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Pathology · Adaptation: endometrial hyperplasia
Sample itemA 50-year-old obese woman with anovulatory cycles has prolonged heavy bleeding. Endometrial biopsy shows crowded glands with a high gland-to-stroma ratio and nuclear atypia. Which statement about the mechanism and risk is correct?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
C. Unopposed oestrogen drives glandular proliferation, and atypical hyperplasia can progress to endometrioid carcinoma
Obesity increases peripheral aromatisation of androgens to oestrone, and anovulation removes progesterone, so oestrogen acts unopposed on the endometrium. This is pathological hyperplasia, a hormone-driven adaptation that reverses when the stimulus is removed. When cytological atypia is present the lesion is a precursor of endometrioid adenocarcinoma, often with PTEN mutations.
Option by option
A. It is physiological hypertrophy of endometrial cells that never progresses once the stimulus is removed
Hyperplasia involves increased cell number, not only hypertrophy, and atypical forms do carry malignant potential.
B. Excess progesterone causes stromal decidualisation, which is the premalignant lesion for endometrial cancer
Progesterone opposes oestrogen and causes secretory change or decidualisation, which is not a precursor of cancer.
C. Unopposed oestrogen drives glandular proliferation, and atypical hyperplasia can progress to endometrioid carcinoma (correct)
Correct. Unopposed oestrogen and atypia explain the risk of endometrioid carcinoma.
D. It arises from TP53 loss in atrophic endometrium and usually progresses to serous carcinoma
TP53-driven serous carcinoma arises from atrophic endometrium through serous intraepithelial carcinoma and is not oestrogen related.
Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.
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