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GCSE/Biology/AQA· Higher tier

B3.3Treating, curing and preventing disease: antibiotics and painkillers, drug discovery and clinical trials, monoclonal antibodies

Notes

Antibiotics, painkillers, drug development and monoclonal antibodies

Once a person is ill, the body's defences may not be enough. Modern medicine treats disease with three classes of drug, plus increasingly with monoclonal antibodies. This is largely a Higher-tier topic.

Antibiotics

Antibiotics are drugs that kill bacteria inside the body. Penicillin (Alexander Fleming, 1928) was the first. Antibiotics target processes specific to bacteria — disrupting cell-wall synthesis or protein synthesis — without harming our cells.

Specific antibiotics for specific bacteria — choosing the right antibiotic matters; broad-spectrum antibiotics are kept in reserve to slow resistance.

Crucially: antibiotics cannot kill viruses. Viruses replicate inside our own cells and don't have bacterial machinery for the drug to attack.

Antibiotic resistance

Random mutations in bacteria can give resistance to an antibiotic. When the antibiotic is used, susceptible bacteria die; resistant ones survive and reproduce — over time, the population becomes resistant. This is natural selection in action (see B6.6).

To slow resistance:

  • Doctors should not over-prescribe antibiotics
  • Patients must finish the course (so all bacteria are killed, not just the susceptible ones)
  • Don't use antibiotics for non-serious viral infections
  • New antibiotic development is too slow to keep up — a major public health concern.

MRSA (methicillin-resistant Staphylococcus aureus) is the GCSE example.

Painkillers

Painkillers (e.g. paracetamol, aspirin) treat symptoms — they don't kill the pathogen. They reduce pain or fever but the immune system still does the work of clearing the infection.

Drug discovery and development

Most drugs originally came from natural sources:

  • Digitalis — from foxglove (heart drug)
  • Aspirin — from willow bark
  • Penicillin — from Penicillium mould (Fleming)

A new drug must be tested in stages:

  1. Preclinical — tested on cells, tissues, then live animals. Checks for toxicity, efficacy and dose.
  2. Clinical phase 1 — small group of healthy volunteers. Find safe dose, monitor side effects.
  3. Clinical phase 2 — small group of patients to check it works.
  4. Clinical phase 3 — large group of patients in a double-blind trial — neither doctor nor patient knows who gets the drug or the placebo (dummy treatment), to remove bias.

Monoclonal antibodies (HT)

A monoclonal antibody is identical antibody molecules produced by a clone of cells, all targeting one specific antigen.

Production:

  1. A mouse is injected with the antigen.
  2. Lymphocytes from the mouse are fused with myeloma (tumour) cells to form hybridomas — cells that divide indefinitely AND produce antibody.
  3. Hybridomas are cloned and the antibody collected.

Uses:

  • Pregnancy tests — detect HCG hormone in urine
  • Diagnosing diseases — measure hormone levels (ELISA)
  • Locating cancer cells — antibody attached to a fluorescent dye
  • Treating cancer — antibody attached to a toxic drug, delivered only to cancer cells (reducing side effects)

Pros: high specificity. Cons: side effects sometimes severe; production was once expensive; ethical issues with mouse use.

Common mistakesCommon mistakes / exam traps

  1. "Antibiotics treat colds" — colds are viral; antibiotics don't help.
  2. "Painkillers kill bacteria" — they don't; they only treat symptoms.
  3. Confusing placebo with control — placebo IS the control treatment in a double-blind trial.
  4. "Resistance evolves because bacteria want to survive" — wrong; it's random mutation followed by natural selection.

Links

Connects to B3.1 (pathogens), B6.6 (natural selection drives resistance) and B6.9 (Darwinian explanation).

AI-generated · claude-opus-4-7 · v3-deep-biology

Practice questions

Try each before peeking at the worked solution.

  1. Question 13 marks

    Antibiotics vs viruses (F/H)

    (F/H1) Explain why antibiotics cannot be used to treat the common cold.

    [Crossover — 3 marks]

    Ask AI about this

    AI-generated · claude-opus-4-7 · v3-deep-biology

  2. Question 24 marks

    Antibiotic resistance evolution (H)

    (H2) Outline how MRSA evolved to be resistant to most antibiotics.

    [Higher tier — 4 marks]

    Ask AI about this

    AI-generated · claude-opus-4-7 · v3-deep-biology

  3. Question 32 marks

    Why finish the course (F)

    (F3) Suggest two reasons why patients should finish the full course of an antibiotic prescription.

    [Foundation — 2 marks]

    Ask AI about this

    AI-generated · claude-opus-4-7 · v3-deep-biology

  4. Question 44 marks

    Drug development stages (H)

    (H4) Describe the main stages of testing a new drug before it can be sold.

    [Higher tier — 4 marks]

    Ask AI about this

    AI-generated · claude-opus-4-7 · v3-deep-biology

  5. Question 53 marks

    Why placebos? (H)

    (H5) Explain why a clinical trial uses a placebo group and is double-blind.

    [Higher tier — 3 marks]

    Ask AI about this

    AI-generated · claude-opus-4-7 · v3-deep-biology

  6. Question 64 marks

    Monoclonal antibody production (H)

    (H6) Describe how monoclonal antibodies are produced.

    [Higher tier — 4 marks]

    Ask AI about this

    AI-generated · claude-opus-4-7 · v3-deep-biology

  7. Question 73 marks

    Monoclonal cancer therapy (H)

    (H7) Explain how monoclonal antibodies can be used to deliver a cancer drug specifically to cancer cells.

    [Higher tier — 3 marks]

    Ask AI about this

    AI-generated · claude-opus-4-7 · v3-deep-biology

Flashcards

B3.3 — Drugs and treatments

10-card SR deck on antibiotics, resistance, drug development and monoclonal antibodies.

10 cards · spaced repetition (SM-2)