Originally described over three hundred years ago, Endometriosis is classically defined as the presence of endometrial glands and stroma in ectopic locations, primarily the pelvic peritoneum, ovaries and rectovaginal septum, affecting 6-10% of women of reproductive age. The prevalence of this condition in women, experiencing pain, infertility or both is as high as 35-50%. \nPathogenesis\n is not fully understood However genetic predisposition and immunological changes have been reported to clearly play a role. Several hypotheses have been used to explain the various manifestations of the disease and its various locations \n1. The Retrograde Menstruation Theory \n2. The Mullerian Metaplasia Theory \n3. The Lymphatic Spread Theory \n4. The Hematogenous Spread Theory \nThe Retrograde Menstruation Theory of Sampson: \nThe Retrograde Menstruation Theory of Sampson proposes that endometrial fragments that are shed during menstruation are transported through the fallopian tubes, then implants themselves and grow in various intra-abdominal sites. (These endometrial fragments are viable and capable of growing in vivo and in vitro) Though retrograde menstruation explains the physical displacement of endometrial fragments into the peritoneal cavity, additional steps are necessary for the development of endometriotic implants. Escape from immune clearance, attachment to the peritoneal epithelium, invasion of the epithelium, the establishment of local neurovascular and continued growth and survival are necessary if endometriosis is to develop from the retrograde passage of endometrium. Collectively, investigations involving the pathophysiology of endometriosis have revealed several well-supported molecular hallmarks of this disease:\nGenetic predisposition\nEstrogen dependence\nProgesterone resistance\nInflammation\nThe Mullerian Metaplasia Theory of Meyer:  \nThe Mullerian Metaplasia Theory of Meyer proposes that endometriosis results from the metaplastic transformation of the peritoneal mesothelium to the endometrium under the influence of certain unidentified stimuli.\nThe Lymphatic Spread Theory of Halban: \nThe Lymphatic Spread Theory of Halban suggests that the lymphatics draining the uterus transport endometrial tissue to the various pelvic sites where it grows ectopically\nThe Haematogenous Spread Theory: \nThe Haematogenous Spread Theory explains the presence of endometrial tissue in distant sites (lung, axilla and forehead). Sites of occurrence Most commonly found in the dependent portions of the pelvis \n1. Ovaries (2 out of 3 women with endometriosis) \n2. Broad ligament \n3. Peritoneal surfaces of the cul-de-sac (uterosacral ligaments and post Cervix) \n4. Rectovaginal septum. \nQuite frequently in the recto-sigmoid colon, appendix and vesicouterine fold of the peritoneum involved. Laparotomy scars esp after C-section or myomectomy or after the uterine cavity has been entered. Pathology The islands of endometriosis are sensitive to ovarian hormones. Estrogen causes proliferation. Regression of corpus luteum and removal of estrogen and progesterone causes them to slough. This sloughed debris induces a profound inflammatory response that causes significant pain and long term fibrosis. Microscopical appearance Depends on site, size, time since implantation and day of the menstrual cycle. Colour is a good indicator and is determined by the vascularity of the lesion, the presence of fibrosis, the size of the lesion and the presence of residual sloughed material. It varies from red, brown, black, white – yellow. Newer implants: Red, blood-filled active lesions. Older lesions: Scarred with a puckered appearance. Microscopically 2 out of 4 must be present in the biopsied specimen to confirm Dx \n1. Endometrial epithelium \n2. Endometrial glands \n3. Endometrial stroma \n4. Hemosiderin laden macrophages \nRisk factors of endometriosis \nMany patients are asymptomatic. Others usually have no positive signs on examination.\n

Endometriosis - Pathogenesis & ComplicationsDisclaimer

Endometriosis - Pathogenesis & Complications
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