6.3 Haematology and Haemostasis

Blood Cells and Normal Values

Erythropoiesis is driven by erythropoietin from renal peritubular fibroblasts in response to hypoxia, which is why chronic kidney disease causes a normocytic anaemia. Red cells survive about 120 days, which is why glycated haemoglobin reflects average glycaemia over the preceding 8 to 12 weeks.

Primary Haemostasis

Vessel injury exposes subendothelial collagen and von Willebrand factor.

1. Adhesion — platelet glycoprotein Ib binds von Willebrand factor, tethering platelets to the subendothelium.
2. Activation — thromboxane A2, ADP and thrombin activate platelets, which change shape and degranulate.
3. Aggregation — glycoprotein IIb/IIIa receptors bind fibrinogen, cross-linking platelets into a primary plug.

Drug targets map directly onto this sequence: aspirin irreversibly acetylates cyclooxygenase-1 and abolishes thromboxane A2 production for the 7 to 10 day lifespan of the platelet; clopidogrel, ticagrelor and prasugrel block the P2Y12 ADP receptor.

Secondary Haemostasis

The coagulation cascade converges on the conversion of prothrombin to thrombin and fibrinogen to fibrin.

• Extrinsic pathway — tissue factor plus factor VII. Measured by prothrombin time and reported as INR. This is the pathway that warfarin monitoring reflects.
• Intrinsic pathway — factors XII, XI, IX and VIII. Measured by activated partial thromboplastin time (APTT). Prolonged in haemophilia A and B.
• Common pathway — factors X, V, II (prothrombin) and I (fibrinogen).

Vitamin K is required for gamma-carboxylation of factors II, VII, IX and X plus proteins C and S. Warfarin inhibits vitamin K epoxide reductase, and because factor VII has the shortest half-life the INR rises before full anticoagulation is achieved.

Direct oral anticoagulants bypass this system entirely: apixaban, rivaroxaban and edoxaban inhibit factor Xa directly, and dabigatran inhibits thrombin. They have predictable pharmacokinetics, a peak effect at 1 to 3 hours and a short half-life of roughly 10 to 14 hours in normal renal function, which is why SDCEP advises timing rather than routine testing.

Fibrinolysis

Plasminogen is converted to plasmin by tissue plasminogen activator, and plasmin degrades fibrin. Saliva is rich in plasminogen activators, which is one reason oral wounds re-bleed and why tranexamic acid, a lysine analogue that blocks plasminogen binding to fibrin, is so effective as a 5% mouthwash after dental extractions.

Exam link. An isolated prolonged APTT with a normal prothrombin time and a normal platelet count in a young male with a bleeding history after a childhood extraction is haemophilia until proven otherwise, and the correct next step is liaison with the haemophilia centre before any invasive dentistry.

Interpreting a Coagulation Screen

Examiners expect candidates to read a basic haematology and coagulation screen and to say what it implies for dental treatment. The prothrombin time, expressed as the international normalised ratio (INR), tests the extrinsic and common pathways and is prolonged by warfarin, liver disease and vitamin K deficiency. The activated partial thromboplastin time (APTT) tests the intrinsic and common pathways and is prolonged in haemophilia A and B, in von Willebrand disease and by unfractionated heparin. A prolonged thrombin time points to a fibrinogen problem or to direct thrombin inhibition. Platelet count below 100 × 10⁹/L raises concern and below 50 × 10⁹/L is associated with a significant bleeding risk from surgical procedures.

The mental model to carry into the exam is that primary haemostasis failures — thrombocytopenia, platelet dysfunction, von Willebrand disease — produce immediate oozing from the whole socket at the time of surgery, together with mucocutaneous signs such as petechiae, purpura and epistaxis. Secondary haemostasis failures — the clotting factor deficiencies — produce initial haemostasis followed by delayed rebleeding hours later, together with deep bleeding into muscles and joints. That distinction, rather than the biochemistry of each factor, is what SBA stems test.

Anaemia and the Oral Cavity

Red cell indices generate a second reliable question type. A microcytic, hypochromic picture with low mean corpuscular volume suggests iron deficiency and demands a cause — in adults, gastrointestinal blood loss until proven otherwise. A macrocytic picture suggests vitamin B12 or folate deficiency, alcohol excess or hypothyroidism. Deficiency anaemias of any type can present orally with angular cheilitis, atrophic glossitis, recurrent aphthous ulceration and candidal infection, which is why the standard investigation of recurrent aphthae is a full blood count with haematinics — ferritin, vitamin B12 and folate. The examinable safety point is that an unexplained anaemia found through oral signs must be referred for investigation of its cause and not simply treated with replacement therapy.