Animal Physiology — IB Biology HL Study Guide (HL Extension)

For: IB Biology HL candidates sitting IB Biology HL.

Covers: IB Topic 11 (HL only) — antibody production and immune response, kidney function and osmoregulation, hormones in sexual reproduction (menstrual cycle), muscle contraction (sliding filament).

A note on the practice questions: All worked questions in the "Practice Questions" section below are original problems written by us in the IB Biology HL style for educational use. They are not reproductions of past IBO papers.

1. Why Animal Physiology Matters in HL

Topic 11 (HL only) extends SL Topic 6 (Human Physiology) with mechanism: how immune cells make antibodies, how the kidney filters and reabsorbs, what hormones control reproduction, how muscle contraction works at the molecular level. About 8-12% of HL Paper 1+2 directly.

2. Antibody production and immunity

Pathogens (bacteria, viruses, fungi) carry antigens — molecules the immune system recognises.

Specific immune response has two arms:

Humoral (antibody-mediated):

1. Pathogen ingested by macrophage → presents antigen on MHC II.
2. Helper T cell with matching receptor binds → activates.
3. Helper T activates B cell with matching B-cell receptor.
4. B cell proliferates → most differentiate into plasma cells producing antibodies; some become memory B cells for future exposure.

Cell-mediated: cytotoxic T cells kill infected body cells displaying antigen on MHC I.

Vaccination = introducing weakened/killed antigen → produces memory cells → future exposure produces rapid secondary response (faster, higher antibody titre).

Monoclonal antibodies: produced from one B cell clone → all identical, highly specific. Used in pregnancy tests, cancer treatment.

3. Kidney function and osmoregulation

The nephron is the functional unit. ~1 million per kidney.

Stages:

1. Ultrafiltration (Bowman's capsule): blood pressure forces small molecules out of glomerular capillaries into capsule. Cells and plasma proteins stay in blood.
2. Selective reabsorption (proximal convoluted tubule): glucose, amino acids, salts, ~70% water reabsorbed actively into peritubular capillaries.
3. Loop of Henle: counter-current multiplier. Descending limb permeable to water (water leaves); ascending limb pumps Na⁺/Cl⁻ out (water can't follow). Creates salt gradient in medulla.
4. Distal convoluted tubule: fine-tuning of Na⁺, K⁺, water reabsorption (regulated by hormones).
5. Collecting duct: final water reabsorption depending on ADH (antidiuretic hormone).

Osmoregulation:

• High blood osmolarity (dehydration) → hypothalamus → posterior pituitary releases ADH → collecting duct walls become more permeable to water → more water reabsorbed → concentrated urine.
• Low osmolarity → less ADH → dilute urine.

Diabetes insipidus = ADH deficiency → excessive dilute urine.

4. Sexual reproduction hormones

Menstrual cycle (~28 days), four hormones interacting:

• FSH (follicle-stimulating hormone): from pituitary. Stimulates follicle growth in ovary.
• LH (luteinising hormone): from pituitary. Triggers ovulation; converts ruptured follicle to corpus luteum.
• Oestrogen: from follicle. Builds up endometrium.
• Progesterone: from corpus luteum. Maintains endometrium.

Phases:

1. Follicular (days 1-13): FSH ↑ → follicle grows → oestrogen ↑.
2. Ovulation (~day 14): high oestrogen → LH surge → egg released.
3. Luteal (days 15-28): corpus luteum makes progesterone → endometrium maintained.
4. Menstruation (days 1-5 of next cycle): if no implantation, corpus luteum degenerates → progesterone drops → endometrium sheds.

If pregnancy: hCG from embryo maintains corpus luteum → progesterone maintained → no menstruation.

IVF (in vitro fertilisation): hormones induce multiple follicle development → eggs collected → fertilised in lab → embryos implanted.

5. Muscle contraction — sliding filament

Skeletal muscle is striated, made of sarcomeres between Z-discs. Sarcomere components:

• Thick filaments (myosin): centre. Have heads sticking out.
• Thin filaments (actin): attached to Z-discs. Have tropomyosin and troponin regulating myosin binding sites.

Contraction cycle (each turn shortens sarcomere slightly):

1. Calcium release: Ca²⁺ from sarcoplasmic reticulum binds troponin → tropomyosin shifts → exposes myosin-binding sites on actin.
2. Cross-bridge formation: myosin head binds actin.
3. Power stroke: myosin head pivots, pulling actin toward sarcomere centre. ADP + Pi released.
4. Detachment: ATP binds myosin → head releases actin.
5. Recocking: ATP hydrolyses → myosin head returns to high-energy position, ready for next cycle.

When motor neuron stops firing, Ca²⁺ pumped back into SR → tropomyosin re-covers binding sites → muscle relaxes.

ATP requirement: contraction (cross-bridge cycling), relaxation (Ca²⁺ pump), maintaining membrane potential. Cramps occur when ATP runs out → cross-bridges stuck.

6. Worked Example

A patient with type 1 diabetes is given an insulin injection.

(a) Explain how insulin lowers blood glucose at the cellular level. (b) Compare and contrast type 1 vs type 2 diabetes. (c) Why must type 1 diabetics inject rather than take oral insulin?

Solution.

(a) Insulin (a peptide hormone, ~51 amino acids) binds insulin receptors on liver, muscle, and adipose cell membranes. Receptor activation triggers GLUT4 glucose transporters to move from intracellular vesicles to plasma membrane. GLUT4 then facilitates glucose uptake from blood into cells. Liver also stores glucose as glycogen. Net effect: blood glucose drops.

(b) Type 1: autoimmune destruction of pancreatic β-cells → no insulin production. Treatment: insulin replacement. Onset usually childhood. Type 2: insulin resistance — cells respond poorly to insulin. β-cells initially produce more, eventually decline. Treatment: lifestyle, oral hypoglycaemics, sometimes insulin. Onset usually adulthood, linked to obesity.

(c) Insulin is a peptide; oral insulin would be digested by stomach proteases (broken into amino acids, lose function). Injection bypasses the digestive system.

7. Common Pitfalls

• B cell vs T cell roles: B cells make antibodies (humoral); T cells either help (helper T) or kill (cytotoxic T). Don't conflate.
• ADH not insulin: ADH controls water reabsorption; insulin controls glucose. Different glands, different targets.
• Sliding filament — filaments don't change length: actin and myosin slide past each other. Sarcomere shortens but individual filaments don't.
• LH and FSH source: both from anterior pituitary, not the ovary.

8. Practice Questions

1. Why does a person with damaged kidneys sometimes need dialysis? Which nephron functions does dialysis replicate?
2. Trace what happens hormonally if a pregnant woman's corpus luteum is removed at week 3 vs week 12 of pregnancy.
3. Explain at the molecular level why rigor mortis (stiffness after death) occurs.

9. Quick Reference Cheatsheet

• B cell → antibody (humoral). Cytotoxic T → kill infected cells (cell-mediated).
• Vaccination → memory cells → faster secondary response.
• Nephron: ultrafiltration → selective reabsorption → Loop of Henle (counter-current) → DCT → collecting duct (ADH-regulated).
• Menstrual cycle: FSH → follicle/oestrogen → LH surge → ovulation → corpus luteum → progesterone.
• Muscle: ATP + Ca²⁺ → cross-bridge cycling → sarcomere shortens.

10. What's Next

Animal Physiology is the final HL extension topic. It connects to Topic 6 (SL Human Physiology) for digestive/respiratory/circulatory systems and Topic 8 (Metabolism) for muscle ATP needs. Use Ollie for any specific physiology problem.