All subjects · Biology · WBI11 (Unit 1)

Atherosclerosis and blood clotting

Cardiovascular disease (CVD) usually starts with damage inside an artery. A plaque builds up, and a blood clot can then block the vessel.

How atherosclerosis develops

1. The endothelium (inner lining) of an artery is damaged, for example by high blood pressure or chemicals from cigarette smoke.

2. An inflammatory response follows: white blood cells move into the artery wall.

3. Cholesterol and other lipids from the blood build up with the white cells under the endothelium (a fatty streak).

4. Calcium salts and fibrous tissue accumulate, forming a hard plaque (atheroma).

5. The artery narrows and loses elasticity, which raises blood pressure and makes further damage more likely: a positive feedback loop.

The clotting cascade

When a vessel wall is damaged:

1. Platelets stick to exposed collagen and release thromboplastin.

2. Thromboplastin, with calcium ions (and vitamin K-dependent clotting factors), converts prothrombin into thrombin.

3. Thrombin, an enzyme, converts soluble fibrinogen into insoluble fibrin.

4. Fibrin threads form a mesh that traps red blood cells and platelets, forming a clot.

Clots and CVD

A plaque that breaks open triggers clotting inside the artery. The clot (thrombus) may block the artery there, or break off and block a smaller vessel downstream.

Narrowed coronary arteries alone can cause chest pain (angina) during exercise.

Worked example

Put in order: fibrinogen to fibrin; damage exposes collagen; prothrombin to thrombin; thromboplastin released.

  1. Damage exposes collagen and platelets stick.
  2. Thromboplastin is released.
  3. Prothrombin is converted to thrombin.
  4. Thrombin converts fibrinogen to fibrin.

Answer: Collagen exposed, thromboplastin released, prothrombin to thrombin, fibrinogen to fibrin.

Key idea: Endothelial damage, inflammation, lipid build-up and plaque formation narrow arteries. Thromboplastin turns prothrombin to thrombin, which turns fibrinogen to fibrin: a clot that can block a coronary or brain artery.

Check yourself

  1. What is usually the first step in atherosclerosis?
    • Formation of a fibrin mesh
    • A heart attack
    • Calcium deposits in veins
    • Damage to the endothelium of an artery
    Show answer

    Damage to the endothelium of an artery. Damage to the lining triggers the inflammatory response.

  2. What does thrombin do?
    • Converts prothrombin into thromboplastin
    • Converts soluble fibrinogen into insoluble fibrin
    • Breaks down a clot
    • Carries oxygen
    Show answer

    Converts soluble fibrinogen into insoluble fibrin. Thrombin is the enzyme that makes fibrin.

  3. Which ion is needed for prothrombin to be converted to thrombin?
    • Sodium ions
    • Chloride ions
    • Iron ions
    • Calcium ions
    Show answer

    Calcium ions. Calcium ions are a cofactor in clotting.

  4. Why does atherosclerosis tend to get worse over time?
    • Narrowed arteries raise blood pressure, which causes more endothelial damage
    • Plaques dissolve and reform
    • White blood cells remove cholesterol
    • Arteries become more elastic
    Show answer

    Narrowed arteries raise blood pressure, which causes more endothelial damage. Raised pressure damages the endothelium further: positive feedback.

  5. A clot blocks a coronary artery. What is the most likely result?
    • A stroke
    • Increased elasticity of the aorta
    • A heart attack, as heart muscle is deprived of oxygen
    • Faster gas exchange in the lungs
    Show answer

    A heart attack, as heart muscle is deprived of oxygen. Coronary arteries supply the heart muscle itself.

  6. Why does fibrin form a clot but fibrinogen does not?
    • Fibrin is insoluble and forms a mesh of threads
    • Fibrin is soluble in plasma
    • Fibrinogen is a red blood cell
    • Fibrinogen contains no protein
    Show answer

    Fibrin is insoluble and forms a mesh of threads. Insoluble fibrin threads trap blood cells.

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Last updated 7 November 2026. Spotted a mistake? Tell us.