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Pathology of Uterine corpus. Dr. Sufia Husain, 2018
- 1. Sufia Husain. Pathology Department KSU,Riyadh March 2018 Reference: Robbins & Cotran Pathology and Rubin’s Pathology The Uterine Corpus Pathology
- 2. Uterus with bilateraltube and ovaries, posterior view http://pixgood.com
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- 5. Lecture Outline Lecture: Endometrialhyperplasia, uterine cancer and fibroids (leiomyomas). At the end of this lecture, the student should know: Lesions of endometrium of uterus: know the risk factors, clinical presentation, macroscopic and histological features of Endometrial hyperplasia Endometrial carcinoma Lesions of myometrium of uterus: Leiomyoma : understand the pathology and clinical features of uterine leiomyomas andis aware that leiomyoma (fibroid) is the commonest neoplasm arising in the female genital tract. Leiomyosarcoma
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- 7. Endometrial hyperplasiais a process in which there is a proliferation of endometrial glands resulting in an increase in the gland/stroma ratio of the endometium when compared to normal. It is induced by persistent, prolonged stimulation of the endometrium by high levels of estrogen. The endometrial hyperplasia may progress to endometrial carcinoma. The risk of developing carcinoma depends on the level and duration of the estrogen excess, the severity of the endometrial hyperplasia and associated cellular atypia. Endometrial Hyperplasia
- 8. Causes of EndometrialHyperplasia: any condition in which there is high estrogen level can lead to endometrial hyperplasia e.g. a.Anovulatory menstrual cycles (failure of ovulation). b.Excessive endogenous production of estrogen (by the body) e.g. in polycystic ovary syndrome (Stein-Leventhal syndrome), granulosa cell tumors of the ovary cortical stromal hyperplasia (excessive ovarian cortical function) a.Exogenous administration or intake of estrogenic steroids without counter balancing progestins, over a long period of time. Endometrial Hyperplasia: causes
- 9. • Mild typeof hyperplasia tends to occur in younger patients. Most of the mild hyperplasia cases regress, either spontaneously or after treatment. • The more severe type of hyperplasia occur mainly in perimenopausal or postmenopausal women. This form has a significant premalignant potential. • Patients with endometrial hyperplasia usually present with abnormal uterine bleeding. Endometrial Hyperplasia: clinical
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- 11. Endometrial Hyperplasia: classification Inendometrial hyperplasia there is proliferation of both glands and stroma but the proliferation of the glands is much more leading to over crowding of glands. Endometrial hyperplasia is classified based on (A) and (B): CLASSIFICATION OF ENDOMETRIAL HYPERPLASIA: I. Simple hyperplasia • Without atypia • With atypia II. Complex hyperplasia • Without atypia • With atypia Note: atypia/ pleomorphism = loss of polarity, vesicular nuclei, prominent nucleoli, rounded cells.
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- 13. Simple hyperplasia(cystic hyperplasia): glands are varibly shaped and sized and cystically dilated with abundant cellular stroma and give a "Swiss Cheese" appearance. There is a mild increase in the gland-to-stroma ratio These lesions rarely progress to adenocarcinoma Simple hyperplasia may progress to cystic atrophy Simple hyperplasia without atypia
- 15. Uncommon Ithas the Architecture of simple hyperplasia, but there is cytologic atypia within the glandular epithelial cells 10% of such lesions progress to carcinoma Simple hyperplasia with atypia
- 16. Proliferation ofendometrial glands resulting in complex crowded glands with papillary infoldings and irregular shapes. The crowded glands are back- to-back with very little intervening stroma. The epithelial cells remain cytologically normal. 3% progression to carcinoma Complex hyperplasia without atypia
- 18. Complex proliferationof endometrial glands (back-to- back irregular glands) with atypia. The nuclei show loss of polarity and are enlarged and rounded and may have irregular nuclear membranes Commonly about 30% of women with this diagnosis have carcinoma somewhere in the uterus when a hysterectomy is performed About 30% progress to carcinoma Complex hyperplasia with atypia
- 20. Some endometrialhyperplasia revert to normal spontaneously or with medical treatment, others persist as hyperplasia, and a few progresses to endometrial adenocarcinoma. The risks for developing adenocarcinoma in each are as follows: Simple hyperplasia without atypia — 1% Complex hyperplasia without atypia — 3% Simple hyperplasia with atypia (simple atypical hyperplasia) — 10% Complex hyperplasia with atypia (complex atypical hyperplasia) — 30% Atypical hyperplasia in postmenopausal women appears to have a higher rate of progression to adenocarcinoma. Endometrial Hyperplasia: Clinical behavior and premalignant potential
- 21. Obesity Westerndiet Nulliparity Diabetes Mellitus Hypertension Hyperestrinism Endometrial Hyperplasia, Risk Factors
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- 23. Endometrial adenocarcinoma This is acommon neoplasm in women. Overall it is the fifth commonest cancer in women. •Endometrial cancers arise mainly in postmenopausal women •They cause postmenopausal bleeding •Early detection and cures are possible •These tumors are classified into two broad categories: Type I carcinomas (also known as endometrioid carcinoma): accounts for 80% of endometrial cancers. It is the most common type. e.g. endometrioid adenocarcinoma and its variants. Type II carcinomas: they are papillary serous carcinoma and clear cell carcinoma. Papillary serous is the more common form of type II carcinoma. www.healthtap.com
- 24. • Endometrioid carcinomais associated with estrogen excess and endometrial hyperplasia. The majority of the carcinomas are well differentiated. • Endometrial hyperplasia is a precursor to endometrioid carcinoma • Risk factors for type I are they same as that of endometrial hyperplasia and include: Obesity Western diet Nulliparity Diabetes Mellitus Hypertension Hyperestrinism Estrogen therapy chronic anovulation Late menopause Tamoxifen therapy High socioeconomic status. The disease may follow atypical hyperplasia but may occur independently of it especially in older patients. Type I endometrial carcinoma/ endometrioid carcinoma
- 25. Usual sequence ofevents in Type I endometrioid carcinoma http://quizlet.com/22858165/srwk3
- 26. 1. Majority ofendometrioid carcinomas have PTEN gene mutations. 2. Also there maybe inactivation of DNA mismatch repair genes 3. p53 mutations is seen in half of the poorly differentiated endometrioid carcinomas. Type I endometrioid carcinoma: genetics http://www.proteinatlas.org/images_dictionary/endometrial_cancer__1__figo_1__overview.jpg
- 27. Endometrial carcinoma Picture Takenfrom Robbins and Cotran Pathologic basis of disease. 8th edition, Chapter 21, 2010 Sanders
- 28. Type II endometrialcarcinomas: Serous carcinoma Serous carcinoma arises in older women, with endometrial atrophy (small atrophic uterus). They occur in late in life, about one decade later than type I carcinoma There is no association with hyperestrinism or preexisting hyperplasia They represent 15% of cases of all endometrial carcinoma Mutations in p53 are present in at least 90% of serous endometrial carcinoma The precursor of serous carcinoma is endometrial intraepithelial carcinoma (its like carcinoma in situ) These tumors are large bulky poorly differentiated tumors which invade early into the myometrium and have a poor prognosis. Extrauterine extension is common. http://quizlet.com/22858165/srwk3
- 29. CHARACTERISTICS OF TYPEI AND TYPE II ENDOMETRIAL CARCINOMAS FEATURES TYPE I TYPE II HISTOLOGIC TYPE Endometriod adenocarcinoma Serous or clear cell carcinoma AGE Premenopausal and perimenopausal (50-60 yrs) Post menopausal (~ 70 yrs) UNOPPOSED ESTROGEN Present Absent PRECURSOR LESION Hyperplasia with atypia Endometrial intraepithelial carcinoma GROWTH Slow growing Rapidly progressing GRADE Low High MYOMETRIAL INVASION Usually superficial Usually deep PROGNOSIS Favorable Poor GENETIC ALTERATIONS NOTED PTEN, microsatellite instability P53 mutations
- 30. • Most patientsare between 50 and 60 years. • Many of the patients tend to be nulliparous and obese. • Patients have abnormal vaginal bleeding and excessive leucorrhea. • Elderly women present with postmenopausal bleeding. • The diagnosis of endometrial cancer must be confirmed by biopsy or curettage and histologic examination of the tissue. Endometrial adenocarcinoma: clinical features http://upload.wikimedia.org/wikipedia/commons/0/00/Endometrial_hyperplasia.jpg
- 31. Grossly: Maylook close to normal or exophytic or infiltrative Microscopy: Both type I and II are adenocarcinomas. In both cases tumors originate in the endometrium and can eventually infiltrate the underlying myometrium, enter vascular spaces and metastasize to lymph nodes. Serous carcinoma has much greater cytologic atypia and are more poorly differentiated and is therefore more aggressive Tumor spreads by: Direct myometrial invasion with extension to the periuterine structures Through lymphatics to lymph nodes In the late stages, metastasize to the lungs, liver, bones, others Endometrial carcinoma: basic morphology
- 32. • Clinical behaviorof endometrial adenocarcinoma depends on the histologic type, the grade (degree of differentiation) and the stage (extent of spread). • Endometrioid carcinoma (type I) has a better prognosis than the other histologic types. • Serous carcinomas (type II) have poorer prognosis • Stage is the major determinant of survival. Endometrial adenocarcinoma: prognosis
- 33. How endometrial carcinoma canspread (stages 1, 2 and 3 of endometrial carcinoma) "Diagram showing stage 1A and 1B, 2 and 3A to 3C cancer of the womb CRUK 196, 206 and 224" by Cancer Research UK - Original email from CRUK. Licensed under CC BY-SA 4.0 via Wikimedia Commons - http://commons.wikimedia.org/wiki/File:Diagram_showing_stage_1A and 1B , 2_and3A_to_3C_cancer_of_the_womb_CRUK_206.svg#/media/File:Diagram_showing_stage_1A_and_1B,_2 and 3A_to_3C__cancer_of_the_womb_CRUK 196 and 206 and 224.svg
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- 35. • Leiomyoma isa benign tumor of smooth muscle origin. • It is the most common neoplasm of the female genital tract and probably the most common neoplasm in women. • The tumor is estrogen responsive. Estrogen stimulates their growth. Leiomyomas often increases in size during pregnancy and decrease in size after menopause. • About 40% of leiomyomas have an associated chromosomal abnormality • They are benign tumors with no appreciable malignant potential (incidence of malignant transformation to sarcoma is 0.1-0.5%). Leiomyoma (fibroid) of uterus
- 36. Clinical features Itcan be single or multiple (mostly multiple). Irregular abnormal bleeding and sometimes pelvic pain. It may cause anemia from heavy bleeding. Can have urinary frequency if the fibroid is compressing the urinary bladder. It may interfere with implantation and therefore cause infertility. In pregnant women it may cause abortion, obstructed labor, post partum hemorrhage etc. Alternatively it maybe entirely asymptomatic Leiomyoma (fibroid) of uterus
- 37. Leiomyoma may belocated anywhere in the myometrium. • Submucosal tumors are present immediately below the endometrium. • Intramural tumors, the most common, lie within the myometrium. • Subserosal fibroids lie beneath the serosal surface of the uterus or are pedunculated and attached to the serosa. • Pedunculated ones may loose their connection to the uterus forming a "parasitic leiomyoma". Uterine Leiomyoma http://www.fibroidoptions.com/images/fibroid1.jpg http://www.humpath.com/IMG/jpg/uterine_leiomyoma_0412_3.jpg
- 38. Leiomyoma gross: Well circumscribed,spherical, dense and firm-to- hard masses. Cut section shows whorled, tan-white cut surfaces. "Leiomyoma" by Ed Uthman from Houston, TX, USA - Leiomyoma. Licensed under CC BY 2.0 via Wikimedia Commons - http://commons.wikimedia.org/wiki/File:Leiomyoma.jpg#/media/File:Leiomyoma.jpg
- 39. Leiomyoma: Microscopically, thereare interlacing bundles of smooth muscle cells with collagenous stroma between bundles. The individual muscle cells are uniform in size and shape. They have the characteristic oval to elongated nucleus. Mitotic figures are scarce. http://pixgood.com/myometrium.html http://pixgood.com/leiomyoma-histology.html
- 40. It isthe malignant tumor of the smooth muscle. It is rare. Sites include the uterus and soft tissue Poor prognosis. Leiomyosarcoma
Editor's Notes
- #13 Schematic diagram depicting the development of type I endometrial carcinoma arising in the setting of hyperplasia. The most common molecular genetic alterations are shown at the time they are most likely to occur during the progression of the disease. *MI, microsatellite instability.
- #26 Schematic diagram depicting the development of type I endometrial carcinoma arising in the setting of hyperplasia. The most common molecular genetic alterations are shown at the time they are most likely to occur during the progression of the disease. *MI, microsatellite instability.