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| Atypical 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 estro- gen 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 |
| General Microscopic Description •glands exhibit crowding and often show budding or dilatation •stratified nuclei with mitotic activity •cells lose orientation to the lumen •nucleoli become prominent, nuclei become hyperchromatic or show nuclear clearing or vesiculation •no necrosis or stromal desmoplasia |
| Clinical Correlation •asymptomatic or post-menopausal bleeding |
| References • Cotran RS, Kumar V, Robbins SL: Robbins Pathologic Basis of Disease. 5th ed. Philadelphia, W.B. Saunders, 1994, pp. 1057-8 |
| Atypical Hyperplasia |
| Synopsis by: Melinda Sanders M.D. (T84000M72005)[19] |
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