First principle: menstruation is a progesterone‑withdrawal event
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Progesterone withdrawal triggers prostaglandin release, spiral‑artery vasoconstriction, ischaemic breakdown, and controlled shedding of the functionalis, with regeneration from the basalis.
Reasoning to abnormal bleeding
- PGF₂α drives both the vasoconstriction and the myometrial cramping → the mechanism of primary dysmenorrhoea (Concept 15) and the rationale for NSAIDs.
- Local haemostasis (vasoconstriction + platelet/fibrin plug) limits loss; defects (e.g. von Willebrand disease) → heavy menstrual bleeding.
- Unopposed estrogen (no progesterone to withdraw from in an orderly way) → irregular, unpredictable breakdown (Concept 14).
Discriminators
| Bleeding pattern | Mechanistic clue |
|---|---|
| Heavy but regular, cyclical | ovulatory; structural (fibroid/adenomyosis) or haemostatic |
| Irregular, unpredictable | anovulatory / unopposed estrogen |
| Postcoital | cervical (Concept 38) |
| Postmenopausal | endometrial malignancy until excluded 🚩 |
Pitfalls
- Attributing heavy regular menstrual bleeding to "hormones" without excluding structural causes (fibroid, adenomyosis) and coagulopathy.
Pearls
- 🎯 Menses = progesterone withdrawal → PGF₂α → ischaemic shedding. This one mechanism yields NSAID logic, dysmenorrhoea, and the anovulatory‑bleeding pattern.
- 🩺 Ask every adolescent with menorrhagia since menarche about bleeding history — inherited coagulopathy is under‑diagnosed.
Next → How do I turn cycle physiology into fertile‑window logic and correctly timed tests? (Concept 13).