When blood vessel walls are damaged or blood flows very slowly , a blood clot is far more likely to form.
When platelets come into contact with the damaged vessel wall they change from flattened discs to spheres with long thin projections.
There cell surfaces change, causing them to stick to the exposed collagen in the wall and to each other to form a temporary platelet plug. They also release substances that activate more platelets.
The direct contact between blood and collagen within the damaged artery causes a series of complex series of chemical changes in the blood.
A cascade of changes results in the soluble plasma protein called prothrombin being converted into thrombin, which is an enzyme that catalyses the conversion of another soluble plasma protein, fibrinogen, into long insoluble strands of the protein fibrin.
These fibrin strands form a tangled mesh that traps blood cells to form a clot.
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