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ENDOMETRIOSIS

ENDOMETRIOSIS. PRESENTER: JOY WILLIAMS 8 TH DEC 2009. OUTLINE. INTRODUCTION INCIDENCE PATHOPHYSIOLOGY PATHOLOGY CLASSIFICATION CLINICAL FEATURES INVESTIGATION TREATMENT PROGNOSIS CONCLUSION. INTRODUCTON. Is the presence of functioning endometrial tissue outside the uterine cavity.

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ENDOMETRIOSIS

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  1. ENDOMETRIOSIS PRESENTER: JOY WILLIAMS 8TH DEC 2009

  2. OUTLINE • INTRODUCTION • INCIDENCE • PATHOPHYSIOLOGY • PATHOLOGY • CLASSIFICATION • CLINICAL FEATURES • INVESTIGATION • TREATMENT • PROGNOSIS • CONCLUSION

  3. INTRODUCTON • Is the presence of functioning endometrial tissue outside the uterine cavity. • One of the first definitive description of endometriosis as a specific clinical condition was by Sampson in 1921. • Is one of the commonest benign gynaecological conditions.

  4. INCIDENCE • 21% of women with infertility, 15% with chronic abdominal pain, and 6% of women undergoing sterilization has endometriosis at laparoscopy. • This condition is most common among 25-35 years age group,but can occur at any age from menarche to menopause.

  5. PATHOPHYSIOLOGY • The precise aetiology remains unknown. Several theories exist to explain the process through which this condition develops and clinical evidence to support these concepts: -menstrual regurgitation and implantation -coelomic epithelium transformation -Genetic and immunological factors -Vascular and lymphaticspread

  6. Menstrual regurgitation & implantation -it has been suggested that endometriosis results from retrograde menstruation of viable endometrial glands & tissue within the menstrual fluid and implants on the peritoneal surface. • Coelomic epithelium transformation -the cells lining d mullerian duct, peritonium, n of d ovary has a common origin. Its been proposed dat these cells undergoes de-differentiation n are then transformed to endometrial cells, which is due to hormonal stimuli of ovarian origin by unidentified chemical subst from uterine endometrium.

  7. Genetic and immunological factors -it alters d susceptibility of a women n allow development of endometriosis. • Vascular and lymphatic spread -vascular n lymphatic embolization to distant sites has been demonstrated n explains d rare findings of endometriosis in sites outside d peritoneal cavity, such as joints, skin, lung ,kidney

  8. PATHOLOGY • Free implants: hav a polypoidal cauliflower-like structure n grows along d surface or cover a cystic structure. Its compose of surface epithelium, glands n stroma. • Enclosed implants: d implants is covered with a surface layer of peritoneum n thus located within tissue or part of free growing lesion. Consist of stroma n glands.

  9. Healed lesion: hav d feature of cysticaly dilated glands containing thin glandular epithelium supported by small numbers of stromal cells surrrounded by connective tissue. Comprises of glands.

  10. Classification / Staging • Ranges from Stage I (Minimal) to Stage IV (Severe) • Staging Involves Location and Depth of Disease, Extent of Adhesions

  11. CLINICAL FEATURES • Patients hav extremely variable symptoms, some may vary depending on d site of d ectopic endometrial lesion. • Signs n symptoms are; -chronic pelvic pain, dysmenorrhea -abnormal uterine bleeding -infertility -deep dyspareunia -pelvic mass(endometrioma) -misc: tenesmus, haematuria, LBP, hemoptysis

  12. DIAGNOSIS • Inconclusive: -Hx -Phy exams -Imaging studies: ultrasound, MRI -CA 125 • Laparoscopy ‘gold standard’ • Laparotomy • Biopsy

  13. Treatment: Overall Approach • Recognize Goals: – Pain Management – Preservation / Restoration of Fertility • Discuss with Patient: – Disease may be Chronic and Not Curable – Optimal Treatment Unproven or Nonexistent

  14. Pain Management: Medical Therapy • NSAIDs • OCPs (Continuous) • Progestins • Danazol • GnRH-a • GnRH-a + Add-Back Therapy • Misc: Opoids, TCAs, SSRIs

  15. Continuous OCPs • “Pseudopregnancy” (Kistner) • ? Minimizes Retrograde Menstruation • Lower Fertility Rates than Other Medical Treatments • Choose OCPs with Least Estrogenic Effects, Maximal Androgenic / Progestin Effects

  16. Progestins • May be as Effective as GnRH-a for Pain Control • MPA 10-30 mg/day, DP 150 mg Semi-Monthly • May be Taken Long-Term • Relatively Inexpensive • Side-Effects: AUB, Mood Swings, Weight Gain, Amenorrhea

  17. Danazol • Weak Androgen • Suppresses LH / FSH • Causes Endometrial Regression, Atrophy • Expensive • Side-Effects: Weight Gain, Masculinization, Occ. Permanent Vocal Changes

  18. GnRH-a • Initially Stimulate FSH / LH Release • Down-Regulates GnRH Receptors–”Pseudomenopause” • Long-Term Success Varies • Expensive • Use Limited by Hypoestrogenic Effects • May be Combined with Add-Back (? >1 Year )

  19. Surgical Treatment (Laparoscopy / Laparotomy) • Resection of endometrioma • Lysis of adhesions, cul-de-sac reconsruction • Uterosacral nerve ablation • Presacral neurectomy • Appendectomy • Uterine suspension (?efficacy) • Hysterectomy +/- BSO

  20. PROGNOSIS • Endometriosis may recur after medical or surgical tx n tends to regress spontaneously after d menopause.

  21. Conclusion • Endometriosis is a Common, Chronic Disease • Typical Symptoms Include Pain, Infertility, Abnormal Uterine Bleeding • The Optimal Treatment Remains Unclear • Surgical Excision is the Most Efficacious Approach with Respect to Fertility • Better Medical Therapies are Needed

  22. THANK YOU!!!!!!!!!!!!!!

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