CFB OG04 Menstrual Disorders
Menstrual disorders are abnormalities in the frequency, duration, amount, or regularity of menstrual bleeding, including conditions such as amenorrhea, oligomenorrhea, menorrhagia, dysmenorrhea, and premenstrual syndrome.
Menstrual Disorders
This lecture (CFB OG04) by Dr. Charleen Cheung is one of the highest-yield O&G topics for the Fourth Summative. It is a foundational lecture that spans essentially all menstrual complaints a woman of reproductive age can present with. The examiners love this topic because it tests physiology, clinical reasoning, investigation ordering, and management stepladders — all in one stem.
The big idea: Understand the hypothalamic-pituitary-ovarian (HPO) axis, define what "normal" menstruation is, classify abnormal uterine bleeding (AUB) using the FIGO systems, work through the clinical assessment systematically, choose appropriate medical or surgical treatments, and approach amenorrhoea/dysmenorrhoea as distinct but related problems.
Learning objectives (from slide outline):
- Physiology of the menstrual cycle
- Normal menstruation and its parameters
- AUB — FIGO System 1 (symptoms) and System 2 (causes/PALM-COEIN)
- Clinical assessment of AUB (history, examination, investigations)
- Treatment of AUB (medical and surgical)
- Dysmenorrhoea — primary vs. secondary
- Oligo-amenorrhoea — definitions, causes, workup, PCOS
- Case-based integration
1. Physiology of the Menstrual Cycle
The HPO axis is the master regulatory circuit for menstruation. Interruption at any level results in menstrual disturbance, ranging from irregular cycles to complete amenorrhoea. [1]
Hypothalamus → GnRH (pulsatile)
↓
Anterior Pituitary → FSH + LH
↓
Ovary → Estrogen (follicular phase) + Progesterone (luteal phase)
↓
Endometrium → Proliferative → Secretory → Withdrawal bleed (menstruation)Why pulsatile GnRH matters: GnRH is released in pulses. Fast pulses favour LH secretion; slow pulses favour FSH. This is why continuous GnRH agonist (GnRHa) therapy down-regulates the axis after initial stimulation — it abolishes the pulsatility, leading to chemical menopause.
Feedback loops:
- Negative feedback: Estrogen + progesterone suppress GnRH/FSH/LH during most of the cycle.
- Positive feedback: Rising estradiol in the late follicular phase triggers the LH surge → ovulation.
- After ovulation, the corpus luteum produces progesterone. If no pregnancy, the corpus luteum regresses → progesterone drops → endometrial shedding (menstruation).
| Phase | Dominant Hormone | Endometrial Event | Approximate Day (28d cycle) |
|---|---|---|---|
| Menstrual | ↓ Progesterone (withdrawal) | Shedding of functional layer | Day 1–5 |
| Proliferative | Estrogen | Gland + stroma growth, ↑ thickness | Day 6–14 |
| Secretory | Progesterone | Glands become tortuous, stromal decidualization | Day 15–28 |
Estrogen drives the proliferative phase; progesterone drives the secretory phase. [1]
Why this matters clinically:
- Unopposed estrogen (no progesterone) → continuous endometrial proliferation → hyperplasia → cancer risk.
- This is why PCOS patients (chronic anovulation = no progesterone) need cyclic progestogen.
The STRAW (Stages of Reproductive Aging Workshop) staging system classifies a woman's reproductive life from menarche through post-menopause. [1]
The key clinical transition is the menopausal transition (perimenopause), characterised by:
The slide further distinguishes the transition stages:
| STRAW stage | Clinical description |
|---|---|
| −2: Early menopausal transition | Cycle length differs from normal by > 7 days; FSH is increasing |
| −1: Late menopausal transition | At least 2 skipped cycles with an interval of amenorrhoea ≥60 days; FSH is increasing |
| 0: Final menstrual period (FMP) | Menopause is recognised retrospectively after 12 months of amenorrhoea |
| +1: Early postmenopause | Approximately the first 1 year after the FMP; FSH remains increased |
| +2: Late postmenopause | Begins after the early postmenopausal stage |
The menopausal transition is characterised by erratic hormone levels. The slide gives an average age of menopause of approximately 51 years. [1]
- Variable cycle length (initially shorter, then longer)
- Fluctuating FSH
- Eventually > 12 months of amenorrhoea = menopause (diagnosed retrospectively)
2. Normal Menstruation — What Is Normal?
FIGO System 1 defines the normal parameters of menstruation and standardises the terminology for abnormalities. [1]
AUB may also be described by its time course as acute, intermittent, or chronic. FIGO System 1 additionally records unscheduled bleeding on progestin ± estrogen gonadal steroids, including bleeding while using pills, rings, patches, or injections. [1]
| Parameter | Normal Range | Abnormality |
|---|---|---|
| Frequency | 24–38 days | < 24d = frequent; > 38d = infrequent |
| Regularity | Variation ≤ 7–9 days | Variation ≥ 8–10 days = irregular |
| Duration of flow | ≤ 8 days | > 8 days = prolonged |
| Volume of flow | 5–80 mL | > 80 mL = heavy menstrual bleeding (HMB) |
| Intermenstrual bleeding | None | IMB (new in 2018): early, mid, or late cycle |
Age-Specific Duration Thresholds
Normal duration of flow varies with age:
- 18–25 years: ≤ 9 days
- 26–41 years: ≤ 7 days
- 42–45 years: ≤ 9 days
This is a slide-specific detail that could appear as an MCQ distractor. [1]
FIGO has abandoned the following traditional terms: dysfunctional uterine bleeding (DUB), menorrhagia, metrorrhagia, menometrorrhagia, polymenorrhoea, oligomenorrhoea, hypermenorrhoea, hypomenorrhoea, etc. [1]
Why abandoned? These terms were inconsistently defined across textbooks and across countries, causing confusion in clinical communication. FIGO now recommends describing AUB in terms of the four parameters above.
However, the lecture still defines the old terms because:
- Many senior clinicians still use them.
- Examiners may still use them in stems.
- You need to recognise what they mean.
| Old Term | Meaning |
|---|---|
| Menorrhagia | Prolonged or excessive bleeding at regular intervals |
| Metrorrhagia | Irregular, frequent uterine bleeding of varying amounts but not excessive |
| Menometrorrhagia | Prolonged or excessive bleeding at irregular intervals |
| Polymenorrhoea | Regular bleeding at intervals < 21 days (luteal phase defect) |
| Oligomenorrhoea | Bleeding at intervals > 35 days and < 6 months (prolonged follicular phase) |
| Amenorrhoea | No uterine bleeding for ≥ 6 months |
| Intermenstrual | Uterine bleeding between regular cycles |
DUB Is an Abandoned Term
"Dysfunctional uterine bleeding" (DUB) = AUB in the absence of recognisable pathology or pregnancy. It is no longer recommended by FIGO. In modern classification, this would fall under AUB-E (endometrial dysfunction) or AUB-O (ovulatory dysfunction) in the PALM-COEIN system. Do NOT use DUB in your exam answers unless quoting an old definition. [1]
History should assess: duration/days of bleeding, presence & size of clots, and symptoms of anaemia. [1]
Pictorial Bleeding Assessment Chart (PBAC):
- A semi-objective tool where patients score pads/tampons per day by degree of soaking, plus clot size.
- A PBAC score ≥ 100 has sensitivity and specificity > 80% for diagnosing menorrhagia (HMB). [1]
3. Abnormal Uterine Bleeding (AUB)
AUB is a common clinical problem affecting up to 15–25% of women during reproductive years, causing significant physical, emotional, sexual, social, and financial burdens and impaired quality of life. [1]
FIGO System 2 classifies the causes of AUB using the PALM-COEIN mnemonic. [1]
| Category | Mnemonic | Structural? | Details |
|---|---|---|---|
| P — Polyp | P | Structural | Endometrial or cervical; usually benign; lifetime prevalence 8–35% |
| A — Adenomyosis | A | Structural | Endometrial tissue in myometrium; prevalence ~20–35% in AUB |
| L — Leiomyoma (fibroid) | L | Structural | Benign myometrial overgrowth; 40% of reproductive-age women |
| M — Malignancy & hyperplasia | M | Structural | Endometrial hyperplasia/cancer; atypical hyperplasia has 30–40% malignancy risk |
| C — Coagulopathy | C | Non-structural | e.g. von Willebrand disease, platelet disorders |
| O — Ovulatory dysfunction | O | Non-structural | Anovulation → unopposed estrogen → irregular shedding |
| E — Endometrial | E | Non-structural | Primary endometrial dysfunction (prostaglandins, fibrinolysis) |
| I — Iatrogenic | I | Non-structural | IUCD, hormones, anticoagulants, SSRIs, antipsychotics, tamoxifen |
| N — Not otherwise classified | N | Non-structural | Rare or unclear causes |
HMB = excessive menstrual blood loss which interferes with the woman's physical, emotional, social and material quality of life, and which can occur alone or in combination with other symptoms. [1]
- Can be assessed subjectively (patient's perception of impact on QoL) or objectively ( > 80 mL per cycle).
- Affects 15–25% of women of reproductive age. [1]
Complication of HMB: Iron Deficiency Anaemia
The major complication of HMB is iron deficiency anaemia (IDA). [1]
- The 2024 DH Population Health Survey (2020–2022) found:
- Local prevalence of iron deficiency (based on serum ferritin) was 5.7%.
- Remarkable difference between men and women of reproductive age — women are far more affected.
- Findings are likely due to regular and heavy menstrual blood loss. [1]
Why this matters: Always check haemoglobin in a woman with HMB. Chronic IDA from HMB is extremely common and often under-recognised. Symptoms include fatigue, pallor, palpitations, SOB on exertion, dizziness, and even pica. [7]
The lecture provides a comprehensive DDx list beyond PALM-COEIN: [1]
| Category | Examples |
|---|---|
| Pregnancy complications | Miscarriages, ectopic pregnancy, APH |
| Benign pelvic pathology | Cervical polyp, endometrial polyp, leiomyoma, adenomyosis |
| Systemic illness | Hepatic disease, renal disease, haematological/coagulopathy |
| Genital tract infections | Cervicitis, endometritis |
| Malignancy | Cervical, vaginal, endometrial, ovarian |
| Endocrine | Thyroid, hyperprolactinaemia, Cushing's, adrenal, PCOS, anovulatory |
| Trauma | Laceration/abrasion, foreign body |
| Stress | Emotional, excessive exercise |
| Medications/Iatrogenic | IUCD, hormones, anticoagulants, SSRIs, antipsychotics, tamoxifen, herbals (ginseng) |
3.4 Structural Causes — Key Details from the Lecture
May be endometrial or cervical. Usually benign. Lifetime prevalence 8–35%. The size, number, and location of the polypi determine symptoms. [1]
- Can cause HMB, IMB, or post-menopausal bleeding.
- Diagnosed by ultrasound, SIS, or hysteroscopy.
- Treatment: hysteroscopic polypectomy.
Presence of endometrial tissue in the uterine muscle. Pathogenesis still poorly understood. Prevalence estimated 20–35% in women with AUB. [1]
- Classically: heavy painful periods (HMB + dysmenorrhoea) in a multiparous woman with a bulky, tender uterus.
- Diffuse form → globally enlarged uterus; focal form → adenomyoma.
- MRI is slightly more sensitive than USS for diagnosis.
- Definitive treatment: hysterectomy (for those who have completed family).
Benign overgrowth of myometrium. Can occur in various sites and may be multiple. 40% of reproductive-age women. May be asymptomatic. [1]
- Submucosal fibroids → most likely to cause HMB (distort the endometrial cavity).
- Intramural fibroids → can cause HMB if large.
- Subserosal fibroids → typically cause bulk symptoms (pressure, urinary frequency), NOT bleeding.
- Fibroids do not typically present with dysmenorrhoea (important DDx point from the dysmenorrhoea section). [1]
The slide further classifies fibroids by their relationship to the endometrium and serosa:
| Type | Description |
|---|---|
| 0 | Pedunculated intracavitary submucosal fibroid |
| 1 | Submucosal, < 50% intramural |
| 2 | Submucosal, ≥50% intramural |
| 3 | Contacts the endometrium and is 100% intramural |
| 4 | Intramural |
| 5 | Subserosal, ≥50% intramural |
| 6 | Subserosal, < 50% intramural |
| 7 | Subserosal pedunculated |
| 8 | Other site, such as cervical or parasitic |
Hybrid leiomyomas involve both the endometrium and serosa and are labelled with two numbers. The first describes the endometrial relationship and the second the serosal relationship; for example, 2–5. [1]
Endometrial hyperplasia = irregular proliferation of the endometrial glands with an increase in the gland-to-stroma ratio. It is a precursor of endometrial cancer. [1]
Revised WHO Classification (2014):
| Type | Risk of Malignancy | Treatment |
|---|---|---|
| Hyperplasia WITHOUT atypia | < 5% in 20 years | Progestogen + surveillance |
| Atypical endometrial hyperplasia | 30–40% | Hysterectomy recommended |
Risk factors for endometrial cancer (per HKCOG guideline): [1]
- Obesity
- PCOS
- Lynch syndrome
- Family history of gynaecological and gastrointestinal malignancy
- Unopposed estrogen therapy
- Tamoxifen therapy
- Persistent or long-standing AUB
- No response to medical treatment
Endometrial Cancer in Young Women
Although endometrial cancer is uncommon in women aged < 40, its number is increasing. The incidence rises sharply at age 50 (66 per 100,000) and peaks at 50–54. But even at age 30, incidence is ~4 per 100,000 — so do NOT dismiss AUB in young women with risk factors. [1]
This is directly testable: the 2020 Minicase Case 3 involves a 55-year-old with postmenopausal bleeding on unopposed estrogen — they want you to say endometrial cancer and order endometrial biopsy + TVUSS. [3]
4. Clinical Assessment of AUB
The lecture provides a systematic 8-point history framework: [1]
| # | Domain | Key Points |
|---|---|---|
| 1 | Bleeding pattern | Quantity, frequency of pad changes, presence of clots, timing in cycle, impact on QoL |
| 2 | Symptoms of anaemia | Headache, palpitations, SOB, dizziness, fatigue, pica |
| 3 | Sexual/reproductive history | Contraception use, STI history, cervical screening, possibility of pregnancy, desire for future pregnancy, known infertility |
| 4 | Associated symptoms | Fever, chills, ↑ abdominal girth, pelvic pressure/pain, bowel/bladder dysfunction, vaginal discharge/odour |
| 5 | Symptoms of systemic cause | Overweight, obesity, PCOS features, hypothyroidism, hyperprolactinaemia, hypothalamic/adrenal disorder |
| 6 | Chronic medical illness | Inherited bleeding disorders (coagulopathy, platelet disorders), SLE/CTD, liver disease, renal disease, CVD |
| 7 | Medications | Hormonal contraceptives, anticoagulants, SSRIs, antipsychotics, tamoxifen, herbals (ginseng) |
| 8 | Family history | Coagulation/thromboembolic disorders, hormone-sensitive cancers |
Structured Screening for Coagulopathy
A positive bleeding-disorder screen is present if any one of the following applies:
- HMB has been present since menarche.
- There has been postpartum haemorrhage, surgery-related bleeding, or bleeding associated with dental work.
- At least two of the following are present: bruising 1–2 times per month, epistaxis 1–2 times per month, frequent gum bleeding, or a family history of bleeding symptoms.
A positive screen warrants further evaluation, including consideration of haematology consultation. [1]
Physical examination has TWO components: general and pelvic. [1]
General:
- Vital signs: BP, pulse, weight, BMI
- Neck: thyroid examination
- Abdomen: tenderness, distension, striae, mass, organomegaly
- Skin: pallor, bruising, petechiae, signs of hirsutism (male hair pattern, acanthosis nigricans)
Pelvic:
- Inspection: vulva, vagina, cervix, anus, urethra → exclude local lesion such as cervical polyp
- Bimanual examination: uterus size/shape/tenderness, adnexal masses
- Rectal examination: if rectal bleeding suspected or risk of concomitant pathology
- Opportunistic investigations: Pap smear, cervical/vaginal cultures if STI risk
Exam Tip: Physical Examination for AUB
In past papers (2018 Q11a), they ask "what aspects of the physical examination will you focus on?" The marking scheme typically wants: abdominal examination (for pelvic mass) and pelvic/vaginal examination (speculum + bimanual to assess cervix, uterine size, adnexal masses). Always mention BOTH. [2]
4.3 Investigations
The lecture provides a tiered investigation approach: [1]
Routine/First-line:
- Pregnancy test — ALWAYS first in reproductive age
- CBC with Hb and platelets — assess for anaemia and thrombocytopenia
- Cervical screening (Pap smear) — if not up to date
- Endocervical swab for Chlamydia — if postcoital or intermenstrual bleeding
NOT routinely recommended (only if indicated):
- Ferritin (if anaemia found)
- Female hormonal profile (if amenorrhoea/PCOS suspected)
- Thyroid function (only if symptomatic)
- Clotting profile (if HMB since menarche or family history of bleeding disorder)
Endometrial assessment:
- Endometrial aspiration (Pipelle) — outpatient, adequate samples 87–97%, detects 67–96% of endometrial carcinoma; blind sampling may miss focal lesions
- Pelvic ultrasound — first-line imaging for AUB
- Saline infusion sonohysterography (SIS) — better for polyps and submucosal fibroids
- Hysteroscopy — gold standard for visualising endometrial cavity; allows targeted biopsy
USS is the first-line imaging modality for AUB. [1]
When to order USS:
- Uterus palpable abdominally
- Pelvic mass present
- Failed medical treatment
USS cannot replace endometrial biopsy. [1]
Endometrial thickness thresholds (postmenopausal women):
| Condition | Average ET |
|---|---|
| Normal postmenopausal | 4 mm |
| Endometrial polyp | 10 mm |
| Endometrial hyperplasia | 14 mm |
| Endometrial carcinoma | 20 mm |
Prediction of endometrial pathology in premenopausal women by ET is NOT reliable — ET can vary from 4 mm in the follicular phase to 16 mm in the luteal phase. [1]
SIS involves instilling 5–15 mL normal saline into the uterine cavity via an infant feeding tube. It provides better detection of endometrial polyps and submucosal fibroids, with pooled sensitivity of 93–94% and specificity of 81%. [1]
MRI is more sensitive than TVUSS for identifying fibroids (especially submucosal) and slightly more sensitive for adenomyosis. However, the benefit must be weighed against waiting time and cost. Therefore, MRI is NOT routinely recommended for all AUB. [1]
Most common outpatient device. Adequate samples 87–97% of the time. Detects 67–96% of endometrial carcinoma. Simple, quick, safe, convenient. Limitation: blind sampling — may miss a focal lesion. [1]
HKCOG recommends endometrial biopsy:
- For all women with AUB at or above age 40
- In women with risk factors for endometrial carcinoma irrespective of age
- Those with persistent symptoms
- Those having failed medical treatment [1]
Allows visualisation of the whole endometrial cavity and cervical canal. Allows targeted endometrial biopsy. Can be done without anaesthesia via vaginoscopic approach. HK study: successful in 92% of patients outpatient. Risks: perforation, infection, false passage. [1]
5. Management of AUB
Management principles: establish cause → explanation/counselling → observation → correction of anaemia → control of bleeding symptoms. [1]
| Intervention | Details |
|---|---|
| D&C (Dilatation and Curettage) | Provides immediate haemostasis; no long-term effects |
| IV Premarin (conjugated estrogen) | For acute severe bleeding; stabilises the endometrium |
5.2 Short-Term Medical Treatment
Inhibit cyclo-oxygenase → reduce endometrial prostaglandin levels → ↓ menstrual flow by 33–55% (1A evidence). Also improve dysmenorrhoea in up to 70%. More effective than placebo; less effective than TXA, danazol, or Mirena. [1]
| Drug | Dose |
|---|---|
| Mefenamic acid | 250–500 mg TDS |
| Naproxen | 250–500 mg BD |
| Ibuprofen | 600 mg daily |
Anti-fibrinolytic agent. Blocks plasminogen. 1 g up to QID during days of heavy menses. Reduces blood loss by 40–50% per cycle (1A evidence). Less effective than LNG-IUS; more effective than placebo, NSAIDs, and luteal-phase progestins. [1]
- 36.3% reduction with TXA vs. 10.9% with placebo.
- Probably improves QoL.
- Cautious with contraceptive pills use and history of VTE (limited data). [1]
Contain estrogen + progestogen. Prevent proliferation of endometrium. Additional advantages: contraception, ↓ dysmenorrhoea, cycle control. Option of extended-cycle use for women with dysmenorrhoea or pelvic pain. [1]
- COC over 6 months reduces HMB from 12% to 77% (vs. 3% placebo).
- More effective than placebo; less effective than LNG-IUS.
- COC and contraceptive vaginal ring have similar effects (COC: greater likelihood of nausea).
Used in the LUTEAL phase only (short cycle) = NO benefit for heavy bleeding, only for cycle regularity. [1] Used throughout follicular AND luteal phases (long cycle, 21 days/cycle) = reduces blood loss by ~83%. [1]
- Norethisterone 15 mg daily for 21 days.
- Side effects: breast tenderness, water retention, weight gain, headache, acne.
- Less effective than LNG-IUS and tranexamic acid.
Critical Exam Point: Luteal-Phase-Only Progestin Does NOT Reduce HMB
Short-cycle (luteal-phase only) progestin is for CYCLE REGULARITY only, not for reducing heavy bleeding. To reduce blood loss, you must use a LONG-CYCLE (21-day) regimen. This is a common exam trap. [1]
Medroxyprogesterone acetate 150 mg IM every 12 weeks. No studies available specifically for AUB/menorrhagia. High rate of amenorrhoea ( > 50% at 1 year). Side effects: unpredictable spotting, decreased BMD. [1]
5.3 Long-Term Medical/Procedural Treatment
Prevention of endometrial proliferation. Licensed for management of menorrhagia. Reduces blood loss up to 71–96%. Also improves dysmenorrhoea. Full benefit may not be seen for 6 months. 20–80% amenorrhoeic in 1 year. [1]
Why LNG-IUS is the gold standard medical treatment for HMB:
- It delivers progesterone directly to the endometrium → profound endometrial suppression with minimal systemic absorption.
- This avoids systemic side effects of oral progestins.
- It also provides excellent contraception.
- Multiple Cochrane reviews show it is the most effective non-surgical treatment.
| Treatment | Relative Effectiveness |
|---|---|
| LNG-IUS (Mirena) | Most effective medical treatment |
| Danazol | ↑ effective but more side effects |
| Tranexamic acid | ↑ effective than NSAIDs/oral progestins |
| COC | Moderate |
| NSAIDs | Moderate; also ↓ dysmenorrhoea |
| Luteal-phase progestin | Least effective (cycle regularity only) |
5.4 Other Interventional/Surgical Options
- Interventional radiology procedure; embolises uterine arteries to reduce blood supply to fibroids.
- Preserves the uterus but may affect fertility.
- Alternative to surgery for symptomatic fibroids.
A non-invasive technique using focused ultrasound energy to ablate fibroids. [1]
First generation: hysteroscopic resection/ablation. Effective in 87–97% of women. Amenorrhoea rates 23–60%. 6–20% require further intervention. Second generation: without direct visualisation — devices like heated balloon, microwave, radiofrequency. [1]
- NOT suitable for women who want future pregnancy (destroys endometrium).
- Requires reliable contraception post-procedure (pregnancy after ablation is dangerous).
- Surgical removal of fibroids while preserving the uterus.
- For women who want to retain fertility.
- Can be hysteroscopic (submucosal), laparoscopic, or open.
Surgical treatment is indicated when: medical therapy fails/is not tolerated; patient's choice/QoL impact; concomitant uterine pathology. [1]
- Definitive treatment — removes the uterus entirely.
- Approaches: abdominal, vaginal, or laparoscopic.
- Complications (commonly examined — 2018 Q11d): [2]
- Intraoperative: haemorrhage, injury to bladder/ureter/bowel
- Postoperative: infection (wound/pelvic), VTE, vault haematoma
- Long-term: vault prolapse, premature ovarian failure (if oophorectomy), psychological impact
Management according to causes: [1]
- Cervical polyp → simple avulsion
- CIN/CA of the cervix → colposcopy, excision, radiotherapy
- Endometrial/fibroid polyp → hysteroscopic excision
6. Dysmenorrhoea
Dysmenorrhoea = painful cramps occurring with menstruation. One of the most common causes of pelvic pain. Prevalence up to 80%. [1]
| Feature | Primary | Secondary |
|---|---|---|
| Definition | Absence of underlying pathology | Results from specific pelvic pathology |
| Onset | Typically 6–12 months after menarche | Any time, but often later in reproductive life |
| Peak prevalence | Late teens / early twenties | Depends on cause |
| Mechanism | ↑ Prostaglandins → myometrial contractions → ischaemia → pain | Depends on pathology |
The lecture lists: [1]
- Endometriosis — cyclic (can be non-cyclic)
- Adenomyosis
- Pelvic inflammatory disease — chronic pelvic pain
- Fibroids — fibroid polyp, associated with HMB; fibroids do NOT typically present with dysmenorrhoea
- Interstitial cystitis
- Irritable bowel syndrome
Diagnosis is clinical. USS pelvis to exclude ovarian cyst. Gold standard for diagnosing endometriosis is laparoscopy. [1]
Medical Treatment Ladder:
| Line | Treatment | Notes |
|---|---|---|
| First line | NSAID (e.g. mefenamic acid) | Inhibits prostaglandin synthesis |
| First line (hormonal) | COC pills — 2nd generation pills recommended | Suppresses ovulation → ↓ prostaglandin production |
| Second line | Progestogen (oral, IM, intrauterine, subcutaneous) | Endometrial suppression |
| Third line | GnRH agonist + add-back HRT if long-term use > 6 months | Creates pseudo-menopause; add-back HRT prevents bone loss |
Why add-back HRT with GnRHa? GnRHa causes profound hypoestrogenism → hot flushes, bone loss, vaginal dryness. Add-back estrogen/progestogen at low doses prevents these side effects while maintaining the therapeutic benefit on the pelvic pathology. Without add-back, GnRHa should not be used for > 6 months.
7. Amenorrhoea / Infrequent Periods
Infrequent period: reduction in frequency of periods where intervals vary between 6 weeks and 6 months. [1] Amenorrhoea: complete cessation of periods for > 6 months. [1]
- Primary amenorrhoea: absence of spontaneous onset of periods by age 16
- Secondary amenorrhoea: absence of periods for 6 months or more when a patient has regular periods before, OR 12 months or more when the patient has irregular cycles
7.2 Causes of Amenorrhoea
Interruption of the HPO axis results in amenorrhoea. [1]
- Pre-puberty, pregnancy, lactation, menopause
Congenital:
- Absence of uterus (with or without absent vagina) — e.g. Mayer-Rokitansky-Küster-Hauser (MRKH) syndrome
- Androgen Insensitivity Syndrome (AIS) — 46,XY individual with female external phenotype, testes (intra-abdominal), absent uterus, blind-ending vagina; previously called "testicular feminisation"
- Outflow tract obstruction — imperforate hymen or transverse vaginal septum → haematocolpos (blood accumulates in vagina) → cyclical pain with no visible menses
Acquired:
- Endometrial damage: traumatic (Asherman's syndrome — intrauterine adhesions, often post-D&C or post-infection), chronic endometritis (pelvic TB), endometrial resection/ablation
- Cervical stenosis (extremely rare): surgical trauma, infective
- Vaginal stenosis (extremely rare): chemical inflammation
The lecture organises endocrine causes by level of the HPO axis: [1]
| Level | Causes |
|---|---|
| Ovarian | Ovarian failure: genetic (Turner syndrome 45,X), autoimmune, post-surgery/chemo/radiotherapy, galactosaemia, idiopathic. PCOS |
| Pituitary | Pituitary failure: adenoma, infarction (Sheehan's syndrome), infection (encephalitis), irradiation. Hyperprolactinaemia: prolactinoma, primary hypothyroidism, chronic renal failure, drug-induced |
| Hypothalamic | Congenital: Kallmann syndrome (GnRH deficiency + anosmia). Functional: weight loss, anorexia nervosa, excessive exercise, psychological stress, debilitating illness |
| Others | Thyroid disease, adrenal disease |
Sheehan's Syndrome: Postpartum pituitary necrosis due to hypovolaemic shock during delivery. The pituitary enlarges in pregnancy (due to lactotroph hyperplasia) and is vulnerable to ischaemia if there is significant haemorrhage. Presents with failure to lactate (↓ prolactin) and amenorrhoea (↓ LH/FSH), plus features of other pituitary hormone deficiencies. [8]
Kallmann Syndrome: Failure of GnRH neurons to migrate from the olfactory placode to the hypothalamus during embryogenesis → GnRH deficiency + anosmia (loss of smell). Presents with primary amenorrhoea in females or delayed puberty in males. [8]
The lecture provides a comprehensive amenorrhoea-specific history checklist: [1]
- Detailed menstrual history — menarche, cycle length and duration
- Sexual and contraceptive history
- Secondary sexual characteristics (breast development, axillary/pubic hair)
- Cyclical abdominal pain (suggests outflow obstruction)
- Marked weight loss or gain
- Hyperandrogenism — acne, excessive hair, baldness
- Presence of galactorrhoea
- Vasomotor symptoms — hot flushes, night sweats (suggests ovarian failure)
- Symptoms of intracranial SOL — headache, vomiting, visual disturbance
- Psychological stress or excessive exercise
- Drug history
- History of previous surgery — surgical TOP, endometrial ablation
- Family history of early menopause, PCOS
Key examination points: [1]
- Height, weight, BMI
- Secondary sexual characteristics (Tanner staging)
- Galactorrhoea
- Hyperandrogenism (acne, excessive hair, baldness)
- Gynaecological examination: imperforate hymen, presence of uterus/vagina
- Detailed neurological examination including smell and ophthalmic examinations (Kallmann → anosmia; pituitary tumour → bitemporal hemianopia)
Hormonal profile interpretation: [1]
| FSH/LH | E2 | Interpretation | Level of Defect |
|---|---|---|---|
| Low | Low | Hypogonadotrophic hypogonadism | Hypothalamic or pituitary |
| High | Low | Hypergonadotrophic hypogonadism (ovarian insufficiency) | Ovary |
- If hyperprolactinaemia is found → MRI pituitary to exclude adenoma [1]
- Thyroid function tests
- Pelvic USS: presence and configuration of uterus, ovarian morphology (PCO features)
PCO Morphology ≠ PCOS
The lecture specifically states: PCO morphology on scanning does NOT equal PCOS. Up to 20% of normal women have polycystic ovarian morphology on USS. PCOS is a clinical syndrome diagnosed by the Rotterdam criteria. [1]
Rotterdam Criteria (2003)
Diagnosis requires 2 out of 3: [1]
- Oligo- and/or anovulation
- Clinical and/or biochemical signs of hyperandrogenism (and exclusion of other aetiologies: CAH, androgen-secreting tumours, Cushing's syndrome)
- Polycystic ovaries on scanning (≥ 12 follicles of 2–9 mm in at least one ovary OR ovarian volume > 10 cm³)
The updated assessment criteria also define clinically important cycle abnormalities by time since menarche:
- More than 1 to less than 3 years after menarche: cycle length < 21 or > 45 days.
- More than 3 years after menarche to perimenopause: cycle length < 21 or > 35 days, or fewer than 8 cycles per year.
- More than 1 year after menarche: any cycle interval > 90 days.
- Primary amenorrhoea by age 15, or more than 3 years after breast development, should prompt assessment.
- In adolescents with irregular cycles and hyperandrogenism, ultrasound is not indicated for diagnosis; reassessment is recommended rather than relying on polycystic ovarian morphology.
- In adults with irregular cycles and hyperandrogenism, ovarian ultrasound is not necessary to establish the diagnosis once other causes have been excluded. [1]
The lecture also mentions 2018 updated international assessment criteria for PCOS, which refine the ultrasound criteria and emphasise anti-Müllerian hormone (AMH) as an alternative to ultrasound in adults.
Why PCOS causes AUB: Chronic anovulation → no corpus luteum → no progesterone → unopposed estrogen → continuous endometrial proliferation → irregular shedding → irregular/heavy bleeding, AND increased risk of endometrial hyperplasia/cancer.
Why PCOS patients with poor compliance need endometrial assessment (Miss B case): 10 years of unopposed estrogen = significant endometrial cancer risk. This is the concern when Miss B returns with irregular heavy bleeding after defaulting follow-up. [1]
8. Case Scenarios (from the Lecture)
19-year-old student, good past health, menarche 13, regular cycles, stressful studies, weight loss 5 lb in 2 months, amenorrhoea 4 months. [1]
Approach:
- Sexually active? → Pregnancy test
- Thyroid symptoms/signs? → TFT
- BMI
- Both negative → likely hypothalamic cause (stress + weight loss)
- Management: optimise body weight + option of OCP for cycle regulation + contraception
6 months later: Good compliance to OCP, monthly withdrawal bleeding, but now c/o intermenstrual and postcoital spotting.
- Further investigation: endocervical swab for Chlamydia (sexually active + IMB/postcoital bleeding → STI screening). Also consider cervical screening if not done.
28-year-old, menarche 12, irregular 45–90 day cycles, normal flow, no pain, not sexually active. P/E: overweight, moderate acne and hair growth over face/limbs. [1]
Assessment:
- Clinically compatible with PCOS (oligomenorrhoea + hyperandrogenism + overweight).
- Menstrual management: cyclic Provera (medroxyprogesterone) for withdrawal bleeding if no periods for 3 months → prevents endometrial hyperplasia.
10 years later (defaulted): Irregular heavy bleeding for 3 months, pregnancy excluded.
- Concern: endometrial hyperplasia / endometrial cancer (10 years of unopposed estrogen from chronic anovulation).
- Action: endometrial biopsy (Pipelle), pelvic USS.
40-year-old, para 2, tubal ligation done, increasingly painful periods for 2 years, 16 weeks' gravid uterus on exam, Hb 9.8 g/dL. [1]
Most likely diagnosis: Adenomyosis (painful HMB + bulky uterus in a multiparous woman). Differential: Uterine fibroids (but fibroids typically don't cause dysmenorrhoea unless degenerating/submucosal).
Investigations:
- CBC (already showing anaemia — Hb 9.8)
- Pelvic USS (assess uterine pathology)
- Endometrial biopsy (age ≥ 40 with AUB → HKCOG guideline)
- Iron studies
Management:
- Correct anaemia (oral iron ± IV iron)
- Family complete + tubal ligation done → can consider definitive treatment: hysterectomy
- If wants to try medical first: LNG-IUS, GnRHa
- NSAID for dysmenorrhoea
10. Exam Intelligence
| Year | Question | Topic | Key Points Tested |
|---|---|---|---|
| 2018 Q11 | 46F with HMB + irregular periods | PE focus areas, investigations, DDx, hysterectomy complications | [2] |
| 2019 Q1 | 36F G2P2, HMB cycling 2–5 weeks | Initial investigations, structural causes, next step after failed COC | [3] |
| 2020 Minicase 3 | 55F with IMB + hot flushes → 2 years on unopposed estrogen | DDx of IMB in perimenopause, endometrial cancer risk factors, investigations | [4] |
| 2020 SAQ Q1 | 30F with vaginal spotting, 8/52 amenorrhoea, +ve PT, adnexal mass | Ectopic pregnancy exclusion, history, physical signs | [5] |
| 2020 SAQ Q9 | 28F acute severe lower abdominal pain, PV bleeding, LMP 6/52 ago | Ectopic pregnancy — investigations and management | [5] |
| 2024 MCQ Q13 | 40F LMP 8/52, left lower abd pain, TVUSS findings | Ectopic pregnancy management (serial β-hCG vs. laparoscopy) | [9] |
| Trap | Correct Approach |
|---|---|
| Using "DUB" or "menorrhagia" as a diagnosis | Use FIGO terminology: AUB-O, AUB-E, HMB, etc. |
| Thinking luteal-phase progestin reduces HMB | It only regulates cycles; use long-cycle (21-day) progestin for blood loss reduction |
| Ordering endometrial biopsy for all young women with AUB | HKCOG: biopsy if ≥ 40, or if risk factors, persistent symptoms, or failed medical Rx |
| Using endometrial thickness to predict pathology in premenopausal women | Not reliable — ET varies with cycle phase |
| Confusing PCO morphology with PCOS | PCO on scan ≠ PCOS; PCOS requires 2/3 Rotterdam criteria |
| Forgetting pregnancy test as the first investigation | Always first in any reproductive-age woman with AUB |
"Name 4 initial investigations for AUB" (common SAQ):
- Urine pregnancy test — to exclude pregnancy
- Complete blood count — to assess for anaemia
- Pelvic ultrasound — to assess for structural pathology
- Endometrial biopsy (Pipelle) — especially if ≥ 40 or risk factors
"Give 4 structural causes of HMB":
- Endometrial polyp
- Adenomyosis
- Leiomyoma (fibroid) — especially submucosal
- Endometrial hyperplasia / malignancy
"Name 3 complications of hysterectomy":
- Haemorrhage (intraoperative)
- Injury to adjacent organs (bladder, ureter, bowel)
- Infection (wound, pelvic abscess)
High Yield Summary
- Summary
-
- Always do a pregnancy test first in any reproductive-age woman with AUB. 2. FIGO System 1 defines normal menstruation by 4 parameters: frequency (24–38d), regularity (variation ≤7–9d), duration (≤8d), and volume (5–80 mL). IMB added in 2018. 3. FIGO System 2 (PALM-COEIN): Structural (Polyp, Adenomyosis, Leiomyoma, Malignancy) vs. Non-structural (Coagulopathy, Ovulatory dysfunction, Endometrial, Iatrogenic, Not classified). 4. HKCOG: Biopsy all women with AUB aged ≥ 40, or those with risk factors for endometrial cancer regardless of age. 5. LNG-IUS (Mirena) is the most effective medical treatment for HMB (71–96% reduction). 6. Luteal-phase-only progestin is for cycle regularity ONLY — does NOT reduce HMB. 7. Tranexamic acid reduces blood loss by 40–50%; more effective than NSAIDs; cautious with VTE history. 8. Endometrial hyperplasia without atypia has < 5% cancer risk (treat with progestogen); with atypia has 30–40% risk (hysterectomy). 9. PCOS diagnosis = 2/3 Rotterdam criteria. PCO morphology ≠ PCOS. 10. Amenorrhoea workup: Hormonal profile → low FSH/LH/E2 = hypogonadotrophic (hypothalamic/pituitary); high FSH/LH, low E2 = ovarian insufficiency. 11. Dysmenorrhoea: First-line = NSAID (mefenamic acid); hormonal first-line = COC (2nd gen); GnRHa is third-line with add-back HRT if > 6 months.
-
Active Recall - Menstrual Disorders
[1] Lecture slides: CFB (OG04) Menstrual Disorders.pdf [2] Past papers: 2018 Fourth Summative SAQ.pdf (Question 11) [3] Past papers: 2019 Fourth Summative SAQ.pdf (Question 1) [4] Past papers: 2020 Fourth Summative Minicases.pdf (Case 3) [5] Past papers: 2020 Fourth Summative SAQ.pdf (Questions 1 and 9) [6] Senior notes: Adrian Lui Gynecology Notes.pdf (Chapter 2 — Menstrual Disorders) [7] Senior notes: Block A - Pallor_ diagnosis of anaemia; nutritional anaemia; anaemia of systemic diseases.pdf [8] Senior notes: Block A - I keep on bumping into people on my side_ pituitary tumours; hypopituitarism.pdf [9] Past papers: 2024 Fourth Summative MCQ.pdf (Question 13)
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