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Q1: Definition, classification and the diagnostic reflex (2 min)
- Define menopause. The permanent cessation of menstruation, defined retrospectively as 12 consecutive months of amenorrhoea in a woman of the expected age without any other pathological or physiological cause.
- Average age and the abnormal thresholds? Average 50 to 52 years (range 45 to 55); early menopause is 40 to 45; premature ovarian insufficiency is before 40.
- The diagnostic reflex in a 51-year-old with hot flushes — do you measure FSH? No. Menopause is a clinical diagnosis in a woman over 45 with typical symptoms; FSH measurement is not routinely required and fluctuates wildly in the perimenopause.
- When DO you measure FSH? Under 45 with symptoms, after hysterectomy (no menstrual marker), suspected POI (over 25 IU/L on two samples 4 to 6 weeks apart), or when contraception can be stopped. Always exclude pregnancy first.
Q2: Pathophysiology — the 'why' behind every symptom (3 min)
- Walk me through the HPO axis in menopause. Depletion of the ovarian follicle pool → the ovary stops producing oestradiol and inhibin → loss of negative feedback → FSH (and LH) rise (FSH over 25 to 30 IU/L is diagnostic in a younger woman).
- Why does the perimenopause paradoxically show high oestradiol at times? The high FSH over-drives the few remaining follicles each cycle; inhibin B is low so FSH is unchecked; cycles are often anovulatory → the heavy irregular bleeding of the transition.
- Mechanism of the hot flush. Loss of oestradiol narrows the hypothalamic thermoneutral zone; small core-temperature rises trigger an exaggerated, noradrenergically mediated heat-dissipation response (sweating, flushing, palpitation, then a chill).
- Mechanism of bone loss. Oestrogen normally restrains osteoclasts via the RANKL / osteoprotegerin axis; loss of oestrogen → unopposed resorption — about 10 percent cortical and 15 percent trabecular loss in the first 5 years.
- Mechanism of GSM. Loss of oestrogen's trophic effect on the vulvar, vaginal and lower-urinary-tract epithelium → thinning, loss of glycogen and lactobacilli, raised vaginal pH (over 5), dryness, dyspareunia, recurrent UTI.
- Explain the 'timing hypothesis'. HRT initiated within 10 years of menopause or under age 60 has a neutral or favourable cardiovascular profile (slows early atherogenesis); the WHI excess cardiovascular risk applied principally to women starting over 60.
Q3: HRT — the uterus rule, the route, the progestogen (3 min)
- A woman with a uterus starts HRT — what is the non-negotiable rule? Oestrogen + a progestogen (or the levonorgestrel IUS). Unopposed systemic oestrogen causes endometrial hyperplasia and cancer.
- After hysterectomy? Oestrogen alone (add a progestogen transiently only if residual endometriosis).
- Which route of oestrogen, and why? Oral (convenient but higher VTE/stroke); transdermal patch or gel (preferred when VTE risk, migraine with aura, obesity, hypertriglyceridaemia, gallstones, smoking over 35 — bypasses the first-pass hepatic effect); vaginal (for GSM only, minimal systemic absorption).
- Which progestogen, and why? Micronised progesterone or dydrogesterone — neutral breast and vascular profile, preferred by NICE and NAMS. Medroxyprogesterone acetate was the WHI trial agent, less preferred. Norethisterone and the levonorgestrel IUS are practical alternatives.
- Cyclical versus continuous combined? Cyclical (sequential) — continuous oestrogen with a progestogen for 12 to 14 days each month — for the perimenopause and within 1 to 2 years of the last period. Continuous combined — daily oestrogen plus progestogen — for women more than 1 to 2 years postmenopausal (bleed-free after a few months).
- The perimenopausal woman who needs contraception? HRT does not suppress ovulation — add a separate contraceptive until 2 years of amenorrhoea under 50 or 1 year over 50; the COCP may be used off-label until 50 in non-smokers without contraindications.
Q4: Premature ovarian insufficiency and the contraindications (3 min)
- A 34-year-old amenorrhoeic woman with FSH 42 IU/L twice — diagnosis and management? Premature ovarian insufficiency. Work up (karyotype, FMR1 fragile-X premutation, adrenal and thyroid antibodies, pelvic ultrasound, baseline DEXA) and treat with combined HRT or the COCP until age 51 — this is physiological replacement and the risks quoted for older-start HRT do not apply. Fertility via oocyte donation IVF; contraception (spontaneous ovulation may resume).
- Absolute contraindications to systemic oestrogen? Current or past breast cancer, oestrogen-sensitive cancer, active liver disease, personal history of VTE or ischaemic stroke, unexplained vaginal bleeding until investigated, pregnancy.
- Breast cancer survivor with severe flushes on tamoxifen? Avoid systemic oestrogen; first-line non-hormonal — venlafaxine or escitalopram (avoid paroxetine — it inhibits CYP2D6 and reduces tamoxifen's activation), gabapentin, clonidine, CBT; vaginal oestrogen only with oncology input.
- What is compounded 'bioidentical' hormone therapy and what is the official position? A compounding pharmacy's individualised mix of oestrogen, progesterone and other hormones, titrated to salivary hormone levels. Not recommended by NAMS, NICE, IMS or EMAS — variable pharmacokinetics, no efficacy or safety data, and salivary monitoring is unreliable. Licensed micronised progesterone and 17-beta-oestradiol are themselves bioidentical and quality-controlled.
Q5: Red flags and the safety-net (2 min)
- A 56-year-old three years past her last period has one episode of painless vaginal bleeding — what do you do? Endometrial cancer until proven otherwise. Examine (speculum and bimanual), arrange transvaginal ultrasound, and endometrial biopsy if the endometrial thickness exceeds 4 to 5 mm; hysteroscopy with targeted biopsy if sampling is inadequate or bleeding recurs. About 5 to 10 percent of women with PMB have endometrial cancer.
- Unscheduled bleeding on HRT? Investigate the same way — never attribute it to the drug without excluding endometrial pathology.
- How long do you continue HRT and how do you stop? Individualised — review annually; the aim is the lowest effective dose for the shortest necessary time, but there is no mandatory stop-date; taper or stop abruptly when symptoms resolve (no safety requirement to wean, though tapering reduces rebound).
- Name the four landmark sources you would cite in an essay. WHI 2002 (PMID 12117397) — the original combined CEE+MPA trial; Manson 2013 (PMID 24084921) — the 13-year extended follow-up and the timing hypothesis; NAMS 2022 Position Statement (PMID 35797481) — current US guidance; Santoro JCEM 2021 (PMID 33095879) — the menopause transition review.