The underlying mechanism of primary<unk>  is the contractions of the muscles of the uterus which induce a local ischemia. During an individual's menstrual cycle, the endometrium thickens in preparation for potential pregnancy. After ovulation, if the ovum is not fertilized and there is no pregnancy, the built-up uterine tissue is not needed and thus shed. Prostaglandins and leukotrienes are released during menstruation, due to the build up of omega-6 fatty acids. Release of prostaglandins and other inflammatory mediators in the uterus cause the uterus to contract and can result in systemic symptoms such as nausea, vomiting, bloating and headaches or migraines. Prostaglandins are thought to be a major factor in primary<unk> . When the uterine muscles contract, they constrict the blood supply to the tissue of the endometrium, which, in turn, breaks down and dies. These uterine contractions continue as they squeeze the old, dead endometrial tissue through the cervix and out of the body through the vagina. These contractions, and the resulting temporary oxygen deprivation to nearby tissues, are thought to be responsible for the pain or cramps experienced during menstruation. Compared with non-dysmnenorrhic individuals, those with primary<unk>  have increased activity of the uterine muscle with increased contractility and increased frequency of contractions.
Dysmenorrhea
Interstitial cystitis
Hypomenorrhea
Pelvic inflammatory disease
Blennorrhoea
Ectopic pregnancy
Amenorrhea
Pelvic pain