Secondary dysmenorrhea

Introduction to secondary dysmenorrhea Secondary dysmenorrhea (secondarydysmenorrhoea) is caused by pelvic organic disease, pelvic examination and other auxiliary examinations often have abnormal findings, which can identify the cause of secondary dysmenorrhea. Secondary dysmenorrhea has provable pathological changes that cause menstrual pain. Endometriosis is a common cause of dysmenorrhea, and a small number of women can also have cervical stenosis (secondary to conical resection, freezing or electrocautery), caused by uterine muscle adenopathy; pain occurs in the uterus trying to expel tissue from the cervix When a pedicled submucosal fibroid or an endometrial polyp is expelled from the uterus, it sometimes causes spastic pain. Pelvic inflammation can cause extensive, persistent pain in the lower abdomen, which tends to worsen during menstruation, and other causes of dysmenorrhea are unknown. basic knowledge The proportion of illness: 0.3% Susceptible people: women Mode of infection: non-infectious Complications: bloating, bloating, endometriosis

Secondary dysmenorrhea

Disease factors (35%):

Secondary pain is often associated with pelvic organic diseases. Common secondary dysmenorrhea: endometriosis, adenomyosis, endometrial polyps, uterine fibroids, submucosal fibroids, intrauterine adhesions Cervical stenosis, uterine malformation, pelvic inflammatory disease (acute, chronic), pelvic congestion syndrome, intrauterine device, hymen atresia, vaginal diaphragm and so on.

Environmental factors (25%):

Other studies have shown that special occupational and working conditions are also related to dysmenorrhea. Women who have been exposed to mercury for a long time and have benzene compounds (even at low concentrations) have an increased incidence of dysmenorrhea. The cold working environment is also related to dysmenorrhea.

Other factors (5%):

Early menarche or long menstrual period, women with more menstrual flow, severe dysmenorrhea, taking contraceptives, the incidence of dysmenorrhea is significantly reduced.

Pathogenesis

Prostaglandins and secondary dysmenorrhea: studies have shown that some patients with secondary dysmenorrhea caused by endometriosis and uterine adenoma also produce excessive PGs, which may be one of the causes of dysmenorrhea, anti-prostaglandin synthesis The preparation also has the effect of relieving dysmenorrhea. The exact relationship between PGs and the pain mechanism of endometriosis is still under investigation. Normal endometrium, normal myometrium, ectopic endometrium, uterine fibroids, normal ovary and The affected ovarian sections were incubated in vitro, and the concentration of 6-keto PGF1a (a metabolite of PGI2), TXB2 (a metabolite of TXA2), PGE2 and PGF2a in the culture medium was found. The results showed that the ectopic endometrial tissue was found. The production of PGs is significantly higher than other groups, especially 6-keto PGF1a, which produces the most ectopic tissue in the endometrium; in severe dysmenorrhea and non-dysmenorrhea, there is a significant difference in the production of PGs, especially severe dysmenorrhea. Muscle adenoma tissue produces a large amount of 6-keto PGF1a, and other studies have shown that the concentration of PGF2a in the peritoneal fluid is significantly increased after the experimental animal is induced with endometriosis; the abdomen of patients with endometriosis The concentration of liquid PGs is also higher than that of the control, suggesting that PGFI2 can cause hyperalgesia in endometriosis menstrual period. In addition, uterine adenomy can cause severe pain, which may be the close proximity of endometrial tissue to uterine muscle, and the location of PGs. Increased absorption and activity, inflammatory responses around the site of ectopic endometrial implantation may be regulated by PGs as PGs regulate inflammatory responses in some tissues.

Cyclooxygenase (C0X) is the rate-limiting enzyme of PGE2 synthesis. Human endometrial glands contain high levels of COX. Immunohistochemistry, RTPCR and Western blot analysis revealed that COX is high in ectopic endometrial tissue. Expression, high activity of COX-2 and abnormal PG production play a role in the pathophysiology and disease progression of endometriosis, which is highly expressed in peritoneal macrophages of patients with endometriosis, It may be related to the increase of PGE2 and play an important role in the development of endometriosis. The PG in peritoneal fluid of patients with endometriosis increases, while the PG in follicular fluid is not different from the control.

Side effects of the intrauterine device (IUD) include menorrhagia, secondary dysmenorrhea, which may be due to damage to the endometrium or leukocyte infiltration in the vicinity of the IUD, which may enhance the biosynthesis of PGs, making women using IUD Corresponding to the activity of uterine muscle, in the experimental animals using IUD, the release of PGs increased, IUD is associated with increased uterine hypertrophy and PGF production, in the uterine horn of IUD, the composition and concentration of uterine PGF and uterine vein The level of PGF in the blood increased. In the ewes, the content of PG in the uterus of the IUD was also significantly increased. In the human study, volunteers wearing the shield-shaped IUD were found to have no symptoms. There was no PGF2a in the endometrium. Increased synthesis; the use of drug-added IUD may be related to the amount of PG produced by the endometrium. For example, wearing metal IUD may release metal ions, which may facilitate the synthesis of PGF2a and inhibit the synthesis of PGE2, but studies have also been reported in IUD. In 1 to 5 months, 14 women had a significant increase in PGE but not PGF in the endometrium. In women with IUD, due to the mechanism of excessive release of PG, PG inhibitors To effectively relieve dysmenorrhea.

Prostaglandin theory itself does not explain some of the other changes in primary dysmenorrhea and secondary dysmenorrhea, increased age and number of births, socioeconomic status, alcohol can reduce the occurrence and/or severity of dysmenorrhea; smoking, Exposure to cold working conditions can increase primary dysmenorrhea, and other factors that directly or indirectly affect development and severity require further study.

Secondary dysmenorrhea prevention

1. Active prevention and treatment of primary disorders leading to secondary dysmenorrhea.

2. Pay attention to menstrual hygiene, avoid strenuous exercise and excessive cold stimulation, and usually strengthen physical exercise and enhance physical fitness.

3. Avoid unclean sex life, pay attention to contraception, try to avoid uterine cavity operation.

4. Regular gynecological census, early detection of disease, early treatment.

Secondary dysmenorrhea complications Complications, abdominal distension, bloating, endometriosis

Secondary pain often has different symptoms, accompanied by abdominal distension, lower abdomen, and traction pain is often more obvious. Most of the pain occurs before the menstrual cramps, peaks in the first half of the menstrual period, and then alleviate until the end. However, dysmenorrhea of endometriosis may also occur shortly after menarche. The beginning of sexual life can reduce the incidence of dysmenorrhea.

Secondary dysmenorrhea symptoms common symptoms lower abdominal pain secondary dysmenorrhea bloating endometriosis uterus transposition period before and after abdominal pain

Secondary pain often has different symptoms, accompanied by abdominal distension, lower abdomen, traction pain is often more obvious, pain occurs before menstruation, peak in the first half of menstruation, later reduced until the end, but endometriosis Dysmenorrhea may also occur shortly after menarche, the beginning of sexual life, which can reduce the incidence of dysmenorrhea.

According to the primary disease combined with symptoms can be diagnosed.

Secondary dysmenorrhea

Secondary dysmenorrhea is mainly to help diagnose by asking about medical history, physical examination and auxiliary examination. Gynecological internal examination can be found that the uterus is harder to enlarge, less active, or in the uterine rectal sinus and hard irregular nodules or masses, tenderness is obvious. Auxiliary examination mainly includes pelvic B-ultrasound, hysterosalpingography, hysteroscopy, laparoscopy and histopathology.

Diagnosis and diagnosis of secondary dysmenorrhea

Secondary dysmenorrhea should first find the primary lesion, pay attention to the identification of primary dysmenorrhea, complete history, age of onset, progression of the disease, the nature of the disease, accompanied by symptoms and other helpful differential diagnosis.

Primary dysmenorrhea: mostly menarche and dysmenorrhea symptoms, diagnosis of primary dysmenorrhea gynecological examination without positive signs for the diagnosis of primary dysmenorrhea is mainly to rule out the existence of pelvic organic lesions. Take a complete medical history, do a detailed physical examination (especially gynecological examination), exclude endometriosis, adenomyosis, pelvic inflammation.

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