Endometriosis is a common benign gynecologic disorder defined as the presence of endometrial glands and stroma outside of the normal location.
- Never giving birth
- Early menarche
- Late menopause
- Heavy menstrual periods that last longer than seven days
- Having higher levels of estrogen in your body or a greater lifetime exposure to estrogen your body produces
- One or more relatives (mother, aunt or sister) with endometriosis
- Reproductive tract abnormalities
- Reproductive outflow tract obstruction
- Environmental Toxins-TCDD(tetrachlorodibenzo-p-dioxin ) and dioxin-like compounds are waste by-products of industrial processing. Ingestion of contaminated foods or accidental contact is the most common method of exposure.
Most commonly, endometriosis is found in the dependent areas of the pelvis. The ovary, pelvic peritoneum, anterior and posterior cul-de-sacs, and uterosacral ligaments ,the rectovaginal septum, ureter, the bladder, pericardium, surgical scars, and pleura may be affected. Endometriosis has been identified on all organs except the spleen.
- Pain -Endometriosis is a common cause of pelvic pain, which in affected women can vary greatly and may be cyclic or chronic. Cause of this pain is proinflammatory cytokines and prostaglandins released by endometriotic implants into the peritoneal fluid. Endometriosis pain may result from neuronal invasion of endometriotic implants that subsequently develop a sensory and sympathetic nerve supply
- Dysmenorrhea(pain and cramping menses)
- Dyspareunia (Pain with intercourse)
- Excessive bleeding( heavy menstrual periods )
- Bleeding between periods (intermenstrual bleeding)
- Infertility-Adhesions that are caused by endometriosis may impair normal oocyte pick-up and transport by the fallopian tube
- Defecatory Pain Painful defecation develops.
- Dysuria(painful urination and cyclic urinary frequency and urgency)
The earliest and most widely accepted theory describes retrograde menstruation through the fallopian tubes and subsequent dissemination of endometrial tissue within the peritoneal cavity .Refluxed endometrial fragments adhere to and invade the peritoneal mesothelium and develop a blood supply, which leads to continued implant survival and growth.
Uterine hyperperistalsis and dysperistalsis have been noted in women with endometriosis and resulted in subsequent increased endometrial reflux.
Women with amenorrhea due to outflow tract obstruction similarly have a high incidence of endometriosis.
2.Lymphatic or Vascular Spread
Evidence also supports the concept of endometriosis originating from aberrant lymphatic or vascular spread of endometrial tissue
The ovary and the progenitor of the endometrium, the müllerian ducts, are both derived from coelomic epithelium, metaplasia may explain the development of ovarian endometriosis.
Estrogen has been definitively established as having a causative role in the development of endometriosis
Progesterone antagonizes the estrogen effects in normal endometrium during the luteal phase of the menstrual cycle. Endometriosis, however, manifests a relative progesterone-resistant state, which prevents attenuation of the estrogen stimulation in this tissue.
5.Role of the Immune System
Menstrual tissue and endometrium that are refluxed into the peritoneal cavity are usually cleared by immune cells such as macrophages, natural killer (NK) cells, and lymphocytes. For this reason, immune system dysfunction is one likely mechanism for the genesis of endometriosis.
6.Surgical scar implantation. After a surgery, such as a hysterectomy or C-section, endometrial cells may attach to a surgical incision.
Speculum Examination- Examination of the vagina and cervix often reveals blue or red powder-burn lesions may be seen on the cervix or the posterior fornix of the vagina. These lesions may be tender or bleed with contact.
- Blood –CBC, serum human chorionic gonadotropin assay, Serum CA125, Cancer antigen 19-9 (CA 19-9),
- ULTRASOUND ABDOMEN
- MRI ABDOMEN