Endocrine System

Question 1 (12 marks)

(a) [4]

• Fault is in the thyroid gland itself (primary hypothyroidism) (1)
• T4 is low, so the thyroid is failing to produce hormone (1)
• TSH is high — the pituitary is working and responding correctly by trying to stimulate the thyroid (1)
• TRH is high — hypothalamus also responding correctly; if the pituitary/hypothalamus were faulty, TSH/TRH would be LOW, not high (1)

(b) [4]

• Normally T4 exerts negative feedback, inhibiting the hypothalamus (TRH) and pituitary (TSH) (1)
• Because T4 is low, this inhibitory feedback is removed/reduced (1)
• So the hypothalamus releases more TRH (1)
• and the pituitary releases more TSH, in an attempt to drive the failing thyroid (1)

(c) [4]

• Oral thyroxine raises blood T4 to normal levels (1)
• Rising T4 restores negative feedback on the hypothalamus and pituitary (1)
• Therefore TSH falls / returns toward normal (1)
• and TRH falls / returns toward normal (1)

Question 2 (12 marks)

(a) [4]

• Insulin is a peptide/protein hormone (1)
• If swallowed, it would be digested/broken down by proteases (protein-digesting enzymes) in the stomach/gut and become inactive (1)
• Steroid hormones are lipid-based/derived from cholesterol and are not digested by these enzymes (1)
• Steroids can also cross the gut lining (lipid-soluble) and be absorbed intact, so can be taken orally (1)

(b) [6]

• Insulin (peptide): cannot cross the cell membrane (water-soluble) (1); binds to a receptor on the cell surface membrane (1); triggers a second-messenger/signal cascade → rapid response (e.g. glucose transporters moving to membrane) (1)
• Cortisol (steroid): lipid-soluble, crosses the plasma membrane (1); binds to an intracellular/cytoplasmic (or nuclear) receptor (1); the hormone-receptor complex acts on DNA to alter gene transcription/protein synthesis → slower response (1)

(c) [2]

• Insulin produces the faster onset (1)
• because it acts via existing surface receptors and second messengers/pre-made proteins, whereas cortisol must alter gene expression and make new proteins, which takes longer (1)

Question 3 (12 marks)

(a) [5]

• Hormone: insulin (1)
• Source: beta (β) cells of the islets of Langerhans in the pancreas (1)
• Rising blood glucose stimulates its release (1)
• Action 1: increases glucose uptake into cells (e.g. muscle/liver via glucose transporters) (1)
• Action 2: promotes conversion of glucose to glycogen (glycogenesis) in liver/muscle (1)

(b) [4]

• Person Y has insulin resistance — cells respond poorly to insulin (1)
• The pancreas secretes more insulin to compensate for the reduced sensitivity (1)
• But target cells fail to take up glucose despite the high insulin (1)
• So blood glucose remains elevated (characteristic of type 2 diabetes) (1)

(c) [3]

• Hormone: glucagon (1)
• (from alpha cells of the pancreas) — released when glucose falls (1)
• Stimulates breakdown of glycogen to glucose (glycogenolysis) / gluconeogenesis in the liver, raising blood glucose back to normal (1)

Question 4 (12 marks)

(a) [4]

• Hormone: adrenaline (epinephrine) (1)
• Released from the adrenal medulla (1)
• Classified as amino-acid-derived (not a steroid) (1)
• (it is water-soluble and acts via surface receptors — accept for the classification point) (1)

(b) [5]

• Hormone: cortisol (1)
• Hypothalamus releases CRH (corticotropin-releasing hormone) (1)
• CRH stimulates the anterior pituitary to release ACTH (1)
• ACTH stimulates the adrenal cortex to release cortisol (1)
• Cortisol then raises blood glucose (gluconeogenesis) and suppresses immune function; it also exerts negative feedback on hypothalamus/pituitary (1)

(c) [3]

• Immediate response: adrenaline is released directly (nervous stimulation of medulla) and acts via surface receptors/second messengers on pre-existing proteins → effect within seconds (1)
• Long-term response: cortisol is a steroid acting on gene transcription (1)
• New protein/enzyme synthesis takes time, so effects take minutes to hours (1)

Question 5 (12 marks)

(a) [3]

• The LH surge triggers ovulation — release of the mature egg from the follicle (1) (1 for "release of egg")
• LH is released from the anterior pituitary gland (1)

(b) [6]

• Normally, rising oestrogen (late follicular phase) triggers a surge in LH (positive feedback) (1)
• The pill keeps oestrogen and progesterone constantly high (1)
• Constantly high levels exert negative feedback on the hypothalamus and pituitary (1)
• This inhibits release of FSH and LH (1)
• Without an LH surge, ovulation does not occur (1)
• No egg released → cannot be fertilised → contraception achieved (1)

(c) [3]

• Falling progesterone means the uterine lining (endometrium) is no longer maintained (1)
• The lining breaks down and is shed → menstruation (1)
• The fall in progesterone also removes negative feedback, allowing FSH to rise and a new cycle to begin (1)

[
  {"claim": "Q1: Primary hypothyroidism pattern — low T4 with high TSH indicates thyroid gland fault (feedback disinhibited). Represent hormone levels: low T4 -> reduced feedback -> high TSH must be True.",
   "code": "T4_low=True; feedback_inhibition = not T4_low; TSH_high = not feedback_inhibition; thyroid_fault = T4_low and TSH_high; result = (thyroid_fault == True)"},
  {"claim": "Q1c: Giving thyroxine restores T4, so feedback returns and TSH falls.",
   "code": "T4_after=True; feedback_restored=T4_after; TSH_falls=feedback_restored; result = (TSH_falls == True)"},
  {"claim": "Q3b: Insulin resistance means high insulin but high glucose (glucose not lowered).",
   "code": "insulin_high=True; cells_respond=False; glucose_lowered = insulin_high and cells_respond; glucose_stays_high = not glucose_lowered; result = (glucose_stays_high == True)"},
  {"claim": "Q5b: Constant high oestrogen+progesterone -> negative feedback -> no LH surge -> no ovulation.",
   "code": "high_hormones=True; neg_feedback=high_hormones; LH_surge = not neg_feedback; ovulation = LH_surge; result = (ovulation == False)"}
]