Cardiovascular Disease

Blood Clotting Process

• Clot formation is stimulated when there is damage to a blood vessel.
• Damage exposes the collagen fibres in the vessel wall.
• When platelets, a type of blood cell without a nucleus, comes into contact with the damaged vessel wall they change from flattened discs to spheres with long thin projections.
• Their cell surfaces change, causing them to stick t the exposed collagen in the wall and to each other to form a temporary platelet plug, and releases thromboplastin.
• They also release substances that activate more platelets.
• The direct contact of blood with collagen within the damaged vessel wall also triggers a complex series of chemical changes in the blood.
• A cascade of changes results in thromboplastin, when in the presence of calcium ions and vitamin K, converting soluble plasma protein called prothrombin into thrombin.
• Thrombin is an enzyme that catalyses the conversion of another soluble plasma protein fibrinogen into long insoluble strands.
• These fibrin strands form a tangled mesh that traps blood cells to form a clot.

Atherosclerosis

• This process is triggered when damage occurs to the epithelial cells lining an artery wall.
• This starts an inflammatory response and macrophages arrive at the site of damage.
• Macrophages attract chemicals and substances such as cholesterol.
• The macrophages engulf cholesterol and become 'foaming cells'.
• This leads to a fatty deposit known as an atheroma forming on the epithelial lining of the artery.
• Calcium ions, salts and fibrous tissues also build up in the area around the atheroma, turning it into hardened plaque.
• This also hardens the surrounding artery wall, causing it to lose some of its elasticity and narrows the artery lumen.
• Results in hgih blood pressure, which causes a dangerous positive feedback system, i.e. high blood pressure causes further damage to the arteries, the process is self-perpetuating.