partial thromboplastin time

PTT evaluates the intrinsic and common pathways of the coagulation cascade. In the lab, a negatively charged activator (e.g., silica, kaolin) and phospholipid are added to plasma along with calcium, triggering clot formation via factors XII → XI → IX → VIII → X → V → II (prothrombin) → I (fibrinogen). The time to clot formation is measured in seconds (normal range ~25–35 seconds, lab-dependent).

Clinical significance: - Elevated PTT is seen in hemophilia A (factor VIII deficiency) and hemophilia B (factor IX deficiency), von Willebrand disease (due to decreased factor VIII stabilization), factor XI or XII deficiency, and liver disease. - PTT is prolonged by unfractionated heparin, which potentiates antithrombin III to inhibit thrombin and factor Xa; PTT is therefore used to monitor heparin dosing (target usually 1.5–2.5x control). - Lupus anticoagulant (antiphospholipid antibody) paradoxically prolongs PTT in vitro but is associated with a hypercoagulable state and increased thrombosis risk in vivo—classic USMLE trick. - A mixing study (patient plasma + normal plasma) helps distinguish factor deficiency (corrects) from inhibitor presence (does not correct), such as lupus anticoagulant or factor VIII inhibitors. - PTT is normal in factor VII deficiency and mild extrinsic pathway defects, which instead prolong PT.

Contrast with PT/INR, which assesses the extrinsic and common pathways (tissue factor, factor VII, X, V, prothrombin, fibrinogen) and is used to monitor warfarin therapy.

High-yield associations: - Heparin → prolongs PTT (monitor with PTT) - Warfarin → prolongs PT/INR (monitor with PT/INR) - Hemophilia A/B → prolonged PTT, normal PT - Von Willebrand disease → prolonged PTT (due to low factor VIII), normal platelet count usually, abnormal ristocetin test - Lupus anticoagulant → prolonged PTT but hypercoagulable clinically