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| Complex Hyperplasia | ||
| Etiology •associated with unopposed estrogen use •may be exogenous (non-cycled estrogens) but generally •endogenous due to peripheral aromatization of adrenal androgens by adipose in obese women •also associated with granulosa cell tumors and other estrogen producing ovarian tumors as well as polycystic ovary syndrome | ||
| Pathogenesis •estrogen drives continued proliferation of the endometrium •in the absence of progesterone maturation of the endometrium and spiral arteries never occurs, nor does regular menses, | ||
| Epidemiology •obese post-menopausal women •may also have diabetes and hypertension (classic triad) | ||
| General Gross Description •plush, thick, tan endometrium measuring up 1.0 cms •Examples: | ||
| General Microscopic Description •glands exhibit crowding and often show budding •pseudostratified nuclei with mitotic activity •cells retain orientation to the lumen •cell nuclei have small nucleoli and normal chromatin •Examples: | ||
| References • Cotran RS, Kumar V, Robbins SL: Robbins Pathologic Basis of Disease. 5th ed. Philadelphia, W.B. Saunders, 1994, pp. 1057-8 This link will directly take you to the relevant new literature Complex Hyperplasia
| Synopsis by: Melinda Sanders M.D. (T84000M72420)[18]
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