PA29.{2-3,9} | Endometrial Hyperplasia, Carcinoma & Uterine Smooth Muscle Tumors — Summary & Reflection

REFLECT

Take a moment to consider this integrated question before looking at the summary:

A 67-year-old woman with BMI 38, type 2 diabetes, and no prior pregnancies presents with vaginal bleeding. She had her menopause at age 55. TVS shows endometrial thickness of 14 mm. Endometrial biopsy reveals Grade 2 endometrioid adenocarcinoma. MRI shows invasion of 60% of the myometrial thickness with no cervical or adnexal involvement.

Reflect on:
1. Which risk factors for endometrial carcinoma does this woman carry, and through what molecular mechanism do obesity and diabetes increase risk?
2. What is the FIGO stage of this carcinoma, and what does that imply for prognosis and treatment planning?
3. If the histology had instead shown a serous carcinoma in an atrophic background endometrium, how would the molecular profile, precursor lesion, and prognosis differ?
4. If a contemporaneous pelvic ultrasound showed a 6 cm uterine mass with whorled appearance and post-menopausal hormonal cessation had caused it to shrink compared to prior scans, what would be your diagnostic reasoning?

Think through each before moving to the summary. This is the calibre of reasoning expected in clinical viva examinations.

KEY TAKEAWAYS

Core take-aways from this SDL:

Endometrial Hyperplasia:
• Driven by unopposed estrogen — anovulation, obesity, exogenous estrogen, PCOS, tamoxifen.
• Two-tier WHO classification: non-atypical (< 5% progression) vs atypical hyperplasia/EIN (25–40% progression to carcinoma; PTEN loss is the key molecular event).

Endometrial Carcinoma:
• Type I endometrioid (80%): estrogen-driven, perimenopausal, precursor = EIN, PTEN/MSI/KRAS mutations, low-grade, good prognosis.
• Type II serous (10%): non-estrogen, older postmenopausal, atrophic background, precursor = SEIC, TP53-driven, high-grade, poor prognosis.
• Presentation: postmenopausal bleeding (PMB) = investigate immediately.
• Diagnosis: TVS (endometrial thickness) → endometrial sampling (Pipelle/D&C/hysteroscopy).
• FIGO staging: Stage IA (< ½ myometrium) → IB (≥ ½) → II (cervical stroma) → III (beyond uterus) → IV (bladder/bowel/distant).
• Spread: direct, lymphatic (pelvic → para-aortic), transtubal (serous), haematogenous (late).

Uterine Leiomyoma:
• Most common uterine tumour — estrogen and progesterone-dependent, regresses post-menopause.
• Gross: well-circumscribed, whorled, pseudocapsule. Micro: interlacing spindle cells, cigar-shaped nuclei, no atypia, < 5 mitoses/10 HPF.
• Clinical: menorrhagia, bulk symptoms, infertility.

Leiomyosarcoma:
• Arises de novo (not from leiomyoma). Solitary, large, fleshy, necrotic.
• Stanford criteria: severe atypia + ≥ 10 mitoses/10 HPF + tumor cell necrosis.
• Spreads haematogenously (lung). Poor prognosis.
• A post-menopausal fibroid that grows must raise this suspicion.