In this note we start from the statistical consideration on dysmenorrhea, probably ignored by our readers, that as many as 60% or more of women suffer from menstrual pain, while a smaller percentage thankfully acknowledge so important pain during the menstrual event, to have to suspend qulsiasi work or other activities.
The scientific term is “dysmenorrhea,” classical expression with which the medical lexicon is intended to indicate the menstruation which is accompanied by abdominal pain for more than colicky, which sometimes may even precede the bloodstream and be often associated with disturbances of type Systemic and back pain, as we shall see later.
It should be said that many women (and even some physicians) equate, erroneously, menstrual pain to so-called premenstrual syndrome, when it is established that the latter is a clinical event with very different characters and different compared to dysmenorrhea. We will discuss next time. Staying in our theme, and a first distinction can be made between primary and secondary dysmenorrhoea. In the first case, uterine cramps, sometimes disabling, as we mentioned, in women with normal menstrual flow, however, regularly preceded by ovulation, and without clinical evidence of pelvic abnormalities.
It ‘also called dysmenorrhea someone idiopathic or functional (or psychogenic) and that seems determined to be an “ischemic” uterine prostaglandins may be determined by a mechanism not yet fully understood. More precisely, menstrual pains were caused by contractions of the ‘primed uterus, as we just said, from’ too much of a prostaglandin (F2 alpha), particularly substance “hormone” produced during the menstrual cycle occurs when the disintegration of the endometrium.
If the dysmenorrhea, however, is associated with pelvic disease, such as those uterine, adnexal or vaginal, we adopt the definition of secondary dysmenorrhea or symptomatic. Some authors in this group would fall congestive dysmenorrhea, due to congestion of the internal genital organs, dysmenorrhea mambranacea, characterized by expulsion of the uterine lining (endometrium) in laminar form and, finally, obstructive dysmenorrhoea, leading to conditions that hinder the flow of menstrual blood, as can happen in uterine malposition or stenosis of the cervical canal.
Regarding the secondary symptom picture of shapes we have to repeat that predominate type of colic pain in the uterus, like the forms we have defined primitives, with some variation, however, depending on the pelvic disease in question. Pains are intermittent and present for the duration of menstruation typically forms in the uterus, appear only late in the salpingo-ovariti and endometriosis, as they occur in the initial period in cases due to stenosis mechanics and in the hours before the start of flow in those congestive.
But we are interested in conclusion, to point out especially the ‘pathogenetic aspect of most common and widespread, ie the primary or idiopathic dysmenorrhoea, namely, which can not be connected to other organic pathology in the pelvic area. Well, in this form it is able to show, for several years, that in women with severe menstrual pain could show high concentrations of prostaglandin appointed in menstrual blood and, therefore, one could think that the hormone enters the bloodstream during the phase exfoliation of the endometrium and did so vigorously contracting the uterus, causing the typical cramping pain attributed to colon cancer.
With regard to drug therapy, it must always be preceded by the investigations necessary to exclude the presence of organic disease (practically forms of secondary dysmenorrhea), because in that case there must be always the treatment of the underlying disease, such as endometriosis , infections and other diseases which we have already mentioned. Also, note that the care they need to relieve primary dysmenorrhea have effect in the secondary and could mask, in this case, the underlying disease.
The anti-inflammatory drugs (NSAIDs), especially when taken before manifesting menstrual pain, but also immediately after, are able to inhibit the biosynthesis of prostaglandins (and therefore also of the F2 alpha) and consequently the uterine spasms that cause the pain. We can mention some molecules such as indomethacin, diclofenac, ibuprofen, ketoprofen, naproxen, etc. all usable in the specific case with warnings and contraindications that the use of these drugs involves. They also recommended that oral contraceptives, eliminating ovulation, the hormonal changes are also involved related to uterine cramps, though some women do not always respond to this treatment.