Cardiovascular Disease and Risk
Atherosclerosis: damage to the artery endothelium (e.g. high blood pressure, smoking) triggers an inflammatory response; white cells and LDL cholesterol build up as an atheroma (plaque), which hardens and narrows the artery. Plaques can rupture, triggering blood clotting: platelets release thromboplastin → prothrombin → thrombin (needs Ca²⁺, vitamin K) → fibrinogen → fibrin mesh traps cells → thrombus. A clot in a coronary artery causes a heart attack (myocardial infarction); in the brain, a stroke. Risk factors: genes, age, male sex, high blood pressure, smoking, high LDL, obesity, inactivity, high salt. Measures: BMI = mass (kg) ÷ height² (m²), waist-to-hip ratio, energy budget. Treatments: antihypertensives (lower pressure), statins (lower LDL), anticoagulants and platelet inhibitors (reduce clotting; risk of bleeding).
Learning objectives
- Describe atherosclerosis and blood clotting.
- Explain risk factors.
- Calculate BMI and interpret risk data.
- Evaluate treatments.
Why are arteries, not veins, damaged by atherosclerosis?
Core idea
Atherosclerosis can develop for decades without symptoms, until a clot blocks a coronary artery.
Damage to artery linings leads to plaques; a ruptured plaque triggers clotting that can block blood flow to the heart or brain.
Atherosclerosis and thrombosis.
80 kg, 1.80 m.
- Goal
- BMI.
- Strategy
- mass ÷ height².
- Square height.
- Divide.
Summary
- Atheroma and thrombosis.
- Risk factors.
- Treatments and risks.
- Atheroma
- Fatty plaque in an artery wall.
- Thrombosis
- Formation of a blood clot inside a vessel.
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