A Level H2 Biology Human Physiology Quiz

Answer Key - A-Level Biology H2 Quiz: Human Physiology

1. Resting vs Action Potential [2]

• Resting potential: Stable membrane potential (approx -70mV) when not conducting an impulse.
• Action potential: Rapid depolarization and repolarization of the membrane potential when a stimulus exceeds threshold.

2. Voltage-gated $\text{Na}^+$ channels [3]

• Open when the membrane reaches threshold potential.
• Allow $\text{Na}^+$ ions to flood into the axon down the electrochemical gradient.
• Causes rapid depolarization of the membrane.

3. Repolarization [3]

• $\text{Na}^+$ channels close.
• Voltage-gated $\text{K}^+$ channels open.
• $\text{K}^+$ ions diffuse out of the axon, returning the membrane potential to a negative value.

4. All-or-nothing [2]

• If the stimulus is below threshold, no action potential is generated.
• If threshold is reached, a full action potential of constant magnitude is always produced.

5. Synaptic Transmission [5]

• Action potential arrives at presynaptic terminal.
• Voltage-gated $\text{Ca}^{2+}$ channels open $\rightarrow$ $\text{Ca}^{2+}$ influx.
• Vesicles fuse with presynaptic membrane $\rightarrow$ exocytosis of neurotransmitters.
• Neurotransmitters diffuse across synaptic cleft.
• Bind to receptors on postsynaptic membrane $\rightarrow$ open ligand-gated ion channels.

6. $\text{Ca}^{2+}$ Channel Blocker [3]

• Prediction: Synaptic transmission will be inhibited/stopped.
• Explanation: Without $\text{Ca}^{2+}$ influx, synaptic vesicles cannot fuse with the membrane.
• Result: Neurotransmitters are not released into the cleft, preventing the postsynaptic neuron from being stimulated.

7. Neuron vs Hormone [3]

• Neuron: Very fast transmission, short-lived/transient effect.
• Hormone: Slower transmission (via blood), longer-lasting effect.

8. Endocrine vs Exocrine [2]

• Endocrine: Ductless; secrete hormones directly into the blood.
• Exocrine: Have ducts; secrete substances (e.g., enzymes) onto a surface or into a cavity.

9. Low Blood Glucose Feedback [5]

• Stimulus: Blood glucose drops below set point.
• Sensor/Control: $\alpha$-cells in the islets of Langerhans (pancreas) detect the drop.
• Effector: $\alpha$-cells secrete glucagon.
• Action: Liver converts glycogen to glucose (glycogenolysis) and fats/amino acids to glucose (gluconeogenesis).
• Result: Blood glucose rises, inhibiting further glucagon secretion (negative feedback).

10. Hypothalamus and Posterior Pituitary [4]

• Hypothalamus contains osmoreceptors that detect low water potential (high solute conc).
• Hypothalamus produces Antidiuretic Hormone (ADH).
• ADH is transported to and stored in the posterior pituitary.
• Posterior pituitary releases ADH into the blood in response to signals from the hypothalamus.

11. Kidney and Dehydration [5]

• High ADH levels in the blood.
• ADH increases permeability of the collecting duct walls to water (via aquaporins).
• More water is reabsorbed from the filtrate back into the blood/interstitial fluid.
• Volume of urine decreases and concentration of urine increases.
• Water potential of blood is restored.

12. Insulin vs Glucagon [4]

• Insulin: Lowers blood glucose by stimulating glycogenesis (glucose $\rightarrow$ glycogen) in the liver.
• Glucagon: Raises blood glucose by stimulating glycogenolysis (glycogen $\rightarrow$ glucose) in the liver.
• They act antagonistically to maintain a narrow range of blood glucose.

13. Adrenal Medulla [3]

• Secretes adrenaline (epinephrine) and noradrenaline.
• Increases heart rate, breathing rate, and blood glucose (via glycogenolysis).
• Prepares the body for immediate physical action.

14. Type 1 Diabetes Insulin [2]

• Insulin is a protein/peptide; if taken orally, it would be digested by proteases in the stomach/small intestine.
• Must be injected to enter the bloodstream intact.

15. Primary vs Secondary Response [3]

• Primary: Slower onset, lower peak antibody concentration.
• Secondary: Faster onset (due to memory cells), significantly higher peak antibody concentration.

16. Clonal Selection and Expansion [4]

• Selection: A specific antigen binds to a B-cell with a complementary receptor.
• Activation: The B-cell is activated (often with T-helper cell assistance).
• Expansion: The activated B-cell undergoes rapid mitosis to produce a large clone of identical cells.
• Differentiation: These cells become plasma cells (secreting antibodies) and memory cells.

17. B-cells vs T-cells [4]

• B-lymphocytes: Humoral response; produce antibodies that target extracellular pathogens/toxins.
• T-lymphocytes: Cell-mediated response; directly attack and kill infected or abnormal (cancerous) cells.

18. Self vs Non-self [3]

• All nucleated cells have Major Histocompatibility Complex (MHC) markers on their surface.
• These markers are unique to the individual ("self").
• Immune cells recognize foreign antigens that do not possess the correct MHC markers.

19. Antibody Neutralization [3]

• Antibodies bind to specific antigens on the surface of the pathogen.
• This blocks the pathogen's ability to bind to and enter host cells.
• Agglutination: Antibodies can clump pathogens together, making them easier for phagocytes to ingest.

20. Fever as Defense [4]

• Inhibits the growth/replication of some pathogens (temperature-sensitive).
• Increases the metabolic rate of the host, speeding up the immune response (e.g., faster leukocyte migration).
• Increases the activity of enzymes involved in the inflammatory response.