Dysmenorrhea pathophysiology
|
Dysmenorrhea Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Dysmenorrhea pathophysiology On the Web |
|
American Roentgen Ray Society Images of Dysmenorrhea pathophysiology |
|
Risk calculators and risk factors for Dysmenorrhea pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Vishnu Vardhan Serla M.B.B.S. [2]
Primary Dysmenorrhea
Pathophysiology
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.