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DSE Biology Diagnostic: Human Reproduction and Homeostasis

Unit Test 1: Hormonal Control of the Menstrual Cycle​

Question

The menstrual cycle is controlled by four main hormones: FSH, LH, oestrogen, and progesterone.

(a) Describe the role of FSH in the menstrual cycle and explain how it is involved in follicle development. [2 marks]

(b) Describe the role of LH and explain the significance of the "LH surge" around day 14. [3 marks]

(c) The graph below shows the blood concentration of oestrogen and progesterone during a typical 28-day menstrual cycle. There are two peaks of oestrogen: one around day 12--13 and another smaller rise around day 21. Explain the hormonal mechanism responsible for the first peak of oestrogen and explain why this peak leads to the LH surge. [4 marks]

Worked Solution

(a) FSH (follicle-stimulating hormone) is secreted by the anterior pituitary gland. It stimulates the development of a Graafian follicle in the ovary and stimulates the follicle cells to produce oestrogen.

(b) LH (luteinising hormone) is secreted by the anterior pituitary gland. The LH surge (a sharp increase in LH concentration around day 14) triggers ovulation: the release of the secondary oocyte from the Graafian follicle. After ovulation, LH also stimulates the remnants of the follicle to develop into the corpus luteum, which secretes progesterone.

(c) The first oestrogen peak (around day 12--13) is caused by the developing Graafian follicle, which is stimulated by FSH to produce increasing amounts of oestrogen.

Mechanism of the LH surge: Initially, oestrogen has a negative feedback effect on FSH and LH secretion, keeping their levels relatively low. However, when oestrogen concentration rises above a critical threshold (high level sustained for approximately 36 hours), the feedback switches to positive feedback: the high oestrogen concentration now stimulates the anterior pituitary to secrete more LH (and also more FSH). This positive feedback loop causes a rapid and large increase in LH -- the LH surge -- which triggers ovulation.

Unit Test 2: Blood Glucose Regulation​

Question

After a meal rich in carbohydrates, blood glucose concentration rises. The body responds to return blood glucose to normal (approximately 90 mg/100 cm3^{3}).

(a) Describe how the pancreas detects the rise in blood glucose concentration and the hormonal response that follows. [3 marks]

(b) Explain how insulin lowers blood glucose concentration. Your answer should include the effect on (i) liver cells, (ii) muscle cells, and (iii) body cells in general. [4 marks]

(c) If blood glucose concentration falls too low (hypoglycaemia), the pancreas secretes glucagon. Describe two ways in which glucagon raises blood glucose concentration. [3 marks]

Worked Solution

(a) The pancreas acts as both an endocrine gland and a receptor. When blood glucose concentration rises above normal, this is detected by the islets of Langerhans in the pancreas. Specifically, the beta (β\beta) cells of the islets detect the elevated glucose and respond by secreting more insulin into the bloodstream.

(b) Insulin lowers blood glucose by:

(i) Liver cells: Insulin stimulates hepatocytes to convert excess glucose into glycogen (glycogenesis) for storage. It also inhibits the breakdown of glycogen into glucose (glycogenolysis) and inhibits gluconeogenesis (the conversion of amino acids and other non-carbohydrates into glucose).

(ii) Muscle cells: Insulin stimulates muscle cells to take up glucose from the blood (by increasing the number of glucose transporter proteins, GLUT4, in the cell membrane) and to convert it into glycogen for storage.

(iii) General body cells: Insulin increases the permeability of cell membranes to glucose, allowing more glucose to enter cells by facilitated diffusion. Inside cells, glucose is used in respiration to produce ATP, lowering blood glucose concentration.

(c) Glucagon raises blood glucose by:

  1. Glycogenolysis: Glucagon stimulates liver cells to break down stored glycogen into glucose, which is released into the bloodstream.
  2. Gluconeogenesis: Glucagon stimulates liver cells to convert amino acids (and other non-carbohydrate sources such as lactate) into glucose, which is released into the blood.

Unit Test 3: Immune Response -- Primary vs Secondary​

Question

A person is vaccinated against a specific bacterial pathogen. Six weeks later, the same person is exposed to the live pathogen but does not become ill.

(a) Describe the primary immune response that occurs after vaccination, including the roles of B-lymphocytes, plasma cells, and memory cells. [4 marks]

(b) Explain why the person does not become ill after exposure to the live pathogen six weeks later, referring to the secondary immune response. [4 marks]

(c) A student claims that antibiotics would be an effective treatment if the person had become ill. Evaluate this claim, distinguishing between bacterial and viral pathogens. [3 marks]

Worked Solution

(a) Primary immune response after vaccination:

  1. The vaccine contains antigens from the pathogen (or a weakened/inactivated form of the pathogen).
  2. Macrophages (phagocytes) engulf and process the antigens, presenting them on their cell surface (antigen presentation).
  3. A specific B-lymphocyte (B-cell) with complementary surface receptors (antibodies) binds to the antigen. This activates the B-cell.
  4. The activated B-cell divides by mitosis (clonal selection) to produce a clone of identical B-cells.
  5. Some of these develop into plasma cells, which secrete large quantities of specific antibodies that bind to the antigen, marking the pathogen for destruction by phagocytes (opsonisation).
  6. Other B-cells develop into memory cells, which remain in the blood for a long time (years or even a lifetime), providing immunological memory.

(b) Upon exposure to the live pathogen six weeks later:

The memory B-cells (from the vaccination) recognise the specific antigens on the pathogen. They rapidly divide and differentiate into plasma cells, producing a large quantity of antibodies in a very short time. This is the secondary immune response:

  • The response is faster (antibodies are produced within hours rather than days).
  • The response is stronger (a much larger quantity of antibodies is produced).
  • The antibodies quickly bind to and neutralise the pathogen before it can multiply and cause illness (the pathogen is destroyed before the population reaches the threshold needed to cause symptoms).

(c) The claim is partially correct but imprecise. Antibiotics are effective against bacterial pathogens because they target specific bacterial structures or processes (e.g. cell wall synthesis, protein synthesis on 70S ribosomes, DNA replication). They can kill or inhibit the growth of bacteria.

However, antibiotics are not effective against viral pathogens because viruses lack the structures and metabolic processes that antibiotics target (viruses have no cell wall, no ribosomes, and replicate inside host cells). For viral infections, the immune system must be relied upon, or antiviral drugs may be used.

The student should have specified that antibiotics are only effective against bacterial infections, not all pathogens.

Integration Test 1: Negative Feedback in Thermoregulation​

Question

(a) Describe how the body responds to a decrease in core body temperature (below 37∘C37^{\circ}C), including the role of the hypothalamus and the effectors involved. [5 marks]

(b) Explain why the thermoregulatory mechanism is an example of negative feedback. [2 marks]

(c) A person with a fever has a body temperature of 39.5∘C39.5^{\circ}C. Explain why the body does not trigger the cooling mechanisms described in part (a) to bring the temperature back to 37∘C37^{\circ}C. [3 marks]

Worked Solution

(a) Response to decreased core body temperature:

  1. Thermoreceptors in the skin detect the decrease in temperature and send nerve impulses to the hypothalamus (the body's thermoregulatory centre in the brain).

  2. The hypothalamus sends nerve impulses to various effectors:

    • Vasoconstriction: Arterioles near the skin surface constrict (narrow), reducing blood flow to the skin surface. This reduces heat loss by radiation and convection from the skin.

    • Piloerection: Hair erector muscles contract, causing body hairs to stand erect. This traps a layer of insulating air next to the skin, reducing heat loss.

    • Shivering: Skeletal muscles undergo rapid, involuntary contractions (shivering). This increases the rate of respiration in muscle cells, generating more heat as a by-product.

    • Increased metabolic rate: The hypothalamus stimulates the thyroid gland (via TSH from the anterior pituitary) to release more thyroxine, which increases the basal metabolic rate, generating more heat from cellular respiration.

    • Behavioural responses: The person may curl up, put on more clothes, or seek warmth.

(b) This is negative feedback because the body's response (warming mechanisms) works to reverse the change that triggered it. The initial stimulus (a decrease in temperature) is counteracted by the response (heat-generating and heat-conserving mechanisms), bringing the temperature back towards the normal set point (37∘C37^{\circ}C). Once the temperature returns to normal, the thermoreceptors stop signalling and the response ceases. The feedback opposes the original change.

(c) During a fever, the set point of the hypothalamus is raised (e.g. from 37∘C37^{\circ}C to 39.5∘C39.5^{\circ}C) by chemicals called pyrogens (released by white blood cells in response to infection). The hypothalamus now considers 39.5∘C39.5^{\circ}C as the "normal" temperature.

At the new set point, the body actually triggers heat-generating mechanisms (shivering, vasoconstriction) to raise the body temperature to 39.5∘C39.5^{\circ}C, rather than cooling mechanisms. The cooling mechanisms are only triggered when the temperature exceeds the new set point (above 39.5∘C39.5^{\circ}C). When the infection is cleared and pyrogens are removed, the set point returns to 37∘C37^{\circ}C and the body triggers cooling (sweating, vasodilation) to bring the temperature back down.

Integration Test 2: Reproductive Systems and Gametogenesis​

Question

(a) Describe the process of spermatogenesis in the seminiferous tubules of the testis, from the division of a spermatogonium to the formation of spermatozoa. Include the type of cell division involved. [4 marks]

(b) Compare the products of meiosis in spermatogenesis and oogenesis with respect to (i) the number of functional gametes produced, and (ii) the timing of meiosis completion. [3 marks]

(c) After fertilisation, the zygote undergoes a series of mitotic divisions (cleavage) to form a blastocyst. Describe the structure of the blastocyst and explain the role of the trophoblast in implantation. [4 marks]

Worked Solution

(a) Spermatogenesis:

  1. Spermatogonium (diploid, 2n2n) divides by mitosis to produce more spermatogonia (ensuring a continuous supply).
  2. A spermatogonium grows and becomes a primary spermatocyte (diploid, 2n2n).
  3. The primary spermatocyte undergoes the first meiotic division (meiosis I) to produce two secondary spermatocytes (haploid, nn). This is the reduction division.
  4. Each secondary spermatocyte undergoes the second meiotic division (meiosis II) to produce two spermatids (haploid, nn). Each primary spermatocyte thus produces four spermatids.
  5. The spermatids undergo differentiation (maturation) into spermatozoa (sperm cells), developing a tail (flagellum) for motility, an acrosome containing digestive enzymes, and a streamlined head.

(b) Comparison:

(i) Number of functional gametes:

  • Spermatogenesis: Four functional spermatozoa are produced from each primary spermatocyte.
  • Oogenesis: Only one functional ovum (secondary oocyte) is produced from each primary oocyte. The other three cells are polar bodies, which degenerate. This ensures the ovum retains maximum cytoplasm and nutrient reserves.

(ii) Timing of meiosis completion:

  • Spermatogenesis: Begins at puberty and is continuous throughout life. The entire process (from spermatogonium to spermatozoon) takes approximately 64--74 days.
  • Oogenesis: Begins before birth (during fetal development). Primary oocytes begin meiosis I but arrest at prophase I. Meiosis I is completed at ovulation (one per menstrual cycle), and meiosis II is completed only if fertilisation occurs. The process spans many years.

(c) Blastocyst structure: By approximately day 5 after fertilisation, the embryo has developed into a blastocyst, a hollow ball of cells consisting of:

  • An outer layer of cells called the trophoblast
  • An inner cell mass (embryoblast) at one pole
  • A fluid-filled cavity (blastocoel) in the centre

Role of the trophoblast in implantation:

  1. The trophoblast cells secrete enzymes that digest and break down the endometrium (uterine lining), allowing the blastocyst to burrow into and embed itself in the uterine wall.
  2. The trophoblast develops finger-like projections (chorionic villi) that increase the surface area for exchange and eventually contribute to the formation of the placenta.
  3. The trophoblast produces hCG (human chorionic gonadotropin), which maintains the corpus luteum (and thus progesterone secretion) to sustain the endometrium during early pregnancy.

Integration Test 3: Homeostasis and Immune System Interaction​

Question

A person has type 1 diabetes mellitus, in which the beta cells of the pancreas are destroyed by the body's own immune system (an autoimmune disease).

(a) Explain why type 1 diabetes is classified as an autoimmune disease, and describe the normal role of T-killer cells that is going wrong in this condition. [3 marks]

(b) Explain the consequences of beta cell destruction on blood glucose regulation, and describe how a person with type 1 diabetes must manage their condition. [4 marks]

(c) People with type 1 diabetes are advised to monitor their blood glucose levels regularly and to be aware of the symptoms of hypoglycaemia (low blood glucose). Describe three symptoms of hypoglycaemia and explain the physiological basis for one of them. [4 marks]

Worked Solution

(a) An autoimmune disease is one in which the body's immune system mistakenly attacks and destroys the body's own healthy tissues, failing to distinguish between self and non-self.

In type 1 diabetes, T-killer cells (cytotoxic T-cells) -- which normally recognise and destroy virus-infected cells or abnormal cells -- incorrectly identify the beta cells of the islets of Langerhans as "foreign" or abnormal. The T-killer cells bind to the beta cells and release enzymes (perforins) that create pores in the beta cell membranes, causing the beta cells to lyse and die. This destroys the body's ability to produce insulin.

(b) Consequences of beta cell destruction:

  • Without beta cells, the pancreas cannot produce insulin.
  • Without insulin, blood glucose concentration cannot be regulated. After eating, blood glucose rises to dangerously high levels (hyperglycaemia) because glucose cannot enter cells efficiently and the liver continues to produce glucose.
  • Excess glucose is excreted in urine (glycosuria), leading to frequent urination and dehydration. Long-term complications include damage to blood vessels, nerves, kidneys, and eyes.

Management:

  • Regular insulin injections (subcutaneous) to replace the missing insulin. The dose must be matched to food intake and activity level.
  • Regular monitoring of blood glucose levels using a glucose meter.
  • Careful dietary management (controlling carbohydrate intake).
  • Regular exercise to improve glucose uptake by muscles.

(c) Three symptoms of hypoglycaemia:

  1. Trembling/shaking
  2. Sweating
  3. Confusion/dizziness
  4. Rapid heartbeat (palpitations)
  5. Irritability
  6. Blurred vision

Physiological basis of trembling: When blood glucose falls too low, the brain (which relies almost exclusively on glucose as its energy source) detects the energy deficit. The hypothalamus triggers the sympathetic nervous system as an emergency response, causing the release of adrenaline. Adrenaline stimulates glycogenolysis (breakdown of glycogen to glucose) in the liver and muscles. The adrenaline also causes widespread effects including increased heart rate, sweating, and involuntary muscle contractions (trembling/shaking) as the body attempts to generate heat and mobilise energy reserves rapidly.