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Endometriosis

Endometriosis. “ Presence of endometrial tissue outside the lining of the uterine cavity” or “Proliferation of endometrium in any site other than the uterine mucosa”. Definition. Age: common in reproductive period True Incidence Unknown: ? 1-5% & 30 – 50 % infertility.

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Endometriosis

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  1. Endometriosis

  2. “Presence of endometrial tissue outside the lining of the uterine cavity” or “Proliferation of endometrium in any site other than the uterine mucosa” Definition

  3. Age: common in reproductive period True Incidence Unknown: ? 1-5% & 30 – 50 % infertility. Does NOT Discriminate by Race. Histology: Endometrial Glands with Stroma +/- Inflammatory Reaction. Herdietary (↑↑ among sisters). Epidemiology

  4. - Pelvic - Extra pelvic Umbilicus. Scars (Lap.). Lungs & plura. Others. Sites

  5. Uterine= Adenomyosis (50%). Extraut: - Ovary 30% - Pelvic peritoneum 10%. - F. tube. - Vagina. -Bladder & rectum. - Pelvic colon. - Ligaments. Pelvic Endometriosis

  6. Endometrial implantation theory Retrograde Vascular and lymphatic Mechanical Immunological and genetic theory Composite theory Theories of histiogenesis

  7. In situ development Coelomic metaplasia theory Induction theory Embryonic cell nest Wolffian ducts Mullerian ducts Germinal epithelium of ovary Theories Of Histiogenesis continue

  8. 1. Hyperoestrinism: a) Fibroid & metropathia hemorrhagica. b) Delayed marriage, infertility. c) Oestrogen secreting tumours of the ovary e.g. granulosa & theca cell tumours, or with prolonged oestrogen therapy. 2. Cervical Stenosis. 3. Insufflation. 4. Curettage. Predisposing Factors

  9. The endometrium in an ectopic site escapes immune surveillance and continues to grow, probably there is a deficiency in CMI, or the amount of regurgitated endometrium exceeds the capacity of cytotoxic cells. TSG may be deleted and or inactivated. The percentages of Tc and NKC in the peripheral blood in endometriosis is not different from control, however their cytotoxicity is so diminished to allow growth of endometriotic implants. Peritoneal fluid macrophages increase in number and activity. IL-1/TNF-, PGE2, IL-8, MCP-1, and C3 increase being macrophage products CMI fault

  10. Peritoneal fluid macrophages are in excess and active. TH/Ts ratio decreases in pregnancy, malignancy, and endometriosis. Peritoneal fluid E2 is high and support the growth of endometriotic implants via EGF/TGF-. Peritoneal fluid chemokines are high and correlate with the stage of the disease. Cytokines and endometriosis

  11. B-cells CD4 cell is the master of immune orchestra Macrophages NKCs TC-cells NKCs IL2 IL4 IFN- CD4 (T-Helper) TGF- IL10 Ts Th/Ts ratio: Increases in autoimmune diseases Decreases in pregnancy, malignancy endometriosis and AIDS

  12. Endometriosis shares SLE More in females Run in families Autoantibodies Response to danazol Both can be combined Endometriosis differs from SLE HLA-unassociated Does not satisfy Witebsky postulate Is endometriosis an autoimmune disease?

  13. Endometriosis is often misdiagnosed leading to delays in treatment sometimes for several years. Delay in diagnosis: Progression of symptoms. Increasing infertility till completed reproductive failure. Diagnosis

  14. Symptoms (history). Signs (Exam). Investigations. DD. Diagnosis Cont…

  15. Asymptomatic. Pain (DYS…….): - Dysmenorrhea (crescendo = progessive) - Dyspareunia. - Dyschesia. - Dysuria. Backache. Acute abdomen. premenst. Tension syndrome. Symptoms

  16. Bleeding: - Menorrhagia. - Cyclic hematuria during menstruation. - Cyclic bleeding per rectum during menstruation. - Vicarious menstruation. Infertility. Mass Intermittent pyrexia. Symptoms cont…

  17. Pelvic examination may reveal: 1. Pelvic tenderness. 2. Fixed retroverted uterus. 3. Nodularity of the Douglas pouch and uterosacral ligaments. 4. Ovaries may be enlarged and tender . Ovarian cyst may be detected. Signs

  18. 1. Laparoscopy . 2. Cystoscopy and proctosigmoidoscopy. 3. Histopathological examination. 4. Imaging. 5. Serum CA - 125. 6. ? IL-8 & CEA. Investigations

  19. Value: It permits a “see and treat” approach, although its effectiveness may be limited by the nature of the disease and the surgeon's skill. Laparoscopy

  20. Appearance: Endometriosis May Appear Brown Black (“Powderburn”) Clear (“Atypical”) Endometriosis May Be Associated with Peritoneal Windows Laparoscopy cont….

  21. 1. Ovarian cysts. 2. Pelvic inflammatory disease . 3. Other causes of nodularity in Douglas pouch as tuberculous peritoni­tis and metastases of ovarian cancer. 4. Causes of haematuria , bleeding per rectum and acute abdominal pain if the patient is presented by one of these symptoms. 5. Asymmetrical enlarged uterus. Differential diagnosis

  22. Formed by invagination of the ovarian cortex after accumulation of menstrual debris from bleeding of endometriotic implants. Ovarian Endometriosis (Endometrioma)

  23. Chocolate cyst of the ovaryEndometrioma

  24. Nodules are formed by hyperplasia of smooth muscles and fibrous tissue surrounding the infiltrated tissue. No cyclical bleeding as the endometriotic tissue are enclosed in nodules. Rectovaginal Septum Endometriosis

  25. Several Proposed Schemes. Revised AFS System: Most Often Used. Ranges from Stage I (Minimal) to Stage IV (Severe). Staging Involves Location and Depth of Disease, Extent of Adhesions. Classification / Staging

  26. Stage I (minimal) 1 – 5. Stage II (mild) 6 – 15. Stage III (moderate) 16 – 40. Stage IV (severe) > 40. Revised AFS 1985

  27. Control of pain Control of bleeding Restoration of fertility Reduction of implant volume CA125 Second look laparoscopy Improvement of the score Management goals

  28. Age. Symptoms. Stage. Infertility. Treatment : Consideration

  29. The presence of endometriosis does not generally impair the results of IVF but it increases the risk of infection. It is preferable not to cauterize ovarian endometrioma if IVF or ICSI is indicated for fear of destruction of ovarian tissues. Endometriosis & IVF

  30. Lines are Expectant treatment Medical treatment Hormonal treatment Conservative surgery Extirpative surgery Combined treatment Choice depends Patient Age Need for children Disease Extent Manifestations Association Other pathology Systemic illness Lines of treatment

  31. Young , asymptomatic infertile patient with mild endometriosis. If pregnancy is not achieved within 12 - 18 months of observation: - hormonal or surgical treatment is indicated . Expectant treatment

  32. Symptomatizing patients with minimal or mild lesions: 1. Analgesics : for pain. 2. Prostaglandin inhibitors. 3. Pregnancy. 4. Opoids. 5. NSAID. (II) Medical Treatment

  33. Oestrogen. Combined oestrogen-progestogen Pills. Progestins. Danazol. GnRH agonists. (Ill) Hormonal treatment

  34. 1. Small endometriotic; lesions. 2. Recurrence after conservative surgery. 3. Preoperative for 6-12 weeks to decrease size. 4. Postoperative for residual lesions. 5. When operation is contraindicated or refused by the patient. Indications of Hormonal ttt

  35. (A) Pseudopregnancy : 1. Combined low - dose contraceptive pills(6 - 18 months to inhibit ovulation and menstruation and induce decidualization to endometriotic tissues). or 2. Progestins (to avoid oestrogen's side effects medroxy progesterone acetate Depo medroxy progesterone acetate (DMPA) can be given in a dose of 150 mg IM every I - 3 months . Aim of the hormonal therapy

  36. (B) Pseudomenopause (induction of amenorrhoea) by: 1. Danazol. 2. Gn RH analogues. 3. Gestrinone. 4. Gossypol. Aim of the hormonal therapy cont….

  37. Weak Androgen (isoxazole derivative of 16 – alpha ethinyl testosterone). Suppresses LH / FSH. Causes Endometrial Regression, Atrophy. Expensive. Dose 400 – 800 mgm orally /day/ 6 – 9 months. Side-Effects: Weight Gain, Masculinization, Occ. Permanent Vocal Changes Danazol

  38. 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 ), using E2/progesterone preparation. GnRH-a

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