The digestive system is an organ system that breaks food into small soluble molecules so they can be absorbed into the blood.
Order of organs: mouth → oesophagus → stomach → small intestine → large intestine → rectum → anus (with the liver and pancreas attached as accessory organs).
Mechanical digestion = chewing (teeth) and churning (stomach muscles). Chemical digestion = enzymes from glands and the pancreas.
Bile is made in the liver, stored in the gall bladder and released into the small intestine. It emulsifies fats (large droplets → small droplets) and neutralises stomach acid.
Absorption of digested food happens in the small intestine through villi; water absorption happens in the large intestine.
Three tissues build the gut wall: muscular (peristalsis), glandular (enzymes/mucus) and epithelial (lining).
Enzymes are biological catalysts — proteins that speed up reactions without being used up.
Each enzyme has a specifically shaped active site that fits only one substrate. This is the lock-and-key model.
Enzymes have an optimum temperature (around 37 °C in humans) and an optimum pH.
Above the optimum temperature OR at an extreme pH, the active site changes shape — the enzyme is denatured and stops working.
Denaturation is NOT 'death' (enzymes were never alive) and is usually irreversible.
Specification reference: enzymes are central to digestion (4.2.2.3) and underpin RP5 — effect of pH on amylase activity.
4.2.2.1 — Name each organ of the human digestive system and state its function.
4.2.2.1 — Distinguish digestion from absorption and state where each happens.
4.2.2.1 — Describe the role of bile and explain why emulsification increases the rate of fat digestion.
4.2.2.1 — Relate the structure of villi to their function in absorption.
4.2.2.2 — Describe enzymes as biological catalysts and proteins.
4.2.2.2 — Use the lock-and-key model to explain substrate specificity.
4.2.2.2 — Describe and explain the effect of temperature and pH on enzyme activity.
4.2.2.2 — Define denaturation and explain it in terms of active site shape.
4.2.2.3 — Name the three classes of digestive enzymes and the food groups they digest.
4.2.2.3 — State the products of digestion of carbohydrates, proteins and lipids.
4.2.2.3 — State where each enzyme is produced and where it acts.
4.2.2.3 — Explain the role of bile in fat digestion (emulsification + pH).
4.2.2.4 — Describe the reagent, method and positive result for the iodine test for starch.
4.2.2.4 — Describe the Benedict's test for reducing sugars and identify a positive result.
4.2.2.4 — Describe the biuret test for protein.
4.2.2.4 — Describe the ethanol emulsion test for lipids.
4.2.2.4 — Apply the tests to identify unknown food samples.
4.2.3.1 — Describe the structure of the human heart including the four chambers, valves and major associated blood vessels.
4.2.3.1 — Explain how the heart functions as a double pump linked to the lungs and the rest of the body.
4.2.3.1 — Identify the natural pacemaker in the right atrium and explain the use of artificial pacemakers to correct heart rate irregularities.
4.2.3.1 — Compare the structure and function of arteries, veins and capillaries, linking structure to function.
4.2.3.2 — Identify the four components of blood and state their functions.
4.2.3.2 — Describe how red blood cells are adapted for transporting oxygen (biconcave shape, no nucleus, haemoglobin).
4.2.3.2 — Explain the role of white blood cells (phagocytes and lymphocytes) in defence against disease.
4.2.3.2 — Explain the role of platelets in blood clotting and why this matters for wound healing.
4.2.3.3 — Explain how coronary heart disease develops and its effect on the heart muscle.
4.2.3.3 — Evaluate the benefits and risks of using stents and statins to treat coronary heart disease.
4.2.3.3 — Describe how faulty heart valves can be treated by valve replacement (biological and mechanical) and explain advantages and disadvantages of each.
4.2.3.3 — Evaluate the use of donor hearts, mechanical hearts and artificial hearts to treat heart failure.
4.2.3.4 — Define health and distinguish between communicable and non-communicable diseases.
4.2.3.4 — Describe how different diseases may interact — defective immunity, immune triggers for allergies, mental illness following physical illness, viruses leading to cancers.
4.2.3.4 — Identify common lifestyle risk factors for non-communicable disease and explain how each increases disease risk.
4.2.3.4 — Distinguish between correlation and causation when interpreting health data.
4.2.3.5 — Define a risk factor and distinguish correlation from causation.
4.2.3.5 — Describe lifestyle risk factors for cardiovascular disease, type 2 diabetes and liver/brain disease.
4.2.3.5 — Discuss the human and financial costs of non-communicable diseases to individuals, local communities, the NHS and the country.
4.2.3.5 — Interpret data and graphs showing the correlation between lifestyle factors and disease incidence.
4.2.3.6 — Describe cancer as the result of changes in cells that lead to uncontrolled growth and division.
4.2.3.6 — Distinguish between benign and malignant tumours.
4.2.3.6 — List and describe risk factors for cancer (genetic and lifestyle).
4.2.3.6 — Explain how secondary tumours form by metastasis.
Study notes
1
Organs of the digestive tract
Mouth, oesophagus, stomach, small intestine, large intestine — with the liver and pancreas as accessory organs.
Food takes a one-way trip through the digestive tract. At each station something specific happens:
Organ
Mechanical job
Chemical / other job
Mouth
Teeth chew (increase surface area); tongue rolls food into a bolus
The small intestine is where most chemical digestion finishes AND where absorption happens.
Common pitfall
Saying digestion happens 'in the stomach'. Only protein digestion really starts there — most chemical digestion is in the small intestine.
2
Digestion vs absorption
Digestion = breakdown of large food into small soluble molecules. Absorption = those molecules crossing the gut wall into the blood.
Examiners regularly catch students mixing these two up.
Digestion is the chemical breakdown of large insoluble food molecules (starch, proteins, fats) into small soluble ones (sugars, amino acids, fatty acids + glycerol). This is mostly done by enzymes (see 4.2.2.2 and 4.2.2.3).
Absorption is the movement of those soluble products through the wall of the small intestine and into the blood (or lymph, for fats). It happens mainly across the villi.
Villi adaptations (mirror the alveoli adaptations from gas exchange):
A huge total surface area (millions of villi, each with microvilli on its epithelial cells).
Walls only one cell thick — short diffusion distance.
A dense network of capillaries to carry absorbed glucose, amino acids and minerals away, maintaining a steep concentration gradient.
A lacteal in the middle for absorbing fatty acids and glycerol into the lymph.
In the large intestine, water from undigested food is absorbed back into the blood. What's left forms faeces, stored in the rectum, removed through the anus.
Digestion = chemical breakdown by enzymes.
Absorption = transport across the gut wall.
Most absorption is in the small intestine; water absorption is in the large intestine.
Villi: large SA, thin walls, good blood supply — same logic as alveoli.
3
Bile: emulsifier and neutraliser
Made in the liver, stored in the gall bladder, released into the small intestine. Emulsifies fats and neutralises stomach acid.
Bile is not an enzyme — it doesn't catalyse a reaction. It does two physical/chemical jobs:
Emulsifies fats. Large fat droplets are broken into many small droplets. This dramatically increases the surface area of the fat for lipase to work on, so fat digestion happens faster.
Neutralises stomach acid. Food entering the small intestine from the stomach is at pH ~2. Bile is alkaline, raising the pH to around 7–8. This is the optimum pH for the enzymes (lipase, pancreatic amylase, pancreatic protease) working in the small intestine.
If the bile duct is blocked (e.g. by a gall stone), fats are poorly digested and the patient may have pale, fatty stools.
Bile is made by the liver, stored in the gall bladder.
Released into the small intestine via the bile duct.
Two jobs: emulsify fats AND neutralise stomach acid.
Bile is not an enzyme — it doesn't break chemical bonds.
Common pitfall
Saying 'bile digests fats'. Bile only physically breaks up fat droplets; lipase chemically digests them.
Linking back to 4.2.1, the wall of the gut contains:
Muscular tissue — circular and longitudinal muscle layers contract in rhythmic waves (peristalsis) to push food along.
Glandular tissue — gastric glands in the stomach release pepsin and hydrochloric acid; intestinal glands secrete mucus and enzymes.
Epithelial tissue — lines the inner surface of the gut, protecting against acid and enzymes and (in the small intestine) absorbing nutrients.
This is the classic AQA "three tissues" answer you should be able to reel off.
Muscular tissue moves food.
Glandular tissue makes enzymes, acid and mucus.
Epithelial tissue lines and absorbs.
5
What is an enzyme?
A protein that catalyses (speeds up) a specific reaction without being used up.
An enzyme is a biological catalyst. Like all catalysts, it speeds up a reaction without being changed or used up — one enzyme molecule can catalyse the same reaction thousands of times per second.
All enzymes are proteins. Their shape is determined by the precise sequence of amino acids in their polypeptide chain. A small region of that folded protein is the active site — the pocket where the substrate fits.
The lock-and-key model:
The substrate (e.g. starch) is the "key".
The active site of the enzyme (e.g. amylase) is the "lock".
They fit together to form an enzyme-substrate complex.
The substrate is then broken down (or built up) into products which leave, freeing the enzyme to bind another substrate.
Because only one substrate shape fits the active site, each enzyme is specific to its substrate. Amylase only digests starch; protease only digests proteins; lipase only digests lipids.
Lock-and-key: only a substrate with the correct shape fits the active site.
Enzymes are proteins.
Active site shape is complementary to one substrate only — specificity.
The enzyme is not used up — it can catalyse another reaction immediately.
Common pitfall
Calling enzymes 'living'. Enzymes are protein MOLECULES — they were never alive, so they can't 'die'.
6
Effect of temperature
Rate rises with temperature until the optimum, then crashes as the enzyme denatures.
As temperature rises from 0 °C, enzyme and substrate molecules move faster. Successful collisions happen more often, so the rate of reaction increases.
This continues until you reach the optimum temperature — about 37 °C for human enzymes (body temperature). At the optimum, rate is at its peak.
Heating beyond the optimum causes the enzyme's protein structure to vibrate so much that the bonds holding the active site shape begin to break. The active site changes shape and no longer fits the substrate. The enzyme is denatured, and the rate of reaction crashes towards zero.
Key idea: denaturation changes the enzyme's shape, not its existence. The protein is still there; the active site just doesn't work.
Cold doesn't denature enzymes — it just slows them down. Warm them back up and they work again.
Rate rises with temperature up to the optimum (~37 °C in humans).
Above optimum, active site shape changes — denatured.
Denaturation is usually irreversible.
Cold = slow, NOT denatured.
Common pitfall
Saying enzymes are 'killed' at high temperature. They aren't alive. Use denatured.
7
Effect of pH (and RP5)
Each enzyme has an optimum pH. Far from optimum, the active site shape changes and the enzyme is denatured.
Like temperature, pH affects the bonds that hold the active site shape. Each enzyme has its own optimum pH:
Enzyme
Where it works
Optimum pH
Salivary amylase
Mouth
~7
Pepsin (stomach protease)
Stomach
~2
Pancreatic amylase / lipase
Small intestine
~8
Move too far from the optimum and the active site distorts — denatured.
Required Practical 5 (RP5): effect of pH on amylase activity
You investigated how pH affects the rate at which amylase digests starch:
Add buffer solutions at different pH (e.g. 3, 5, 7, 9, 11) to amylase + starch in a series of test tubes.
Every 10–30 seconds, take a drop and add it to iodine solution in a spotting tile.
Iodine stays orange-brown when starch is gone; turns blue-black when starch is present.
The time taken for the iodine to stop going blue-black = how long the amylase took to digest the starch.
Shorter time = faster rate = closer to optimum pH (around pH 7 for salivary amylase).
Control variables: temperature (use a 30–35 °C water bath), volume + concentration of enzyme and substrate, time between sampling.
Every digestive enzyme on the AQA spec belongs to one of three families. Learn the enzyme → substrate → products triangle for each.
Enzyme
Substrate (food it digests)
Products
Carbohydrase (e.g. amylase)
Starch / complex carbohydrates
Simple sugars (e.g. maltose, then glucose)
Protease (e.g. pepsin)
Proteins
Amino acids
Lipase
Lipids (fats and oils)
Fatty acids + glycerol
Each enzyme is specific (lock-and-key, 4.2.2.2) — amylase can't digest proteins; lipase can't digest starch.
The classic AQA three-row table — learn it!
Carbohydrase = starch → sugars (amylase is the main example).
Protease = protein → amino acids.
Lipase = lipid → fatty acids + glycerol.
Each enzyme only digests its own substrate (specificity).
Common pitfall
Writing 'lipase digests lipids into glycerol' (missing fatty acids) or 'into glucose' (wrong). Always fatty acids + glycerol.
10
Where each enzyme is produced
Amylase: salivary glands, pancreas, small intestine. Protease: stomach, pancreas, small intestine. Lipase: pancreas, small intestine.
Examiners love the question 'name three sites of production'. Learn this table.
Enzyme
Made in
Acts in
Amylase (carbohydrase)
Salivary glands; pancreas; small intestine
Mouth; small intestine
Protease (pepsin in the stomach; trypsin from pancreas)
Stomach; pancreas; small intestine
Stomach; small intestine
Lipase
Pancreas; small intestine
Small intestine
The pancreas is the all-rounder — it secretes all three enzymes into the small intestine. The small intestine also makes its own enzymes that finish digestion.
Notice that all three enzymes finish their work in the small intestine. This is why bile (which neutralises stomach acid and emulsifies fats) and the structure of villi (for absorption) matter so much.
Amylase: salivary glands, pancreas, small intestine.
Protease: stomach, pancreas, small intestine.
Lipase: pancreas, small intestine.
Pancreas secretes all three.
All three finish in the small intestine.
11
Bile and the small intestine
Bile emulsifies fats (more SA for lipase) and neutralises stomach acid (right pH for enzymes).
Bile is produced by the liver, stored in the gall bladder, and released into the small intestine through the bile duct.
Two jobs:
Emulsifies fats — breaks large fat droplets into many small ones. This increases the surface area of the lipid for lipase to act on, so fat digestion happens faster.
Neutralises hydrochloric acid from the stomach. Bile is alkaline, so it raises the pH in the small intestine from about 2 to about 8. This is the optimum pH for pancreatic enzymes (lipase, amylase, trypsin).
Bile is not an enzyme. It doesn't break chemical bonds — it just physically increases the rate at which lipase can work and creates the right pH for enzyme activity.
Bile = made in liver, stored in gall bladder, acts in small intestine.
Emulsifies fats (more SA for lipase).
Neutralises stomach acid (right pH for enzymes).
Bile is NOT an enzyme.
Common pitfall
Saying 'bile breaks down fats'. Bile EMULSIFIES — lipase BREAKS DOWN.
12
What happens to the products?
Glucose → respiration. Amino acids → new proteins. Fatty acids + glycerol → respiration or storage.
After digestion in the small intestine, the products are absorbed (4.2.2.1) and used by the body:
Glucose is used in respiration (4.4) to release energy, or stored as glycogen in the liver/muscles.
Amino acids are used to build new proteins — enzymes, muscle, hormones. Excess amino acids are deaminated in the liver and the nitrogen excreted as urea.
Fatty acids and glycerol can be used in respiration, built back into lipids for cell membranes, or stored as body fat.
This links digestion to respiration (4.4), homeostasis (4.5) and protein synthesis (4.6).
Reagent: iodine solution (also called iodine in potassium iodide solution).
Method:
Grind/dissolve the food sample in a small amount of distilled water in a test tube or on a spotting tile.
Add a few drops of iodine solution.
Observe the colour.
Result:
Blue-black = starch present.
Orange-brown / yellow (iodine's own colour) = no starch.
This is the test you used in RP5 to time amylase activity — the iodine turns blue-black while starch is still there; once amylase has digested it, iodine stays orange-brown.
Safety: iodine stains skin and clothes; wear an apron and eye protection.
Add roughly equal volumes of food solution and Benedict's solution to a test tube.
Place the test tube in a hot water bath at 60–80 °C for 5 minutes.
Observe the colour change.
Result (colour shows ROUGH amount of sugar):
Stays blue = no reducing sugar.
Green = trace.
Yellow = low.
Orange = medium.
Brick-red = high.
Safety: Benedict's contains copper ions (irritant); the water bath is hot — use eye protection and tongs.
Reducing sugars include glucose, fructose, maltose and lactose. The reagent works because copper(II) ions are reduced to copper(I) oxide (a brick-red precipitate) by the sugar's aldehyde/ketone group.
Reagent: Benedict's solution.
Must heat in a water bath (60–80 °C).
Positive: colour gradient from green → yellow → orange → brick-red (more sugar = more red).
Tests for reducing sugars only (sucrose doesn't react).
Common pitfall
Saying 'Benedict's turns red'. There's a whole gradient — your written answer should match the colour to the amount of sugar.
Reagent: biuret solution (alternatively, sodium hydroxide solution followed by a few drops of copper sulfate solution).
Method:
Add the food solution to a test tube.
Add about the same volume of biuret reagent.
Mix gently. Do NOT heat.
Observe the colour.
Result:
Blue = no protein.
Purple / violet / lilac = protein present.
Safety: sodium hydroxide is corrosive — wear eye protection and wash off skin contact immediately. Avoid mixing on the skin.
Reagent: biuret solution (NaOH + CuSO₄).
No heating.
Positive: purple/violet.
Negative: stays blue (biuret's own colour).
Common pitfall
Saying 'biuret turns pink'. AQA wants purple/violet or lilac. Pink is not accepted.
16
4. Ethanol emulsion — lipid test
Shake sample with ethanol, then add water. Cloudy white emulsion = lipid present.
Reagent: ethanol, then distilled water.
Method:
Add a small piece of the food to a dry test tube.
Add a few cm³ of ethanol. Shake to dissolve any lipid.
Pour the ethanol layer into a second test tube containing distilled water.
Observe immediately.
Result:
Clear = no lipid.
Cloudy white emulsion = lipid present.
The lipid dissolves in the ethanol but is insoluble in water. When the ethanol-lipid mixture is poured into water, tiny lipid droplets form a milky emulsion.
Safety: ethanol is highly flammable — keep away from naked flames (no Bunsen burner nearby).
Reagent: ethanol then distilled water.
Positive: cloudy white emulsion.
Negative: clear.
Ethanol is flammable — no Bunsen.
Common pitfall
Saying 'turns white' isn't enough. Use cloudy white emulsion for full marks.
17
Applying the tests to unknown foods
Real foods often contain several food groups. Test for each one separately.
If you're given an unknown food (e.g. milk, bread, an energy bar) and asked which nutrients it contains, run all four tests on separate samples (or sub-samples):
Test 1 — iodine for starch.
Test 2 — Benedict's for reducing sugar (with heating).
Test 3 — biuret for protein.
Test 4 — ethanol emulsion for lipid.
Each test is independent. Record the colour observed, the food group identified, and any quantitative comparison (e.g. "sample A gave brick-red Benedict's = lots of sugar; sample B gave green = small amount").
Common exam scenario: comparing two food labels' claims using these tests as evidence.
Each test is independent — run on a separate sample.
Record colour AND identify the food group.
Benedict's colour gradient lets you compare quantities semi-quantitatively.
18
Structure of the heart (4.2.3.1)
Four chambers, four valves and four major vessels. Learn the names and the order.
The human heart is a muscular organ in the centre of the chest, slightly to the left. It is divided into two sides by a thick wall called the septum, so that oxygenated and deoxygenated blood never mix.
The four chambers:
Chamber
What it does
Right atrium
Receives deoxygenated blood from the body via the vena cava
Right ventricle
Pumps deoxygenated blood to the lungs via the pulmonary artery
Left atrium
Receives oxygenated blood from the lungs via the pulmonary vein
Left ventricle
Pumps oxygenated blood to the body via the aorta
The left ventricle has a much thicker muscular wall than the right ventricle, because it has to generate the pressure needed to pump blood all the way around the body. The right ventricle only has to push blood the short distance to the lungs.
The four valves ensure blood flows in one direction only:
Tricuspid valve — between right atrium and right ventricle.
Bicuspid (mitral) valve — between left atrium and left ventricle.
Pulmonary semilunar valve — at the base of the pulmonary artery.
Aortic semilunar valve — at the base of the aorta.
The heart muscle (the cardiac muscle of the walls) is supplied with oxygen and glucose by the coronary arteries, which branch off the aorta. Blockage of these is the cause of coronary heart disease (4.2.3.3).
The four chambers, four valves and four major vessels. Note the thicker wall of the left ventricle.
Four chambers: right atrium, right ventricle, left atrium, left ventricle.
Septum keeps oxygenated and deoxygenated blood separate.
Left ventricle has the thickest muscular wall — pumps blood around the whole body.
Valves (tricuspid, bicuspid, two semilunar) prevent backflow.
Major vessels: vena cava in, pulmonary artery out (right), pulmonary vein in, aorta out (left).
Common pitfall
Mixing up the pulmonary artery (carries DEOXYGENATED blood AWAY from the heart) and the pulmonary vein (carries OXYGENATED blood TO the heart). These are the only artery/vein that 'break the rule' on oxygenation.
19
The heart as a double pump
Two circuits in one pump: pulmonary (lungs) and systemic (body).
Humans have a double circulatory system — blood passes through the heart twice for every full circuit of the body.
Pulmonary circuit (right side of the heart):
Deoxygenated blood from the body enters the right atrium via the vena cava.
It is pumped into the right ventricle, then out through the pulmonary artery to the lungs.
In the lungs, gas exchange occurs — oxygen is absorbed, carbon dioxide is released.
Systemic circuit (left side of the heart):
Oxygenated blood from the lungs enters the left atrium via the pulmonary vein.
It is pumped into the left ventricle, then out through the aorta to the rest of the body.
Cells respire using the oxygen and produce CO₂, which travels back to the heart.
Why is a double circulation useful? It allows blood to be pumped at high pressure to the body without damaging the delicate lung capillaries. Pressure drops as blood passes through the lung capillaries, so the left side needs to re-pressurise it. This gives mammals a high metabolic rate.
Double circulation = blood goes through the heart twice per body circuit.
High pressure delivery + safe low-pressure lung circulation.
20
Natural and artificial pacemakers
Cells in the right atrium set the rhythm; artificial devices can correct it.
Your resting heart rate (around 60–80 beats per minute for a healthy UK teenager) is controlled by a group of specialised cells called the natural pacemaker, located in the wall of the right atrium. This is the sinoatrial node (SAN), though AQA accepts simply 'a group of cells in the right atrium'.
The pacemaker sends out small electrical impulses that spread through the heart muscle, causing the atria to contract first, then the ventricles. This coordinated electrical sequence produces a regular, effective heartbeat.
When the natural pacemaker fails — for example, if it fires too slowly (bradycardia), too fast (tachycardia) or irregularly (arrhythmia) — a doctor may fit an artificial pacemaker. This is a small electrical device implanted under the skin near the collarbone. Thin wires carry electrical impulses to the heart muscle, keeping the heartbeat regular.
Modern artificial pacemakers monitor the heart's own rhythm and only fire when needed, extending battery life to 5–10 years before replacement.
Natural pacemaker = group of cells in the wall of the right atrium.
Arteries carry blood at high pressure (because the heart has just pumped it). Their thick, muscular and elastic walls stretch and recoil to maintain the pressure surge with each heartbeat.
Veins carry blood at low pressure (most of the pressure has been lost passing through capillaries). They have a wide lumen for easier flow, and valves prevent blood flowing backwards as it slowly returns to the heart. Skeletal muscle contractions help squeeze blood along veins.
Capillaries are the exchange vessels. Their walls are just one cell (endothelium) thick, so the diffusion distance for oxygen, glucose, carbon dioxide and other substances is as short as possible. They are also permeable — small molecules and water can pass through.
Three vessels, three adaptations. Wall thickness, lumen size and valves all match function.
Artery: thick wall, narrow lumen, no valves — high pressure away from heart.
Vein: thinner wall, wide lumen, valves — low pressure back to heart.
Capillary: one cell thick, very narrow lumen — short diffusion distance for exchange.
Structure–function: every feature serves a job.
Common pitfall
Writing that 'arteries always carry oxygenated blood'. The pulmonary artery is the exception — it carries deoxygenated blood to the lungs.
22
The four components of blood (4.2.3.2)
Blood is a TISSUE made of plasma + three types of cells (RBC, WBC, platelets).
Blood is classified as a tissue (4.2.1) — a group of similar cells working together. Despite being a liquid, it contains specialised cells suspended in a liquid background.
Component
What it looks like
Main function
Plasma
Pale yellow liquid (about 55 % of blood volume)
Transports dissolved substances + heat around the body
Red blood cells (RBCs)
Small biconcave discs, no nucleus, red colour
Carry oxygen from lungs to body cells
White blood cells (WBCs)
Larger, with a nucleus; several types
Defence against pathogens
Platelets
Tiny cell fragments
Help blood clot at wounds
In 1 mm³ of blood there are roughly 5 million red cells, 5,000–10,000 white cells and 250,000 platelets. Red cells massively outnumber the others — they're the workhorses of oxygen transport.
The four components — what AQA expects you to identify on a labelled diagram.
Plasma transports CO₂, urea, hormones, nutrients, antibodies AND heat.
Plasma is the pale yellow liquid (mostly water) that makes up just over half of blood by volume. Almost everything else in blood — cells, dissolved gases, food molecules, waste products — is carried in plasma.
Plasma transports:
Carbon dioxide from respiring tissues to the lungs (dissolved in plasma as hydrogencarbonate ions, mostly).
Urea from the liver (where amino acids are broken down) to the kidneys (where it is excreted in urine).
Hormones from glands to their target organs (e.g. insulin from pancreas to liver and muscles).
Dissolved food molecules — glucose, amino acids — absorbed from the small intestine to body cells.
Antibodies produced by white blood cells to fight pathogens.
Heat generated by respiring cells (especially the liver and muscles) is distributed around the body — important in thermoregulation (4.5).
The plasma is also where the red and white blood cells and platelets float. Without plasma, the cells couldn't travel and dissolved substances couldn't be carried.
Writing 'plasma carries oxygen'. Oxygen is carried by RED BLOOD CELLS, not plasma. Plasma carries CO₂.
24
Red blood cells — oxygen transport
Biconcave, no nucleus, packed with haemoglobin → carry as much O₂ as possible.
Red blood cells (RBCs, erythrocytes) are specialised to carry oxygen from the lungs to every cell in the body. They have several structural adaptations:
1. Biconcave disc shape — concave on both sides. This gives them a large surface area to volume ratio, so oxygen can diffuse in and out quickly.
2. No nucleus — when red cells mature, they expel their nucleus. This frees up internal space for more haemoglobin, the oxygen-carrying protein.
3. Packed with haemoglobin — each red cell contains about 270 million haemoglobin molecules. Each haemoglobin has an iron-containing centre that binds oxygen:
In the lungs (high O₂): haemoglobin + oxygen → oxyhaemoglobin (a reversible reaction).
In respiring tissues (low O₂): oxyhaemoglobin → haemoglobin + oxygen.
The oxygen is then released to the cells, which use it in respiration (4.4).
4. Small and flexible — they can squeeze through narrow capillaries (about 7 µm diameter, only slightly wider than a single RBC).
UK adults make about 2 million new red blood cells per second in the bone marrow to replace the same number that die after their ~120-day lifespan.
Worked exam phrasing for full marks:
"Red blood cells have a biconcave disc shape, giving a large surface area for diffusion of oxygen. They contain no nucleus, which leaves more space for haemoglobin. Haemoglobin binds oxygen in the lungs to form oxyhaemoglobin, which is then transported to body cells where the oxygen is released."
Biconcave disc → large surface area to volume ratio.
Saying 'red cells have no nucleus to fit through capillaries'. The reason for no nucleus is more room for haemoglobin. Flexibility (and small size) is what helps them through capillaries.
25
White blood cells and platelets
WBCs defend against pathogens; platelets clot blood at wounds.
White blood cells (WBCs) are part of the body's immune system. There are several types — AQA expects you to know two:
Phagocytes — engulf and digest pathogens (bacteria, viruses, fungi). The phagocyte recognises the pathogen, surrounds it with its cell membrane, then digests it inside the cell using enzymes. This is called phagocytosis.
Lymphocytes — produce antibodies, special proteins that lock onto specific antigens (markers) on pathogens. The antibodies clump pathogens together or mark them for destruction. Lymphocytes also produce antitoxins that neutralise toxins released by some bacteria.
WBCs have a nucleus (unlike RBCs) and are larger. There are far fewer of them — about 1 WBC per 700 RBCs.
Platelets are not whole cells — they are small fragments of cells made in the bone marrow. Their function is blood clotting:
When a blood vessel is damaged, platelets stick together at the wound site.
They release chemicals that trigger a chain of reactions, converting the soluble protein fibrinogen in plasma into insoluble fibrin.
Fibrin forms a mesh of fibres that traps red blood cells, forming a clot.
The clot dries to form a scab, preventing further blood loss and stopping pathogens entering.
People with low platelet counts (e.g. in haemophilia or some leukaemia patients) bruise easily and bleed for longer than normal.
Phagocytes ENGULF pathogens (phagocytosis).
Lymphocytes PRODUCE antibodies (specific to one antigen) and antitoxins.
Saying 'white blood cells kill bacteria' is too vague — say 'phagocytes engulf them' OR 'lymphocytes produce antibodies'. Two different mechanisms.
26
What is coronary heart disease? (4.2.3.3)
Fatty deposits clog the coronary arteries → cardiac muscle starved of O₂ → heart attack.
The heart muscle, like any other tissue, needs a constant supply of oxygen and glucose for aerobic respiration (4.4) to keep contracting. This supply comes through the coronary arteries, which branch off the aorta as soon as it leaves the left ventricle.
In coronary heart disease (CHD), layers of fatty material (cholesterol, fat and other substances) build up on the inside of the coronary arteries. This process is called atherosclerosis. Two consequences follow:
The lumen narrows. Less blood can flow through, so less oxygen reaches the heart muscle. The cardiac muscle has to respire anaerobically to keep going — but anaerobic respiration produces only a small amount of energy and lactic acid. This can cause pain (called angina), especially during exercise when the muscle needs more energy.
A clot can block the artery completely. If a piece of fatty material breaks off, a blood clot can form on it (using platelets). When the artery is fully blocked, the part of the heart muscle supplied stops getting any oxygen — those cells die. This is a heart attack (myocardial infarction).
Risk factors for CHD include a diet high in saturated fat and salt, lack of exercise, smoking, obesity, high blood pressure, family history and increasing age. In the UK, CHD remains a leading cause of death (Office for National Statistics figures, 2024).
CHD is non-communicable — it isn't caused by a pathogen and can't be passed from person to person.
Coronary arteries supply the heart muscle with O₂ and glucose.
CHD = fatty material narrows the lumen of coronary arteries.
Reduced blood flow → less O₂ for cardiac muscle → angina or heart attack.
Non-communicable (not caused by pathogens).
Linked to lifestyle (diet, smoking, exercise) and family history.
Common pitfall
Saying CHD is 'caused by a virus' or 'passed on like a cold'. CHD is non-communicable.
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Stents — opening up the artery
A small mesh tube props the artery open and restores blood flow.
A stent is a small mesh tube made of metal (usually stainless steel). It is inserted into a narrowed coronary artery and expanded so that it props the artery open. Blood can then flow normally through the lumen again.
How stents are fitted:
A catheter (thin tube) with a deflated balloon and stent on the end is fed up through an artery (usually from the groin or wrist) into the heart.
At the narrowed point, the balloon is inflated, which expands the stent against the artery wall.
The balloon is removed, leaving the stent in place permanently.
Advantages of stents:
Effective for a long time (often years).
Surgery is relatively quick and recovery is fast.
Lowers the risk of a heart attack.
Disadvantages of stents:
Risk of complications during surgery (e.g. infection, bleeding, damage to the artery).
Risk of a clot forming on the stent itself (called thrombosis) — patients usually take blood-thinning drugs afterwards.
Doesn't treat the underlying cause — fatty material continues to build up elsewhere.
Stent = small metal mesh tube inserted into a narrowed coronary artery.
Cons: surgical risks, possible clotting on the stent, doesn't fix the cause.
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Statins — reducing cholesterol
Drugs that lower blood cholesterol so fatty deposits build up more slowly.
Statins are drugs that reduce the level of low-density lipoprotein (LDL) cholesterol in the blood. LDL cholesterol is the 'bad' cholesterol that contributes to fatty deposits in arteries.
Effect on CHD:
Less cholesterol in the blood → fatty material builds up more slowly in the coronary arteries.
Slows the progression of CHD.
May also slightly increase 'good' cholesterol (HDL).
Advantages of statins:
Reduce the risk of heart attack and stroke.
Inexpensive and easy to take (a daily tablet).
Benefit lasts as long as the drug is taken.
Disadvantages of statins:
Must be taken regularly for life.
Possible side effects: muscle pain, headaches, kidney problems, liver damage (rare).
Don't immediately help patients who already have severely narrowed arteries — these patients may still need stents.
In the UK, statins are one of the most commonly prescribed medicines on the NHS, with millions of UK adults taking them daily.
Statins and exercise reduce CHD risk; smoking and inactivity raise it. Treatment is most effective alongside lifestyle change.
Statins reduce blood LDL ('bad') cholesterol.
Slows the rate at which fatty material builds up in arteries.
Cons: lifelong use, possible muscle/liver side effects, don't fix existing narrowing immediately.
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Faulty valves and heart failure
Faulty valves can be replaced (biological or mechanical). Severe heart failure needs a transplant or artificial heart.
Heart valves can fail in two ways:
They don't open fully (restricting blood flow), or
They don't close fully (allowing blood to flow backwards — called leaky valves).
Faulty valves can be replaced by valve replacement surgery. Two options:
Type
Source
Pros
Cons
Biological
From pigs, cows or human donors
No need for blood-thinning drugs long-term; works like a normal valve
Wears out (often 10–15 years); may need replacing
Mechanical
Man-made (titanium and polymers)
Lasts a lifetime — no wear-out
Need to take blood-thinning drugs to prevent clots forming on the surface
Heart failure — when the heart can no longer pump effectively — can be treated with:
Donor heart (transplant) — the gold standard for severe cases, but there are very few donors in the UK and the recipient must take immunosuppressant drugs for life to prevent rejection.
Artificial / mechanical heart — used as a bridge to transplant (keeping the patient alive while waiting), or in some cases as a long-term solution. They are bulky, the patient must carry a battery pack, and there is a risk of blood clots and infection.
Evaluating treatments is a key AQA skill. A good answer compares the cost, risk and quality of life for each option. For example:
"A donor heart restores normal function and lets the patient live a full life, but donor hearts are scarce. A mechanical heart is more readily available but requires the patient to carry equipment and take blood thinners; it is better used as a bridge to transplant than as a long-term treatment."
Faulty valves: don't open fully OR don't close fully.
Treatment: biological valve (no anticoagulants but wears out) vs mechanical valve (lifelong, but needs anticoagulants).
Heart failure: donor heart (best long-term, scarce, rejection risk) vs artificial heart (bridge to transplant, bulky, clot risk).
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Defining health (4.2.3.4)
WHO: health is physical + mental + social well-being. Not just absence of disease.
The World Health Organization (WHO) defines health as:
"A state of complete physical, mental and social well-being — and not merely the absence of disease or infirmity."
This is the definition AQA uses in mark schemes. The key idea is that health is much broader than being free from disease. A person can be physically well but mentally unwell (e.g. clinical depression), or physically and mentally well but socially isolated — all three dimensions matter.
Disease is just one factor affecting health. Other factors include:
Diet — too much or too little of specific nutrients.
Stress — chronic stress impairs the immune system and increases risk of cardiovascular disease.
Life situation — housing, income, safety, relationships.
Access to healthcare — preventive screening, vaccines, medicines.
For UK GCSE Biology students, the headline message is: 'health' is more than 'not ill'.
WHO definition: physical + mental + social well-being.
Health is not just absence of disease.
Affected by diet, stress, life situation, healthcare access — and by disease.
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Communicable vs non-communicable diseases
Communicable = caused by pathogens, transmissible. Non-communicable = not contagious.
Diseases are classified into two big groups in the AQA spec:
Type
Caused by
Transmissible?
Examples
Communicable
Pathogens (bacteria, viruses, fungi, protists)
Yes
Flu, measles, TB, malaria, athlete's foot, rose black spot
Non-communicable
Lifestyle, genetics, environment
No
CHD, type 2 diabetes, most cancers, lung disease (from smoking), liver damage (from alcohol)
The distinction matters because prevention and treatment strategies are different:
Communicable disease prevention: hygiene, vaccination, isolating patients, treating with antibiotics/antivirals.
In the UK, the rise in non-communicable disease over the last 50 years has shifted NHS spending dramatically — chronic conditions like CHD, type 2 diabetes and cancer now account for the majority of the healthcare budget.
Communicable = pathogens, transmissible.
Non-communicable = lifestyle/genetics/environment, not transmissible.
Different prevention strategies for each.
Common pitfall
Calling cancer 'a virus you can catch'. Most cancers are non-communicable. A few (e.g. cervical cancer caused by HPV) involve a virus, but the cancer itself is not contagious.
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How diseases interact
Diseases don't happen in isolation — one can trigger or worsen another.
AQA's spec lists four ways diseases can interact. You should be able to give examples.
1. Defective immune system → more vulnerable to infections. Conditions like HIV/AIDS, leukaemia or genetic immune disorders weaken the immune system, so patients catch communicable diseases (e.g. pneumonia, TB) more easily. Pre-2020 NHS data shows HIV patients are 50–100× more likely to develop active TB.
2. Some viruses trigger cancers. Certain viruses can damage DNA in cells they infect, increasing the chance of uncontrolled cell division. Examples: HPV (cervical cancer), Hepatitis B/C (liver cancer), Epstein-Barr virus (some lymphomas). This is why HPV vaccination is offered to UK teenagers.
3. Immune reactions can trigger allergies. When the immune system overreacts to a substance (e.g. pollen, dust mites, peanuts), it can trigger asthma, eczema or hayfever. Asthma rates in UK children have risen significantly over the past 50 years.
4. Severe physical illness can lead to mental illness. Cancer diagnoses, chronic pain, long-term disability and heart attacks frequently lead to depression and anxiety. The connection goes both ways — chronic mental illness can also worsen physical health.
The big idea: the body is a system. A problem in one place often spreads to others.
Diet, smoking, alcohol, lack of exercise — UK's biggest preventable causes of disease.
A risk factor is anything that increases the chance of developing a disease. AQA lists the main lifestyle risk factors for non-communicable disease in UK populations.
Strong risk factor for type 2 diabetes, CHD, joint problems, cancer.
Body Mass Index (BMI) and waist:hip ratio are common measures used by UK doctors.
Other risk factors:
Ionising radiation (UV, X-rays) → DNA damage → cancer (skin, others).
Carcinogens (chemicals like asbestos, tar) → cancer.
Combined effect: lifestyle risk factors usually act together. A UK adult who smokes, eats a poor diet and does no exercise has a much higher CHD risk than someone with just one of these factors.
Smoking remains the single biggest preventable cause of premature death in UK adults. Lifestyle factors often combine.
Diet: saturated fat/sugar/salt → CHD, obesity, type 2 diabetes.
Smoking: lung cancer, COPD, CHD, fetal harm.
Alcohol: liver disease, brain damage, fetal alcohol syndrome, some cancers.
Inactivity + obesity: type 2 diabetes, CHD, joint disease.
In health science, correlation means two variables tend to change together. Causation means one variable directly causes a change in the other.
A famous example: in the 1950s, doctors noticed that smokers had higher lung-cancer rates than non-smokers. This was a strong correlation. But it took further work to show causation — namely:
Identifying carcinogens (chemicals in tar) that damage DNA in lung cells.
Reproducing the effect in animal studies.
Watching lung-cancer rates fall in populations that quit smoking.
Once a biological mechanism is found AND multiple independent studies confirm it, scientists can be confident there's a causal link.
Common pitfalls when reading health data:
Confounding variables. People who smoke may also drink more, exercise less and eat worse. Any correlation needs to control for these other factors.
Reverse causation. Does X cause Y, or does Y cause X? E.g. does stress cause illness, or does illness cause stress?
Coincidence. Two unrelated things can correlate by chance, especially with small samples.
For AQA, you should be able to describe a correlation in data and then carefully state whether causation has been established. Examiner reports flag students who jump straight from 'X is linked to Y' to 'X causes Y' without acknowledging the difference.
Correlation = change together; causation = direct cause.
Need biological mechanism + repeated studies to prove cause.
Watch for confounding variables, reverse causation, coincidence.
Smoking → lung cancer is established (mechanism + decades of data).
Common pitfall
Writing 'the graph shows that X causes Y' when the data only show a correlation. Use 'X is linked to Y' or 'there is a correlation between X and Y' unless causation has been clearly established.
Non-communicable diseases are now the biggest killer in the UK. They develop slowly over years — so the lifestyle choices a 15-year-old makes today can change the chance of disease at 50.
Non-communicable = cannot be passed from person to person.
Causes are multifactorial: lifestyle + genetics + environment.
NCDs include CVD, type 2 diabetes, many cancers, liver disease.
Common pitfall
Calling type 2 diabetes 'infectious'. It isn't — your pancreas/insulin response changes due to diet and weight.
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What is a risk factor?
A risk factor raises the chance of disease but doesn't always cause it on its own.
A risk factor is something that increases the probability that a person develops a disease. Risk factors can be:
Aspects of lifestyle — diet, smoking, exercise, alcohol.
Substances in the body or environment — high blood cholesterol, ionising radiation, asbestos.
Causal mechanism vs correlation. A correlation shows two things vary together. A causal mechanism is the biological reason one drives the other. For example, smoking and lung cancer are correlated AND causal because tobacco smoke contains carcinogens (tar) that damage DNA in lung cells. The link between obesity and type 2 diabetes is also causal — excess fat causes cells to become less responsive to insulin.
By contrast, a graph showing that ice-cream sales and drownings rise together is a correlation only — temperature is the hidden third factor.
Tar in tobacco smoke contains carcinogens — the link is also causal.
Risk factor = increases chance of disease.
Correlation = two variables move together.
Causation = a biological mechanism links them.
Smoking → lung cancer is BOTH correlation and causation.
Common pitfall
Writing 'smoking causes lung cancer in everyone'. It increases risk — many smokers do not get lung cancer; some non-smokers do.
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Cardiovascular disease, type 2 diabetes and obesity
Obesity, high-fat diets and inactivity raise CVD and type 2 diabetes risk through cholesterol, blood pressure and insulin resistance.
Cardiovascular disease (CVD) includes coronary heart disease, heart attack and stroke. Lifestyle risk factors:
High saturated fat diet → high LDL cholesterol → fatty plaques in coronary arteries → narrowed arteries → angina/heart attack.
Type 2 diabetes is caused when body cells stop responding well to insulin (insulin resistance). The pancreas still makes insulin but it stops working effectively. Key risk factor: obesity, especially fat stored around the abdomen.
Obesity (body mass index over 30) is itself driven by an energy imbalance — eating more energy than is used in respiration over months/years. The UK has rising rates in 11-15 year-olds, which is why this topic is on the spec.
CVD risk factors: high fat diet, smoking, inactivity, high BP.
Type 2 diabetes — strongly linked to obesity and inactivity.
Obesity = BMI > 30; abdominal fat is the worst kind.
All three are partly preventable through diet and exercise.
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Alcohol, smoking in pregnancy and carcinogens
Alcohol damages the liver and brain; smoking and alcohol in pregnancy harm the fetus; carcinogens cause cancer.
Alcohol in excess damages the liver (cirrhosis, liver cancer) because the liver detoxifies ethanol and cells die in the process. It also damages brain function — long-term heavy drinking is linked to memory loss and reduced cognitive ability.
NCDs cost the NHS billions per year and shorten lives — examiners reward answers that mention multiple levels of cost.
For 6-mark evaluate questions, structure your answer around three levels of cost:
Level
Costs
Individual
Shorter life, reduced quality of life, loss of income, family stress.
Local community
Lost workforce productivity, demand on local GP surgeries, social care for sick relatives.
National (NHS / country)
NHS spending on treatment (estimated £6+ billion/year on obesity-related care alone in the UK), lost tax revenue, public health campaign spending.
Lifestyle change is cheaper than treatment — which is why the UK government runs campaigns like Change4Life and smoking-cessation services.
Individual: shorter life, lost earnings.
Community: workforce loss, GP demand.
National: NHS spending in billions, lost tax revenue.
Prevention is much cheaper than treatment.
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What is cancer?
Cancer is uncontrolled cell division forming a tumour, caused by mutations in genes controlling the cell cycle.
Normally the cell cycle (4.1.2.2) is tightly controlled — cells divide only when needed, e.g. to replace dead cells. Cancer happens when mutations damage the genes that control this cycle. Cells then divide uncontrollably, forming a mass called a tumour.
A tumour is just a lump of cells growing where they shouldn't. The behaviour of the tumour decides whether it is dangerous.
Mutations can be caused by:
Carcinogens — chemicals like tar in tobacco smoke, asbestos fibres.
This is THE classic AQA exam question. Learn the exact wording.
Feature
Benign tumour
Malignant tumour (cancer)
Growth
Slow, contained in a membrane
Faster, irregular
Invades nearby tissue?
No
Yes
Spreads to other parts of the body?
No
Yes — through blood and lymph
Forms secondary tumours?
No
Yes (metastasis)
Life-threatening?
Usually not
Often, if not treated
Metastasis = the spread of malignant cells via the blood or lymph to form secondary tumours in other organs. This is why cancer is so dangerous — a tumour that starts in the breast can spread to the lungs, bones or liver.
Benign = contained. Malignant cells travel via blood/lymph to form secondary tumours.
Benign — local, contained, not life-threatening.
Malignant — invades, spreads via blood/lymph.
Secondary tumours = metastasis.
Common pitfall
Writing 'benign tumours are healthy'. Even benign tumours can press on organs (e.g. brain) and cause problems — they just don't spread.
Smoking → lung, mouth, throat cancer (tar contains carcinogens).
Excess alcohol → liver, mouth, throat cancer.
Obesity → linked to bowel, breast (post-menopausal), pancreatic cancers.
UV light (sunbathing, sunbeds) → skin cancer (melanoma).
Diet — low fibre/high processed meat linked to bowel cancer.
Genetic risk factors:
Inherited mutations in genes such as BRCA1 / BRCA2 raise breast and ovarian cancer risk.
Family history of cancer raises personal risk (genes you inherited from your parents).
Environmental / occupational:
Asbestos → mesothelioma (lung).
Ionising radiation (X-rays, gamma) → various cancers.
Some viruses — HPV (cervical), Hepatitis B (liver).
Most cancers result from a combination of factors over years. Lifestyle changes lower — but don't remove — the risk.
Lifestyle: smoking, alcohol, obesity, UV, diet.
Genetic: inherited mutations e.g. BRCA1/2.
Environmental: asbestos, ionising radiation, some viruses.
Often a combination of factors.
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Screening and treatment (context only)
Early detection through screening saves lives; treatment uses surgery, radiotherapy and chemotherapy.
Although treatment isn't on the AQA spec in detail, examiners often set application questions about UK NHS programmes. Know these in outline:
NHS screening programmes — breast (mammogram), cervical (smear), bowel (FIT test). These catch tumours early when treatment is more likely to work.
Surgery — removes the tumour.
Radiotherapy — uses ionising radiation to kill cancer cells.
Chemotherapy — uses drugs that stop dividing cells (so it has side effects on healthy dividing cells like hair and gut).
The key biology link: because cancer cells divide more often than most healthy cells, radiotherapy and chemotherapy harm them more — but healthy fast-dividing cells (hair, gut, bone marrow) also suffer.
Screening = early detection.
Treatments target dividing cells.
Side effects on hair/gut because those cells also divide quickly.
Quick recap
Mouth → oesophagus → stomach → small intestine → large intestine → rectum → anus.
Liver makes bile; gall bladder stores it; pancreas makes amylase, protease, lipase.
Bile emulsifies fats AND neutralises stomach acid.
Three gut tissues: muscular, glandular, epithelial.
Enzymes are proteins that catalyse specific reactions.
Lock-and-key: substrate shape must match active site shape.
Optimum temperature ~37 °C for human enzymes; optimum pH varies by enzyme.
Denaturation = shape of active site changed, substrate no longer fits.
RP5: pH on amylase, timed with iodine spotting tile.
Amylase (carbohydrase) → starch → sugars.
Protease → protein → amino acids.
Exam tips
Always say 'bile emulsifies fats' (not 'digests') and link it to surface area for lipase.
When asked to describe peristalsis, mention 'wave-like contractions of muscular tissue' to score the mark.
Don't confuse the small intestine (digestion + absorption) with the large intestine (water absorption only).
Use the phrase 'active site is complementary to the substrate'. The word 'complementary' is an examiner keyword.
Don't say enzymes are 'killed'. Use denatured.
If a question asks about temperature OR pH, your explanation chain is the same: bonds break → shape changes → active site no longer fits → no complex.
For RP5, the dependent variable is 'time taken for iodine to stay orange-brown' (or 'time to digest starch'). State control variables (temperature, volumes, concentrations).
Use exact AQA product names: sugars (not 'sugar molecules'), amino acids, fatty acids and glycerol.
If a question gives a marks-per-point structure, name the enzyme, substrate and products separately.
Always link bile to surface area (emulsification) AND pH (neutralises acid). Two marks.