Condition | Cause | Pathology/Histology | Clinical Features | Other Features |
Proliferative Enodmetrium | · Straight glands · Narrow lumens · Pallisading nuclei · Ovoid nuclei · Mitoses | |||
Early Secretory Endometrium | First manifestation of effect of ovulation on endometrium | · Glands remain straight · Lumens remain narrow · Subnuclear vacuoles appear | 24-36 hours after ovulation | |
Mid Secretory Endometrium | · Glands become coiled · Vacuoles no longer present in glands · Secretory product appears in lumen | Postovulatory days 5-9 | ||
Late Secretory Endometrium | · Intralumenal secretions are spent · Stromal predecidua appears · First predecidua around spiral arteries · Later predecidua beneath surface | Postovulatory days 10-14 | ||
Menstrual Endometrium | · Stromal collapse · Fribrin thrombi and blood · Glands are broken apart · Glands have no secretions | |||
Hyper-secretory Endometrium of Pregnancy | · Arias-Stella reaction · large, hyperchromatic nuclei · prominent cytoplasmic vacuolization | |||
Atrophic endometrium | · short glands · glandular cells – flat, without significant mitotic activity | |||
Dysfunctional Uterine Bleeding | · anovulatory bleeding · luteal phase defect | |||
Unopposed Estrogen | · proliferative glands · stromal breakdown · fibrin thrombi · wreathing of stroma by glandular cells | |||
Contraceptives | Combined oral agents | · mix of proliferative and secretory changes · long use · atrophic glands · stromal predecidual pattern dominates | ||
Depoprovera | · unopposed progesterone | |||
Tamoxifen | · inc risk of carcinoma · inc incidence of polyps · large, mucinous metaplasia, fibrotic | |||
Endometrial Hyperplasia | · unopposed estrogen stimulation – exogenous, endogenous · no progestational stimulation | · simple or complex architecture · typical or atypical nuclei | Vaginal bleeding, 60s Risk factors – obesity, diabetes, nulliparity, early menarche, late menopause | Complex atypical hyperplasia progresses to carcinoma – 1/3 T – hysterectomy, hormonal manipulation |
Endometrial Carcinoma Type 1 Endometrioid | · PTEN gene mutation à cell growth and apoptosis | · squamous or mucinous | Grade determines prognosis T – hysterectomy, good survival Low grade – hormonal | |
Endometrial Carcinoma Type 2 Unfavorable Histology | · serous-p53 mutations | · clear cell | Early spread outside uterus long term survival uncertain |
Saturday, May 07, 2005
Gynecological Pathology Endometrium
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