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PH-RO12

Endometrial hyperplasia and adenomyosis

How unopposed oestrogen causes endometrial hyperplasia, how a PTEN-deficient clone forms atypical hyperplasia (the precursor of endometrioid carcinoma), and how endometrium within the uterine muscle (adenomyosis) causes heavy, painful periods.

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  • 5 steps · 10 questions
  • 3D anatomy, affected parts marked

By the end, you can

  • Explain how unopposed oestrogen from anovulation, obesity or tamoxifen leads to endometrial hyperplasia.
  • Distinguish hyperplasia without atypia from atypical hyperplasia (endometrioid intraepithelial neoplasia) by clonality, microscopy and risk of carcinoma.
  • Describe adenomyosis and how injury to the junctional zone may let endometrium grow into the muscle.
  • Relate the gross and microscopic appearance of adenomyosis to a diffusely enlarged, globular uterus.
  • Explain why hyperplasia causes irregular bleeding and adenomyosis heavy, painful periods, and contrast both with endometriosis.
  • Recognise the classic microscopy, sampling methods and ultrasound and MRI signs of both conditions, and explain how progestogens (including the levonorgestrel intrauterine system), GnRH analogues and hysterectomy act on their mechanisms.

What it is

Both are disorders of the endometrium: too much of it, or in the wrong layer. Endometrial hyperplasia is an overgrowth of endometrial glands, crowded relative to the stroma, usually driven by oestrogen without enough progesterone; it divides into hyperplasia without atypia and atypical hyperplasia (endometrioid intraepithelial neoplasia), the precursor of endometrioid carcinoma. Adenomyosis is endometrial glands and stroma within the myometrium, with overgrowth of the muscle around them; unlike endometriosis, the tissue stays within the uterus.

4 types to tell apart
Hyperplasia without atypia
A diffuse, polyclonal response to oestrogen: more glands than usual, irregular in size and shape, but with nuclei like those of normal proliferative endometrium. Older systems split it into simple and complex hyperplasia.
Atypical hyperplasia (EIN)
A clonal proliferation of crowded glands whose cells differ from the background endometrium, often with loss of PTEN; a precancerous lesion. Older systems called it simple or complex atypical hyperplasia.
Diffuse adenomyosis
Foci scattered through the wall, often more in the posterior wall, giving a uniformly enlarged, globular uterus.
Focal adenomyosis and adenomyoma
A localised area of adenomyosis; an adenomyoma is a nodule of endometrial glands and stroma in overgrown smooth muscle, without the pseudocapsule that lets a fibroid shell out cleanly.

US spelling: oestrogen → estrogen.

Normal function

Endometrium, junctional zone and myometrium

The and of the uterus are lined by the endometrium: simple columnar epithelium forming tubular glands in a cellular stroma. Its deep basal layer persists and rebuilds the superficial functional layer after each period. There is no submucosa: the basal layer rests directly on the smooth muscle of the myometrium along an irregular border.

The innermost myometrium, the junctional zone, differs from the outer muscle: its cells are more tightly packed with less matrix between them, and on MRI it shows as a dark inner band. It contracts in waves that help carry sperm towards the tubes and push menstrual tissue out.

Oestrogen drives proliferation of glands and stroma in the first half of the cycle. After ovulation, progesterone from the corpus luteum stops that proliferation and differentiates the lining; its withdrawal then triggers complete, orderly shedding. Without progesterone, both the brake and the regular reset are lost.

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