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This Concept Map, created with IHMC CmapTools, has information related to: Endometriosis, E2, IL-1beta, TNF and IL6 ???? dymenorrhea/pelvic pain, estrone by the enzyme 17 beta-hydroxydehydrogenase TYPE II, Roberta Trout presents with dymenorrhea/pelvic pain, GnRH from the hypothalamus so with GnRH analogs chronically provided you get the suppression of FSH and LH via downregulation of GnRH receptors, endometriotic implants which can respond to hormone changes, similar to the endometrium of the uterus, leads to suppress follicular growth and ovulation which may reduce endometriosis Endometriosis, initiate inflammation resulting in pelvic pain which leads to her symptoms of dymenorrhea/pelvic pain, Timing: after ovulation until next menses Physiology: high levels of progesterone will stabilize endometrium to help with implantation. Secretion from the glands is facilitated. If blastocyst does not implant within 9-11 days after ovulation and form a placental membrane to form Beta-HCG, the corpus luteum will regress and stratum functional will be shed (menses). Cycle will repeat. Flow of Menses Irregularly: retrograde menstruation out of the uterine tubes into the peritoneal cavity, Timing: spans from the start of menses to ovulation Physiology: Increased amounts of estrogen which causes the stratum functionale to start proliferating and spiral arteries and glands are developing. Estrogen will increase progesterone receptor synthesis to enable endometrium to respond to progesterone the next phase is the secretory phase, progesterone by the actions of 3-beta-hydroxysteroid dehydrogenase which is then acted upon by 17-alpha- hydroxylase to generate, Estrogen ???? The synthesis of estrogen homrones, which is theorized to be caused from metastatic changes, oral contraceptives which help to minimize pain and regulate menstrual flow, impairment of ovarian, tubal, peritoneal, and endometrial function which leads to defective folliculogenesis, and implantation which ultimately leads to infertility, Roberta Trout Diagnosed with Endometriosis, androstenedione which can be acted upon by 17-b HSD, the menstrual cycle which normally functions through phases in the ovary, anatomic distortion such as deep ovarian endometriomas and/or major pelvic adhesions with obliteration of normal pelvic organ organization which can lead to pain due to the associated overproduction of inflammatory mediators such as prostaglandins, metalloproteinases, cytokines, and chemokines, GnRH from the hypothalamus which stim the stimulate the release of, endometriotic implants which can initiate inflammation resulting in pelvic pain