Part 1 Science Notes
MRCOG Part 1
Pathology
Gynaecological Pathology
Cervical Pathology
Cervical Intraepithelial Neoplasia (CIN)
- CIN 1: mild dysplasia, lower 1/3 of epithelium; most regress spontaneously (60%)
- CIN 2: moderate dysplasia, lower 2/3; intermediate regression/progression
- CIN 3: severe dysplasia / carcinoma in situ, full thickness; 30-50% progress to invasive cancer over 10-30 years
- HPV types: 16 and 18 cause ~70% of cervical cancers; 6 and 11 cause genital warts (NOT cancer)
- HPV vaccination: 9-valent vaccine (Gardasil 9) covers types 6, 11, 16, 18, 31, 33, 45, 52, 58
Cervical Screening (UK Programme)
- Uniform 5-yearly interval for ages 25-64 with an HPV-negative result (extended from the previous 3-yearly-under-50/5-yearly-50+ split, effective 1 July 2025 — see NHS cervical screening programme guidance)
- First invitation at age 24.5
- HPV primary screening (since 2019): HPV test first → if positive → cytology triage on the same sample; if HPV-negative, routine recall in 5 years regardless of age
- HPV-vaccinated individuals still require screening — the vaccine does not cover all oncogenic HPV subtypes
- Colposcopy: acetic acid (white areas = acetowhite = abnormal); iodine (Schiller's test: normal epithelium stains brown; abnormal does not take up iodine)
Cervical Cancer
- Squamous cell carcinoma (80%), adenocarcinoma (20%)
- FIGO staging: Stage I (confined to cervix), Stage II (beyond cervix, not to pelvic wall), Stage III (pelvic wall/lower vagina/hydronephrosis), Stage IV (bladder/rectum/distant)
- Treatment: early (IA1-IB1) — surgery; advanced — chemoradiotherapy (cisplatin-based)
Endometrial Pathology
Endometrial Hyperplasia
- Without atypia: low risk of progression to cancer (<5%); managed with progestogens (LNG-IUS first-line) or observation
- With atypia (endometrial intraepithelial neoplasia): 30-40% risk of progression or concurrent cancer; hysterectomy recommended (unless fertility desired → high-dose progestogens with close surveillance)
- Risk factors: unopposed oestrogen (obesity, PCOS, tamoxifen, oestrogen-only HRT without progestogen), nulliparity, late menopause
Endometrial Cancer
- Most common gynaecological cancer in developed countries
- Type 1 (80%): endometrioid; oestrogen-dependent; younger, obese patients; better prognosis; often preceded by hyperplasia
- Type 2 (20%): serous, clear cell; NOT oestrogen-dependent; older patients; poorer prognosis; not preceded by hyperplasia
- FIGO staging: I (confined to corpus), II (cervical stromal invasion), III (local spread: serosa, adnexa, vagina, nodes), IV (bladder/bowel mucosa or distant)
- Treatment: total hysterectomy + BSO ± lymphadenectomy ± adjuvant therapy
Ovarian Tumours
Classification
| Category | Examples | Key Features |
|---|---|---|
| Epithelial (60-70%) | Serous (most common), mucinous, endometrioid, clear cell, Brenner | Most common in postmenopausal; serous can be high-grade (aggressive) or low-grade |
| Germ cell (15-20%) | Mature teratoma (dermoid cyst — most common benign), immature teratoma, dysgerminoma, yolk sac tumour, choriocarcinoma | Young women; dermoid: hair, teeth, fat, thyroid (struma ovarii); dysgerminoma = seminoma equivalent |
| Sex cord-stromal (5-8%) | Granulosa cell tumour, fibroma, thecoma, Sertoli-Leydig cell tumour | Granulosa cell: produces oestrogen → endometrial hyperplasia/cancer; Sertoli-Leydig: virilisation |
Tumour Markers
- CA-125: epithelial ovarian cancer (not specific — elevated in endometriosis, fibroids, pregnancy, peritonitis)
- AFP: yolk sac tumour, immature teratoma
- hCG: choriocarcinoma, dysgerminoma (some)
- LDH: dysgerminoma
- Inhibin: granulosa cell tumour
- RMI (Risk of Malignancy Index): CA-125 × ultrasound score × menopausal status; RMI ≥250 → refer to cancer centre
Gestational Trophoblastic Disease (GTD)
| Type | Features |
|---|---|
| Complete mole | 46,XX (all paternal origin — androgenetic); no fetal tissue; "snowstorm" USS; very high hCG; 15-20% risk of malignant transformation |
| Partial mole | 69,XXX or 69,XXY (triploid); some fetal tissue present; lower hCG than complete; 0.5-5% malignancy risk |
| Choriocarcinoma | Highly malignant; follows molar pregnancy (50%), miscarriage (25%), normal pregnancy (25%); haematogenous spread (lung most common); very sensitive to chemotherapy (cure rate >95%) |
- Follow-up: serial hCG monitoring through specialist centres (Charing Cross, Sheffield, Dundee)
- Advise against pregnancy until hCG normalised and follow-up complete
Vulval Pathology
- Lichen sclerosus: white atrophic plaques; itching; affects vulva perianally ("figure-of-eight"); 3-5% risk of vulval SCC; treat with potent topical steroids (clobetasol); lifelong follow-up
- VIN (vulval intraepithelial neoplasia): usual type (HPV-related, younger) vs differentiated type (non-HPV, associated with lichen sclerosus, higher malignancy risk)
- Vulval cancer: SCC most common (90%); presents as lump/ulcer; staging includes inguinal lymph node assessment; sentinel node biopsy increasingly used
Fibroids (Leiomyomas)
- Most common benign uterine tumour; oestrogen and progesterone dependent
- Types: submucosal (most symptomatic — menorrhagia), intramural, subserosal
- Degeneration types: hyaline (most common), red/carneous (in pregnancy — acute pain), cystic, calcific, sarcomatous (<0.5%)
- Treatment: medical (tranexamic acid, GnRH agonists, ulipristal), surgical (myomectomy, hysterectomy), UAE (uterine artery embolisation)
Important Facts for MRCOG
- HPV 16 and 18: cause 70% of cervical cancers; HPV 6 and 11: cause warts only
- Endometrial hyperplasia with atypia: 30-40% malignancy risk → hysterectomy recommended
- Type 1 endometrial cancer: endometrioid, oestrogen-dependent, better prognosis
- Granulosa cell tumour: produces oestrogen → endometrial hyperplasia; marker = inhibin
- Complete mole: 46,XX (all paternal); partial mole: triploid
- Choriocarcinoma: highly chemo-sensitive; cure rate >95%
- Lichen sclerosus: 3-5% risk of vulval SCC; treat with clobetasol
- Red degeneration of fibroids: occurs in pregnancy; managed conservatively
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