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Female Genital Tract Pathology

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Female Genital Tract Pathology

Female Genital Tract Pathology

  1. 1. THE FEMALE GENITAL TRACT CRISBERT I. CUALTEROS,M.D. http://crisbertcualteros.page.tl
  2. 24. CERVICAL CANCER clinical course and management <ul><li>Cytologic screening </li></ul><ul><ul><li>Papanicolaou smear </li></ul></ul><ul><ul><li>HPV testing </li></ul></ul><ul><li>Histologic diagnosis and removal of precancers </li></ul><ul><li>Surgical removal of invasive cancers with adjunctive radiation and chemotherapy </li></ul><ul><li>Vaccines for preventing of HPV infection or treating existing disease </li></ul>
  3. 28. DYSFUNCTIONAL UTERINE BLEEDING <ul><li>ANOVULATORY CYCLE </li></ul><ul><ul><li>Results in excessive and prolonged estrogenic stimulation without the development of the progestational phase that regularly follows ovulation </li></ul></ul><ul><ul><li>Most common at menarche and perimenopausal period </li></ul></ul><ul><li>INADEQUATE LUTEAL PHASE </li></ul><ul><ul><li>Occurrence of inadequate corpus luteum function and low progesterone output, with an irregularly ovulatory cycle </li></ul></ul><ul><li>ENDOMETRIAL CHANGES ENDUCED BY ORAL CONTRACEPTIVES </li></ul><ul><ul><li>Common response pattern is a discordant appearance between glands and stroma, usually with inactive glands amid a stroma showing large cells with abundant cytoplasm reminiscent of the decidua of pregnancy </li></ul></ul><ul><li>MENOPAUSAL & POSTMENOPAUSAL CHANGES </li></ul><ul><ul><li>Anovulatory cycle  ovarian failure and atrophy of the endometrium </li></ul></ul><ul><ul><li>Mild hyperplasia with cystic dilation of glands  cystic atrophy </li></ul></ul>
  4. 34. PTEN <ul><li>Tumor suppressor gene </li></ul><ul><li>Deletion/inactivation </li></ul><ul><li>Encodes a phosphatase with dual lipid and protein specificity </li></ul><ul><li>Most impt fxn: lipid phosphatase blocking Akt phosphorylation in the P13K pathway </li></ul><ul><li>If absent, endometrial cells become more sensitive to stimulation by estrogens  may be integral--hyperplasia & cancer </li></ul><ul><li>Inactivation is seen: </li></ul><ul><ul><li>63% - premalignant endometrial hyperplasia </li></ul></ul><ul><ul><li>50-80% - endometrial carcinoma </li></ul></ul><ul><ul><li>43% - premenopausal women </li></ul></ul><ul><li>Loss of PTEN expression may be an early step in endometrial carcinogenesis </li></ul>
  5. 35. CARCINOMA OF THE ENDOMETRIUM <ul><li>55-65 yo </li></ul><ul><li>Higher frequency is seen with: </li></ul><ul><ul><li>Obesity </li></ul></ul><ul><ul><li>Diabetes (abn. glucose tolerance >60%) </li></ul></ul><ul><ul><li>Hypertension </li></ul></ul><ul><ul><li>Infertility ( single, nulliparous, history of functional menstrual irregularities consistent with anovulatory cycles) </li></ul></ul><ul><li>Infrequently, both endometrial & breast CA arise in the same patient. </li></ul>
  6. 37. ENDOMETRIAL CANCER <ul><li>85% are adenocarcinomas characterized by more or less well-defined gland patterns closely resembling normal endometrial epithelium (endometrioid tumors) </li></ul><ul><li>3-step grading system </li></ul><ul><ul><li>Grade 1 – well-differentiated, with easily recognizable glandular patterns </li></ul></ul><ul><ul><li>Grade 2 – moderately differentiated, showing well-formed glands mixed with solid sheets of malignant cells </li></ul></ul><ul><ul><li>Grade 3 – poorly differentiated, char. by solid sheets of cells with barely recognizable glands and a greater degree of nuclear atypia and mitotic activity </li></ul></ul><ul><li>Papillary serous carcinomas and clear cell carcinomas are managed as grade 3 carcinomas irrespective of histologic pattern. </li></ul>
  7. 38. ENDOMETRIAL CANCER <ul><li>20% of endometrioid carcinomas contain foci of squamous differentiation. </li></ul><ul><li>Adenoacanthoma – benign squamous elements + WD adenoCA </li></ul><ul><li>Adenosquamous carcinoma – malignant squamous elements + MD or PD adenoCA </li></ul><ul><li>Current classification systems grade the carcinomas based on glandular differentiation alone and use the term squamous differentiation for tumors falling into these categories. </li></ul>
  8. 43. OVARIAN CANCER <ul><li>Risk factors </li></ul><ul><ul><li>Nulliparity </li></ul></ul><ul><ul><li>Family history </li></ul></ul><ul><ul><li>Heritable mutations </li></ul></ul><ul><li>Genetic factors </li></ul><ul><ul><li>Increase susceptibility in mutations in both BRCA1 and BRCA2 </li></ul></ul><ul><ul><ul><li>BRCA1 mutations occur in 5% <70 yo </li></ul></ul></ul><ul><ul><ul><li>BRCA1 or BRCA2 mutations occur in 20-60%, 70 yo </li></ul></ul></ul><ul><ul><li>30% express high levels of HER2/neu (ERB-B2) oncogene  poor prognosis </li></ul></ul><ul><ul><li>50% has mutations in tumor-suppressor gene p53 </li></ul></ul>
  9. 49. ENDOMETRIOID TUMORS (OVARY) <ul><li>Presence of tubular glands bearing a close resemblance to benign or malignant endometrium </li></ul><ul><li>15-30% of endometrioid CA of the ovary are accompanied by a CA of the endometrium, and the relatively good prognosis in such cases suggests that the two may arise independently rather than by metastatic spread from one another. </li></ul>
  10. 67. CHORIOCARCINOMA <ul><li>Rapidly invasive, widely metastasizing malignant neoplasm: </li></ul><ul><ul><li>Lungs (50%) </li></ul></ul><ul><ul><li>Vagina (30-40%) </li></ul></ul><ul><ul><li>Brain, liver, kidney </li></ul></ul><ul><li>Responds well to chemotherapy – 100% cure or remission </li></ul><ul><li>By contrast, nongestational chorioCA are much more resistant to therapy </li></ul><ul><li>Preceded by: </li></ul><ul><ul><li>50% - hydatidiform mole </li></ul></ul><ul><ul><li>25% - previous abortion </li></ul></ul><ul><ul><li>22% - normal pregnancy </li></ul></ul><ul><ul><li>Ectopic pregnancy, genital & extragenital teratomas </li></ul></ul><ul><li>Does not produce chorionic villi </li></ul><ul><li>Abnormal proliferation of both cytotrophoblast & syncytiotrophoblast </li></ul><ul><li>Titers of HCG are elevated to levels above those encountered in H. moles </li></ul>
  11. 70. THANK YOU

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