Endometrial hyperplasia pathophysiology: Difference between revisions
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==Genetics== | ==Genetics== | ||
==References== | ==References== |
Revision as of 15:40, 7 March 2016
Endometrial hyperplasia Microchapters |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Soujanya Thummathati, MBBS [2]
Overview
Pathophysiology
Pathogenesis
- Endometrial hyperplasia is a condition of excessive proliferation of the endometrial cells (inner lining of the uterus) associated with an increased gland to stroma ratio.
- The proliferative phase is the second phase in normal mentrual cycle when estrogen causes the lining of the uterus to proliferate. As the ovarian follicles mature, they begin to secrete increasing amounts of estradiol, and estrogen. The estrogens initiate the formation of a new layer of endometrium in the uterus, histologically identified as the proliferative endometrium.[1]
- The majority of cases of endometrial hyperplasia result from high concentrations of estrogen combined with insufficient concentration of the progesterone-like hormones which normally counteract the proliferative effects of estrogen on the endometrial tissue.[2]
- Unopposed oestrogen stimulation may be either from an endogenous or exogenous source.[3][2]
- Excessive endogenous estrogen in pre or perimenopausal women may result from chronic anovulation caused by obesity and/or polycystic ovary disease, and estrogen producing tumours (e.g. granulosa cell tumour).
- Excessive exogenous estrogen may result from hormone replacement therapy or non-prescription herbal medications.
Elevated endogenous estrogen in premenopausal or perimenopausal
women commonly arises from chronic anovulation
because of obesity and/or polycystic ovary disease.
Women may have increased estrogen because of the
peripheral conversion in adipose tissue of androstenedione
to estradiol, leading to endometrial stimulation, which can
occasionally result in endometrial hyperplasia and carcinoma
Microscopic Pathology
- Prolonged estrogenic stimulation results in larger, more complex, and proliferating endometrial glands.[3]
Gallery
-
Diagram illustrating how the uterus lining builds up and breaks down during the menstrual cycle[4]
-
Low magnification micrograph of simple endometrial hyperplasia without nuclear atypia. Normal gland-to-stroma ratio (~1:3); proliferating pseudostratified glandular epithelium; irregular endometrial glands: dilated glands or glands with variable size; non-ovoid/non-circular glands[5]
Genetics
References
- ↑ Menstrual cycle. Wikipedia. https://en.wikipedia.org/wiki/Menstrual_cycle Accessed on March 7, 2016
- ↑ 2.0 2.1 Endometrial hyperplasia. Wikipedia. https://en.wikipedia.org/wiki/Endometrial_hyperplasia Accessed on March 7, 2016.
- ↑ 3.0 3.1 Owings RA, Quick CM (2014). "Endometrial intraepithelial neoplasia". Arch Pathol Lab Med. 138 (4): 484–91. doi:10.5858/arpa.2012-0709-RA. PMID 24678678.
- ↑ Menstrual cycle. Wikipedia. https://en.wikipedia.org/wiki/Menstrual_cycle Accessed on March 7, 2016
- ↑ Endometrial hyperplasia. Wikipedia. https://en.wikipedia.org/wiki/Endometrial_hyperplasia#/media/File:Simple_endometrial_hyperplasia_-_low_mag.jpg Accessed on March 7, 2016