A Level H1 Biology Human Physiology Quiz

A-Level Biology H1 Quiz – Human Physiology

Answer Key and Marking Scheme

Section A: Multiple Choice (5 × 1 mark = 5 marks)

1. B – The acidic environment of the stomach destroys many pathogens before they can establish an infection; it is a non‑specific chemical barrier.

2. C – B lymphocytes mature in the bone marrow and, upon activation, differentiate into plasma cells that secrete antibodies.

3. C – HIV infects and destroys helper T cells, weakening the immune system.

4. C – The primary immune response has a longer lag phase (several days) before antibody levels rise, whereas the secondary response is much faster.

5. C – Malaria is caused by the protozoan Plasmodium; tuberculosis is bacterial, influenza is viral, cholera is bacterial.

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Section B: Structured Questions (5 × 2 marks = 10 marks)

6. Distinguish between innate and adaptive immunity.

• Innate immunity is non‑specific, present from birth, and provides immediate defence (e.g., skin, phagocytosis) without memory.
• Adaptive immunity is highly specific to a particular pathogen, develops more slowly, and produces immunological memory (e.g., antibody production by B cells).

[2 marks: 1 for innate features, 1 for adaptive features; accept equivalent points.]

7. Outline the role of helper T cells.

• Helper T cells recognise antigen‑MHC class II complexes on antigen‑presenting cells (e.g., macrophages).
• They become activated and release cytokines, which stimulate B cells to divide and differentiate into plasma cells, and also activate cytotoxic T cells.

[2 marks: 1 for recognition/activation, 1 for role in stimulating B and T cells.]

8. Explain how vaccination leads to immunological memory.

• A vaccine contains a harmless form of the antigen (e.g., inactivated pathogen, part of a pathogen).
• This triggers a primary immune response, during which memory B and memory T cells are produced.
• These memory cells remain in the body and, upon subsequent exposure to the actual pathogen, mount a rapid, strong secondary response.

[2 marks: 1 for primary response producing memory cells, 1 for rapid secondary response.]

9. State two ways HIV evades the immune system.

1. HIV infects and destroys helper T cells, crippling the coordination of the immune system.
2. The virus mutates rapidly, altering its surface antigens so that existing antibodies and memory cells no longer recognise it.

[2 marks: 1 for each correctly stated evasion mechanism.]

10. Describe how a phagocyte destroys a bacterium.

• The phagocyte is attracted to the bacterium by chemotaxis; it engulfs the bacterium by extending pseudopodia.
• The bacterium is enclosed in a phagosome, which fuses with a lysosome to form a phagolysosome.
• Lysosomal enzymes and reactive oxygen species digest the bacterium, and the debris is expelled by exocytosis.

[2 marks: 1 for phagocytosis/engulfment, 1 for digestion by lysosomal enzymes.]

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Section C: Data‑Response and Application (15 marks)

11. (a) Primary response labelled as the first lower curve after A; secondary response labelled as the high curve after B. [1 mark]

(b) After the primary response, antibody concentration declines as the plasma cells die off; however, memory cells remain. The slow shape between A and B reflects the primary lag phase, the peak, and the decline. [2 marks: 1 for decline, 1 for memory cell mention.]

(c) The secondary response is faster and larger because memory B and T cells are already present. Upon re‑exposure, memory cells quickly proliferate and differentiate into plasma cells, producing large amounts of antibodies in a short time. [2 marks: 1 for memory cells, 1 for rapid proliferation.]

12. (a) Correct labelling: antigen‑binding site at the tips of the Y arms, variable region at the tips (including the binding site), constant region at the stem of the Y. [2 marks: 1 for each correct label, or 2 marks if all three correctly placed.]

(b) The variable region has a unique three‑dimensional shape that is complementary to a specific antigen, allowing the antibody to bind through non‑covalent interactions (lock‑and‑key fit). [1 mark]

13. (a) Tuberculosis – bacterium; Influenza – virus; Malaria – protoctist (protozoan). [2 marks: 1 for two correct, 2 for all three correct.]

(b) Antibiotics target specific bacterial structures (e.g., cell wall, ribosomes) that are absent in viruses and protoctists. [1 mark]

14. (a) Disease rate in vaccinated group = 25/5000 = 0.005 (0.5%); disease rate in control = 250/5000 = 0.05 (5%).
Protection = (0.05 – 0.005)/0.05 × 100 = 90%.

[2 marks: 1 for correct rates, 1 for correct calculation.]

(b) The control group allows a comparison to see the natural infection rate without the vaccine, confirming that the lower rate in the vaccinated group is due to the vaccine and not to other factors. [1 mark]

15. (a) The bacterium has a cell wall (visible as a distinct outer layer) that is absent in the virus; alternatively, the bacterium is much larger. [1 mark]

(b) Viruses lack the cellular machinery for replication; they must enter a host cell and use its ribosomes, enzymes, and ATP to reproduce. Most bacteria possess their own ribosomes and metabolic pathways, so they can reproduce outside a host cell. [2 marks: 1 for lack of machinery, 1 for bacterial self‑sufficiency.]

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Section D: Extended Response (20 marks)

16. Compare B and T lymphocytes.

• Maturation: B cells mature in the bone marrow; T cells migrate to and mature in the thymus.
• Receptors: B cell receptors are membrane‑bound antibodies (immunoglobulins) that recognise intact antigens; T cell receptors (TCRs) recognise processed antigen fragments presented on MHC molecules.
• Functions: Activated B cells give rise to plasma cells that secrete antibodies (humoral immunity); T cells are involved in cell‑mediated immunity – helper T cells activate B cells and cytotoxic T cells, while cytotoxic T cells directly kill virus‑infected cells.

[4 marks: 1 for maturation site, 1 for receptor type, 2 for comparison of functions; allow equivalent detail.]

17. Advantages and limitations of vaccination programmes.

• Advantages: Vaccines stimulate long‑lasting immunity (memory cells) without causing disease; they protect individuals and contribute to herd immunity, reducing the spread of pathogens; they have eradicated diseases like smallpox and reduced the incidence of measles, polio, etc.
• Limitations: Some vaccines require cold storage and trained personnel, making global distribution difficult; antigenic variation (e.g., influenza) means vaccines must be reformulated; individuals with compromised immunity may not respond; public distrust (“anti‑vax” movements) can reduce uptake.

[5 marks: 3 for advantages (at least two points), 2 for limitations (at least two points); credit well‑developed explanations.]

18. How antibiotics work and resistance development.

• Antibiotics inhibit bacterial growth by targeting specific bacterial features: e.g., penicillin prevents peptidoglycan cross‑linking in the cell wall, leading to lysis; tetracyclines bind to bacterial ribosomes and inhibit protein synthesis.
• Resistance can arise through spontaneous mutation or horizontal gene transfer (e.g., plasmids carrying resistance genes). Bacteria with resistance genes survive antibiotic treatment and reproduce, passing the trait to offspring. The antibiotic acts as a selective pressure, leading to an increase in the proportion of resistant bacteria over time.

[4 marks: 2 for mechanisms of antibiotics, 2 for explanation of resistance development.]

19. Body’s defence against pathogens (non‑specific and specific).

• Non‑specific (innate): physical barriers – skin, mucous membranes; chemical defences – lysozyme in tears, stomach acid; phagocytosis by neutrophils and macrophages; inflammatory response (histamine release, increased blood flow).
• Specific (adaptive): humoral immunity – B cell activation by helper T cells, clonal expansion, plasma cells produce antibodies; cell‑mediated immunity – cytotoxic T cells kill infected cells. Memory cells ensure rapid response upon re‑exposure.
• Examples: skin prevents entry; if pathogen breaches skin, phagocytes engulf it; if infection persists, specific antibodies tag the pathogen for destruction.

[4 marks: 2 for innate components with examples, 2 for adaptive components with explanation; allow equivalent depth.]

20. Herd immunity and its importance.

• Herd immunity occurs when a sufficiently high proportion of a population is immune to a disease (through vaccination or prior infection) so that the chain of transmission is broken, protecting unvaccinated individuals.
• Measles example: measles is highly contagious; vaccination coverage of about 95% is needed to achieve herd immunity. When coverage drops, outbreaks occur.
• Importance: protects vulnerable groups who cannot be vaccinated (e.g., infants, immunocompromised), reduces overall disease prevalence, can lead to disease elimination (e.g., polio).

[4 marks: 1 for definition, 1 for measles/disease linkage, 2 for evaluation of importance; credit specific references to measles data.]

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END OF ANSWER KEY