Polycystic ovary syndrome — structured SAQ (15 marks)

(a) Rotterdam criteria verbatim and phenotype (3 marks)

One mark per point, maximum three. ^[1][2]

• Rotterdam 2003 verbatim: the syndrome is present when two of the following three are present, after exclusion of other aetiologies (congenital adrenal hyperplasia, androgen-secreting tumours, Cushing's syndrome): (1) oligo-anovulation; (2) hyperandrogenism (clinical or biochemical); (3) polycystic ovarian morphology on ultrasound.
• This patient meets all three: (1) oligomenorrhoea (cycles 40–60 days); (2) clinical hyperandrogenism (mFG 9, above the Caucasian threshold of 8); (3) PCOM (22 follicles per ovary and ovarian volume 14 mL, exceeding the 2023 threshold of 20 follicles or 10 mL).
• Phenotype A (classic, full phenotype) — hyperandrogenism + anovulation + PCOM — the phenotype carrying the highest cardiometabolic and endometrial-cancer risk.^[1]

(b) Lifelong cardiometabolic and psychological surveillance (4 marks)

One mark per surveillance domain. ^[2]

• Glycaemic: annual HbA1c and/or fasting glucose for life; baseline 75 g 2-hour OGTT, then every 1–3 years (more frequently if obese, gaining weight, or with a first-degree family history of T2DM). Lifetime T2DM risk is around 4x.
• Lipid and cardiovascular: lipid profile every 1–2 years; blood pressure at every visit. Subclinical atherosclerosis and later-life cardiovascular event risk are elevated.
• Hepatic and sleep: ALT/AST for NAFLD (present in 30–60%); screen for obstructive sleep apnoea with STOP-BANG.
• Psychological and oncological: screen for depression, anxiety and eating disorders (PHQ-9, GAD-7) at every visit — 3–4x more common in PCOS. Counsel on the ~3x endometrial-cancer risk (up to 9x with obesity) and ensure regular withdrawal bleeding or use the COCP.^[2]

(c) OHSS-aware IVF pathway (5 marks)

One mark per measure, maximum five. ^[2][5]

• Frame the risk: PCOS patients carry a 2–3x baseline OHSS risk because of the exaggerated follicular cohort.
• GnRH antagonist protocol (not the long agonist protocol) — shorter gonadotrophin exposure, lower follicular synchrony.
• GnRH-agonist trigger (triptorelin 0.2 mg) instead of hCG for final oocyte maturation — the shorter luteinising half-life halves OHSS risk.
• Freeze-all strategy with elective single frozen embryo transfer in a subsequent cycle, separating stimulation from implantation.
• Metformin 1500–2000 mg daily continued through stimulation — independently reduces OHSS risk.
• Cycle cancellation thresholds: apply strict cancellation rules for excessive follicular response.^[5]

(d) The single most important rule-out test (3 marks)

One mark per point. ^[4]

• Morning seventeen-hydroxyprogesterone (seventeen-hydroxyprogesterone), drawn in the early follicular phase (day 3–5), fasting, in the morning (peak ACTH).
• Rationale: non-classic 21-hydroxylase deficiency (congenital adrenal hyperplasia) affects 1–10% of hyperandrogenic women and mimics PCOS, but is treated with glucocorticoids (to suppress ACTH-driven androgen excess), not letrozole or the COCP. Labelling a woman with CAH as PCOS denies her the correct treatment.
• Interpretation: a raised baseline requires an ACTH (Synacthen) stimulation test with confirmation of the stimulated peak. Note that seventeen-hydroxyprogesterone is falsely elevated in the luteal phase and in pregnancy — timing matters.^[4]