GC114 Climacteric Symptoms Menopause And Related Illness; Amenorrhoea
Climacteric symptoms encompass the vasomotor, psychological, and urogenital manifestations arising from ovarian hormone decline during the menopausal transition, while amenorrhoea refers to the absence of menstruation due to physiological, pathological, or iatrogenic causes.
Climacteric Symptoms, Menopause & Related Illness; Amenorrhoea
This lecture is a two-part powerhouse that covers the full spectrum of absent periods — from the teenager who has never menstruated, to the woman whose periods stopped unexpectedly, to the woman going through the menopausal transition. These are bread-and-butter O&G topics that examiners love because they test your ability to think systematically through the hypothalamic-pituitary-ovarian (HPO) axis, correlate hormone patterns with diagnoses, and counsel patients about hormone replacement therapy (HRT) — a topic with nuanced risks and benefits.
Learning Objectives [1]:
Amenorrhoea:
- Define primary and secondary amenorrhoea
- Know the causes (organized by anatomical level)
- Take appropriate history, examine, investigate systematically
- Describe management principles for each cause
Menopause & Climacteric:
- Define climacteric, menopause, perimenopause
- Describe symptoms and long-term health consequences
- Manage climacteric symptoms including HRT risks/benefits
- Understand HRT regimens and routes of administration
How this fits clinically and in exams: Amenorrhoea questions appear almost every year in the Fourth Summative — as EMQs matching clinical scenarios to diagnoses, SAQs asking for investigations/management, and MCQs testing definitions and hormone patterns. Menopause/HRT questions test your understanding of the WHI trial, contraindications, and non-hormonal alternatives. The 2022 past paper had a full EMQ section on amenorrhoea [9]. The 2024 MCQ tested sexual dysfunction in menopausal women [10].
Part 1: Amenorrhoea
Amenorrhoea is the absence of menstrual periods. It is a SYMPTOM, NOT a diagnosis. [1]
This is a critical exam point. You must always look for the underlying cause. Think of amenorrhoea like "anaemia" — it tells you something is wrong, but you need to find out what.
| Type | Definition | Key Notes |
|---|---|---|
| Primary amenorrhoea | Absence of menstruation by age 16 | Investigate by age 14 if NO secondary sexual characteristics [1] |
| Secondary amenorrhoea | Absence of menstruation for 6 months in a woman who has previously menstruated | Must have previously had functioning ovaries, responsive endometrium, and patent outflow tract [1] |
Critical Concept
All causes of secondary amenorrhoea can also present as primary amenorrhoea. For example, PCOS can present as primary amenorrhoea if it suppresses ovulation from the start. However, with primary amenorrhoea, you must ALSO think about congenital/genetic abnormalities (e.g., Turner syndrome, AIS, Müllerian anomalies) that wouldn't cause secondary amenorrhoea. [1]
Why these definitions matter from first principles:
- For menstruation to occur, you need: (1) a functioning hypothalamus pulsing GnRH, (2) a responsive anterior pituitary making FSH/LH, (3) ovaries that respond to gonadotrophins to produce oestrogen and progesterone, (4) an endometrium that proliferates and then sheds, and (5) a patent outflow tract (cervix, vagina) for blood to exit.
- A problem at ANY of these levels causes amenorrhoea. This is why we organize causes anatomically.
1.2 Causes of Amenorrhoea — Systematic Classification
Causes are organized by level: Physiological → Hypothalamus/CNS → Pituitary → Ovary → Outflow tract/Uterus → Thyroid → Adrenal [1]
Always rule out pregnancy first! [1] — This is literally a standalone slide in the lecture. In an OSCE, if you forget to ask about pregnancy or order a pregnancy test, you will lose marks.
| Physiological Cause | Explanation |
|---|---|
| Pre-pubertal / constitutional delay | Normal variant; puberty just hasn't started yet |
| Pregnancy & lactation | hCG maintains corpus luteum → high progesterone suppresses HPO axis. Prolactin during lactation suppresses GnRH |
| Certain contraceptives | Depo-Provera, hormonal IUDs, continuous COC — all suppress the HPO axis or thin the endometrium |
| Postmenopausal | Ovarian follicle depletion → no more oestrogen production |
CNS effects: weight loss, over-exercise, stress, eating disorders (e.g., anorexia nervosa) [1]
Why these cause amenorrhoea: The hypothalamus is exquisitely sensitive to energy balance. When the body perceives energy deficit (low body fat, excessive exercise, psychological stress), it suppresses GnRH pulsatility. This is an evolutionarily adaptive mechanism — the body "decides" it's not a good time to reproduce. The result: low FSH, low LH, low oestradiol → functional hypothalamic amenorrhoea.
| Hypothalamic Cause | Key Features |
|---|---|
| Functional (weight loss, exercise, stress, anorexia nervosa) | Most common hypothalamic cause; reversible with lifestyle change |
| Kallmann's syndrome | Congenital GnRH deficiency + anosmia (failure of GnRH neurons to migrate from olfactory placode). Primary amenorrhoea with absent secondary sexual characteristics [1][2] |
| Idiopathic hypogonadotrophic hypogonadism | Same as Kallmann's but without anosmia |
| Tumours (e.g., craniopharyngioma) | Compress hypothalamus; also think of other space-occupying lesions |
Sheehan's syndrome, prolactinomas, non-functioning adenoma, iatrogenic (surgery, radiotherapy), hyperprolactinaemia, thyroid dysfunction [1]
| Pituitary Cause | Mechanism |
|---|---|
| Sheehan's syndrome | Post-partum pituitary necrosis from haemorrhagic shock. The pituitary enlarges during pregnancy (lactotroph hyperplasia) making it vulnerable to ischaemia. Classically: inability to lactate → then gradual panhypopituitarism |
| Prolactinomas | Secrete excess prolactin → prolactin inhibits GnRH pulsatility → low FSH/LH → amenorrhoea + galactorrhoea |
| Hyperprolactinaemia (non-tumour) | Drugs (antipsychotics, metoclopramide), hypothyroidism (high TRH stimulates prolactin), stalk effect from large non-functioning tumours compressing the stalk (loss of dopamine inhibition) |
| Non-functioning adenoma | Mass effect → compresses normal pituitary tissue → hypopituitarism [2][3] |
Past Paper Alert (2020 SAQ Q6)
A woman with secondary amenorrhoea, galactorrhoea, prolactin 4× upper normal, normal IGF-1, pituitary macroadenoma. Asked: causes of hyperprolactinaemia, why bromocriptine restored menstruation, tumour type when no shrinkage on bromocriptine. Answer: (a) Prolactinoma OR stalk compression from non-functioning adenoma; (b) Bromocriptine = dopamine agonist → lowers prolactin → restores GnRH pulsatility → menstruation resumes; (c) Non-functioning pituitary macroadenoma (because prolactinomas should shrink with dopamine agonists). [8]
Premature ovarian insufficiency (POI), gonadal agenesis/dysgenesis, iatrogenic, autoimmune, PCOS [1]
Premature Ovarian Insufficiency (POI):
- Loss of ovarian function before age 40
- Confirm diagnosis: FSH > 25 IU/L on TWO occasions, at least 4 weeks apart [1]
- Causes: chromosomal (Turner 45,X — most common genetic cause), autoimmune, iatrogenic (chemo/radiotherapy), Fragile X premutation, idiopathic
- Investigations: karyotype, Fragile X premutation, anti-thyroid Ab, anti-adrenal Ab, DXA scan [1]
Gonadal dysgenesis (Turner syndrome 45,X):
- Short stature, webbed neck, shield chest, streak gonads
- Primary amenorrhoea with absent breast development but normal pubic hair (adrenal androgens intact)
- See 2022 MCQ Q25: 18-year-old, height 147cm, no breasts, normal pubic hair, 45,X → this is Turner syndrome [9]
Polycystic Ovary Syndrome (PCOS):
Rotterdam Criteria — need 2 out of 3:
- Oligo-anovulation
- Clinical / biochemical hyperandrogenism
- Sonographic features: follicle number per ovary > 20 and/or ovarian volume ≥ 10 mL [1]
Why PCOS causes amenorrhoea: Excess androgens (from ovarian theca cells stimulated by chronically elevated LH) are peripherally converted to oestrone. This chronic oestrogen exposure without ovulation means no progesterone is produced → no organized secretory endometrium → no shedding → amenorrhoea or oligomenorrhoea. The chronic unopposed oestrogen also increases the risk of endometrial hyperplasia and cancer.
Cervical/vaginal atresia, transverse vaginal septum, imperforate hymen, absence of vagina/uterus, Asherman syndrome, TB endometritis [1]
| Condition | Key Feature | Exam Clue |
|---|---|---|
| Imperforate hymen | Cyclical lower abdominal pain with haematocolpos | Primary amenorrhoea + normal secondary sexual characteristics + cyclic pain + USG shows blood collection. 2022 MCQ Q24 [9] |
| Transverse vaginal septum | Similar to imperforate hymen but higher up | Primary amenorrhoea + haematocolpos |
| Mayer-Rokitansky-Küster-Hauser (MRKH) syndrome | Congenital absence of uterus and upper 2/3 of vagina | 46,XX, normal ovaries and secondary sexual characteristics, primary amenorrhoea. Often associated with renal tract anomalies [1] |
| Asherman syndrome | Intrauterine adhesions from excessive curettage or infection | Secondary amenorrhoea after uterine instrumentation. 2022 MCQ Q22: woman with amenorrhoea after surgical TOP complicated by PID [9] |
| TB endometritis | Granulomatous destruction of endometrium | Secondary amenorrhoea in TB-endemic settings |
46,XY karyotype, androgen receptor mutation → non-virilisation of genitalia → female phenotype. Undescended gonads, no axillary/pubic hair, some breast development (peripheral conversion of androgen → oestrogen). [1]
This is a classic exam favourite. The 2022 MCQ Q23 tested this: 19-year-old girl, primary amenorrhoea, normal breast development, NO pubic hair, height 170cm → AIS [9].
Why no pubic hair but breasts present? Pubic/axillary hair depends on androgen action at the hair follicle — in AIS, the androgen receptor is non-functional, so no hair growth. Breast development occurs because testosterone is peripherally aromatized to oestradiol, and the oestrogen receptor is normal.
1.3 Evaluation of Amenorrhoea
Onset and duration, previous menstruation, pubertal development, PMH, drug history, nutrition/stress/weight change, galactorrhoea/headache/visual disturbance, menopausal symptoms, thyroid symptoms, hyperandrogenic symptoms, family history [1]
Why each matters:
- Previous menstruation → distinguishes primary from secondary
- Pubertal development → tells you about oestrogen exposure (breasts) and androgen exposure (pubic hair)
- Drug history → OCPs, antipsychotics (prolactin), chemotherapy
- Weight change/nutrition/stress → functional hypothalamic amenorrhoea
- Galactorrhoea/headache/visual disturbance → pituitary tumour
- Hyperandrogenic symptoms (acne, hirsutism) → PCOS, CAH
Body height/weight, stigmata of chromosomal abnormality, hirsutism/virilisation, secondary sexual characteristics, goitre, galactorrhoea, visual field, abdominal mass, genital tract development [1]
Exam-relevant points:
- Short stature + webbed neck = Turner syndrome
- Tall + no pubic hair + breast development = AIS
- Hirsutism + acanthosis nigricans + obesity = PCOS
- Blue/bulging hymen = imperforate hymen with haematocolpos
First-line:
FSH, LH, E2, PRL, TFT, testosterone, progestogen challenge test, USG pelvis [1]
Always rule out pregnancy first! [1]
Second-line (depending on clinical suspicion):
Androgens (SHBG, 17-OH progesterone), E+P withdrawal test, GnRH stimulation test, karyotype (primary amenorrhoea, POI), Fragile X premutation, 3D USG/MRI pelvis, USG renal tract, pituitary MRI, visual field perimetry, laparoscopy/hysteroscopy, autoimmune screening [1]
This is a critical exam slide — the flowchart approach to amenorrhoea [1]:
This is the single most testable concept. Learn to interpret the hormone results:
| Pattern | FSH/LH | E2 | Withdrawal Bleed | Diagnosis | WHO Class |
|---|---|---|---|---|---|
| ↑ FSH/LH, ↓ E2 | High | Low | No | POI / Gonadal failure (ovaries can't respond → pituitary pushes harder) | Class 3: Hypergonadotrophic hypogonadism [1] |
| ↓ FSH/LH, ↓ E2 | Low | Low | No | Hypothalamic/Pituitary failure (no signal to ovaries) | Class 1: Hypogonadotrophic hypogonadism [1] |
| Normal FSH/LH, Normal E2 | Normal | Normal | Yes (in PCOS) / No (outflow) | PCOS or outflow tract problem | Class 2: Normogonadotrophic anovulation [1] |
Why the Progestogen Challenge Test Works
You give exogenous progestogen (e.g., Provera) for 5–10 days. If the patient bleeds after stopping, it means: (1) there IS oestrogen present (endometrium was primed), and (2) the outflow tract is patent. This points to anovulation (e.g., PCOS) as the cause. If NO withdrawal bleed occurs, either oestrogen is too low to prime the endometrium (hypothalamic/pituitary/ovarian failure) OR the endometrium/outflow tract is damaged (Asherman's, anatomical).
1.6 Management Principles
Amenorrhoea is a symptom, NOT a diagnosis. Treat the underlying cause. Do not forget PHYSIOLOGICAL causes! [1]
Environmental causes → lifestyle modification, reassurance, ± psychological treatment. Primary amenorrhoea or no obvious external cause → pituitary MRI, ± GnRH stimulation test, visual field perimetry. Neurosurgical treatment for hypothalamic-pituitary lesions. Induction of puberty by oestrogen in primary amenorrhoea. Maintenance HRT to protect bone (except transient secondary causes). Fertility treatment: gonadotrophins. [1]
Why HRT for bone? Without oestrogen, bone resorption exceeds formation → progressive bone loss → osteoporosis. Young women with hypogonadism are at particular risk because they may never achieve peak bone mass.
Weight reduction. Menstrual regulation to prevent endometrial hyperplasia/CA: periodic progestogen for withdrawal bleeding or COC pills. Hirsutism: COC pills, cosmetic measures, anti-androgens. Fertility: ovulation induction by letrozole / gonadotrophin. Monitor for long-term metabolic disorder. [1]
Why prevent endometrial hyperplasia? Chronic unopposed oestrogen (from peripheral aromatization of androgens) without cyclical progesterone keeps stimulating endometrial proliferation → hyperplasia → risk of endometrial carcinoma. Regular progestogen exposure induces secretory change and shedding.
Confirm: FSH > 25 IU/L × 2 (≥4 weeks apart). Investigations: karyotype, Fragile X, autoimmune antibodies, DXA. Induction of puberty if primary amenorrhoea. Maintenance HRT until age 51 (average natural menopause age). HRT in POI does NOT increase breast cancer risk above the general population. Fertility: oocyte donation, adoption. [1]
High Yield: POI and HRT
HRT in POI is not "extra" hormones — it is REPLACEMENT of what the body should be making at that age. Therefore, there is no increase in breast cancer risk compared to the general population. HRT should continue until age 51. [1]
Thyroid disorder → treat accordingly. Hyperprolactinaemia → dopaminergic drugs (bromocriptine, cabergoline), rarely neurosurgery. CAH → endocrine management. [1]
Confirm with 3D USG / MRI pelvis ± laparoscopy/hysteroscopy. Check for associated renal tract anomalies. Surgical correction. Vaginal dilation (for MRKH or AIS). Address fertility and sexuality issues. [1]
Part 2: Climacteric & Menopause
| Term | Definition |
|---|---|
| Climacteric | The years of waning ovarian function, marking the transition from reproductive to non-reproductive state [1] |
| Menopause | The permanent cessation of ovarian function and fertility — a specific event (the final menstrual period), diagnosed RETROSPECTIVELY after 12 months of amenorrhoea in a previously cycling woman [1] |
| Perimenopause | The period beginning with the first clinical/biological/endocrinological features of approaching menopause, ending 12 months after the final menstrual period [1] |
Why "retrospective"? Because you can't be sure a period is the "last" one until enough time has passed without another. Hence the 12-month criterion.
| Type | Definition | Key Point |
|---|---|---|
| Natural menopause | Spontaneous amenorrhoea for 12 months without other cause, mean age 51 years [1] | Clinical diagnosis in healthy women > 45 |
| Artificial/induced menopause | Sudden termination of menstrual life due to surgery, radiotherapy, or chemotherapy [1] | Often more severe symptoms due to abrupt hormone withdrawal |
| Premature ovarian insufficiency | Loss of ovarian function before age 40 [1] | Needs HRT until age 51 |
The fundamental change: depletion of ovarian follicles → loss of oestrogen and progesterone production → loss of negative feedback on pituitary → FSH and LH rise.
- Oestradiol drops dramatically
- FSH rises (earliest and most reliable marker)
- The remaining oestrogen source is peripheral aromatization of adrenal androgens (androstenedione → oestrone) in adipose tissue — this is a much weaker oestrogen
A clinical diagnosis in healthy women > 45 years — amenorrhoea for 12 months. No adequate biological marker. FSH rises some years before menopause. High FSH is supportive in special circumstances. [1]
When might you check FSH? In women under 45 with amenorrhoea (to distinguish POI from other causes), or when clinical diagnosis is uncertain (e.g., woman on progesterone-only contraception who has amenorrhoea anyway).
2.5 Climacteric Symptoms
At least 1/3 of most women's lifespan in developed countries is spent in the postmenopausal years. [1]
Hot flushes, sweating, palpitation, dizziness [1]
Mechanism: Oestrogen withdrawal narrows the thermoneutral zone in the hypothalamus. Small increases in core body temperature that would normally be tolerated now trigger the body's heat-dissipation response → peripheral vasodilation (flushing), sweating. Noradrenaline and serotonin neurotransmitter changes in the thermoregulatory centre are involved.
Loss of energy/drive, loss of concentration, irritability, anxiety, depression, mood fluctuations, sleep disturbances [1]
Can be multifactorial: Bio-psycho-social factors! [1]
Why biopsychosocial? The woman going through menopause may simultaneously be dealing with children leaving home ("empty nest"), ageing parents, relationship changes, career stress, and body image concerns. Oestrogen decline affects serotonin and noradrenaline neurotransmission in the brain, contributing to mood changes, but the psychosocial context often amplifies symptoms.
Dyspareunia (from atrophic change), decreased libido. Can be multifactorial. [1]
The 2024 MCQ Q6 tested: The MOST COMMON cause for low coital frequency in Hong Kong Chinese menopaused women is "no sexual desire" (decreased libido) [10]. This is important — it's not just vaginal dryness. Loss of desire is the predominant complaint.
Vaginal: dryness, burning, pruritus, dyspareunia, prolapse. Urinary: urgency, frequency, dysuria, UTI, incontinence, voiding difficulties. [1]
Why both vaginal and urinary? The lower vagina, urethra, and trigone of the bladder all derive from the urogenital sinus and are all oestrogen-responsive tissues. Oestrogen deficiency causes thinning of the epithelium, loss of glycogen, change in vaginal pH (becomes more alkaline), altered flora → increased susceptibility to infections and atrophic symptoms.
2.6 Longer-Term Health Conditions
Incidence increases after menopause. Oestrogen is probably protective to vasculature and has favourable effect on lipid profile. [1]
Why protective? Pre-menopausal oestrogen: (1) promotes vasodilation via NO, (2) has anti-atherosclerotic effects on vessel walls, (3) improves lipid profile (↑HDL, ↓LDL). After menopause, these protective effects are lost, and CVD risk rises to match men.
Oestrogen deficiency leads to bone loss. Postmenopausal osteoporosis is an important risk factor for fracture. [1]
Mechanism: Oestrogen normally suppresses osteoclast activity (by reducing production of RANKL and pro-resorptive cytokines like IL-6, TNF-α). Without oestrogen, osteoclast activity increases → net bone resorption → bone loss → osteoporosis.
WHO Criteria for Osteoporosis: [1]
| Category | T-score |
|---|---|
| Normal | < 1 SD below young adult mean |
| Low bone mass (Osteopenia) | 1–2.5 SD below young adult mean |
| Osteoporosis | > 2.5 SD below young adult mean |
| Severe osteoporosis | > 2.5 SD below + one or more fragility fractures |
FRAX tool should be used to assess 10-year fracture probability, incorporating clinical risk factors beyond BMD alone [1].
Musculoskeletal: laxity of soft tissue, reduced muscular strength, backache, joint pains. Dementia and cognitive decline. [1]
2.7 Management of Menopause
Three management principles:
- Holistic bio-psycho-social approach for general health
- Management of menopausal symptoms
- Prevention of chronic health conditions [1]
Address bone health, smoking cessation, alcohol use, cardiovascular risk assessment and management, cancer screening and prevention [1]
Air conditioning, dressing in layers, avoiding alcohol and spicy food, reducing obesity, reducing stress [1]
HRT is effective for treatment of severe climacteric symptoms and improves QoL. Can prevent/delay bone loss and reduces both vertebral and non-vertebral fractures. For atrophic symptoms — topical oestrogen. [1]
HRT Regimens:
| Situation | Regimen | Rationale |
|---|---|---|
| Without uterus | Oestrogen alone | No risk of endometrial hyperplasia/cancer without a uterus |
| With uterus — Sequential (cyclical) | Oestrogen + Progestogen for 12-14 days/cycle → scheduled bleeding | Progestogen opposes oestrogen's proliferative effect on endometrium → prevents hyperplasia |
| With uterus — Continuous combined | Oestrogen + Progestogen daily → non-bleeding regime | More suitable for women > 2 years post-menopause [1] |
| Tibolone | Synthetic compound with oestrogenic, progestogenic, and some androgenic metabolites | Alternative for women who want a non-bleeding HRT |
Why add progestogen if the uterus is intact? Unopposed oestrogen stimulates endometrial proliferation → increased risk of endometrial hyperplasia and carcinoma. Adding progestogen for at least 12 days per cycle induces secretory change and shedding, protecting the endometrium [1][4].
Oestrogen Types and Routes:
Natural oestrogens preferred: 17β-oestradiol (Estrofem®), conjugated equine estrogens (Premarin®). Preparations: oral, transdermal patch, gel. Implant and vaginal ring not available in HK. [1]
Why transdermal may be preferred in some patients: Transdermal oestrogen bypasses first-pass hepatic metabolism → avoids increase in hepatic clotting factor synthesis → lower VTE risk compared to oral. Also avoids the triglyceride increase seen with oral oestrogen.
Progestogen Types:
Oral progestogen. Mirena® (levonorgestrel-releasing intrauterine system) [1]
Mirena provides local progestogenic effect on the endometrium with minimal systemic progestogen exposure — useful in women who have side effects from systemic progestogens.
HRT Principle:
Use the lowest possible dose for the shortest possible duration for symptom relief. No universal rule — tailored to individual's condition and need. [1]
Special situation — POI: HRT till age 51. No increase in breast cancer risk compared to general population. [1]
Risks of HRT: carcinoma of breast, VTE, stroke, gallbladder disease [1]
The Women's Health Initiative (WHI) study is the landmark trial [1]:
E+P arm (women with uterus, CEE + MPA):
| Outcome | Effect | Additional Events per 10,000 women/year |
|---|---|---|
| CHD | ↑ (29% increase) | +7 |
| Stroke | ↑ | +8 |
| Invasive breast cancer | ↑ | +8 |
| VTE | ↑ | +18 |
| Colorectal cancer | ↓ (benefit) | -6 |
| Hip fracture | ↓ (benefit) | -5 |
| Endometrial cancer | Neutral | — |
E-only arm (women without uterus, CEE alone):
| Outcome | Effect | Events per 10,000 women/year |
|---|---|---|
| Stroke | ↑ | +12 |
| Hip fracture | ↓ (benefit) | -6 |
| Breast cancer | Neutral/slight decrease | Not statistically significant increase |
| CHD | Neutral | — |
The 'Window of Opportunity' Hypothesis
The WHI study enrolled women with mean age 63 — much older than the typical woman starting HRT for menopausal symptoms (around 50-55). Some data suggest benefits in CHD prevention if HRT is started before age 60 and/or within 10 years of menopause. [1] This is the "timing hypothesis" — early initiation may be cardioprotective, while late initiation may be harmful.
Common Exam Trap
Students often state "HRT causes heart disease" as a blanket statement. The nuance is: the WHI showed increased CHD in the combined E+P arm in older women (mean age 63). For younger symptomatic women starting HRT around menopause, the cardiovascular risk is much lower and there may even be benefit. The exam expects you to know the WHI findings AND the timing nuance.
Severe liver disease, cerebrovascular disease, DVT/PE, oestrogen-dependent tumours (breast, uterus), undiagnosed uterine bleeding [1]
Why each matters:
- Liver disease → oestrogen is hepatically metabolised; may worsen liver dysfunction and increase clotting factors
- Cerebrovascular disease/DVT/PE → oestrogen increases VTE risk
- Oestrogen-dependent tumours → oestrogen fuels tumour growth
- Undiagnosed uterine bleeding → must rule out endometrial pathology before starting HRT
Annual monitoring for continual need. Well-women check-up. Side effects (breast tenderness, fluid retention, bloating, nausea, headache, irregular bleeding) — usually transient. Report unscheduled bleeding promptly if it occurs after 3 months. Cessation: tapering vs abrupt stop (no proven difference in clinical outcome); warn about symptom recurrence. [1]
Evidence conflicting. Limited data on long-term safety. Beware of unregulated preparations. [1]
| Symptom | Non-Hormonal Option |
|---|---|
| Vasomotor | Clonidine, gabapentin, relaxation, lifestyle modifications [1] |
| Mood symptoms | Psychological counselling/therapy, antidepressants [1] |
| Vaginal atrophy | Lubricants, moisturisers [1] |
| Osteoporosis prevention/treatment | Calcium, vitamin D, weight-bearing exercise, avoid smoking/excessive alcohol/caffeine. Raloxifene (SERM), bisphosphonates, denosumab (RANK ligand inhibitor) [1][4] |
| Cardiovascular health | Exercise, avoid smoking, control HT/DM/hyperlipidaemia/obesity [1] |
Raloxifene detail (from osteoporosis lecture): SERM — oestrogen agonist on bone (↓vertebral fractures by 40% but NOT non-vertebral), oestrogen antagonist on breast and endometrium (↓ER+ breast cancer risk). Side effects: VTE, hot flushes, leg cramps. Should be discontinued during immobilisation [4].
Integration with Related Material
From the psychiatry sexual function lecture [11][12]: menopause is listed as a cause of female sexual interest/arousal disorder (lack of hormones → decreased interest, vaginal dryness) and female orgasmic disorder (damage to vasculature/nerves, hormonal changes). Treatment includes HRT, treat medical conditions, adjust medications, sex therapy, couples therapy.
Sheehan's syndrome and prolactinomas connect directly to the pituitary tumours lecture [2][3]. The order of anterior pituitary hormone loss in hypopituitarism is classically GH → FSH/LH → ACTH → TSH [3]. In women, FSH/LH deficiency manifests as amenorrhoea + infertility + climacteric symptoms + decreased BMD.
The osteoporosis lecture [4] emphasises that HRT is mainly an option for young postmenopausal women with climacteric symptoms. For older women with high fracture risk, more potent agents (bisphosphonates, denosumab) are preferred. HRT inhibits bone resorption by decreasing calcium excretion and reducing cytokine production by stromal cells.
From the DVT/PE lecture [6]: pregnancy and oestrogen use create a hypercoagulable state. This is why VTE is a risk of HRT and a contraindication in women with prior DVT/PE. Transdermal oestrogen has lower VTE risk than oral.
Likely Exam Questions
- EMQ: Match the diagnosis — A 19-year-old with primary amenorrhoea, breast development, NO pubic hair → AIS [9]
- EMQ: Match the diagnosis — A 16-year-old with primary amenorrhoea, normal secondary sexual characteristics, cyclic pain, haematocolpos → Imperforate hymen [9]
- EMQ: Match the diagnosis — A 28-year-old with secondary amenorrhoea after repeated surgical TOP complicated by PID → Asherman syndrome [9]
- MCQ: Most common cause of low coital frequency in menopausal HK Chinese women? → No sexual desire [10]
- MCQ: HRT in a woman with an intact uterus — why must progestogen be added? → To prevent endometrial hyperplasia/cancer from unopposed oestrogen
-
"A 30-year-old woman presents with secondary amenorrhoea for 8 months. Describe your approach to investigation." → Pregnancy test first → FSH, LH, E2, PRL, TFT, testosterone → Progestogen challenge test → USG pelvis → interpret based on hormone pattern → further investigations as indicated
-
"List 4 risks and 2 benefits of combined HRT from the WHI study." → Risks: CHD, stroke, breast cancer, VTE. Benefits: reduced hip fractures, reduced colorectal cancer.
-
"A 17-year-old girl presents with primary amenorrhoea. She has no breast development, normal pubic hair, and is 148 cm tall. Karyotype is 45,X. What is the diagnosis and outline management." → Turner syndrome (POI/gonadal dysgenesis). Management: oestrogen for puberty induction, long-term HRT for bone protection until age 51, monitor cardiovascular/renal associations, fertility counselling (oocyte donation).
-
"Define menopause and perimenopause." → Menopause: permanent cessation of ovarian function, diagnosed retrospectively after 12 months amenorrhoea. Perimenopause: period from first features of approaching menopause to 12 months after final menstrual period.
High Yield Summary
Amenorrhoea:
- Primary = no menses by age 16; Secondary = no menses for 6 months in previously menstruating woman
- ALWAYS rule out pregnancy
- Organize causes by HPO axis level: hypothalamus → pituitary → ovary → outflow tract → other endocrine
- Three hormone patterns: ↑FSH (ovarian failure), ↓FSH (hypothalamic/pituitary), normal FSH (PCOS/outflow)
- Progestogen challenge test differentiates anovulation (+bleed) from oestrogen deficiency or outflow problem (−bleed)
- PCOS: Rotterdam 2/3 criteria; manage with weight loss, menstrual regulation, anti-androgens, ovulation induction
- POI: FSH > 25 × 2 (≥4 weeks apart); HRT until 51; no increased breast CA risk
- AIS: 46,XY, female phenotype, no pubic hair, breast development
Menopause:
- Clinical diagnosis at > 45 years: 12 months amenorrhoea; mean age 51
- Symptoms: vasomotor, psychological, sexual, urogenital atrophy
- Long-term: CVD, osteoporosis, musculoskeletal, cognitive decline
- HRT: effective for symptoms; use lowest dose, shortest duration; add progestogen if uterus intact
- WHI: E+P increases CHD, stroke, breast CA, VTE; decreases colorectal CA, hip fractures
- Contraindications: liver disease, CVA, DVT/PE, oestrogen-dependent tumours, undiagnosed bleeding
- Non-hormonal: clonidine/gabapentin (vasomotor), antidepressants (mood), lubricants (atrophy), bisphosphonates/raloxifene/denosumab (osteoporosis)
Active Recall - Lecture Notes
[1] Lecture slides: GC 114. Climacteric symptoms menopause and related illness; amenorrhoea.pdf [2] Senior notes: Block A - I keep on bumping into people on my side_ pituitary tumours; hypopituitarism.pdf [3] Senior notes: Ryan Ho Endocrine.pdf (Section 5.3 Hypopituitarism) [4] Senior notes: Block A - Back pain in an elderly woman_ osteoporosis and related fractures.pdf (HRT and Raloxifene sections) [5] Senior notes: Ryan Ho Fundamentals.pdf (Sections 3.8.1.2–3.8.1.3 Hypothyroidism, Thyroid) [6] Senior notes: Block A - Leg swelling and chest pain_ deep vein thrombosis; pulmonary embolism; Thrombophilia.pdf (Pregnancy and estrogen VTE) [7] Lecture slides: Block C - Climacteric symptoms_ menopause and related illness; amenorrhoea.pdf [8] Past papers: 2020 Fourth Summative SAQ.pdf (Question 6) [9] Past papers: 2022 Fourth Summative MCQ.pdf (Questions 22–25, Section VI Amenorrhoea) [10] Past papers: 2024 Fourth Summative MCQ.pdf (Question 6) [11] Medicine lecture slides: MBBS4 Sexual function t Dysf140824.pdf (Slides 26–27, 44) [12] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (Hypopituitarism section)
GC113 Can We Get Married Pre-marital, Pre-pregnancy And Pre-natal Counselling
Pre-marital, pre-pregnancy, and pre-natal counseling is a comprehensive genetic and medical assessment provided to couples before marriage, conception, or during pregnancy to identify hereditary disorders, optimize maternal-fetal health, and guide informed reproductive decision-making.
GC115 I Am Pregnant Medical Problems Complicating Pregnancy
Pre-existing or newly arising medical conditions—such as hypertension, diabetes, thyroid disorders, cardiac disease, or thromboembolic disease—that complicate pregnancy and require specialized management to optimize maternal and fetal outcomes.