Endocrine System

Question 1 (10 marks)

(a) Endocrine vs exocrine (6 — 1 mark per correct contrast point, max 6):

Why: the defining structural difference (ducts vs bloodstream) drives all the functional differences — blood distribution means widespread, slower, sustained action.

(b) Pancreas as mixed gland (4):

• "Mixed" = has both endocrine and exocrine functions (1).
• Endocrine: islets of Langerhans secrete insulin/glucagon into the blood (1) — no duct (1).
• Exocrine: acinar cells secrete digestive enzymes/pancreatic juice (amylase, lipase, trypsinogen) into the duodenum via the pancreatic duct (1).

Question 2 (12 marks)

(a) Two mechanisms traced (8):

Steroid hormone (lipid-soluble) — 4 marks:

1. Being lipid-soluble, it diffuses directly through the phospholipid plasma membrane (1).
2. Binds an intracellular / cytoplasmic (or nuclear) receptor forming a hormone–receptor complex (1).
3. Complex enters nucleus and binds DNA/response elements, acting as a transcription factor (1).
4. Alters gene transcription → mRNA → new protein synthesis = cellular response (1).

Peptide hormone (water-soluble) — 4 marks:

1. Being water-soluble it cannot cross the membrane; binds a cell-surface receptor (1).
2. Activates a membrane transducer/G-protein → enzyme (e.g. adenylate cyclase) (1).
3. Produces a second messenger (e.g. cAMP) inside the cell (1).
4. Second messenger activates a cascade (kinases) → activates existing enzymes = response (1).

Why they differ: driven by solubility. Lipid-soluble steroids pass the membrane and act on genes directly; water-soluble peptides are blocked by the membrane, so they need a surface receptor + second-messenger relay.

(b) Slower but longer-lasting (4):

• Steroids act via new gene expression/protein synthesis, which takes time to occur (1) → slow onset (1).
• The newly made proteins persist, and the hormone–receptor complex has lasting genomic effects (1) → prolonged action, whereas peptide second-messenger cascades are quickly reversed/degraded (1).

Question 3 (10 marks)

Pathway (6):

$\text{Hypothalamus} \xrightarrow{\text{TRH}} \text{Anterior pituitary} \xrightarrow{\text{TSH}} \text{Thyroid gland} \xrightarrow{T_3/T_4} \text{Target tissues (↑metabolism)}$

• Hypothalamus releases TRH (thyrotropin-releasing hormone) (1) → to anterior pituitary (1).
• Anterior pituitary releases TSH (thyroid-stimulating hormone) (1) → to thyroid (1).
• Thyroid releases thyroxine T₄ / triiodothyronine T₃ (1) → act on tissues raising metabolic rate (1).

Negative feedback (4):

• Rising T₃/T₄ in blood is detected and inhibits the hypothalamus (less TRH) and anterior pituitary (less TSH) (2 — 1 each site).
• Less TSH → thyroid secretes less T₃/T₄ (1).
• This keeps hormone level oscillating around a set-point, preventing over/under-production = homeostatic stability (1).

Question 4 (12 marks)

(a) After the meal — high glucose (6):

• Hormone: insulin (1), secreted by β-cells of islets of Langerhans (1).
• Actions (any 3, 1 each):
  • Increases glucose uptake into cells (GLUT4) (1)
  • Stimulates glycogenesis — glucose → glycogen in liver/muscle (1)
  • Promotes conversion to fat / lipogenesis and protein synthesis (1)
  • Inhibits gluconeogenesis (1)

(b) Overnight fast — low glucose (4):

• Hormone: glucagon (1), from α-cells of islets of Langerhans (1).
• Actions (2, 1 each):
  • Glycogenolysis — glycogen → glucose in liver (1)
  • Gluconeogenesis — new glucose from amino acids/glycerol (1)

(c) Antagonistic pair (2):

• They have opposite effects on blood glucose (insulin lowers, glucagon raises) (1); balancing the two around a set-point maintains stable blood glucose = homeostasis via negative feedback (1).

Question 5 (8 marks)

(a) Short vs long term (6):

• Short-term (fight-or-flight): adrenaline (epinephrine) + noradrenaline (1) from the adrenal medulla (1); rapid effects — ↑heart rate, ↑glucose release, bronchodilation, pupil dilation (1).
• Long-term: cortisol (glucocorticoids) (and aldosterone) (1) from the adrenal cortex (1); slower — sustained gluconeogenesis, protein/fat breakdown, ↑blood glucose (1).

(b) Harm of prolonged cortisol (2): suppresses the immune system (raises infection risk) / causes muscle wasting / raises blood pressure / persistent hyperglycaemia — any valid, well-explained point (2).

Question 6 (8 marks)

Hormones & sources (4 — 1 each):

• FSH — anterior pituitary; stimulates follicle growth (1).
• LH — anterior pituitary; triggers ovulation, forms corpus luteum (1).
• Oestrogen — developing follicle (ovary); repairs/thickens endometrium (1).
• Progesterone — corpus luteum (ovary); maintains endometrium (1).

Ovulation trigger — feedback switch (4):

• In the follicular phase, low/moderate oestrogen exerts negative feedback, keeping FSH/LH low (1).
• As the follicle matures, oestrogen rises to a high threshold level (1).
• High oestrogen now exerts positive feedback on the hypothalamus/pituitary (1).
• This causes a sharp LH surge (and FSH) ~day 14 → ovulation (release of the egg) (1).

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  {"claim":"Menstrual cycle is ~28 days with ovulation at midpoint (~day 14)","code":"cycle_length=28; ovulation_day=cycle_length/2; result = (ovulation_day==14)"},
  {"claim":"Q4 mark breakdown sums to 12","code":"result = (6+4+2==12)"},
  {"claim":"Total paper marks sum to 60","code":"result = (10+12+10+12+8+8==60)"},
  {"claim":"Insulin and glucagon act antagonistically: net effect of both balanced is zero change in set-point direction","code":"insulin_effect=-1; glucagon_effect=+1; result = (insulin_effect+glucagon_effect==0)"}
]