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Q1: Definition, classification and clinical presentation (2 min)
- Define endometriosis. Functional endometrial glands AND stroma outside the uterine cavity, responsive to cyclic hormones. Distinguish from adenomyosis (endometrium within the myometrium — enlarged, boggy, tender uterus with menorrhagia).
- Name the three phenotypes and the commonest site. Superficial peritoneal (red/black 'powder-burn'/white opacified lesions), ovarian endometrioma ('chocolate cyst'), and deep infiltrating endometriosis (DIE). Ovary is the commonest site overall.
- State the classic triad and an atypical presentation. Triad: secondary dysmenorrhoea + deep dyspareunia + chronic pelvic pain; infertility may be the only feature. Atypical: asymptomatic infertility; teenager with refractory dysmenorrhoea; catamenial pneumothorax/haemoptysis (thoracic); cyclical scar nodule (caesarean/episiotomy scar).
- Key pearl: pain severity does NOT correlate with rASRM stage — a few deep nodules can cause excruciating pain while extensive superficial disease is silent.
Q2: Pathophysiology (2 min)
- Leading theory of origin? Sampson's retrograde menstruation — necessary but not sufficient (occurs in up to 90 per cent of women, only 10 per cent develop disease). Alternative theories: coelomic metaplasia, Müllerian remnants, lymphatic/vascular spread, induction theory.
- Three molecular hallmarks? (1) Oestrogen dependence — implants overexpress aromatase, make their own oestradiol; (2) progesterone resistance — reduced PR-B, low 17-beta-HSD type 2 (the molecular lynchpin); (3) chronic inflammation — macrophage IL-1, IL-6, IL-8, TNF-alpha and PGE2 drive pain and adhesions (PGE2 upregulates aromatase in a positive-feedback loop).
- Why does it cause infertility? Anatomic distortion (adhesions, tubal block), ovulatory dysfunction (luteinised unruptured follicle), peritoneal inflammation (cytokines toxic to gametes/embryos), impaired oocyte quality, and impaired implantation (progesterone resistance).
Q3: Investigations (2 min)
- First-line imaging and the pathognomonic finding? Transvaginal ultrasound — ground-glass echogenic content, no papillary projections, thick wall, no internal Doppler flow = ovarian endometrioma.
- Role of CA-125? Non-specific, NOT diagnostic (raised in malignancy, PID, pregnancy, menstruation); used in work-up of an adnexal mass and to monitor known disease — a normal value does not exclude endometriosis.
- When is MRI used? To map deep infiltrating endometriosis before surgery (bowel, bladder, ureter, rectovaginal septum). Endometriomas are T1-hyperintense with T2 'shading sign'.
- Is laparoscopy always required before treatment? No — a clinical-plus-imaging diagnosis permits empiric hormonal therapy. Laparoscopy (with histology) is the gold standard but is reserved for refractory disease, suspected malignancy, or when surgery is planned.
Q4: Management (3 min)
- Pain ladder (drug, dose, route): Step 1 — NSAIDs (ibuprofen 400 mg PO TDS) + continuous combined OCP. Step 2 — progestogen: dienogest 2 mg PO OD, LNG-IUS (Mirena), DMPA 150 mg IM every 3 months. Step 3 — GnRH agonist goserelin 3.6 mg SC every 4 weeks + add-back (tibolone 2.5 mg PO OD); OR oral GnRH antagonist relugolix combination OD / elagolix 150 mg OD or 200 mg BD.
- Why add-back? GnRH agonists cause hypo-oestrogenic bone loss (limit 6 months without add-back); add-back counteracts this and allows up to 12 months or longer without reducing efficacy.
- Surgery: excision preferred over ablation for DIE; cystectomy (stripping) preferred over drainage/ablation for endometrioma (lower recurrence, but counsel on ovarian-reserve loss). Hysterectomy + BSO reserved for completed-family refractory disease.
- Infertility: surgery improves fertility only in early-stage (rASRM I to II) disease; medical suppression does NOT improve spontaneous fertility (it suppresses ovulation); IVF is most effective for advanced disease; use the Endometriosis Fertility Index to guide strategy.
Q5: Complications, prognosis and pitfalls (2 min)
- Complications: infertility; chronic pelvic pain with central sensitisation; reduced quality of life/work productivity; small but real risk of malignant transformation (clear-cell / endometrioid ovarian carcinoma); surgical loss of ovarian reserve, ureteric/bowel injury, adhesions; medical hypo-oestrogenic bone loss.
- Prognosis: chronic, relapsing, NOT curable but manageable. Recurrence 20 to 40 per cent at 5 years after surgery (lower with post-operative hormonal suppression). Disease regresses after menopause (but HRT — especially oestrogen-only — may reactivate it). Pain usually improves in pregnancy.
- Pitfalls: normalising severe dysmenorrhoea (average diagnostic delay 6 to 10 years); over-operating (repeat laparoscopies cause adhesions); missing ureteric DIE (silent hydronephrosis, irreversible renal loss — always check the ureters and renal function); assuming a complex adnexal mass is an endometrioma without excluding malignancy.