Endometrial Hyperplasia
Endometrial hyperplasia is a proliferation of endometrial glands relative to stroma, primarily caused by unopposed estrogen. It is a significant risk factor for the development of endometrioid adenocarcinoma.
1. Pathophysiology & Risk Factors
- Mechanism: Chronic estrogen stimulation without progesterone opposition leads to continuous mitotic activity in the endometrium.
- Risk Factors: Anovulatory cycles (e.g., PCOS), obesity (peripheral conversion of androgens to estrogen), estrogen-secreting tumors (granulosa cell tumors), and hormone replacement therapy (without progesterone).
2. Classification
| Type | Key Features |
|---|---|
| Hyperplasia without Atypia | Increased gland-to-stroma ratio; architectural crowding but no significant nuclear atypia. |
| Atypical Hyperplasia | Architectural crowding plus cytological atypia (enlarged, round nuclei, loss of polarity). |
3. Exam Must-Knows
- Clinical Presentation: Postmenopausal bleeding or abnormal uterine bleeding in perimenopausal women.
- Malignancy Risk: Atypical hyperplasia is a direct precursor to adenocarcinoma; hysterectomy is often indicated.
Pathology Board Hint: For board exams, always identify the root cause: unopposed estrogen. If you see a patient with PCOS or obesity presenting with irregular bleeding, consider hyperplasia. Atypical hyperplasia is the “high-risk” category that needs immediate surgical evaluation.