Cancer is NOT the commonest cause → there are many many more benign causes ^[2]

The key mental model is anatomical classification — start from below and work upwards:

Common Causes listed on GC 112 slide: Fibroid, endometrial polyps, pregnancy-related, hyperplasia, dysfunctional uterine bleeding, anovulation, cervical erosion, cervical polyp, atrophic vaginitis, lacerations — these can be benign or malignant and can arise from any part of the genital tract ^[1]

First triage before classification: assess haemodynamic stability, quantify current blood loss, obtain IV access/resuscitate if unstable, check haemoglobin and perform a pregnancy test in anyone with pregnancy potential. Anticoagulation can worsen bleeding but must not be assumed to be the only cause without anatomical/endometrial assessment.

• Anovulation/DUB: The most common cause of endometrial bleeding is irregular ovulation causing irregular periods ^[2]. Without ovulation, there is no progesterone to stabilize the endometrium, leading to erratic shedding.
• Fibroids: Submucosal fibroids distort the endometrial cavity and increase surface area, causing heavy menstrual bleeding (HMB).
• Endometrial polyps: Focal endometrial overgrowths that cause intermenstrual or post-menopausal bleeding.
• Cervical ectropion (erosion): Columnar epithelium extends onto ectocervix; fragile, bleeds on contact. Common with OCP use, pregnancy.
• Atrophic vaginitis: Post-menopausal oestrogen deficiency → thin, fragile vaginal mucosa → bleeding with minimal trauma.

Ask where the patient is in her reproductive life: ^[1]

• Pre-menarche? → Think trauma, foreign body, precocious puberty, rare tumours (sarcoma botryoides)
• Pregnant? → Must exclude pregnancy-related causes (miscarriage, ectopic, molar pregnancy)
• Peri-menopausal? → Anovulatory cycles are common, but persistent AUB or endometrial-cancer risk factors require sampling; the slide's fixed “> 40” cutoff has been superseded by age/risk-based guidance
• Post-menopausal? → Must exclude endometrial cancer; also consider atrophic vaginitis, cervical cancer

Key questions: ^[1]

• Amount? — Quantify: number of pads/tampons, flooding, clots, haemodynamic symptoms
• Regular or irregular bleeding? — Regular heavy = structural cause (fibroid); irregular = anovulation or pathology
• Intermenstrual bleeding (IMB)? — Bleeding between periods → think polyps, cervical pathology, endometrial cancer
• Postcoital bleeding (PCB)? — Bleeding after intercourse → cervical ectropion, cervical polyp, cervical cancer

Provoking factors: Trauma? Stress? ^[1] Associated symptoms: Pain? Urinary/bowel symptoms? ^[1]

• Pain suggests adenomyosis, endometriosis, infection, or advanced malignancy
• Urinary/bowel symptoms suggest large pelvic mass or advanced cancer invading adjacent organs

Contraceptive history — Can she be pregnant? Is she on hormones? ^[1] Cervical screening history (HPV testing and/or cytology according to the local programme) ^[1] Obstetric history ^[1] Drug history — Anticoagulation? HRT? ^[1] Family history — FHx of Ca ovary / breast / colon etc? ^[1]

Why each matters:

• Contraceptives: OCPs can cause breakthrough bleeding; missing pills → pregnancy risk
• Cervical screening: no regular screening increases the risk of undetected HPV-related precancer/cancer. Hong Kong now uses primary HPV testing in Department of Health services for ages 30–64, while ages 25–29 use cytology ^[11]
• Anticoagulants: Warfarin, DOACs can exacerbate or cause vaginal bleeding
• HRT: Unopposed oestrogen → endometrial hyperplasia → cancer
• Family history: Lynch syndrome (hereditary nonpolyposis colorectal cancer / HNPCC) confers 15–60% lifetime risk of endometrial cancer ^[1]

Pallor (anaemia from chronic blood loss), bleeding tendency (petechiae, bruising), constitutional signs (weight loss, cachexia suggesting malignancy) ^[1]

Inspection: Scars / distention / signs of pregnancy? ^[1] Palpation: Mass? Tenderness? ^[1] Percussion: Ascites? (suggests advanced ovarian cancer) ^[1] Auscultation: Fetal heart? (pregnancy) ^[1]

Speculum examination: Can you see an abnormality? Lesion on vulva / vagina / cervix ^[1] Bimanual: Uterine size, adnexal masses ^[1] Rectal examination — assesses parametrial involvement in cervical cancer ^[1]

Cervical smear — screening for CIN/cervical dysplasia ^[1] Colposcopy — magnified examination of cervix after applying acetic acid; identifies abnormal areas for biopsy ^[1] Cervical biopsy — definitive tissue diagnosis ^[1]

Reading the cervix photograph: the smooth pink ectocervix with a central os is a speculum view, not a diagnosis by itself. Screening samples exfoliated cells/HPV from an asymptomatic cervix; colposcopy magnifies the transformation zone and directs biopsy. A symptomatic friable, ulcerated or exophytic lesion needs urgent specialist assessment and tissue diagnosis, even if the last screen was normal.

Current Hong Kong screening context: screening is for asymptomatic people aged 25–64 who have ever had sexual experience. Ages 25–29 use cytology; ages 30–64 may use HPV testing every 5 years, co-testing every 5 years or cytology under the programme schedule. Department of Health services transitioned to primary HPV testing for ages 30–64 in 2023 ^[11].

Endometrial aspirate (e.g., Pipelle) — office-based blind sampling; first-line in AUB from age 45, or younger with persistent bleeding, failed treatment or unopposed-oestrogen risk ^[12] Hysteroscopy with targeted biopsy — direct visualisation of the uterine cavity; especially valuable for focal lesions, inadequate/negative blind sampling with persistent bleeding, or discordant imaging

Reading the procedure diagrams: a Pipelle passes through the cervix and samples endometrium by suction, but can miss a focal polyp. Hysteroscopy distends the cavity and lets the operator distinguish a smooth focal polyp from irregular/friable malignant tissue and biopsy it directly.

Ultrasound — transvaginal (TVS) or transabdominal (TAS) ^[1]

• On TVUS, identify the midline endometrial echo and measure the double-layer thickness in the sagittal plane. The lecture's ≥5 mm threshold is historical; older ACOG guidance used > 4 mm in an initial PMB episode, while an April 2026 ACOG update recommends TVUS plus endometrial tissue sampling for most patients with PMB. Persistent/recurrent bleeding requires histology regardless of a thin stripe ^[13]. Follow the local pathway.

This table synthesizes the MCQ theme from the 2021 Fourth Summative ^[6]:

• 7th most common female cancer in Hong Kong in the slide's 2020 registry snapshot ^[1] — retain as historical local context, not a current rank
• Vaccination and effective screening reduce cervical-cancer burden, but the slide's local table actually shows a small positive 10-year ASR change (+1.2%) and a small mortality decline (−0.4%); do not invent a local downward incidence trend from the rank alone

Reading the 2020 registry figures: the table reports 556 registered cases, 159 deaths, age-standardised incidence 7.6 per 100,000 and 5-year relative survival 65.8% (2010–2018 cohort). The stage pie shows I 26.8%, II 22.1%, III 23.7%, IV 15.1% and 12.2% unstaged. These are dated population observations—not fixed personal survival estimates or current service performance.

Persistent high-risk human papillomavirus (HPV) — causes virtually all cervical cancers; HPV16/18 are especially important ^[1] Earlier sexual exposure, multiple partners or a partner with HPV exposures — epidemiologic proxies for acquiring persistent HPV, not moral labels Smoking — impairs local cervical immunity ^[1] Lower socio-economic class — reduced access to screening ^[1] Long-duration combined oral contraceptive use — a modest association that diminishes after stopping; it is not explained simply by “ectropion allowing HPV access” Immunosuppression — HIV, transplant patients; impaired HPV clearance ^[1]

Age: Median 55 ^[1] Bleeding pattern: Postcoital bleeding — the hallmark symptom ^[1] Associated symptoms: ^[1]

• Early disease — not much (asymptomatic; picked up on screening)
• Late disease — back pain / leg oedema (pelvic sidewall involvement, lymphatic obstruction)

Contraceptive/Sexual history: Sexually active (or had been), ? OC pills ^[1] Cervical screening history: no regular HPV/cytology screening ^[1] Obstetric history: Parous ^[1] Family history: Probably not related (cervical cancer is NOT a hereditary cancer) ^[1]

This slide contrast means cervical cancer is predominantly infection-driven rather than a classic hereditary-cancer syndrome; it does not mean family history or rare genetic susceptibility can never modify risk.

Growth on cervix: exophytic (cauliflower), endophytic (infiltrative, barrel shape), ulceration ^[1]

Reading the paired speculum images: the upper cervix is smooth with an intact surface; the lower image shows an irregular, friable, ulcerated exophytic mass with contact bleeding. Describe what is visible—site, size, exophytic/endophytic pattern, ulceration and bleeding—then biopsy. Do not diagnose or exclude invasion by appearance alone.

For diagnosis: Take a biopsy ^[1] For management planning: ^[1]

• Blood tests: CBP, RFT, LFT
• Selected biomarkers/tumour markers may support prognosis or surveillance, but SCC antigen is not a substitute for biopsy and is not a generic diagnostic test
• Imaging: CT / MRI / PET-CT to assess renal tract, extent of spread, lymph node involvement

Why RFT? Cervical cancer commonly causes ureteric obstruction → hydronephrosis → renal impairment. This is staging-relevant (Stage IIIB).

Local spread: Direct extension to parametrium, vagina, bladder, rectum ^[1] Distal spread: Lymphatic → pelvic lymph nodes → para-aortic lymph nodes; haematogenous spread to lungs, liver, bone (rare, late) ^[1]

Reading the spread diagrams: direct spread proceeds from cervix into upper vagina/parametria, then pelvic sidewall, ureters, bladder or rectum. Lymph drains through paracervical/obturator/internal and external iliac chains, then common iliac and para-aortic nodes. Hydronephrosis can therefore reflect ureteric compression at the pelvic sidewall.

Cervical cancer uses Clinical / Pathology / Imaging staging ^[1]

This is important — cervical cancer staging is NOT purely surgical (unlike endometrial cancer). Imaging and clinical examination contribute.

Detailed substaging (high yield for written exams):

The survival percentages are broad 2020-registry teaching estimates, not individual prognoses. Histology, nodal burden, tumour biology, treatment and contemporary outcomes all matter.

Reading the staging cartoon: stage I stays within the cervix; stage II extends to upper vagina/parametrium without pelvic sidewall; stage III reaches lower vagina/sidewall, causes hydronephrosis, or includes pelvic/para-aortic nodes; stage IV invades bladder/rectal mucosa or spreads distantly.

Treatment modalities: Surgery, Radiotherapy, Chemotherapy, Targeted therapy / immunotherapy ^[1]

Advantages of surgery over radiotherapy: preserves ovarian function, avoids long-term morbidities of radiotherapy ^[1]

Surgical-route and ovarian nuance: open surgery remains the standard approach when a radical parametrectomy is required because minimally invasive radical hysterectomy produced worse oncologic outcomes; rare highly selected low-risk tumours under expert protocols are exceptions ^[14]. Ovarian preservation/transposition may be considered in younger patients—more readily with squamous histology—but is individualised for histology, stage, genetics and planned radiotherapy.

Long-term RT morbidities include: vaginal stenosis, radiation cystitis, radiation proctitis, lymphoedema, premature ovarian failure (if ovaries irradiated), secondary malignancies.

Stage, lymph node metastasis, histology ^[1]

• Stage is the most important prognostic factor
• Lymph node positivity dramatically worsens prognosis
• Histology: squamous cell carcinoma (most common, ~70–80%) vs. adenocarcinoma (worse prognosis stage-for-stage)

• 4th most common female cancer in Hong Kong in the slide's 2020 registry snapshot ^[1]; the accompanying 2006–2020 plot shows rising age-standardised incidence with comparatively low, fairly stable mortality over that interval
• Predominantly a disease of post-menopausal women
• Most common gynaecological cancer in developed countries

Reading the registry panels: in 2020 the slide reports 1,186 cases, 121 deaths, age-standardised incidence 16.2 per 100,000 and 5-year relative survival 70.4% (2010–2018 cohort). The stage pie is dominated by stage I (68.6%), illustrating the benefit of bleeding as an early warning symptom; 5.8% were stage II, 8.1% stage III, 8.9% stage IV and 8.6% unstaged.

The unifying mechanism is unopposed oestrogen exposure on the endometrium:

Risk factor table from GC 112: ^[1]

Why each matters — first principles:

• Obesity: Adipose tissue contains aromatase → converts androgens to oestrone → chronic oestrogen exposure. Also: higher BMI → lower SHBG → more free oestrogen.
• Nulliparity/late menopause/early menarche: More lifetime ovulatory cycles → more cumulative oestrogen exposure without the protective effect of progesterone in pregnancy.
• PCOS: Chronic anovulation → no progesterone to oppose oestrogen.
• Tamoxifen: Anti-oestrogenic on breast tissue but pro-oestrogenic on endometrium → endometrial hyperplasia/cancer. This is a classic exam question!
• Lynch syndrome (HNPCC): Germline mutation in DNA mismatch repair genes (MLH1, MSH2, MSH6, PMS2). Lifetime endometrial cancer risk 15–60%. Also associated with colorectal cancer.
• Unopposed oestrogen HRT: Without progestogen, oestrogen stimulates endometrial proliferation.

CFB (OG04) also lists these risk factors: Obesity, PCOS, Lynch syndrome, FHx of gynae/GI malignancy, unopposed oestrogen therapy, tamoxifen, persistent/long-standing AUB, no response to medical treatment ^[8]

Abnormal bleeding presentations: ^[1]

• Change in menstrual pattern
• Prolonged bleeding
• Intermenstrual bleeding
• Irregular bleeding
• Post-menopausal bleeding

Key clinical pearl: Unlike cervical cancer (which is asymptomatic early), endometrial cancer presents early with bleeding — this is why prognosis is generally better.

"Corpus cancer — symptomatic at early stage (abnormal bleeding)" ^[1]

Lecture-era rule: “age over 40—sample” ^[1]. Current ACOG reproductive-age guidance uses older than 45 years as a first-line sampling trigger, and samples younger patients with persistent AUB, failed treatment or unopposed-oestrogen risk ^[12].

Post-menopausal bleeding requires prompt endometrial-cancer evaluation. The 5-mm slide threshold is not current; 2026 ACOG recommends TVUS plus tissue sampling for most patients ^[13].

Gold standard — hysteroscopy and biopsy ^[1]

Current investigation algorithm:

1. PMB → prompt specialist pathway; in most patients combine TVUS with endometrial tissue sampling under the current local/ACOG pathway. Persistent or recurrent bleeding needs histology even with a thin endometrium ^[13].
2. Reproductive-age AUB → pregnancy test first; sample at age > 45 or younger when persistent, treatment-resistant or exposed to unopposed oestrogen ^[12].
3. Hysteroscopy with targeted biopsy → use when focal pathology is suspected, office sampling is inadequate/negative despite persistent bleeding, or imaging and histology disagree.

Spread pattern (from GC 112 slide 41, diagram) ^[1]:

1. Direct extension: Through myometrium → serosa → adnexae
2. Downward: To cervix, vagina
3. Lymphatic: To pelvic → para-aortic lymph nodes
4. Transperitoneal: Across peritoneal cavity (peritoneal deposits)
5. Haematogenous: Lungs (late)

Reading the spread figure: arrows show downward cervical/vaginal extension, trans-tubal/adnexal or peritoneal spread, and lymphatic drainage from pelvic/lateral iliac to para-aortic nodes. This explains why myometrial depth, cervical stromal invasion, adnexal/peritoneal disease and nodal level each alter stage and adjuvant therapy.

The deck reproduces FIGO 2009 surgical staging ^[1]. FIGO revised endometrial-cancer staging in 2023 to integrate histologic type, LVSI and molecular classification where available; record the slide table for historical exam interpretation, but do not call modern staging “surgery alone” ^[15].

Detailed substaging:

Why myometrial invasion depth matters: The deeper the invasion, the higher the risk of lymph node metastasis. Stage IA (< 50% myometrial invasion) has excellent prognosis; Stage IB (≥ 50%) has significantly higher LN metastasis risk.

Modern molecular layer: classify tumours, where possible, as POLE-mutated, mismatch-repair deficient (MMRd), no specific molecular profile (NSMP), or p53-abnormal. These groups materially change prognosis and adjuvant-treatment decisions, so an anatomic stage alone is incomplete ^[15][16].

Standard surgery for most operable disease: total hysterectomy + bilateral salpingo-oophorectomy with risk-adapted nodal staging ^[16]

• TH = Total Hysterectomy, BSO = Bilateral Salpingo-Oophorectomy

Minimally invasive hysterectomy is preferred for apparent early-stage disease when feasible; sentinel-node mapping is commonly used for nodal staging rather than routine full lymphadenectomy ^[16]

Adjuvant treatment: ^[1]

• If LN positive → post-op chemo ± RT
• If high-risk group, even if LN negative → can consider brachytherapy ± chemotherapy
• If LN not done → give external RT if high risk

What defines “high risk” now? Risk grouping combines stage, histotype/grade, myometrial invasion, substantial LVSI and molecular class rather than a single old checklist ^[16].

Ovarian and fertility nuance: BSO is standard for most patients, but ovarian preservation can be considered in carefully selected premenopausal patients with low-grade, superficially invasive endometrioid disease, normal ovaries and no hereditary ovarian-cancer risk. Fertility-sparing progestin-based treatment is possible only for highly selected stage IA low-grade endometrioid disease with intensive surveillance; it is not represented in the 2023 slides ^[16].