The clotting cascade

When a blood vessel wall is broken, platelets are exposed to damaged tissue. They become sticky and clump together at the wound site, forming a temporary plug. Platelets also release chemicals that initiate a chain of reactions.

These reactions convert the soluble plasma protein fibrinogen into insoluble fibrin. Fibrin forms a network of threads across the wound. Red blood cells and more platelets become trapped in this mesh, forming a solid blood clot that seals the wound.

Why clotting matters

Clotting serves two vital purposes: it stops blood loss (haemorrhage), maintaining blood volume and pressure; and it prevents pathogens from entering the body through the open wound. The dried surface of a clot forms a scab, which protects the healing tissue beneath.

Without effective clotting, even small cuts could lead to life-threatening blood loss. People with haemophilia produce insufficient clotting factors and bleed for much longer than normal.

Clotting versus immunity

Clotting is a physical defence: it seals the wound as a barrier. It is not the same as the immune response, which involves white blood cells recognising and destroying pathogens. Both contribute to the body's defence, but through different mechanisms.

Inappropriate clotting inside blood vessels (thrombosis) can block blood flow. If a clot forms in a coronary artery already narrowed by atherosclerosis, it can cause a heart attack. This links blood clotting to coronary heart disease.