First principle: no ovulation → no progesterone → unopposed estrogen
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The endometrium proliferates without orderly progesterone withdrawal → erratic bleeding now, and hyperplasia → carcinoma risk later. This links PCOS, obesity, perimenopause and endometrial cancer.
Structure the work‑up: PALM‑COEIN
| Structural (PALM — imaging/biopsy) | Non‑structural (COEIN — history/labs) |
|---|---|
| Polyp | Coagulopathy |
| Adenomyosis | Ovulatory dysfunction |
| Leiomyoma (fibroid) | Endometrial |
| Malignancy/hyperplasia 🚩 | Iatrogenic |
| Not otherwise classified |
Reasoning workflow
- Exclude pregnancy and malignancy risk (age, unopposed‑estrogen risk factors, postmenopausal bleeding). 🚩
- Pattern: regular‑heavy (think structural/haemostatic) vs irregular (think ovulatory dysfunction).
- Investigate: ultrasound ± endometrial biopsy when malignancy risk is present.
Red flags 🚩
- Postmenopausal bleeding, or AUB with atypical hyperplasia risk factors → biopsy the endometrium.
Pitfalls
- Labelling irregular bleeding "hormonal" (COEIN) without excluding a structural cause or hyperplasia, especially in the anovulatory‑obese‑PCOS phenotype.
Pearls
- 🎯 Anovulation = unopposed estrogen = irregular bleeding + hyperplasia risk.
- 🩺 In a chronically anovulatory woman, cyclical or continuous progestin protects the endometrium.
Next → The other common menstrual complaint — pain (Concept 15).