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O&G VivasGynaecological health — menstrual disorders and androgen excess

O&G Vivas · Gynaecological health — menstrual disorders and androgen excess

Polycystic ovary syndrome — structured oral station (12 minutes)

FRANZCOG oral-format station on PCOS: the candidate confirms Rotterdam criteria verbatim, phenotypes the patient, walks the life-stage management ladder, addresses the cardiometabolic and psychological surveillance, and defends the OHSS-aware IVF pathway. Scored against the eight published RANZCOG oral domains.

clinical4 min readSource-verified ·

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FRANZCOGMRCOGABOG
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Target exams

FRANZCOGMRCOGABOG
Prompt
You are the gynaecology registrar in clinic. A 29-year-old presents with irregular cycles (every 40–60 days) since menarche, an mFG score of 9, BMI 31, and a transvaginal ultrasound showing 22 follicles (2–9 mm) per ovary. Morning 17-hydroxyprogesterone, TSH and prolactin are normal. The examiner will ask you to confirm the diagnosis, phenotype the patient, defend the management ladder, and address her psychological burden and her future fertility intentions. You may be shown a transvaginal ultrasound image of a polycystic ovary.

Station format

4 minutes reading, 12 minutes examination, 20 marks, global scoring. The eight published RANZCOG oral domains apply to every station: history and examination; investigations and interpreting results; treatment/management; clinical knowledge; complex, urgent or unusual clinical presentations; rapport with patient, support person or colleague; respect; communication skills. You are marked on how you behave, not only what you know. [2]

Reveal the examiner script and model responsesShowHide

Opening prompt — "What is your working diagnosis and why?"

Model response — Rotterdam verbatim: [1][2]

  • "She meets the Rotterdam 2003 criteria verbatim — any two of three, after exclusion of other aetiologies. She has all three: oligomenorrhoea (cycles 40–60 days), clinical hyperandrogenism (mFG 9, above the Caucasian threshold of 8), and polycystic ovarian morphology (22 follicles per ovary and ovarian volume 14 mL, exceeding the 2023 threshold of 20 follicles or 10 mL)."
  • "That makes her phenotype A — the classic, full phenotype — which carries the highest cardiometabolic and endometrial-cancer risk. The mimics have been excluded: normal 17-OHP excludes non-classic CAH, normal TSH and prolactin exclude thyroid and prolactin disease."[1]

Probe 1 — "What is the single most important rule-out test before labelling a woman with PCOS?"

  • "A morning 17-hydroxyprogesterone, drawn in the early follicular phase (day 3–5), fasting. A baseline over 6 nmol/L is confirmed by an ACTH stimulation test with a peak over 30–65 nmolL. Non-classic 21-hydroxylase deficiency affects 1 to 10% of hyperandrogenic women and is treated with glucocorticoids, not letrozole or the COCP — so labelling a woman with CAH as PCOS denies her the correct treatment."[4]

Probe 2 — "She is anxious and not seeking fertility. What is your management plan?"

  • "I frame PCOS as a chronic disease from the first visit. Lifestyle first — weight loss of 5 to 10% restores spontaneous ovulation in 30 to 60%. Then the combined oral contraceptive pill for cycle control, endometrial protection, acne and hirsutism — choosing one with an anti-androgenic progestogen like drospirenone or cyproterone. The hard threshold is withdrawal bleeding at least every 90 days to protect the endometrium."[2]
  • "And I do not forget the surveillance — annual HbA1c, lipids, blood pressure; baseline OGTT then 1 to 3-yearly; screen for NAFLD, sleep apnoea, and screen explicitly for depression and anxiety, which are 3 to 4 times more common in PCOS."[2]

Probe 3 — "Three years later she is seeking fertility and letrozole has failed. Describe the IVF pathway."

  • "PCOS patients carry a 2 to 3 times baseline risk of ovarian hyperstimulation syndrome because of their exaggerated follicular cohort. My OHSS-aware protocol combines four measures: a GnRH antagonist protocol rather than the long agonist; a GnRH-agonist trigger — triptorelin 0.2 mg — instead of hCG, which halves OHSS risk via its shorter luteinising half-life; a freeze-all strategy with elective single frozen embryo transfer in a subsequent cycle; and metformin 1500 to 2000 mg continued through stimulation. I cancel the cycle if more than 2 dominant follicles over 16 mm develop or oestradiol exceeds 1000 pg/mL."[2][5]

Probe 4 — "She asks if she is going to get diabetes. What do you say?"

  • "I am honest: her lifetime type 2 diabetes risk is around 4 times that of the background population, rising further with obesity. But it is not inevitable — lifestyle, metformin for impaired glucose tolerance, and annual surveillance substantially delay or prevent progression. I would do a baseline 75 g oral glucose tolerance test today and an HbA1c, and set up annual metabolic screening for life."[2]

Probe 5 — "She is frightened this means she will never have children. What do you say?"

This is a scored communication domain — demonstrate it out loud: [2]

  • Move to her eye level, use her name, acknowledge the fear: "PCOS is the commonest cause of fertility difficulty, and it is also one of the most treatable. Letrozole achieves live birth in around 27.5% per cycle, and cumulative rates reach 60 to 70% across cycles. If we need IVF, the modern protocols are very effective. Your fertility is something we plan around, not against. I am not going to send you away to cope alone."[2][3]

Probe 6 — "How would your approach differ if she were 14?"

  • "In an adolescent within 8 years of menarche, irregular cycles and polycystic morphology are physiologic, so I would require all three Rotterdam features before diagnosing PCOS. Treatment focuses on cycle control with the COCP and lifestyle; I avoid fertility drugs and reserve metformin for impaired glucose tolerance. The bar to diagnose and to intervene is higher."[2]
Obstetrics & Gynaecology Pro

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You have read the opening of this viva. The complete unit — every section and its primary-source references — is part of the Obstetrics & Gynaecology fellowship library.

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References5ShowHide
  1. [1]Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus Workshop Group. Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome. Fertil Steril, 2004.PMID 14711538
  2. [2]Teede HJ, Tay CT, Laven JJE, Dokras A, Moran LJ, Piltonen TT, et al. Recommendations from the 2023 International Evidence-based Guideline for the Assessment and Management of Polycystic Ovary Syndrome. Fertil Steril, 2023.PMID 37589624
  3. [3]Legro RS, Brzyski RG, Diamond MP, et al. Letrozole versus clomiphene for infertility in the polycystic ovary syndrome. N Engl J Med, 2014.PMID 25006718
  4. [4]Legro RS, Arslanian SA, Ehrmann DA, et al. Diagnosis and treatment of polycystic ovary syndrome: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab, 2013.PMID 24151290
  5. [5]Fauser BC, Tarlatzis BC, Rebar RW, et al. Consensus on women's health aspects of polycystic ovary syndrome (PCOS): the Amsterdam ESHRE/ASRM-Sponsored 3rd PCOS Consensus Workshop Group. Fertil Steril, 2012.PMID 22153789
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