Primary dysmenorrhea

Introduction to primary dysmenorrhea Primary dysmenorrhea (primarydysmenorrhoea) is functional dysmenorrhea, dysmenorrhea refers to menstrual pain, often sputum, concentrated in the lower abdomen, other symptoms include headache, fatigue, dizziness, nausea, vomiting, diarrhea, low back pain. It is a very common condition among young women. Primary dysmenorrhea is not associated with significant pelvic organic disease. basic knowledge Probability ratio: 2% of specific population Susceptible people: women Mode of infection: non-infectious Complications: anxiety

Primary dysmenorrhea

Age factor (25%):

In the first few months of menarche, there is very little dysmenorrhea, and the subsequent rate increases rapidly. It reaches its peak (82%) at 16 to 18 years old, gradually decreases after 30 to 35 years old, and stabilizes at around 40% in the middle of childbearing age. Later, it will be lower at 20 years old, and the beginning of sexual life can reduce the incidence of dysmenorrhea. The 5-year follow-up survey of Swedish 19-year-old female youth shows that the incidence of dysmenorrhea drops from 72% by the age of 24 To 67%, the severity has also dropped.

Body factor (20%):

The incidence and severity of dysmenorrhea in women with a history of full-term pregnancy delivery are significantly lower than those without pregnancy and pregnancy, but spontaneous abortion or abortion, because near the full term, the adenines of the smooth muscle cells in the uterus are almost all Disappeared, uterine norepinephrine levels also decreased; postpartum, these nerve endings only partially regenerated, uterine norepinephrine levels can not be restored to pre-pregnancy levels, this change in uterine neuromuscular activity after full-term pregnancy can explain full-term postpartum The cause of dysmenorrhea is reduced or disappeared, but the abortion has no such changes. In addition, women with early menarche or long menstrual period, menstrual menstruation, severe dysmenorrhea, and contraceptives, the incidence of dysmenorrhea is significantly reduced, and dysmenorrhea also shows certain family characteristics. The mother and sister of dysmenorrhea often have dysmenorrhea, smokers, reduced dysmenorrhea, cultural level, physical activity and dysmenorrhea.

Occupational factors (25%):

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.

Mental factors (20%):

The relationship between mental factors and dysmenorrhea has been discussed over the years. The results are inconsistent. Some people think that the mental factors of dysmenorrhea women are also very important. They often show self-regulation, relatively depressed, anxiety and introversion. Serious dysmenorrhea is better than dysmenorrhea. Interests and emotions are more feminine, and others believe that mental factors only affect the response to pain, not pathogenic factors.

Pathogenesis

1. Abnormal uterine contractions: the occurrence of primary dysmenorrhea is related to the increase of uterine tension and excessive spasmodic contraction caused by increased uterine muscle activity. In normal menstrual period, the basal tension in the uterine cavity is <1.33 kPa, and the pressure during uterine contraction does not exceed 16kPa, contraction coordination, frequency is 3 ~ 4 times / 10min, dysmenorrhea, the basal tension in the uterine cavity increases, the pressure during uterine contraction exceeds 16 ~ 20kPa, the contraction frequency increases, and becomes uncoordinated or arrhythmic contraction, Due to the abnormal contraction of the uterus, the blood flow to the uterus is reduced, causing uterine ischemia, leading to dysmenorrhea.

It has been found that the causes of excessive contraction of the uterus are: prostaglandins, leukotrienes, vasopressin, oxytocin, and the like.

2. Prostaglandin or leukotriene synthesis and release: In 1957, the smooth muscle stimulator was first found in menstrual blood, and it was called "menstrual irritant". In 1961, several active lipids were found in menstrual blood. Substance, now known as prostaglandin (PGS), is a group of unsaturated, hydroxylated fatty acids with similar chemical structure and physiological activity. It is widely present in human tissues and body fluids with very low levels and strong effects. Prostaglandins are mainly synthesized by phospholipids present in the cell membrane and are a reflection of tissue damage. In normal women, the late luteal phase, the corpus luteum is degraded, the progesterone level is decreased, the lysosomal membrane is unstable, and the phospholipase A2 is released, causing phospholipids. Hydrolysis produces arachidonic acid, which produces different PG species through two pathways:

(1) Prostaglandins such as PGD2, PGE2, PGF2, prostacyclin (PGF2), thromboxane (TX) A2, called cyclooxygenase pathway, non-steroidal anti-inflammatory, under the action of cyclooxygenase The drug blocks the pathway by inactivation of the epoxidase after acetylation.

(2) Under the action of 5-lipoxygenase, leukotrienes are produced, and leukotrienes are powerful vasoactive substances. Different types of PGs exhibit different physiological activities due to structural differences. PGF2a and TXA2 can Stimulate uterine hypercontraction; PGE2 and PGI2 can relax the uterus, and the most relevant PGs for dysmenorrhea are PGF2a. Regulators of prostaglandin biosynthesis include: stimulating factors and inhibitors. Common stimulating factors include fatty acids, trauma, estrogen, progesterone , cAMP, LH, adrenaline; inhibitors include prostaglandin synthesis inhibitors, corticosteroids, and the like.

The endometrium is an important part of the synthesis of prostaglandins. Many evidences indicate that uterine synthesis and release of PG are important causes of primary dysmenorrhea. PGF2a and thromboxane A2 can stimulate excessive contraction of the uterus, resulting in decreased uterine blood flow, most Menstrual blood, uterine lavage fluid, menstrual irrigated fluid, PGF2a concentration and PGF2a/PGE2 ratio in menstrual endometrial and peripheral blood were significantly increased in the menstrual dysmenorrhea, and the symptoms of primary dysmenorrhea could be simulated by intravenous or intrauterine input of PGF2a. Including related systemic symptoms such as: nausea, vomiting, diarrhea, headache, etc., normal endometrium, ability to synthesize PGF2a before menstruation; uterine dysmenorrhea in patients with dysmenorrhea is 7 times that of non-dysmenorrhea women, PG release during menstrual period Mainly within the first 48h, this is consistent with the time of dysmenorrhea symptoms. The PG synthesized in the endometrium is higher than the proliferative phase in the secretory phase, and there is no dysmenorrhea in the ovulation menstrual cycle. The most convincing evidence is: Prostaglandin synthetase inhibitor - Non-steroidal anti-inflammatory drugs can effectively relieve some dysmenorrhea.

In the adjacent muscle cells, the transmission of contractile signals is regulated by gap junctions. During the menstrual period, this transmission activity is more frequent in the myometrium; dysmenorrhea women are more frequent, and it is known that PGF2a can induce gap junctions, which may be caused The mechanism of excessive uterine contraction, the underlying cause of PGF2a overproduction and release is still not fully understood. Some studies have confirmed that human endometrial and myometrial synthesis of PG is affected by the menstrual cycle, high estrogen levels are particularly important, and women with dysmenorrhea have been reported. The estrogen level in the late luteal phase was significantly higher than that in the control group.

The increase of PG level in the blood of women with primary dysmenorrhea not only stimulates the excessive contraction of the myometrium to cause uterine ischemia, but also in the exfoliated endometrium, the lesion continues to produce a small amount of PG, so that the pelvic nerve endings are sensitized to PG. Causes mechanical stimulation or chemical stimuli such as bradykinin and histamine to lower the threshold of pain. The study also found that intrauterine PGE2 and PGF2a in dysmenorrhea and non-dysmenorrhea patients, the uterine muscle response is no different, because PGs rapidly decompose into 15-ketone, 13,14-dihydro-PGF2a, although the plasma concentration of PGF2a in dysmenorrhea women is similar to that of the control, the 15-keto, 13,14-dihydro-PGF2a in normal women's plasma is higher than that in women with dysmenorrhea, indicating the metabolic reduction of PG in dysmenorrhea slow.

The synthesis of prostaglandins in some patients with dysmenorrhea does not increase, but the activity of 5-lipoxygenase pathway is enhanced, which increases the synthesis of leukotrienes. The latter is a powerful vasoconstrictor, which may explain why some patients have Non-steroidal anti-inflammatory drugs are not effective.

3. The role of vasopressin and oxytocin: vasopressin as another important pathogenic factor of dysmenorrhea, has been confirmed by many studies, elevated levels of vasopressin in women with primary dysmenorrhea, this hormone also It can cause the contraction of smooth muscles of the myometrium and arterial wall, and the blood flow of the uterus is reduced. The intravenous injection of hypertonic saline can increase the secretion of vasopressin, enhance the contraction of the uterus, and aggravate the symptoms of dysmenorrhea.

Estrogen can stimulate the release of vasopressin from the pituitary gland. This effect can be counteracted by progesterone. Under normal circumstances, plasma vasopressin levels are highest during ovulation, luteal phase declines, until menstrual period, primary dysmenorrhea women, late The estrogen level in the luteal phase is abnormally elevated, so the vasopressin level is 2 to 5 times higher than that in the normal person on the first day of the menstrual period, resulting in excessive contraction of the uterus and ischemia.

In the past, it was thought that oxytocin had little relationship with dysmenorrhea, but recent studies have confirmed that ovation receptors are also present in non-pregnant uterus. After dysmenorrhea enters hypertonic saline, blood levels of oxytocin are also elevated, vasopressin and oxytocin. Both are important factors in increasing uterine activity leading to dysmenorrhea. Both peptides seem to act through specific vasopressin and oxytocin receptors acting on the uterus. The relative importance of their action depends on the hormonal status of the uterus. Vasopressin may also affect oxytocin receptors in non-pregnant uterus, and oxytocin antagonists, competitive inhibition of oxytocin and vasopressin receptors, can effectively relieve dysmenorrhea (44%), which can also be seen The role of vasopressin and oxytocin in dysmenorrhea.

4. Other

(1) Cervical stenosis: In the past, it was thought that the uterine cervix was not produced, which caused the intrauterine pressure to rise. The menstrual blood flowed back into the pelvic cavity and stimulated the pelvic nerve endings to cause pain. It is now known that menstrual menstrual blood reflux is more common and does not necessarily cause dysmenorrhea.

(2) Other peptides and autonomic nervous system: Endothelin, norepinephrine can also cause uterine muscle and uterine vasoconstriction, leading to dysmenorrhea, autonomic nervous system (choline, adrenergic) peptide energy can also affect Uterine and blood vessels, anterior tibial nerve resection can treat dysmenorrhea, postpartum dysmenorrhea in term pregnancy, and is also associated with a significant reduction in autonomic nerve fibers in the uterus.

(3) Immune system: Recently, some scholars have studied the changes of immune cells and immune responses in patients with dysmenorrhea for the first time. It is found that the mitogen-induced lymphocyte proliferative response is significantly decreased in the 26th day of the cycle, and the monocyte - in the blood on the third day of the cycle. Increased levels of endorphins suggest that dysmenorrhea is a recurrent disease that forms a physical and psychological stress that leads to changes in the immune response. The relationship between dysmenorrhea and immunity remains to be further confirmed. Explore.

Primary dysmenorrhea prevention

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

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

3. Regular gynecological census: early detection of disease, early treatment.

Primary dysmenorrhea complications Complications

Concurrent anxiety and other mental disorders.

Symptoms of primary dysmenorrhea Common symptoms Dysmenorrhea, abdominal pain, menstrual period before and after abdominal pain, menstrual period, abdominal pain, premenstrual syndrome, secondary dysmenorrhea, fatigue, diarrhea, menstrual headache, dizziness

Primary pain often occurs in young women, starting several months after menarche (6 to 12 months), and the incidence begins to decline after 30 years of age. Pain often begins before or after the onset of menstruation and continues during the menstrual period. For the first 48 to 72 hours, the pain is often sputum, sometimes so heavy that it takes hours or days to stay in bed. The pain is concentrated in the middle of the lower abdomen, sometimes with low back pain or radiation to the medial side of the femoral tract.

The determination of the degree of dysmenorrhea is generally based on the degree of pain and the impact on daily activities, systemic symptoms, and the application of painkillers. Mild: There is pain, but it does not affect daily activities, work is rarely affected, and there is no systemic symptoms. Lack of painkillers; moderate: pain affects daily activities, work ability also has a certain impact, few systemic symptoms, need to use painkillers, and effective; severe: pain makes daily activities and work significantly affected, the whole body The symptoms are obvious and the painkillers are not effective.

Primary dysmenorrhea

Excretion check, hormone level check.

B-ultrasound, laparoscopic, hysteroscopy, uterine tubal iodine angiography.

Diagnosis of primary dysmenorrhea

Diagnosis of primary dysmenorrhea, gynecological examination without positive signs for the diagnosis of primary dysmenorrhea, mainly to rule out the existence of pelvic organic lesions, take a complete medical history, do a detailed physical examination (especially gynecological examination), exclude the uterus Endometriosis, adenomyosis, pelvic inflammation, etc.

Differential diagnosis: It should be distinguished from chronic pelvic pain. The pain of chronic pelvic pain has nothing to do with menstruation. It should also be differentiated from secondary dysmenorrhea and early endometriosis.

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