Endometrial Hyperplasia

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  • 1. ENDOMETRIAL HYPERPLASIA
  • 2. ENDOMETRIAL HYPERPLASIA • Endometrial hyperplasia is defined as an increased proliferation of endometrial glands, relative to stroma resulting in increased gland to stromal ratio than normal endometrium. • The proliferative glands vary in size & shape and may shows cytological atypia, which may progress or co- exist with endometrial carcinoma.
  • 3. ENDOMETRIAL HYPERPLASIA Age : Peri-menopausal women, if estrogen level more than progesterone.
  • 4. ENDOMETRIAL HYPERPLASIA Causes of endometrial hyperplasia : Endometrial hyperplasia associated with prolonged estrogen stimulation of the endometrium, which may be due to- 1. Anovulation 2. Increased estrogen production from endogenous source or exogenous estrogen. 3. Obesity 4. Polycystic ovarian disease 5. Functional granulosa cell tumors of ovary 6. Estrogen replacement therapy 7. Cortical stromal hyperplasia 8. Idiopathic.
  • 5. ENDOMETRIAL HYPERPLASIA Molecular genetics : Mutation in PTEN genes ( 20% of hyperplasia )
  • 6. ENDOMETRIAL HYPERPLASIA Classification : According to architectural & cytological factors endometrial hyperplasia divided into four groups- 1. Simple hyperplasia 2. Complex hyperplasia 3. Atypical hyperplasia ( has more change to developed malignancy )
  • 7. ENDOMETRIAL HYPERPLASIA Simple hyperplasia : Glands are various size and irregular shapes with cystic dilatation with mild hyperplasia. Epithelial growth pattern and cytology are similar to those of proliferative endometrium.Mitosis are not prominent. 1% chance of develop carcinoma.
  • 8. ENDOMETRIAL HYPERPLASIA Complex hyperplasia : Increase in the number and size of the glands, marked gland crowding and branching occurs. Gland form finger like projection but not invasion towards stroma, epithelial cell remains cytologically normal. 3% chance to develop carcinoma .
  • 9. ENDOMETRIAL HYPERPLASIA Atypical hyperplasia : In simple atypical hyperplasia, there is cytological atypia within the glandular cells- such as loss of polarity, vesicular nuclei, prominent nucleoli, cells become rounded and loss the normal perpendicular orientation to the basement membrane. 8% may progress to carcinoma.
  • 10. ENDOMETRIAL HYPERPLASIA In complex atypical hyperplasia consists of back-to-back crowding of glands lined by atypical cells. Lipid laden “ foam” cells may be noted in the intervening stroma. 23% to 48% women have the chances to develop carcinoma.
  • 11. ENDOMETRIAL CARCINOMA
  • 12. ENDOMETRIAL CARCINOMA Endometrial carcinoma is the most common invasive cancer of the female genital tract. It is about 7% of all invasive cancer in women.
  • 13. ENDOMETRIAL CARCINOMA Age : • Common in women >40 years of age ( peri & post menopausal women ) • Relatively unknown in young age. • Peak incidence 55 to 65 years of age.
  • 14. ENDOMETRIAL CARCINOMA Risk factor of endometrial carcinoma : 1. Obesity 2. Diabetes 3. Hypertension 4. Infertility 5. Unopposed estrogen stimulation 6. Family history 7. Endometrial atrophy
  • 15. ENDOMETRIAL CARCINOMA Classification : A. According to the clinico- pathological & molecular studies : 1. Type - I 2. Type - II
  • 16. ENDOMETRIAL CARCINOMA B. According to the histopathology---- 1. Endometroid adenocarcinoma 2. Adenocarcinoma with squamous differentiation 3. Adenosquamous carcinoma 4. Serous carcinoma 5. Clear cell carcinoma
  • 17. ENDOMETRIAL CARCINOMA Type - I endometrial carcinoma :  It is the most commonest type, about 80% of all cases. Usually occurs in 55- 65 years. The majority are well differentiated and estrogen related, present histologically as a endometroid tumor associated with atypical endometrial hyperplasia.  Prognosis is better and have superficial myometrial invasion.
  • 18. ENDOMETRIAL CARCINOMA Molecular genetics of Type-I : 1. Mutation in PTEN tumor suppressor gene – 80% 2. PIK3CA mutation – 39% 3. Mutation in KRAS & beta catenin oncogen 4. Mutation in KRAS gene 5. Mutation in p53 gene ( upto 50% in poorly differentiated endometroid carcinoma )
  • 19. ENDOMETRIAL CARCINOMA Type – II tumor :  About 15% of endometrial carcinoma.  It is arise in the sitting of endometrial atrophy. Not related to estrogen stimulation or endometrial hyperplasia. They are poorly differentiated, high grade tumor with poor prognostic cell type like - serous endometrial carcinoma, clear cell tumor.
  • 20. ENDOMETRIAL CARCINOMA  Usually occurs in older or post menopausal women and not related to obesity, HTN, DM.  Develop finger like papillary projection.  Aggressive in behavior.
  • 21. ENDOMETRIAL CARCINOMA Molecular genetics of Type-II : 1. Mutation in p53 gene 2. Aneuploidy 3. PIK3CA
  • 22. ENDOMETRIAL CARCINOMA Endometroid carcinoma :  85% of endometrial carcinoma.  Endometrial carcinoma either localized polypoid tumor or diffuse tumor involving the endometrial surface.
  • 23. ENDOMETRIAL CARCINOMA  Endometrial adenocarcinoma formed well differentiated to poorly differentiated glandular structure mixed with solid sheet of malignant cells. Poorly differentiated type have barely recognizable glands and greater degree of nuclear atypia and mitotic activity.  Upto 20% of endometroid carcinoma contain foci of squamous differentiation.
  • 24. ENDOMETRIAL CARCINOMA Serous carcinoma: Generally arise in the sitting of small atrophic uterus, often form large bulky tumor or deep invasion in to the myometrium. The precursor of serous carcinoma is endometrial intraepithelial carcinoma.
  • 25. ENDOMETRIAL CARCINOMA • Lesion may have papillary growth pattern composed of cells with marked cytological atypia, including high nuclear to cytoplasmic ratio, atypical mitotic figure,heterocromastia and prominent nucleoli. • They can also have predominantly glandular pattern, different from adenocarcinoma by marked cytological atypia.
  • 26. ENDOMETRIAL CARCINOMA Malignant mixed mullarian tumor : MMTs consist of endometrial adenocarcinomas with malignant changes in the stroma.The stroma tends to differentiate into a verity of malignant mesodermal components, including muscle, cartilage and even osteoid. MMTs occur in the post-menopausal women and present with post menopausal bleeding. This is a highly malignant tumor.
  • 27. ENDOMETRIAL CARCINOMA In gross appearance: MMTs are fleshier than adenocarcinomas, may be bulky and polypoid and sometimes protrude through the cervical os. On histology: the tumor consist of adenocarcinoma mixed with malignant mesenchymal elements(striated musce,adipose tissue, bone)
  • 28. ENDOMETRIAL CARCINOMA Grading : The step-grading system applied to endometroid tumor – G1 : Well differentiated adenocarcinoma, less than 5% solid growth.( with easily recognizable glandular pattern ) G2 : Moderately differentiated adenocarcinoma with partly solid growth <50% ( showing well formed glands mixed with solids sheets of malignant cells .
  • 29. ENDOMETRIAL CARCINOMA G3 : Poorly differentiated adenocarcinoma with predominantly solid growth >50% ( solid sheets of cell with barely recognizable gland with greater degree of nuclear atypia and mitotic activity ) All non-endometroid carcinoma classified as grade-3 irrespective of histological pattern.
  • 30. ENDOMETRIAL CARCINOMA Staging : Stage I :Carcinoma is confined to the corpus uteri itself. Stage II :Carcinoma involves the corpus and the cervix. Stage III :Carcinoma extends outside the true but not outside the true pelvis. Stage IV :Carcinoma extends outside the true pelvis or involves the mucosa of the bladder or rectum.
  • 31. ENDOMETRIAL CARCINOMA Route of spread : 1. Direct spread 2. Lymphatic spread and Transtubal spread 3. Heamatogenous spread
  • 32. ENDOMETRIAL CARCINOMA Clinical presentation : 1. Asymptomatic 2. Abnormal uterine bleeding 3. Abnormal menstrual cycle & Menorrhagia 4. Lower abdominal pain & pelvic pain 5. Vaginal discharge in post menopausal women.
  • 33. ENDOMETRIAL CARCINOMA How to diagnosed : 1. Pelvic examination 2. TVS 3. Pap’s smear 4. Endometrial sampling 5. D & C
  • 34. ENDOMETRIAL CARCINOMA Complications : 1. Anemia may result, caused by chronic loss of blood.( This may occur if the women has ignored symptoms of prolonged or frequent abnormal menstrual bleeding.) 2. Perforation of the uterus may occur during D & C or an endometrial biopsy.
  • 35. ENDOMETRIAL CARCINOMA Management : Surgery and Radiation therapy are the only methods of successful treatment.
  • 36. ENDOMETRIAL CARCINOMA Women with the early stage-I disease treatment with surgical hysterectomy either abdominal or vaginal. Women with late stage-I disease and stage-II disease are often offered surgery in combination with Radiation therapy.
  • 37. ENDOMETRIAL CARCINOMA Prognosis : Stage-I & well differentiated endometrial carcinoma – 75% to 80% prognosis Stage-II & III : < 50% prognosis
  • 38. ENDOMETRIAL CARCINOMA Prevention : 1. All women should have regular pelvic examination and pap’s smear ( beginning at the onset of sexual activity or at the age of 20 if not sexually active ) to help detect signs of any abnormal development.
  • 39. ENDOMETRIAL CARCINOMA 2. Women with estrogen replacement therapy should report immediately to the doctor if any of the following symptoms arise I. Bleeding or spotting after intercourse or douching II. Bleeding that lasts longer than 7 days III. Reappearance of blood or staining after 6 months or more of no bleeding at all.
  • 40. THANK YOU