How is the girl's stomachache?

It hurts during the physiological period

My stomach hurts.

Appendicitis can also hurt.

Ectopic pregnancy will hurt one day if it is not found in time.

Dysmenorrhea is periodic lower abdominal pain before and after menstruation, which often occurs before and during menstruation, and occasionally occurs within a few days after menstruation. Lower abdominal pain is spasmodic swelling pain, which can radiate to lumbosacral region, inner thigh and around anus. It may be accompanied by pallor, nausea, vomiting, chills in the whole body or lower abdomen, frequent defecation, and collapse when severe pain occurs. The degree of dysmenorrhea depends on subjective feelings, and there is no objective standard, so the incidence rate is different. According to the survey results of 29 provinces and cities in China (1980), the incidence of dysmenorrhea was 33. 19%, including primary dysmenorrhea (30.06%), mild dysmenorrhea (45.73%), moderate dysmenorrhea (38.8 1%) and severe dysmenorrhea. It is rare that primary dysmenorrhea occurs within half a year after menarche. It is reported that 75% of primary dysmenorrhea occurs within 1 year after menarche, 0/3% in the second year and 50% in the third year. Secondary pain often occurs 2 years after menarche. The age and course of dysmenorrhea in different diseases are different, and the occurrence of dysmenorrhea is different sooner or later.

etiology

Primary dysmenorrhea is generally attributed to the following reasons: endometrial tube shedding (membranous dysmenorrhea), uterine hypoplasia, uterine flexion, cervical canal stenosis, bad posture and physical factors, allergic state and mental factors.

Patients with secondary dysmenorrhea are diagnosed as secondary dysmenorrhea if pelvic organ lesions are found in Shuanghe town. It is often misdiagnosed as primary dysmenorrhea when the local abnormal signs are not obvious, so if dysmenorrhea begins more than 3 years after menarche, the possibility of secondary dysmenorrhea should be considered and further examination should be made.

The common cause of secondary dysmenorrhea in young women is endometriosis, which is very similar to the symptoms of primary dysmenorrhea. If the patient has a family history of progressive dysmenorrhea or endometriosis (one of the mother or sister has this disease), laparoscopic examination should be performed as soon as possible to make a definite diagnosis, and conservative surgery should be performed as soon as possible to preserve fertility.

In addition, the causes of secondary dysmenorrhea are: congenital uterine malformation (including biconical uterus, mediastinal uterus, residual horn uterus, vaginal septum, etc. ), pelvic inflammatory disease, adenomyosis, hysteromyoma, uterine polyp, uterine adhesion, cervical canal stenosis, ovarian cyst, pelvic blood stasis syndrome.

Patients with elevated body temperature during menstruation should consider pelvic inflammatory disease in addition to dysmenorrhea. About 5% of women with intrauterine devices suffer from dysmenorrhea. If there is no infection, the cause of dysmenorrhea may be that the intrauterine device stimulates the endometrium and PGs is released too much, resulting in excessive contraction of uterine muscles.

Patients with uterine malformation and complete obstruction of lower reproductive tract may have periodic lower abdominal pain, no menstrual cramps after menarche, and other secondary sexual characteristics are normal. Periodic lower abdominal pain is secondary to reproductive tract hematocele, which usually occurs within 2 ~ 3 years after breast development. Genital tract malformation, hymen atresia and obstruction of vaginal septum can be easily diagnosed by gynecological examination. However, if one side of the reproductive tract is blocked and the other side is unobstructed due to fusion defects, such as undivided double uterus, blind end of one side of vagina or residual angle of uterus that is not connected with vagina, it is difficult to diagnose. These patients have a history of aggravated dysmenorrhea, and they can touch the lump when they are diagnosed, which is easy to be misdiagnosed as vaginal cyst's or ovarian tumor.

Adenomyosis, endometrial polyps and hysteromyoma are relatively rare among adolescent girls. Dysmenorrhea induced by this lesion mostly occurs after the age of 25, and the type of pain is uncertain and the pain lasts for a long time.

[pathophysiology]

1. The nerves innervating uterus, fallopian tubes and ovaries are composed of sympathetic nerves, parasympathetic nerves and some spinal nerves. Pelvic plexus is mainly composed of: ① sympathetic nerve of presacral plexus; ② Parasympathetic nerves of sacral nerve 2 ~ 4 (including a few sympathetic nerves); ③ Spinal nerve is composed of a few parasympathetic nerves.

Branches of pelvic plexus are distributed in ureter, bladder, rectum and uterus. The nerves in the ovary are multi-source, including the ovarian plexus composed of nerve fibers separated from the renal plexus, fibers from the lower abdominal plexus and pelvic plexus, and sympathetic nerve fibers extending from the uterine body. Ovary is extremely insensitive to nerve stimulation and is mainly regulated by endocrine.

(1) nerve distribution: the pelvic plexus extends to the paracervical plexus on both sides of the cervix, enters the uterus in parallel with the branches of the uterine artery at the isthmus, and extends to the myometrium of the uterus and cervix. The nerve entering the muscular layer continues to branch, passes through the muscular layer parallel to the sagittal artery, reaches the endometrium, and is distributed around the spiral artery. In addition, a few nerves located outside the uterus rise to the bottom of the uterus in parallel with the ascending branch of uterine artery, and are divided into smaller nerve fibers, which are distributed in the ovary and proximal fallopian tube.

(2) Nerve function: The distribution and function of sensory and motor nerve fibers in pelvic sympathetic nerve and parasympathetic nerve are different.

1) sensory nerve: the sensory nerve fibers of sympathetic nerve mainly transmit the pain of uterine body, and transmit it to the center through the thoracic nerve11-12. The sensory nerve fibers of parasympathetic nerve mainly transmit the pain of cervix and upper vagina, and transmit them to the center through sacral nerve 2-4; Pain in urethra and middle and lower vagina passes through pudendal nerve and then through sacral nerve 2-4 to the center. The isthmus and cervix have extremely sensitive sensory nerve plexus, which consists of sympathetic nerve and parasympathetic nerve, so the pain here is transmitted to the center through two kinds of nerve fibers.

2) Motor nerve: the motor nerve fibers of pelvic nerve are output from thoracic nerve 7-8, in which sympathetic nerve contracts the blood vessels of pelvic organs and inhibits the secretion of gastrointestinal glands; Parasympathetic nerves can relax the blood vessels of pelvic organs and stimulate the secretion of gastrointestinal glands.

2. The mechanism of dysmenorrhea The pain of dysmenorrhea comes from multiple sources, including abnormal uterine contraction and uterine ischemia and hypoxia. The periodic changes of sex hormones and the stimulation of uterine isthmus plexus are caused by other factors. This paper mainly discusses the pathogenesis of primary dysmenorrhea.

(1) Abnormal uterine contraction, ischemia and hypoxia: Prostaglandins synthesized in endometrium include PGF20, PGE2, prostacyclin and thromboxane Az. Personal computer, page 100. And thromboxane A: it has contractile effect on uterine muscles and increases uterine muscle tension; Prostaglandin E2 and prostacyclin inhibit uterine muscle contraction and relax cervix. Endometrium can synthesize the above prostaglandins in both proliferative and secretory phases, and the secretory phase is more than the proliferative phase. Especially in the 2-3 days before menstruation, when progesterone drops significantly, prostaglandin secretion increases rapidly. Prostaglandins in normal menstrual cycle are about 395-435n in L- menstrual blood. Prostaglandins not only come from endometrium, but also from platelets in menstrual blood and degenerated endometrium. Therefore, the amount of prostaglandin in menstrual blood can be 10 times higher than that in endometrium, and it can even rise to 7000 N in severe dysmenorrhea. PGF2 is the main component in menstrual blood of patients with L-type dysmenorrhea. , the first day of menstruation increased significantly, PGF2. The content is four times that of normal women. Therefore, PGF2 in menstrual endometrium, menstrual blood and peripheral blood of patients with dysmenorrhea. Level and PGF2. The ratio of PGF _ 2 to PGF _ 2 increased significantly, resulting in strong uterine contraction and dysmenorrhea.

Prostaglandins can also contract gastrointestinal smooth muscle, inhibit gastric acid secretion and affect intestinal water and sodium absorption. When menstruation comes, prostaglandins in menstrual blood can enter the blood circulation and act as its metabolites. When the absorption of prostaglandin increases, it will cause nausea, vomiting, diarrhea and even collapse.

The uncoordinated uterine contraction and the change of uterine muscle tension are also one of the mechanisms leading to dysmenorrhea. It is reported that in non-dysmenorrhea women, the uterine tension in follicular phase and luteal phase is between 10-30 mmHg, and the uterine contraction frequency is 3-4 times per 10 minute, which is coordinated; On the first day of menstrual period, uterine tension rises to 50- 100 mmHg, which can exceed 120- 150 mmHg, dysmenorrhea can reach 200mmHg, and uterine contraction is uncoordinated. This leads to uterine ischemia and hypoxia, causing unbearable colic. In the late luteal phase, lysosomes release phospholipase A unsteadily: it activates cyclooxygenase, increases prostaglandin synthesis, and may also participate in uterine tension and contraction disharmony.

Demers et al. reported that in some patients with primary dysmenorrhea, the increase of 5- lipoxygenase activity leads to the increase of leukotriene (1euxotriene) synthesis, and the increased leukotriene in endometrium has a strong vasoconstrictive effect, and uterine ischemia and hypoxia and the increase of acidic metabolites cause uterine pain.

Eks~om and others found that vasopressin increased in patients with moderate and severe primary dysmenorrhea, which could cause contraction of uterine muscles and vascular muscles, but vasopressin decreased after oral contraceptives, and dysmenorrhea was relieved.

(2) Sensory nerve fibers are stimulated: In addition to excessive contraction of uterine muscle fibers, it can also directly compress sensory nerve fibers in the muscle layer, unruptured endometrium, especially tubular endometrium during membranous dysmenorrhea, and a large amount of menstrual blood or small blood clots directly stimulate sensitive nerve plexus at isthmus and cervix, resulting in pain. In order to expel the tubular endometrium, the strong contraction of uterus is also one of the mechanisms of membranous dysmenorrhea. The dissolved products of menstrual blood and degenerative necrotic tissue also stimulate sensory nerve fibers and cause pain.

(3) Endocrine factors: Dysmenorrhea generally occurs in the menstrual period with ovulation, and it disappears after ovulation is not observed or inhibited. This suggests that dysmenorrhea is related to the changes of sex hormones in menstrual cycle. Milsom and others believe that the imbalance of sex hormones is the cause of dysmenorrhea, and the excessive estrogen in luteal phase promotes vasopressin and PGF2. The increase of synthesis and release can increase the activity of uterine muscles, inhibit the decline of uterine activity after ovulation and eliminate dysmenorrhea.

(4) Nerves and neurotransmitters: There are adrenergic and cholinergic nerves in uterine muscles. It is found that norepinephrine is related to dysmenorrhea, and the nerves in the uterus of guinea pigs will be denatured after pregnancy, and the adrenergic nerves in the human body will also be denatured during pregnancy, resulting in a low level of norepinephrine. The postpartum norepinephrine level did not return to the pre-pregnancy level, which explained the disappearance of postpartum primary dysmenorrhea.

(5) Lower pain threshold: It has been reported that patients with dysmenorrhea have the lowest pain threshold and are the most sensitive to pain compared with those without dysmenorrhea, postmenopausal women and men. After amenorrhea, it is still sensitive to pain, which shows the role of pain threshold in dysmenorrhea.

[Classification and Diagnosis]

Dysmenorrhea is divided into primary and secondary. A complete medical history, onset age, disease progress, disease nature and accompanying symptoms are helpful for differential diagnosis. The key to the diagnosis of primary dysmenorrhea is that gynecological examination has no positive signs, but there may be no positive signs in the early stage of secondary dysmenorrhea. Ultrasound, hysterosalpingography and hysteroscopy can be used to understand the uterus and its accessories; Laparoscopy can directly observe pelvic lesions and can be used for biopsy.

1. Primary dysmenorrhea, without pelvic organic lesions, also known as functional dysmenorrhea, has three characteristics that are of great significance for diagnosis: ① dysmenorrhea ovulates in almost all menstrual cycles; Dysmenorrhea mostly occurs in the first few hours of menstrual period, and the pain disappears within 2 ~ 3 days; ② The pain is in the area above pubic symphysis in the lower abdomen, showing paroxysmal swelling or spasmodic pain. Also pay attention to whether there are psychological factors such as tension, uterine dysplasia, excessive flexion and flexion of the uterus; ③ Membranous dysmenorrhea with tubular endometrial shedding. Pan Lingya and other epidemiological studies found that menarche C5: 12 years old, menstrual period of 7 days, menstrual athletes primary dysmenorrhea may cause endometriosis. Davis was diagnosed as endometriosis by laparoscopy in 49 patients with dysmenorrhea aged 65438 06.6i65438 0.4 years. Schroeder et al. proposed that most of dysmenorrhea in adolescence was caused by endometriosis. Therefore, after the diagnosis of primary dysmenorrhea, patients who may have mild endometriosis should be considered.

2. Secondary dysmenorrhea refers to dysmenorrhea caused by pelvic organic lesions. Because the disease is different, the performance is different.

(1) Pelvic inflammatory disease: adnexitis, periuterine tissue inflammation, etc. Can cause menstrual dysmenorrhea. However, there are also non-menstrual pelvic pain, and menstrual period is aggravated. In acute and subacute attacks, pain has nothing to do with menstrual cycle.

(2) Endometriosis and adenomyosis: Most of them occur in childbearing age. Dysmenorrhea is characterized by progressive aggravation, and severe cases usually have pelvic pain and sexual pain. Gynecological examination involving painful nodules of uterosacral ligament has diagnostic value, and laparoscopy improves the accuracy of diagnosis. The characteristics of dysmenorrhea in adenomyosis are similar to those of endometriosis, but the pain of uterus is the main one, and the uterus can be enlarged. Ultrasound shows that the myometrium of uterus is irregular, which has diagnostic value. May be accompanied by menorrhagia.

(3) Uterine fibroids generally have no dysmenorrhea, and occasionally submucosal fibroids (pedicled) have dysmenorrhea. Uterine myoma with dysmenorrhea can be accompanied by adenomyosis or adenomyoma. There is no dysmenorrhea in hysteromyoma, and it is necessary to check whether there is degeneration in hysteromyoma in the future. Ultrasonic examination is helpful for diagnosis.

Common secondary dysmenorrhea includes endometriosis, adenomyosis, hysteromyoma, endometrial polyp, intrauterine adhesions, and residual horn.