Membership of the Royal College of Obstetricians and Gynaecologists (MRCOG) Gynaecology: Benign, Menstrual and Reproductive Disorders Flashcards

24 sample cards from the Gynaecology: Benign, Menstrual and Reproductive Disorders deck

Sampled from the end of the deck, so these are different cards from the ones shown on the syllabus page.

1. Why and how is endometrial protection provided in women with PCOS?

   Chronic anovulation causes unopposed oestrogen and endometrial hyperplasia risk. Protection is achieved by inducing a withdrawal bleed at least every 3-4 months — via cyclical progestogens, the combined oral contraceptive pill, or the LNG-IUS.

2. What is the first-line agent for ovulation induction in PCOS-related anovulatory infertility?

   Letrozole (an aromatase inhibitor) is now first-line, having superseded clomifene citrate in many guidelines due to higher live birth rates. Metformin may be added, and gonadotrophins or laparoscopic ovarian drilling are second-line.

3. List the main causes of hyperprolactinaemia.

   Physiological (pregnancy, lactation, stress); pituitary tumours (prolactinoma — micro- or macroadenoma); drugs (antipsychotics, metoclopramide, antidepressants, oestrogens); primary hypothyroidism (raised TRH); stalk compression; chronic kidney disease; and macroprolactinaemia (biologically inactive).

4. How does hyperprolactinaemia cause amenorrhoea, and what is the first-line treatment for a prolactinoma?

   High prolactin suppresses GnRH pulsatility, lowering FSH/LH and causing hypogonadotrophic hypogonadism with amenorrhoea and galactorrhoea. First-line treatment is a dopamine agonist (cabergoline preferred, or bromocriptine), which lowers prolactin and shrinks the tumour; surgery is reserved for resistant or compressive cases.

5. What signs distinguish hirsutism from virilisation, and what does rapid virilisation suggest?

   Hirsutism is excess terminal hair in androgen-dependent areas (face, chest, abdomen). Virilisation adds signs of marked androgen excess: clitoromegaly, deepening voice, male-pattern balding, breast atrophy and increased muscle bulk. Rapid-onset virilisation with very high testosterone suggests an androgen-secreting ovarian or adrenal tumour.

6. What tool quantifies hirsutism and what testosterone level raises concern for a tumour?

   The modified Ferriman-Gallwey score grades terminal hair at 9 body sites (0-4 each); a score above the population threshold defines hirsutism. A total testosterone more than twice the upper limit of normal (often quoted as $>5\ \text{nmol/L}$) warrants urgent investigation for an androgen-secreting tumour.

7. What is the biochemical hallmark of non-classic (late-onset) congenital adrenal hyperplasia and how is it confirmed?

   21-hydroxylase deficiency causing raised 17-hydroxyprogesterone (especially an elevated early-morning level). Diagnosis is confirmed with a short Synacthen (ACTH stimulation) test showing an exaggerated 17-OHP rise. It can mimic PCOS with hirsutism and oligomenorrhoea.

8. Describe the cause and typical phenotype of complete androgen insensitivity syndrome (CAIS).

   X-linked loss-of-function mutation in the androgen receptor in a 46,XY individual. Testes produce testosterone and AMH, but tissues cannot respond to androgens: result is a female external phenotype, absent uterus and upper vagina (AMH-driven Müllerian regression), primary amenorrhoea, scant pubic/axillary hair, and intra-abdominal testes (gonadectomy advised due to malignancy risk).

9. In a 46,XX disorder of sexual development, what is the commonest cause of virilised/ambiguous genitalia at birth?

   Congenital adrenal hyperplasia, most often 21-hydroxylase deficiency. Cortisol deficiency drives ACTH and shunts steroidogenesis to androgens, virilising the external genitalia; the salt-wasting form also causes life-threatening hyponatraemia, hyperkalaemia and adrenal crisis in the neonate.

10. How is the menopause diagnosed and what defines perimenopause and premature menopause?

    Menopause is diagnosed clinically as 12 months of amenorrhoea after the final menstrual period (average age ~51 in the UK). Perimenopause is the symptomatic transition with irregular cycles. Premature menopause/POI is menopause before age 40. In women over 45 with typical symptoms, no blood tests are needed for diagnosis.

11. List the common symptoms of the menopause.

    Vasomotor symptoms (hot flushes, night sweats), genitourinary syndrome (vaginal dryness, dyspareunia, urinary frequency/urgency), sleep disturbance, mood changes/anxiety, reduced libido, joint aches, and irregular bleeding during the transition.

12. When is FSH measurement useful in diagnosing menopause/POI?

    FSH is used in women under 45 with suspected menopause, and is required to diagnose premature ovarian insufficiency: two elevated FSH levels (e.g. $>25\text{-}40\ \text{IU/L}$) measured 4-6 weeks apart, alongside amenorrhoea/oligomenorrhoea before age 40.

13. What are the principles of choosing HRT regimens (cyclical vs continuous; with vs without progestogen)?

    Women with a uterus need oestrogen plus a progestogen for endometrial protection; oestrogen-only HRT is given only after hysterectomy. Use sequential (cyclical) combined HRT if perimenopausal/still bleeding, and continuous combined HRT if postmenopausal (>1 year amenorrhoea) to give a bleed-free regimen.

14. What are the main benefits and key risks of HRT?

    Benefits: relieves vasomotor and genitourinary symptoms, improves quality of life, and reduces osteoporotic fracture risk. Risks: oral oestrogen increases VTE risk (transdermal does not increase baseline risk); combined HRT slightly increases breast cancer risk (duration-related); unopposed oestrogen increases endometrial cancer risk.

15. How does transdermal differ from oral oestrogen regarding VTE and stroke risk?

    Transdermal oestrogen avoids hepatic first-pass metabolism and does not increase the risk of venous thromboembolism or stroke above baseline, so it is preferred in women at higher VTE/cardiovascular risk, those who are obese, or who have migraine.

16. What is premature ovarian insufficiency (POI) and what are its major causes?

    Loss of ovarian function before age 40, with amenorrhoea/oligomenorrhoea and raised FSH on two occasions. Causes: idiopathic (commonest), genetic (Turner syndrome, fragile X premutation), autoimmune, and iatrogenic (chemotherapy, radiotherapy, bilateral oophorectomy).

17. Why is hormone therapy recommended in POI, and until what age?

    To control symptoms and, crucially, to protect long-term bone health and cardiovascular health from premature oestrogen deficiency. HRT (or the combined pill) is advised at least until the average age of natural menopause (~51 years); it does not raise breast cancer risk above that of an age-matched menstruating woman.

18. How is osteoporosis defined by bone mineral density (DXA T-score)?

    Using DXA T-scores: normal is $T \geq -1.0$; osteopenia is $-2.5 < T < -1.0$; osteoporosis is $T \leq -2.5$; established (severe) osteoporosis is $T \leq -2.5$ with one or more fragility fractures.

19. What are the first-line pharmacological treatment and key lifestyle measures for postmenopausal osteoporosis?

    First-line: bisphosphonates (e.g. oral alendronate/risedronate) which inhibit osteoclastic bone resorption. Adjuncts: adequate calcium and vitamin D, weight-bearing exercise, smoking cessation, reduced alcohol, and fall prevention. HRT also preserves bone and is useful around the menopause.

20. What is the commonest cause of prepubertal vaginal discharge, and what is a key red flag to exclude?

    Non-specific vulvovaginitis is the commonest cause, due to thin, unoestrogenised vulval skin, poor hygiene and the neutral vaginal pH; managed with hygiene advice and barrier emollients. A persistent, blood-stained or foul discharge raises suspicion of a retained vaginal foreign body, and any discharge should prompt consideration of sexual abuse.

21. What is labial adhesion (fusion) in prepubertal girls and how is it managed?

    Midline fusion of the labia minora due to low oestrogen and minor inflammation, often asymptomatic and found incidentally. Most resolve spontaneously at puberty; symptomatic cases (recurrent infections, dribbling of urine) are treated with topical oestrogen cream, with surgical separation reserved for refractory cases.

22. Describe the normal sequence and Tanner staging of female puberty.

    Sequence: thelarche (breast budding, the first sign) → adrenarche/pubarche (pubic hair) → growth spurt → menarche (last, ~2-2.5 years after thelarche). Tanner stages B1-B5 grade breast development and PH1-PH5 grade pubic hair. Menarche typically occurs at Tanner breast stage 4.

23. Differentiate precocious puberty from delayed puberty by age and define central (true) precocious puberty.

    Precocious puberty: onset of secondary sexual characteristics before age 8 in girls. Delayed puberty: absence of breast development by age 13 (or no menarche by 15). Central (true, GnRH-dependent) precocious puberty is premature activation of the hypothalamic-pituitary-gonadal axis (gonadotrophin-dependent), most often idiopathic in girls; peripheral precocious puberty is gonadotrophin-independent.

24. What are the UK contraceptive considerations for adolescents and the legal framework for under-16s?

    Long-acting reversible contraception (implant, IUS/IUD) is encouraged as it is most effective. Provision to under-16s relies on Fraser guidelines: the young person understands the advice, cannot be persuaded to inform parents, is likely to have intercourse regardless, and their physical/mental health or best interests require treatment without parental consent. Always assess for safeguarding/exploitation.

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