Coronary heart disease: a non-communicable disease - AQA GCSE Biology Exam Questions

Practise 30 exam-style questions on Coronary heart disease: a non-communicable disease for AQA GCSE Biology. Write your answer as you would in the exam and get it marked in seconds against the mark scheme, point by point, with an AI tutor on hand if you get stuck.

30 questions
2–6 marks each
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20 questions, marked as you go

Sample questions with model answers

Here are 4 of the questions in this topic, each with a model answer, an explanation of why it earns the marks and the mark scheme an examiner would use.

Question 1

2 marks

Explain briefly how a faulty heart valve can lead to heart failure.

Model answer

If a valve leaks (regurgitation) or is stenosed, the heart must work harder to maintain output. Over time this increased workload leads to ventricular hypertrophy and ultimately decompensation/heart failure.

Explanation

Faulty valves create abnormal pressures or volumes that force the myocardium to compensate; chronic strain causes structural changes and failure to maintain sufficient circulation.

Mark scheme

1 mark
valve leakage or narrowing increases workload on the heart (volume/pressure overload)
1 mark
chronic overload leads to hypertrophy and eventual heart failure / reduced cardiac output

Question 2

3 marks

Outline two reasons why a patient might not be given a stent even if they have a coronary blockage.

Model answer

If blockage is diffuse or in small distal vessels unsuitable for stent; if patient has allergy to stent material or cannot tolerate dual antiplatelet therapy; previous restenosis or anatomy better treated with bypass surgery; severe comorbidities making procedure high risk.

Explanation

Stents are not always appropriate due to vessel anatomy, patient bleeding risk/contraindications to antiplatelet drugs, or when bypass grafting offers better long-term results.

Mark scheme

1 mark
disease too diffuse / multiple small vessels not suitable for stent
1 mark
patient cannot take antiplatelet therapy / bleeding risk or allergy to stent
1 mark
anatomy better suited to bypass or prior stent failure / restenosis or high surgical risk

Question 3

4 marks

Explain how raised LDL cholesterol leads to atherosclerotic plaque formation.

Model answer

High LDL enters damaged endothelium and is oxidised, attracting macrophages which engulf LDL forming foam cells. Smooth muscle proliferation and extracellular matrix deposition form a fatty streak and later fibrous plaque that narrows the lumen.

Explanation

Atherosclerosis is a process where LDL builds up in the arterial wall, incites inflammation, foam cell formation and smooth muscle response, leading to plaque with a fibrous cap that reduces lumen size and blood flow.

Mark scheme

1 mark
LDL cholesterol accumulates in artery wall / enters intima
1 mark
oxidation / modification of LDL triggers inflammation and macrophage uptake (foam cells)
1 mark
smooth muscle cells proliferate and secrete matrix / cholesterol core forms fatty streak
1 mark
fibrous cap and plaque form narrowing artery lumen

Question 4

5 marks

Design a simple clinical trial outline to test a new drug that reduces LDL cholesterol. Include: control group, randomisation, primary endpoint, and duration.

Model answer

Randomised controlled trial: patients with high LDL randomly assigned to drug or placebo/control; double-blind if possible. Primary endpoint: change in LDL at 6 months or incidence of cardiovascular events over longer follow-up. Duration: e.g. 6–12 months for LDL change, longer (years) for CV outcomes. Include sample size and monitoring for side effects.

Explanation

A valid trial uses random assignment and a control group to reduce bias, a prespecified endpoint (LDL change or CV events) and adequate duration and safety monitoring to determine efficacy and harms.

Mark scheme

1 mark
control group: placebo or standard therapy group
1 mark
randomisation: patients randomly assigned to groups / mention double-blind if possible
1 mark
primary endpoint: change in LDL cholesterol (or % reduction) or CV events
1 mark
duration: e.g. 6–12 months (for LDL change) or longer for clinical events
1 mark
monitor for side-effects / safety and use sufficient sample size
Award for inclusion of safety monitoring or sample size justification.

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