolysis — factor XII activates plasminogen to plasmin, not the coagulation cascade

Explanation

The 'contact pathway' (intrinsic pathway, factor XII, prekallikrein, high-molecular-weight kininogen → XI → IX) was historically considered the initiator of coagulation but has since been recognised as NOT essential for haemostasis. Factor XII-deficient individuals have markedly prolonged aPTT in the lab but have a normal bleeding phenotype — they do NOT bleed excessively. Paradoxically, factor XII deficiency is associated with thrombotic risk (Hageman factor's original patient died of pulmonary embolism). In vivo haemostasis is primarily initiated by the extrinsic pathway (tissue factor/factor VIIa, exposed at vessel injury), with the intrinsic pathway serving as an amplifier. This distinction explains why prolonged aPTT from factor XII deficiency does not require treatment.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.