Dysmenorrhea pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Vishnu Vardhan Serla M.B.B.S. [2]
Pathophysiology
Primary Dysmenorrhea
Primary dysmenorrhea occurs during regular ovulatory cycles. Women with primary dysmenorrhea have increased activity of the uterine muscle with increased contractility and increased frequency of contractions. Prostaglandins are released during menstruation due to destruction of the endometrial cells and the resultant release of their contents.
Release of prostaglandins and other inflammatory mediators in the uterus (womb) is thought to be a major factor in primary dysmenorrhea (Wright et al. 2003). Prostaglandin levels have been found to be much higher in women with severe menstrual pain than in women who experience mild or no menstrual pain. Drugs which inhibit the production of prostaglandins, such as the non-steroidal anti-inflammatory drugs (NSAIDs) Naproxen, Ibuprofen and Mefenamic Acid, can provide relief for the discomfort and other associated symptoms of excessive prostaglandin release, such as nausea, vomiting, and headache.
Secondary Dysmenorrhea
The mechanisms causing the pain of secondary dysmenorrhea are varied and may or may not involve prostaglandins. Some causes of secondary dysmenorrhea are endometriosis, pelvic inflammation, leiomyoma, adenomyosis, ovarian cysts, and pelvic congestions (Hacker et al. 2004). The presence of an IUD (intrauterine device) for contraception may also be a potential cause of menstrual pain, although they usually lead to pelvic pain only around the time of insertion. Some women also find that use of internally-worn menstrual products, such as tampons and menstrual cups, exacerbate menstrual cramps and pain.