# Coagulation Screening > Coagulation screening in MBBS Physiology: PT-INR, aPTT, bleeding time interpretation, mixing studies and the vitamin K dependent factors. - Canonical URL: https://prepelephant.com/topics/mbbs/physiology/coagulation-screening-physiology - Exam / course: MBBS · Subject: Physiology - Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team - First published: 2026-10-02 - Last updated: 2026-10-02 - How to cite: "Coagulation Screening", PrepElephant, https://prepelephant.com/topics/mbbs/physiology/coagulation-screening-physiology ## Direct answer Three tests screen haemostasis: prothrombin time (normal about 11-14 seconds) tracks the extrinsic and common pathways (factors VII, X, V, II, I); activated partial thromboplastin time (about 25-35 seconds) tracks intrinsic plus common (XII, XI, IX, VIII, X, V, II, I); and bleeding time (Ivy method, 2-7 minutes) tests the platelet plug and vessel wall. PT and aPTT prolong together in liver disease, disseminated intravascular coagulation and mixed anticoagulant therapy. Isolated aPTT prolongation suggests heparin contamination, haemophilia A or B, von Willebrand disease or a lupus anticoagulant; isolated PT prolongation appears early in vitamin K deficiency and liver failure because factor VII has the shortest half-life at 4-6 hours. The INR standardises PT for warfarin monitoring (target usually 2-3), and a mixing study separates factor deficiency, which corrects, from inhibitor, which does not. ## What you must remember - **Normal ranges to quote:** PT 11-14 s, aPTT 25-35 s, bleeding time 2-7 min (Ivy), platelets 150,000-400,000 per microlitre (1.5-4 lakh in Indian convention), fibrinogen 200-400 mg/dL, clotting time (Lee-White) 5-10 minutes. - **Vitamin K dependent factors:** II, VII, IX, X plus proteins C and S; factor VII's 4-6 hour half-life makes PT the earliest abnormal test in deficiency — the physiological logic of the newborn's 1 mg intramuscular vitamin K. - **Warfarin numbers:** INR target 2-3 for most indications, 2.5-3.5 for mechanical mitral valves; early protein C depletion explains the transient hypercoagulable window and skin necrosis. - **Heparin monitoring:** aPTT roughly 1.5-2.5 times control for unfractionated heparin; anti-Xa assays for high-dose protocols; protamine reverses. - **Bleeding time logic:** prolonged by thrombocytopenia, uraemic platelet dysfunction, aspirin and von Willebrand disease — but normal in haemophilia, the single most-quoted line in Indian practicals. - **Mixing study:** 1:1 correction means factor deficiency; no correction means an inhibitor (heparin, lupus anticoagulant, acquired factor VIII inhibitor). - **DIC panel pattern:** PT prolonged, aPTT prolonged, platelets low, fibrinogen low (relative to its acute-phase rise) and D-dimer high — all five together make the diagnosis. ## Four panels, four diagnoses Read them as patterns. A boy with haemophilia A: bleeding time normal, platelets normal, PT normal, aPTT markedly prolonged, corrected by mixing — factor VIII deficiency. A woman with menorrhagia since menarche: bleeding time prolonged, aPTT mildly prolonged, platelets normal, ristocetin assay abnormal — von Willebrand disease, where the plug fails and factor VIII is secondarily unstable. A patient on no anticoagulants with an isolated prolonged aPTT that does not correct on mixing, yet a history of thrombosis not bleeding: lupus anticoagulant, the paradox to name deliberately — an in vitro prolongation with in vivo thrombophilia. Finally, a jaundiced septic patient with all three screens deranged plus falling platelets and rising D-dimer: DIC, where consumption outruns production; the fibrinogen may read "normal" only because it is an acute-phase reactant that has fallen from an even higher baseline. ## Where students slip "Bleeding time is normal in haemophilia" is the line most often inverted — platelets and vessel wall are intact, so the plug forms; what fails is the fibrin reinforcement, hence the deep delayed bleeds of haemophilia against the immediate superficial bleeds of thrombocytopenia. The lupus anticoagulant paradox is the second trap: a prolonged aPTT that does not correct on mixing in a patient who clots, not bleeds. Third, the vitamin K question stops at "II, VII, IX, X" without proteins C and S, losing the explanation of warfarin-induced skin necrosis — transient protein C fall before factor X falls. And in Indian practical examinations, platelet counts are still commonly reported in lakhs; converting 1.5-4 lakh to 150,000-400,000 per microlitre on the spot is expected fluency. ## Frequently asked questions ### Which pathways do PT and aPTT evaluate? PT screens the extrinsic (factor VII) plus common pathways; aPTT screens the intrinsic (XII, XI, IX, VIII) plus common pathways, and both use the common factors X, V, II and I. ### Why does PT prolong before aPTT in early liver failure and vitamin K deficiency? Factor VII has the shortest half-life (4-6 hours), so its level falls first, deranging the PT in isolation before other factors decline. ### What is the purpose of a mixing study? Mixing patient plasma 1:1 with normal plasma: correction indicates a missing factor, while persistent prolongation indicates an inhibitor such as heparin, a lupus anticoagulant or an acquired factor inhibitor. ### Why is bleeding time normal in haemophilia? Primary haemostasis — platelet adhesion and aggregation with vessel contraction — is intact; the defect is secondary haemostasis (fibrin clot formation), so the plug bleeds later rather than immediately. ### What INR range is targeted on warfarin? Two to three for most indications including atrial fibrillation and deep vein thrombosis, and 2.5-3.5 for high-risk mechanical mitral valves.