Mounir M F Elhao,Professor of Ob & Gyn . Ain Shams University,Cairo Egypt

1. PREMALIGNANT LESIONS OF THE FEMALE GENITAL ORGANS. Mounir M F Elhao,Professor of Ob & Gyn.Ain Shams University,Cairo Egypt

3. Vulva disorders ranging from vulvadynia to vulvar dystrophy to premalignant vulvar dysplasias. 

4. Premalignant lesions of the vulva. Vulvar dystrophy is another very poorly understood disorder Atrophic type:inwhich the mucous membrane of the vulva (vaginal introitus) changes its appearance.  It can either be thin, pale white, and loses all of its elasticity with atrophy of the labia, especially the labia minora, with fusion of the labia minora over the clitoris.  The mucous membrane then tears with any attempted stretching, such as intercourse, and itches incessantly.  Hypertrophic typeis similar except the epithelium is thickened and contains white plaques.  Again, it causes itching, tears easily, but does not give the atrophy as the atrophic type does.  The hypertrophic kind can have a premalignant tendency

5. Vulvar dysplasia (Means a premalignant lesion of the vulva.)  Mild referred to as VIN-I, Moderate referred to as VIN-IIS Severe referred to as VIN-III, or in situ carcinoma.  ( If left alone, the majority will eventually develop into invasive carcinoma. )

6. TTT OF VIN: Each can be resected locally by simply removing skin-deep tissue.  The cosmetic and therapeutic results are outstanding. 

7. The vagina(Va IN ) Can also have premalignant lesions similar to that described on the vulva, which can be treated in a similar manner.

8. lichen planus   A rare but severe symptom-producing problem of the vagina.  Here the vaginal mucosa completely sloughs leaving bare areas with no epithelium and the vagina is severely scarred.  This can also be treated with steroid creams.

9. PREMALIGNANT LESIONS of the vagina. Vaginal neoplasia is more common in patients who have previously been treated for cervical or vulvar neoplasia. The vaginal apex, in the fornices or about the vestibule and lower vagina .

10. PML of the Endometrium.

11. Endometrial hyperplasias .  Simple hyperplasia - Increased number of glands but regular glandular architecture Complex hyperplasia - Crowded irregular glands Simple hyperplasia with atypia - Simple hyperplasia with presence of cytologic atypia (prominent nucleoli and nuclear pleomorphism) Complex hyperplasia with atypia - Complex hyperplasia with cytologic atypia

12. CGH and Adenomatous Hyperplasia.

13. Endometrial Hyperplasia: Continuous estrogen stimulation that is unopposed by progesterone. This could be due to endogenous estrogen or exogenous estrogenic sources. Endogenous estrogen may be caused by chronic anovulation associated with polycystic ovary syndrome (PCOS) or perimenopause. Obesity also contributes to unopposed estrogen exposure due to chronic high levels of estradiol that result from aromatization of androgens in adipose tissue and conversion of androstenedione to estrone. Endometrial hyperplasia and cancer can also result from estradiol-secreting ovarian tumors such as granulosa cell tumors.

14. Exogenous estrogen without progesterone Has been associated with increased endometrial hyperplasia and adenocarcinoma (Lethaby, 2004). The Postmenopausal Estrogen/Progestin Interventions (PEPI) trial found that unopposed estrogen exposure increased the risk of complex hyperplasia by 22.7% and atypical hyperplasia by 11.8% over 3 years of use compared with a less than 1% increase in placebo controls (PEPI, 1996).

15. TTT of ENDOMETRIAL HYPERPLASIA. Treatment depends on patient symptoms such as • Degree of bleeding, • Presence of cytologic atypia, • Patient's surgical risks, and • wish for future childbearing

16. TTT . Progestins can effectively treat endometrial hyperplasia and they can serve as prevention of recurrence in those with continued risk factors. Hyperplasia without atypia responds well to progestins. More than 98% of women with hyperplasia treated with cyclic progestins saw regression of the disease in 3-6 months (Gambrell, 1995). The PEPI trial showed a 94% normalization of complex or atypical hyperplasia in 45 women treated with progestins (PEPI, 1996). Multiple regiments of progestin therapy have been found effective in reversing hyperplasia.

17. If hyperplasia with atypia is found on dilation and curettage (D&C) or endometrial biopsy, Definitive treatment with hysterectomy is recommended due to the high rate of concurrent endometrial cancer.

18. Pap tests can detect precancerous and cancerous conditions • by collecting cells from the surface of the cervix. Sometimes these cells appear abnormal, or atypical, when looked at under a microscope, but they are not completely cancerous. These are called premalignant or precancerous cells, which means they might turn into cancer if not found and treated early enough. These precancerous lesions are commonly called cervical intraepithelial neoplasia (CIN).

19. The cervix: Squamous Intraepithelial Lesion (SIL) is the abnormal growth of squamous cells on the surface of the cervix.

25. Tools.

27. Most common premalignant disorders vulva, vagina, and cervix.  The cervix is obviously the most common due to the fact that it is reflected in abnormal Pap smears.  There are also ovarian neoplasms that are premalignant

28. Conservative approach to abnormal Pap smears, especially in young women who have not fulfilled their reproductive desires.  This includes colposcopy for identifying and diagnosing the origin of the abnormal Pap smears as well as outpatient management. 

29. Based on location of the lesion, the severity of the pathological abnormalities, and the potential for childbearing.  Each patient is individualized as to whether their proper management would be close follow-up,laser, cryotherapy or LEEP procedures in the office or cold knife conizations under anesthesia

31. Abnormal vessels

36. The surface of the cervix is made up of two different types of cells, squamous epithelial cells (the lining cells of the outer part of the cervix, or ectocervix) and columnar epithelial cells (the lining cells of the inner part of the cervix, or endocervix).

37. Early detection and treatment of precancerous cells can prevent them from becoming cancerous. Otherwise, the abnormal cells can become cancer and spread to other parts of the body.

38. LG- SIL

39. SIL-HG & Carcinoma.

40. Adenocarcinoma in situ.

41. These lesions have also been called squamous intraepithelial lesions (SIL)and there are two types: Low-grade SIL - In this type of SIL, the changes are thought to be just starting. The changes can be in the size, shape, or number of cells that are on the surface of the cervix. In these low-grade lesions, the cells have only a few abnormal characteristics, but are still somewhat similar to the normal cells. Other common names for this low-grade SIL are mild dysplasia or cervical intraepithelial neoplasia type I (CIN 1). High-grade SIL - In this type of SIL, the cells look very abnormal under the microscope. However, these cells are still only on the surface of the cervix. They are not invading the deepest parts of the cervix yet. These lesions are also called moderate or severe dysplasia, CIN II or III or carcinoma in situ (CIS).

42. The next step, in many cases, is a colposcopy( an exam with an instrument that visually magnifies the cervix) Removal of any areas likely to be precancerous or cancerous. Sometimes, the physician and patient may decide to repeat the Pap test later and proceed to colposcopy only if the second test shows more abnormal cells that might need removal.

43. Borderline ovarian tumors • Are a subset of epithelial ovarian tumors that have a very favorable prognosis. The accepted initial treatment is surgical removal of the tumor and biopsies.

44. Frequency: One woman in 55 (1.8%) develops some form of ovarian cancer in her lifetime. Approximately 90% of these cancers are tumors of epithelial origin. If benign lesions are included, epithelial tumors account for 60% of all ovarian tumors.

45. Borderline tumors comprise approximately 15% of all epithelial ovarian tumors. The mean age of occurrence is approximately 10 years younger than that of women with frankly malignant ovarian cancer. Factors reportedly linked with borderline tumors include oral contraceptive use, menarche, age at first pregnancy, age at first delivery, menstrual history, smoking, and family history of ovarian cancer, although none of these has been shown to be statistically significant.

46. Borderline ovarian cancer is staged according to the FIGO classification of ovarian cancer. Many clinicians group stages II-IV together for prognostic consideration. Another common component of staging is the description of the type of implants, as these have significant prognostic value. As opposed to its true malignant counterpart, epithelial ovarian carcinoma, borderline ovarian cancers are often found at early stages.

47. Border line ovarian tumors. Etiology: The etiology of this disease remains unclear because of the small number of cases and the lack of randomized controlled studies. Pathophysiology: The 2 major histologic tumor subtypes are serous and mucinous, with serous being more common. Other much less common tumors include clear cell and endometrioid. Serous tumors are presumed to originate from the germinal epithelium. Mucinous tumors do not have a clearly defined origin. Many authorities consider borderline tumors to occupy an intermediate position between their benign and frankly malignant counterparts.

48. BOT Clinical: These tumors, as with other ovarian tumors, are difficult to detect clinically until they are advanced in size or stage. In one study, the most common presenting symptoms were abdominal pain, increasing girth or abdominal distension, and abdominal mass. Approximately 23% of patients were asymptomatic. When a complex ovarian mass is discovered, surgery is often, if not always, indicated. Preoperatively, borderline tumors are often presumed to be either benign or malignant ovarian masses; regardless, surgery is required to determine the type of mass.