Edexcel A Level Biology: Molecules, Transport and Health — Practice Questions

These are original questions written for Marlbridge, in the style and at the standard of the examination. They are not reproduced past-paper questions — examination boards hold copyright in their own papers. Use these alongside the official past papers available free from your board.

Related: Molecules, Transport and Health revision notes

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Section A

1. Describe the structure of a triglyceride and explain how it differs from a phospholipid. [3]

2. Explain the difference between a saturated and an unsaturated fatty acid, and relate this to melting point. [3]

Section B

3. Describe the cardiac cycle, naming the three stages and stating what happens to the valves in each. [6]

4. Atherosclerosis is a key stage in cardiovascular disease.

(a) Describe how an atheroma forms, starting from damage to the endothelium. [5] (b) Explain how an atheroma can lead to a myocardial infarction. [3]

5. Explain the roles of the following in blood clotting: platelets, thromboplastin, thrombin, fibrin. [4]

6. A study reports that people with higher blood cholesterol have more heart attacks.

(a) Explain why this does not prove that cholesterol causes heart attacks. [2] (b) State three other risk factors for cardiovascular disease and explain one of them. [4]

Section C

7. Explain why haemoglobin’s oxygen dissociation curve is sigmoid (S-shaped) rather than a straight line. [2]

8. Explain the Bohr effect and why it is beneficial in actively respiring tissue. [3]

9. Explain how fetal haemoglobin’s dissociation curve differs from adult haemoglobin’s, and why this allows the fetus to obtain oxygen from the mother’s blood. [3]

10. A patient is prescribed a statin. Explain how statins reduce cardiovascular risk, and state one drawback that must be weighed against this benefit. [3]

11. Describe the food test for a reducing sugar, including the positive result. [3]

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Answers

1. A triglyceride is one glycerol joined to three fatty acids by ester bonds formed in condensation reactions [1] [1]. In a phospholipid, one fatty acid is replaced by a phosphate group, making the molecule partly hydrophilic [1].

2. A saturated fatty acid has no C=C double bonds, so the chains are straight and pack closely, giving strong intermolecular forces and a high melting point — solid at room temperature [1] [1]. An unsaturated fatty acid has one or more C=C bonds causing a kink, so the chains pack less well and the melting point is lower — liquid at room temperature [1].

3. Atrial systole — the atria contract, forcing blood into the ventricles; the atrioventricular valves are open, semilunar valves closed [1] [1]. Ventricular systole — the ventricles contract, pressure rises; the atrioventricular valves close (the first heart sound) and the semilunar valves open, ejecting blood into the aorta and pulmonary artery [1] [1]. Diastole — all chambers relax, pressure falls; the semilunar valves close and the atrioventricular valves open as blood flows in passively [1] [1].

4. (a) The endothelium is damaged, for example by high blood pressure or toxins in smoke [1]. An inflammatory response occurs and white blood cells move into the wall [1]. They accumulate cholesterol from low-density lipoproteins, forming a fatty streak [1]. More cells and fibrous tissue build up, forming a plaque or atheroma [1] which hardens and narrows the lumen of the artery, raising blood pressure further [1]. (b) The rough plaque can rupture, triggering a blood clot (thrombus) [1]. If this blocks a coronary artery [1], the cardiac muscle it supplies is deprived of oxygen and dies [1].

5. Platelets adhere to the damaged surface and release thromboplastin [1]. Thromboplastin catalyses the conversion of prothrombin to thrombin, in the presence of calcium ions and vitamin K [1]. Thrombin then catalyses the conversion of soluble fibrinogen into insoluble fibrin [1]. Fibrin forms a mesh of fibres that traps red blood cells, forming the clot [1].

6. (a) This is a correlation, not causation [1]; a third factor such as diet, obesity or lack of exercise could be causing both the raised cholesterol and the heart attacks [1]. (b) Any three: smoking, high blood pressure, obesity, lack of exercise, diet high in saturated fat, age, genetic predisposition [1] [1] [1]. Explanation, e.g. smoking — carbon monoxide reduces the oxygen-carrying capacity of haemoglobin and nicotine raises blood pressure, both increasing the strain on the heart and the risk of endothelial damage [1].

7. Binding of the first oxygen molecule changes haemoglobin’s quaternary structure [1], making it easier for further oxygen molecules to bind — cooperative binding — so the curve rises steeply once binding begins rather than in a straight line [1].

8. A higher concentration of carbon dioxide, as found in actively respiring tissue, shifts the dissociation curve to the right [1], meaning haemoglobin holds oxygen less tightly at a given oxygen partial pressure [1]. This means haemoglobin releases more oxygen exactly where it is needed most — in tissue that is respiring rapidly [1].

9. Fetal haemoglobin has a higher affinity for oxygen at any given partial pressure, so its curve sits to the left of the adult curve [1]. This allows the fetus to take oxygen from the mother’s blood across the placenta, where the oxygen partial pressure is too low for maternal haemoglobin to release much oxygen [1] but still high enough for fetal haemoglobin to load it [1].

10. Statins inhibit an enzyme in the liver involved in cholesterol synthesis [1], lowering blood LDL cholesterol and reducing the cholesterol available to form atheromas [1]. This benefit must be weighed against side effects such as muscle pain [1].

11. Heat the sample with an excess of Benedict’s reagent in a water bath [1]; a positive result is a colour change from blue through green and orange to a brick-red precipitate of copper(I) oxide [1], and the test can be made semi-quantitative by comparing colours or timing the change [1].

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Where marks are usually lost

• Saying valves are “opened by muscles” — they open and close due to pressure differences.
• Describing atheroma formation without starting at endothelial damage.
• Reversing the fibrinogen–fibrin conversion.
• Treating correlation as proof of cause.