- Tests of coagulation
- Propagation of haemostasis is prevented by TF pathway inhibitor (TFPI), protein C, and antithrombin.
- New theory favours the cell based model of coagulation, placing TF-VIIa complex at the centre of this theory. It has 5 stages
- Initiation
- TF binds to VIIa and in the presence of factor V, converts IX to IXa and X to Xa. Xa binds to prothrombin to generate a small amount of thrombin.
- Amplification
- The small amount of thrombin generated is insufficient to convert fibrinogen to fibrin. Thrombin mediated feedback to amplify the system
- Propagation
- TF-VIIa complex ensures a supply of IXa. IXa with VIIIa activates X to ensure adequate supply of Xa and maintains thrombin burst
- Stabilisation
- High thrombin levels stimulate XIII to cross link soluble monomers and protection of the clot by thrombin activate blue fibrinolysis inhibitor
- Inhibition
- Thrombosis controlled by thrombin activated protein C (aPC) which cleaves Va & Xa. TFPI inhibits TF-VIIa and Xa by binding them and AT inhibits thrombin, IXa and Xa
- Near patient testing
- Haemochron activated clotting time
- Haemochron Jr signature
- CoaguChek
- Platelet function analysing monitor
- TEG
Link:Thromboelastometry
- Fibrinogen level
- APTT
- Reagent used contains no tissue factor unlike the PT. All procoagulants except VII & XIII are measured.
- PT
- Prolonged with deficiencies in I, II, V and X as well as liver disease, vitamin k deficiency, DIC and high dose heparin. The INR standardises the assay and is the ratio of the patient's PT to control plasma PT raised to the power of a correction factor known as the international sensitivity index (ISI)
- CEACCP
Link:ceaccp.oxfordjournals.org/content/7/2/45.full.pdf