Haemostasis, Thrombosis, and Transfusion Science
Normal haemostasis
Understand primary haemostasis (vascular constriction, platelet adhesion via von Willebrand factor to glycoprotein Ib, activation, aggregation via glycoprotein IIb/IIIa and fibrinogen), secondary haemostasis (coagulation cascade, thrombin generation, fibrin formation), and fibrinolysis (plasminogen activators, plasmin, D-dimers). Know the intrinsic (XII, XI, IX, VIII), extrinsic (III, VII), and common (X, V, II, I) pathways and that the PT/INR reflects the extrinsic and common pathway while the APTT reflects the intrinsic and common pathway.
Thrombosis and embolism
Virchow's triad: endothelial injury, stasis or turbulence, and hypercoagulability. Distinguish arterial thrombi (white, platelet-rich, often at atherosclerotic plaques) from venous thrombi (red, fibrin-rich, often in deep veins). Know lines of Zahn, organisation, recanalisation, and embolic complications. Inherited thrombophilias include factor V Leiden, prothrombin G20210A, and antithrombin/protein C/protein S deficiency; acquired causes include malignancy, pregnancy, oral contraceptives, and antiphospholipid syndrome.
Transfusion science
Know ABO and Rh compatibility, the basis of the antibody screen and crossmatch, and the major transfusion reactions. Acute haemolytic reactions are usually ABO-incompatible and complement-mediated; febrile non-haemolytic reactions relate to cytokines and leukocyte antibodies; TRALI involves donor antibodies against recipient leukocytes; TACO is volume overload. Know indications for component therapy (packed cells, platelets, fresh frozen plasma, cryoprecipitate) and the risks of massive transfusion, including dilutional coagulopathy and citrate-induced hypocalcaemia.
Traps
Do not confuse bleeding time (platelet function) with APTT. Heparin potentiates antithrombin; warfarin inhibits vitamin K-dependent factors (II, VII, IX, X) and proteins C and S. A normal PT with prolonged APTT suggests haemophilia or a factor VIII/IX defect.
Rule of thumb
For prolonged APTT with normal PT, think intrinsic pathway; for prolonged PT with normal APTT, think extrinsic pathway or early vitamin K deficiency.