Hematology mnemonic
Coagulation Cascade — Intrinsic, Extrinsic, Common Pathways
The coagulation cascade is memorable when you tie it to PT and PTT. Extrinsic drives PT. Intrinsic drives PTT. Common drives both. That's the exam pattern.
The coagulation cascade appears complex but reduces to three pathways: intrinsic (activated by contact/trauma inside vessels), extrinsic (activated by tissue factor from damaged tissue), and common (where they converge to form fibrin). Every hematology question about bleeding disorders traces back to which pathway is affected and which lab test detects it.
This page gives you the factor list per pathway, the lab test each pathway drives (PT vs PTT), and the classic bleeding disorders with their affected factors.
The three pathways — factors and lab tests
Card the pathway → factor list → lab test triad:
- Extrinsic pathway — Factor VII → PT (prothrombin time). Fastest pathway. Activated by tissue factor.
- Intrinsic pathway — Factors XII → XI → IX → VIII → PTT (partial thromboplastin time). Slower. Activated by contact with negatively charged surfaces (subendothelial collagen).
- Common pathway — Factors X → V → II (prothrombin/thrombin) → I (fibrinogen/fibrin). Affects BOTH PT and PTT if disrupted.
Bleeding disorders by factor
Classic Step 1 associations:
- Hemophilia A — Factor VIII deficiency. X-linked. Prolonged PTT, normal PT. Treat with recombinant VIII.
- Hemophilia B (Christmas disease) — Factor IX deficiency. X-linked. Prolonged PTT, normal PT. Treat with recombinant IX.
- Hemophilia C — Factor XI deficiency. Autosomal recessive, common in Ashkenazi Jews. Mild.
- Von Willebrand disease — most common inherited bleeding disorder. vWF carries VIII, so PTT can prolong. Also affects platelet adhesion → prolonged bleeding time / abnormal ristocetin test.
- Vitamin K deficiency — affects Factors II, VII, IX, X + protein C, S. Prolonged PT first (VII has shortest half-life), then PTT.
- Warfarin — inhibits vitamin K epoxide reductase → same factors as vitamin K deficiency. Monitor with PT/INR.
- Heparin — potentiates antithrombin → inhibits II and X. Monitor with PTT.
- DIC — consumes all factors + platelets → both PT and PTT prolonged, low fibrinogen, elevated D-dimer, low platelets.
The lab test decision tree
Isolated PT prolongation → extrinsic or early warfarin/vitamin K deficiency. Isolated PTT prolongation → hemophilia A/B/C, vWD, heparin, lupus anticoagulant. Both PT + PTT prolonged → common pathway defect, severe vitamin K deficiency, DIC, liver disease.
Anticoagulant mechanisms — high yield
Warfarin: inhibits vitamin K epoxide reductase → depletes II, VII, IX, X and proteins C, S. Onset delayed (days). Reverse with vitamin K + FFP.
Heparin: potentiates antithrombin → inhibits IIa (thrombin) and Xa. Onset immediate. Reverse with protamine.
LMWH (enoxaparin): more Xa selective. No routine monitoring needed.
DOACs — rivaroxaban/apixaban (direct Xa inhibitors), dabigatran (direct thrombin inhibitor). Reverse with andexanet alfa (Xa) or idarucizumab (dabigatran).
Frequently asked questions
Why does Factor VII have the shortest half-life?
Factor VII has a plasma half-life of about 4–6 hours — shorter than any other coagulation factor. This is why PT prolongs first in early warfarin therapy and vitamin K deficiency, before the intrinsic factors deplete.
Why is PT reported as INR now?
PT results vary by lab reagent. INR (International Normalized Ratio) standardizes PT so warfarin dosing can be compared across labs. INR target is typically 2–3 for most indications, 2.5–3.5 for mechanical mitral valves.
What activates the intrinsic pathway physiologically?
Contact with negatively charged surfaces — subendothelial collagen when vessels are damaged. In lab tests, kaolin or silica activates the intrinsic pathway. Note that Factor XII deficiency prolongs PTT but does NOT cause clinical bleeding — a common exam trick.
How does DIC produce both bleeding and clotting?
Widespread intravascular activation consumes clotting factors and platelets (bleeding) while producing microthrombi (clotting). Labs: prolonged PT + PTT, low platelets, low fibrinogen, elevated D-dimer, schistocytes on smear.
What test measures fibrinolysis?
D-dimer measures degradation of cross-linked fibrin. Elevated in DIC, PE, DVT, malignancy. High sensitivity, low specificity.
How many cards does this generate?
60–90 atomic cards covering factors by pathway, bleeding disorders, anticoagulants, and lab test patterns.
Keep exploring
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