## Adenomyosis: Pathophysiology and Clinical Features ### Definition and Pathogenesis **Key Point:** Adenomyosis is the presence of endometrial glands and stroma within the myometrium, typically defined as invagination of the basalis layer at a depth of ≥2.5 mm below the endometrial-myometrial junction (EMJ). **High-Yield:** The invagination theory is the most accepted mechanism: - Disruption of the endometrial-myometrial interface - Increased junctional zone thickness (>12 mm on MRI is suggestive) - Abnormal myometrial contractions - Altered uterine peristalsis ### Myometrial Dysfunction **Clinical Pearl:** Adenomyosis causes: - Increased frequency and amplitude of uterine contractions - Abnormal uterine peristalsis patterns - Impaired embryo transport and implantation - Dysmenorrhea (due to increased prostaglandin production and uterine contractions) - Menorrhagia (due to increased vascularity and angiogenesis) ### Risk Factors and Epidemiology **Mnemonic: CURET** — Curettage, Uterine procedures, Reproductive trauma, Endometriosis, Termination - Age (increases with advancing age, peak in 40–50 years) - Multiparity - Uterine curettage (D&C, miscarriage management) - Termination of pregnancy (medical or surgical) - Cesarean delivery - Myomectomy - Hysteroscopic procedures ### Adenomyosis vs. Endometriosis: Key Differences **Warning:** Adenomyosis and endometriosis are DISTINCT pathological entities, NOT the same condition in different locations. This is a critical distinction frequently tested in NEET PG. | Feature | Adenomyosis | Endometriosis | |---------|------------|---------------| | **Location** | Within myometrium (intrauterine) | Outside uterus (ectopic) | | **Pathogenesis** | Invagination of basalis endometrium | Retrograde menstruation, metaplasia, stem cell migration | | **Age of onset** | Typically 40–50 years | Typically 20–40 years | | **Parity** | More common in multiparous women | More common in nulliparous women | | **Primary symptom** | Menorrhagia + dysmenorrhea | Dysmenorrhea + chronic pelvic pain | | **Infertility mechanism** | Impaired implantation, abnormal contractions | Altered peritoneal fluid, mechanical distortion | | **Imaging (MRI)** | Junctional zone thickening (>12 mm) | Focal lesions, T2 hyperintense or hypointense | | **Histology** | Adenomyotic foci with smooth muscle hyperplasia | Endometrial glands/stroma without smooth muscle proliferation | | **Treatment response** | GnRH agonists, progestins, hysterectomy | Medical (NSAIDs, OCP, progestins) or surgical excision | | **Molecular profile** | Different from endometriosis | Different from adenomyosis | **Key Point:** While adenomyosis and endometriosis can coexist in the same patient ("adenomyotic endometriosis"), they have distinct pathophysiological mechanisms, epidemiologies, and molecular profiles. ### Diagnosis **High-Yield:** - **MRI:** Gold standard for diagnosis (junctional zone thickening, heterogeneous signal intensity) - **Transvaginal ultrasound:** Increasingly used; shows junctional zone abnormalities - **Histopathology:** Definitive diagnosis (endometrial glands ≥2.5 mm into myometrium) ### Clinical Presentation **Mnemonic: DAMP** — Dysmenorrhea, Abnormal uterine bleeding (menorrhagia), Menorrhagia, Pelvic pain - Severe dysmenorrhea (often progressive) - Menorrhagia (heavy, prolonged menstrual bleeding) - Chronic pelvic pain - Infertility (secondary, due to impaired implantation) - Enlarged, boggy uterus on examination [cite:Robbins 10e Ch 22; Park 26e Ch 19]
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