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ENDOMETRIOSIS
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- 2. “Presence of endometrialglands and stroma outside the uterus“ Common in reproductive andadolescentagegroup Prevalence:8-10% Common benign gynaecological condition Similarities to malignancy – disease progression, local invasion, widespread dissemination itis estrogen dependent and its resolve after menopause.
- 3. RISK FACTORS INENDOMETRIOSIS •Menstrual cycle -Early menarche -Heavy menstrual bleeding -Short menstrual cycles •Delayed childbirth – voluntary / involuntary •Nulliparity/ low parity •Higher social class •History of endometriosis in first degree relatives •Lower body mass index •Obstructive Mullerian anomalies •Exposure to dioxins
- 4. Pathogenesis ofendometriosis • Etiologyis unknown • There are several theories 1) Implantationtheory – SAMPSON Endometrial fragments transported through the tubes into the peritoneal cavity by Retrograde menstruation are responsible for the development of endometriosis Endometriosis common in dependent portions of pelvis •Ovary •Cul-de-sac •Uterosacral ligaments •Rectovaginal septum •Posterior surface of uterus
- 5. 2) Coelomic metaplasiatheory - MEYER Cells of original coelomic epithelium can undergo metaplastic changein to endometrial tissue. Thistheorycan explain endometriosis in pleura and peritoneal cavity. 3) Induction theory Degenerating menstrual endometrium releases endogenous factors that induce metaplasia of coelomic epithelium
- 6. 4)Vascular and lymphaticspread Vascularandlymphatic embolization of endometrial tissue canexplain occurrence of endometriotic deposits in cervix, vagina,vulva, GI tract, lungs, pleural cavity, surgical scars, lymph nodes 5) Immunological theory Decreased cellular immunity to endometriotic tissue – reduced clearance from peritoneal cavity – altered function of macrophages 6) Genetic factors – familial predisposition- 7 fold increase in incidence in relatives of women with endometriosis 7) Molecular defects
- 7. Biologically active substancesproduced in ectopic endometrium Cytokines Adhesion to peritoneal surface MMP Invasion VEGF- 1 Angiogenesis Growth factors Growth Oestrogen Proliferative changes Prostaglandins inflammation
- 8. GENETIC FACTORS IMMUNOLOGICAL FACTORS MOLECULAR DEFECTS MECHANICAL FACTORS Implantation of endometrialcells Adhesion to peritoneal surface Angiogenesis Growth of endometrial cells Proliferation Inflammatory reaction endometriosis
- 9. Commonly occur inpelvic • Ovaries • Uterosacral ligament • Pouchof Douglas • Lateral pelvic wall • Ovarian fossa
- 10. Superficial / Peritonealendometriosis Ovarian endometriosis Deep infiltrating endometriosis
- 11. Superficical endometriosis Dependent portionsof pelvis •Ovary •Pelvic peritoneum over anterior and posterior surface of uterus •Cul-de-sac (pouch of douglas) •Uterosacral ligaments •Rectovaginal septum NATURE OF LESION GROSS APPEARANCE EARLY, SUBTLE PAPULAR, VESICULAR HAEMORRHAGIC RED, FLAME SHAPED POWDER BURN PUCKERED, BLUE- BLACK FIBROTIC WHITE OR BLACK/ PIGMENTED
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- 13. TYPICAL FEATURES OFOVARIAN ENDOMETRIOMA
- 14. DEEP INFILTRATIONG ENDOMETRIOSIS •Posteriorpelvic endometriosis •LESIONS EXTEND >5mm beneath the peritoneum •Adhesion formation
- 15. Common sites ofextrapelvic endometriosis
- 16. MICROSCOPIC APPERANCE •BOTH endometrialglands and endometrial stroma •Hemosiderin laden macrophages •Glands – secretory/ proliferative •Deep infiltrating lesions – fibrous and smooth muscle tissue Long duration endometriosis typical endometrial glands and stroma may not be seen POSITIVE HISTOLOY CONFIRMS DIAGNOSIS NEGATIVE HISTOLOGY DOES NOT EXCLUDE ENDOMETRIOSIS
- 17. ENDOMETRIOSIS AND MALIGNANCY Rarelyovarian clear cell carcinoma and endometrioid carcinoma can develop in endometriosis
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- 19. CAUSES OF PAININ ENDOMETRIOSIS Pain ⋉ DEPTH OF ENDOMETRIOSIS
- 20. CAUSES OF INFERTILITYIN ENDOMETRIOSIS Prevalence of endometriosis is 30-45% in infertile women
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- 23. • Laparoscopy inendometriosis Gold standard •Visualization of lesions •Staging the disease •Biopsy for histology •Evaluation of extent of adhesions •Therapeutic intervention if required
- 24. Staging Score Stage 1 minimal 1-5 Stage2 mild 6-15 Stage 3 moderate 16-40 Stage 4 severe >40
- 25. Management • No definitivecure • Short term goals – pain relief , fertility • Long term goals – prevention of disease progression and recurrence
- 26. Medical management Principle isto create aperiod of amenorrhoea sothat endometriosis tissue will undergo atropic changesand endometriosis will undergo regression This canbe achieved by either creatinga situation of pseudo-pregnancy or post menopause
- 27. Drugs used inmedical management of endometriosis P
- 28. NEWER DRUGS INENDOMETRIOSIS
- 29. SURGICAL MANAGEMENT LAPAROSCOPIC UTEROSACRALNERVE ABLATION >3CM
- 30. MANAGEMENT OF DEEPINFILTRATING AND ADVANCED ENDOMETRIOSIS