## Pathophysiology of Uterine Fibroids **Key Point:** Uterine fibroids (leiomyomas) are benign smooth muscle tumors with distinct molecular and cellular characteristics that differentiate them from normal myometrium. ### Correct Statements | Feature | Details | |---------|----------| | **Origin** | Arise from myometrial smooth muscle; composed of smooth muscle cells, fibroblasts, and extracellular matrix | | **Monoclonal origin** | Each fibroid develops from a single transformed smooth muscle cell (demonstrated by cytogenetic and molecular studies) | | **Growth factors** | bFGF, TGF-β, VEGF, and FGF-2 promote fibroid proliferation and angiogenesis | | **Hormone receptors** | Estrogen and progesterone receptors are **INCREASED and ABNORMALLY DISTRIBUTED** in fibroid tissue | ### Why Option 2 Is Incorrect **High-Yield:** Hormone receptor expression in fibroids is **NOT uniform** compared to normal myometrium. Instead: 1. **Increased receptor density** — Fibroids have higher concentrations of estrogen receptors (ER-α and ER-β) and progesterone receptors (PR-A and PR-B) than surrounding normal myometrium. 2. **Altered distribution** — Receptors are abnormally localized within fibroid tissue, contributing to increased hormone sensitivity. 3. **Progesterone resistance** — Despite higher PR expression, fibroids show impaired progesterone signaling, leading to reduced responsiveness to progesterone-based therapies. **Clinical Pearl:** This altered hormone receptor profile explains why fibroids grow during reproductive years (estrogen-dependent) and regress after menopause, and why hormonal therapies (GnRH agonists, levonorgestrel IUD) are effective management options. **Mnemonic:** **HERM** — Hormone receptors are **Higher**, **Expressed abnormally**, and show **Resistance** to progesterone, making fibroids **Myometrium-dependent**.
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