**9. Anticoagulant drugs**

These drugs are used to prevent thrombus formation, or limit the extension of existing thrombus. Venous thrombus consists of a fibrin web with trapped platelets and erythrocytes and is more successfully treated or prevented with anticoagulants than arterial thrombus, which contains proportionally more platelets and less fibrin.


Fig. 4. Causes of a Hypercoagulable State (11)

Blood Protein S and Protein C deficiencies (these normally regulate

coagulation)

suppression)

develop)

Thalassaemia Sickle Cell Disease

adhesion)

perioperatively)

Hyperlipidaemia

Immobility (blood stasis)

Obesity

Fig. 4. Causes of a Hypercoagulable State (11)

fibrinolysis)

Systemic Pregnancy / postpartum

to complement)

**Source Hypercoagulable risk factor (mechanism and notes in brackets)** 

Antithrombin III deficiency (incidence 1 in 5000)

Inherited dysfibrinogenaemia (rare)

ineffective against mutated factor V)

anticoagulant effect of antithrombin III) Sepsis (increased circulating tissue factor)

dysfunction & increased fibrinogen)

vitamin B6 & vitamin B12)

Polycythaemia rubra vera, Thrombocytosis (blood is more viscous

Paroxysmal Nocturnal Haemoglobinuria (excessive RBC sensitivity

Prothrombin 20210 mutation (leads to increased prothrombin levels) Heparin Induced Thrombocytopenia (heparin-associated antibodies

Leiden Factor V mutation - the most common hereditary cause of hypercoagulable state (anticoagulant effect of activated protein C is

Iatrogenic Oestrogen (increases coagulation factors and reduces

Hyperhomocysteinaemia (genetic disorder, treated with folate,

Smoking (mechanisms include endothelial damage and platelet

Congestive Heart Failure (mechanisms include vascular endothelial

Antiphospholipid syndrome, including lupus anticoagulant (either

Malignancy (tumour cells activate clotting cascade and inhibit

primary or secondary to infection, drugs, malignancy) Uraemia (endothelial dysfunction, increased cytokines) Surgery (reduced risk with thromboprophylactic drugs

Diabetes mellitus (increased platelet activation)

Trauma/burns (release of tissue thromboplastin)

Hypothyroidism (increased circulating fibrinogen, FVII)

Hyperthyroidism (increase in circulating FX)

thus prone to stasis – treatment may include bone marrow

