A 43-year-old multiparous woman presents with progressive dysmenorrhea, heavy menstrual bleeding, and chronic pelvic pain over 3 years. On examination, her uterus is diffusely enlarged, globular, soft, and tender. After failed medical therapy, hysterectomy is performed. The gross specimen shows a diffusely thickened myometrium with a trabeculated cut surface. The structures marked **B** in the diagram—small hemorrhagic cystic spaces scattered throughout the myometrium—represent ectopic endometrial tissue. Which of the following best describes the pathophysiological mechanism by which these structures contribute to the patient's heavy menstrual bleeding?
A. Disruption of the spiral arteries in the basal layer of the endometrium leading to abnormal vascularity
B. Increased endometrial surface area and impaired uterine contractility due to ectopic endometrial glands within the myometrium
Invasion of myometrial vessels by adenomyotic lesions resulting in direct arteriovenous fistulae
C.
D. Excessive production of prostaglandins by the ectopic endometrial stroma causing uterine hypercontractility
Explanation
Why option 1 is correct
The small hemorrhagic cystic spaces marked B represent ectopic endometrial glands and stroma invaginated into the myometrium—the hallmark of adenomyosis. These ectopic endometrial foci increase the total endometrial surface area available for menstrual shedding and simultaneously disrupt normal myometrial contractility through smooth muscle hyperplasia and disorganization. Both mechanisms directly cause heavy menstrual bleeding (HMB), which is one of the cardinal clinical features of adenomyosis. Williams Gynecology and FIGO 2018 Classification emphasize that the presence of endometrial glands and stroma >2.5 mm below the endo-myometrial junction (as seen in the histology of this case) defines adenomyosis and explains the bleeding phenotype.
Why each distractor is wrong
Option 2: While adenomyosis does involve disruption of the junctional zone, the primary mechanism of HMB is not abnormal spiral artery architecture but rather the increased endometrial surface and impaired contractility caused by the ectopic endometrial tissue itself. Spiral artery remodeling is more characteristic of endometriosis than adenomyosis.
Option 3: Although prostaglandins are elevated in adenomyosis and contribute to dysmenorrhea and pain, the primary mechanism of HMB is not prostaglandin-induced hypercontractility but rather the enlarged endometrial surface area and contractile dysfunction. Excessive prostaglandins cause cramping pain, not bleeding per se.
Option 4: Arteriovenous fistulae are not a recognized pathophysiological feature of adenomyosis. This mechanism is more relevant to severe endometriosis with deep infiltration or to vascular malformations, not to the ectopic endometrial cysts seen in adenomyosis.
High-YieldNEET PG
Adenomyosis causes HMB through two mechanisms: (1) increased endometrial surface area from ectopic glands, and (2) impaired myometrial contractility from smooth muscle disorganization—not through prostaglandin excess or vascular fistulae.
Williams Gynecology 4e Ch 11; FIGO 2018 Classification
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