STEPTRACKERHEMATOLOGY | PATHOLOGY + PHYSIOLOGY | HIGH-YIELD REVIEW

Hemostasis & Coagulation Tests

Platelet plug first, fibrin mesh second, natural brakes and clot-busting after — and the tests that check each stage.

FOCUS ON
Reading the tests is the core skill. PT checks extrinsic + common (VII, X, V, II, fibrinogen). PTT checks intrinsic + common (XII, XI, IX, VIII …). Bleeding time checks platelet function. A mixing study separates a factor deficiency (corrects) from an inhibitor (does not). Bleeding pattern tells platelets from factors.
STAGE
WHAT HAPPENS
KEY MOLECULES
CLINICAL / DRUG LINK
Vasoconstriction
seconds
Injured vessel narrows to slow flow.
Endothelin, neural reflex
Transient only
Platelet adhesion
primary hemostasis
vWF binds exposed subendothelial collagen; platelets stick via GPIb.
vWF (Weibel-Palade bodies, subendothelium) ↔ GPIb
vWD, Bernard-Soulier
Activation & release
primary
Platelets change shape and empty granules.
Dense: ADP, Ca²⁺, serotonin · α: vWF, fibrinogen, PF4 · TXA₂ made
Aspirin (TXA₂), clopidogrel (ADP P2Y₁₂)
Aggregation
primary
Fibrinogen bridges platelets → weak primary plug.
GPIIb/IIIa ↔ fibrinogen
Glanzmann; abciximab, eptifibatide
Coagulation cascade
secondary hemostasis
Tissue factor + VIIa (extrinsic) and XII → XI → IX + VIII (intrinsic) converge on X + V → thrombin → fibrin; XIII cross-links.
Ca²⁺ and platelet phospholipid surfaces; vitamin K–dependent: II, VII, IX, X, C, S
Hemophilia, warfarin, heparin, DOACs
Natural anticoagulants
limits the clot
Stop the clot spreading beyond the injury.
Antithrombin (thrombin, Xa) · protein C + S (cut Va, VIIIa) · TFPI · PGI₂, NO
Heparin boosts antithrombin; factor V Leiden resists protein C
Fibrinolysis
clean-up
Plasmin cuts fibrin into split products, including D-dimer.
tPA, urokinase: plasminogen → plasmin · α₂-antiplasmin inhibits
Alteplase; tranexamic acid blocks it

Mechanism — the cascade

ExtrinsicTF + VIIa
→
CommonXa + Va
→
Thrombin (IIa)
→
Fibrinogen → fibrinXIII cross-links
IntrinsicXII → XI
→
IXa + VIIIaTenase
→
Activates XJoins common path

Thrombin also feeds back: it activates V, VIII, XI, XIII and platelets, and with thrombomodulin it switches on protein C.

The tests

TEST
MEASURES
PROLONGED BY
PT / INR
VII + common (X, V, II, fibrinogen)
Warfarin, vitamin K deficiency, liver disease, factor VII deficiency
PTT
XII, XI, IX, VIII + common
Heparin, hemophilia A/B, vWD, lupus anticoagulant
Platelet count
Number
ITP, TTP, HUS, DIC, HIT, marrow failure
Bleeding time / PFA
Platelet function
vWD, Glanzmann, Bernard-Soulier, aspirin, uremia
Mixing study
Corrects = factor deficiency
No correction = inhibitor
D-dimer
Cross-linked fibrin breakdown
DIC, DVT/PE (rule-out test)
Platelet-type bleeding
Mucosa (nose, gums, menorrhagia), petechiae, immediate bleeding after cuts
Factor-type bleeding
Deep tissue: hemarthroses, muscle hematomas; delayed rebleeding after surgery

How it's tested

COMMON CONFUSIONFactor VII has the shortest half-life, so early warfarin or early vitamin K deficiency prolongs the PT first.
THE TRAPA prolonged PTT that does not correct with mixing, in a patient with clots, is lupus anticoagulant. An inhibitor does not always mean bleeding.
YOUR APPROACHBleeding pattern (mucosal vs deep) → which tests are abnormal (PT, PTT, count, bleeding time) → mixing study if a factor test is long.

If you see… think…

PT prolonged alone → factor VII deficiency, early warfarin, early vitamin K loss
PTT prolonged alone, bleeding → hemophilia A/B, heparin, vWD
PT, PTT and platelet count all abnormal → DIC
Long bleeding time, normal count → qualitative platelet defect or vWD
PTT corrects with normal plasma → factor deficiency
Petechiae and gum bleeding → primary (platelet) problem
Knee hemarthrosis after minor fall → coagulation factor problem
Aspirin's antiplatelet effect lasts → 7–10 days (platelet lifespan)
Vitamin K–dependent proteins → II, VII, IX, X, protein C, protein S