Atherosclerosis and blood clottingEdexcel International A Level Biology: Revision notes
Section 1
The artery wall and endothelial damage
Artery walls have an inner lining of endothelium, a layer of smooth muscle and elastic fibres, and an outer layer of collagen. The smooth endothelium lets blood flow easily.
Endothelial dysfunction or damage is the first step in atherosclerosis. Common causes are high blood pressure (greater force on the wall), chemicals in cigarette smoke, and high blood concentrations of LDL cholesterol. Once the endothelium is damaged, lipids and white blood cells can enter the wall beneath it.
Section 2
Inflammatory response and plaque formation
At the damaged site an inflammatory response begins:
- Monocytes (white blood cells) move into the artery wall and become macrophages.
- Macrophages take up LDL cholesterol and become lipid-filled foam cells.
- Smooth muscle cells multiply and migrate, and fibrous tissue (collagen) is laid down.
- A raised atheroma (fibrous plaque) forms, which is covered by a fibrous cap.
Calcium salts are later deposited, so the plaque and the artery wall harden.
Describe plaque formation in order: damage, inflammation, macrophages and foam cells, fibrous tissue, narrowing.
Section 3
Effects of atherosclerosis
The plaque narrows the lumen and the wall loses elasticity. Both increase resistance to blood flow, so blood pressure rises. Higher blood pressure then damages the endothelium further, a positive feedback cycle.
Narrowed coronary arteries deliver less oxygen to cardiac muscle, which can cause angina (chest pain on exertion). Narrowing in the arteries of the brain or legs reduces their blood supply too.
A plaque does not usually block the artery by itself. Complete blockage mostly comes from a clot forming on a ruptured plaque.
Section 4
The blood clotting mechanism
When a vessel is damaged, damaged tissue and platelets release thromboplastin, a clotting factor. The reactions are:
- Thromboplastin and Ca²⁺ ions cause prothrombin (an inactive plasma protein) to be converted to thrombin, an enzyme.
- Thrombin converts soluble fibrinogen to insoluble fibrin.
- Fibrin forms a mesh of fibres that traps platelets and red blood cells, forming a clot.
Clotting seals wounds and prevents blood loss and entry of pathogens. Each step is a cascade, so a small stimulus causes a large response.
Section 5
Clotting and cardiovascular disease
If a plaque ruptures, it damages the endothelium and exposes tissue beneath, so platelets and thromboplastin start clotting inside the artery. This clot is a thrombus (thrombosis).
- A thrombus in a coronary artery blocks blood flow to the heart muscle, causing a myocardial infarction (heart attack).
- A piece of thrombus that breaks off is an embolus; if it blocks an artery in the brain it causes a stroke.
Cardiac muscle or brain cells starved of oxygen and glucose cannot respire aerobically and die.
Link each disease to its blocked artery: coronary artery gives myocardial infarction, cerebral artery gives stroke.
That's the notes covered.
Carry on to the next subtopic.
Exam questions on Atherosclerosis and blood clotting
- A post-mortem examination of the coronary artery of a man who died of a heart attack showed a raised, fatty deposit in the artery wall that had narrowed the lumen.Explain how atherosclerosis can lead to raised blood pressure.2 marks
- Blood clotting is a series of reactions. In a laboratory demonstration, a technician starts the clotting of a plasma sample by adding thromboplastin and calcium ions.Explain why it is important that fibrinogen is soluble but fibrin is insoluble.2 marks
- A 62-year-old woman with raised blood pressure and a high blood cholesterol concentration is admitted to hospital with a heart attack. An angiogram shows that one of her coronary arteries is blocked by a blood clot at the site of an atheromatous plaque.Explain how the atheromatous plaque could have led to the formation of the blood clot.3 marks
Written by the Exaim team, led by Shaun Daswani (Head of Upper Secondary, Improve ME Institute; MSc Financial Mathematics, Imperial College London; BSc, UCL) and Jason Daswani (operational lead, Improve ME Institute; LSE).