Central genesis. Antipyretic drugs in the practice of a pediatrician: tactics of choice and rational treatment of fever in children Central genesis of the disease

I. Primary amenorrhea (absence of menstruation in girls 15-16 years old and older, who have never had menstruation).

1) May occur with organic lesions of the central nervous system: brain tumors, chronic meningoencephalitis, arachnoiditis, chronic serous meningitis, epidemic encephalitis;

2) Psychogenic amenorrhea – associated with negative emotions, mental and physical stress;

3) Pathology of the hypothalamic-pituitary region:

Adiposogenital dystrophy is a disease associated with intrauterine infection, toxoplasmosis, and infection in childhood and adolescence. It manifests itself as obesity with pronounced deposition of fat in the pelvis and hips. Skeletal development defects, genital hypoplasia and amenorrhea;

Lawrence-Moon-Beadle syndrome is a hereditary family disease caused by gene defects. It is characterized, in addition to the signs characteristic of adiposogenital dystrophy, by severe mental retardation and numerous developmental defects;

Hand-Schüller-Christian disease is a hereditary disease characterized by dwarfism, sexual infantilism, xanthomatosis, osteoporosis, diabetes insipidus, and endophthalmos;

Pituitary cachexia (panhypopituitrism) is a disease that occurs with hypofunction of the entire pituitary gland and is characterized by dwarfism (dwarfism) with sexual infantilism and amenorrhea.

II. Secondary amenorrhea (cessation of menstruation after having had it at least once):

1. Psychogenic amenorrhea – occurs as a result of acute or chronic emotional and mental trauma.

Under the influence of stress, there is an increase in the release of beta-endorphins, neurotransmitters of the class of endogenous peptides. This leads to a decrease in the formation of dopamine and a decrease in the formation and release of gonadoliberins, which in turn causes a decrease in the release of gonadotropins.

With psychogenic amenorrhea, along with secondary amenorrhea, psychopathic-like disorders are observed, often leading to the development of asthenoneurotic, asthenodepressive or asthenohypochondriacal syndrome.

Hormonal studies reveal the monotonous nature of the content of luteinizing and follicle-stimulating gonadotropins in the blood, the amount of which fluctuates within the lower limit of the basal level. The content of estradiol in the blood is reduced, the karyopyknotic index fluctuates between 25-30% and is also monotonous.

With prolonged psychogenic amenorrhea, the size of the uterus may decrease slightly.

The diagnosis of psychogenic amenorrhea is established on the basis of a typical history and clinical picture. Involvement of hypothalamic structures is confirmed by a positive GnRH test.

Treatment is carried out jointly with a neuropsychiatrist. Mandatory: normalization of living conditions, elimination of stress. Antidepressants and antipsychotics are used (it must be remembered that these drugs increase inhibition of the gonadotropic function of the pituitary gland, which leads to a slower recovery of the menstrual cycle). Normalization of menstrual function and restoration of ovulatory cycles occur after improvement in the mental state of patients. Therapy with vitamins A, E and B is also indicated.

2. Hypothalamic form of secondary amenorrhea (amenorrhea due to weight loss) - develops in girls and young women who use a protein-poor diet for cosmetic purposes.

The cause of amenorrhea in this case is the insufficiency of the pituitary zone of the hypothalamus due to infectious and toxic effects in childhood and puberty. Psycho-emotional stress may be a resolving factor. The volume of adipose tissue, the site of extragonadal estrogen synthesis, plays a certain role.

The clinical picture of this form of amenorrhea is characterized primarily by a decrease in body weight by 15-25% of the age norm, moderate hypoplasia of the mammary glands, external and internal genital organs. A sharp decrease, and sometimes lack of appetite, high performance and social activity.

Treatment includes complete fractional nutrition, the prescription of enzyme preparations, vitamins (B1, B6, C and E), glutamic acid, infusion or decoction of valerian. Psychotherapy is very effective.

As a rule, the menstrual cycle is restored upon reaching body weight corresponding to age standards, however, the menstrual cycle may be erratic.

35.1.Endocrine infertility– infertility caused by ovulation disorders:

1. Anovulation.

Chronic anovulation may be a consequence of dysfunction of the hypothalamic-pituitary system (disturbance in the rhythm and amount of secretion of gonadotropin-releasing hormones and gonadotropic hormones of the pituitary gland), developed as a result of neuroinfection, intoxication, psycho-emotional stress, cerebral trauma, etc. Anovulation is also a symptom of endocrine diseases, namely polycystic ovaries, dysfunction of the adrenal cortex, hyperprolactinemia. Postpartum obesity, hypo- and hyperthyroidism. Itsenko-Cushing's disease, nervous and mental diseases.

Manifestations of chronic anovulation, in addition to infertility, can include menstrual irregularities - dysfunctional uterine bleeding, amenorrhea, oligomenorrhea.

The diagnosis of anovulation is based on data from functional diagnostic tests: monophasic basal temperature, monotonous karyopyknotic index (usually fluctuating within the limits characteristic of the beginning of the first phase of the cycle), absence of the “pupil” symptom, cervical mucus tension 2-6 cm, laparoscopy is used for diagnostic purposes , in which the appearance of the ovaries, the absence of ovulatory stigma and corpora lutea are assessed, non-endocrine causes of infertility are identified - adhesions, the presence of endometrioid ectopia in the pelvis. Additional chromopertubation - the introduction of a dye (indigo carmine, methylene blue) through the external os - makes it possible to establish obstruction of the fallopian tubes or the localization of their obstruction.

2. Luteinization of the unovulated follicle.

It is believed that stress plays a role in the occurrence of this pathology. Hyperprolactinemia and ovarian inflammation.

The diagnosis is very difficult, because Functional diagnostic tests and hormone levels in the blood and urine do not differ from those during the ovulatory cycle. During ultrasound examination and measurement of follicle diameters, a slow gradual decrease in the size of the preovulatory follicle is noted (while ovulation is characterized by the disappearance of the dominant follicle). Laparoscopy performed on the 13-15th day of the cycle reveals a hemorrhagic corpus luteum without ovulatory stigma.

3. Insufficiency of the luteal phase of the cycle (hypofunction of the corpus luteum) – is accompanied by a decrease in the synthesis of progesterone.

The cause of infertility due to insufficiency of the luteal phase of the cycle can be: defective secretory transformations of the endometrium, preventing the implantation of a fertilized egg; decreased peristaltic activity of the fallopian tubes due to progesterone deficiency.

Insufficiency of the luteal phase of the cycle can be observed as a physiological phenomenon after menarche, childbirth, abortion over several menstrual cycles. The causes of insufficiency of the luteal phase of the cycle can be hyperandrogenism of adrenal origin, hyperprolactinemia, inflammatory diseases of the uterus and appendages, hypothyroidism. In addition to infertility, if the luteal phase of the cycle is insufficient, scanty bleeding is observed on the 4-7th day before the next menstruation.

The diagnosis of insufficiency of the luteal phase of the cycle is established on the basis of a shortening of the hyperthermic phase of basal temperature to 4-8 days when the temperature difference in the first and second phases of the cycle is less than 0.4 ° C; reducing the content of pregnanediol in the urine below 3 mg/day, progesterone in the blood below 15 nmol/l on the 4th day of increasing basal temperature; defective phase of secretion in the endometrium 2-3 days before menstruation.

All the numerous variants of endocrine disorders leading to ovulation disorders can be conditionally combined into separate clinical groups, which are characterized by the corresponding symptom complex:

Group I – hypothalamic-pituitary insufficiency (pathological conditions defined as genital underdevelopment);

Group II – hypothalamic-pituitary dysfunction (patients with menstrual disorders);

Group III – ovarian failure;

Group IV – congenital or acquired disorders of the reproductive system;

Group V – hyperprolactinemia in the presence of a tumor in the hypothalamic-pituitary region;

Group VI – hyperprolactinemia without lesions in the hypothalamic-pituitary region;

Group VII – amenorrhea due to a tumor in the hypothalamic-pituitary region.

Treatment of endocrine infertility is carried out for women under 35 years of age in the absence of somatic diseases that are a contraindication to pregnancy and childbirth.

In the presence of endocrine diseases, therapy of the indicated etiology is necessary.

A common method of anovulation is stimulation of ovulation. The following drug administration regimens are used:

1) Clomiphene (clomiphene citrate, clostilbegide) – 50-150 mg from the 5th to the 9th day from the onset of menstruation or from the onset of a drug-induced menstrual reaction. For this purpose, oral contraceptives such as non-ovalone, bisecurin, etc. are used, 1 tablet per day for 7-10 days;

2) Clomiphene in the same dose and at the same time in combination with human chorionic gonadotropin, which is administered after the dominant follicle reaches preovulatory size (at least 18 mm in diameter) at a dose of 4500-3000 units;

3) You can use tamoxifen (zitozonium), which has antiestrogenic activity. The drug is prescribed from the 5th to the 9th day of the cycle at a dose of 10-20 mg per day;

4) Pergonal (human menopausal gonadotropin) from the 5th day of the induced menstrual reaction at a dose of 150 units daily under the control of ultrasound measurement of the diameter of the follicles.

You can use synthetic analogues of gonadotropic releasing hormones of the hypothalamus, which stimulates the release of luteinizing gonadotropin by the pituitary gland and indirectly ovulation in the ovary. The drug is administered intravenously at hourly intervals in the so-called pulsating mode, simulating the release of GnRH by the hypothalamus.

In case of infertility caused by insufficiency of the luteal phase of the cycle, pathogenetic treatment of the diseases that caused this dysfunction of the ovaries is carried out. Hormone replacement therapy is also carried out with corpus luteum preparations or norsteroids, which have a gestagenic effect. Use progesterone 1 ml of 1% solution intramuscularly from the 18-20th day of the cycle for 6-8 days; 17-hydroxyprogesterone capronate 1 ml of 12.5% solution on the 17th or 20th day of the cycle; Norkolut, which is prescribed from the 16th to the 26th day of the cycle at a dose of 5 mg per day. It is recommended to use human chorionic gonadotropin, which stimulates hormonal secretion of the corpus luteum (1000-1500 units intramuscularly on the 2nd, 4th, 6th day of increase in basal temperature). Duration of therapy is 3-4 menstrual cycles.

In case of infertility caused by luteinization of a non-ovulated follicle, stimulation of ovulation is recommended.

It must be remembered that if the dose of drugs that stimulate ovulation is selected incorrectly, a complication may occur - ovarian hyperstimulation syndrome.

The prognosis for restoration of reproductive function with correct identification of the cause of endocrine infertility and timely implementation of adequate therapy is favorable. If a woman has diseases or dysfunction of the endocrine glands, treatment should begin with the treatment of these endocrine diseases. Typically, normalization of the function of the endocrine glands leads to the restoration of the ovulatory menstrual cycle. Only with ongoing anovulation or insufficiency of the luteal phase of the cycle is stimulation of ovulation and the therapy discussed above recommended.

In cases where infertility is associated with dysfunction of the hypothalamic-pituitary system, therapy is ineffective.

If pregnancy occurs after treatment, it is necessary to monitor women from early stages, since these pregnant women constitute a high-risk group for miscarriage in the first trimester of pregnancy.

37.1.Modern means of contraception:

1. Intrauterine contraception:

1) neutral intrauterine devices (IUDs) - the most widely used are the Lips loop (a polyethylene device in the form of a double Latin letter), IUDs in the shape of the letter T and the number 7.

The mechanism of action of neutral IUDs is to disrupt the implantation of a fertilized egg, which is associated with accelerated peristalsis of the fallopian tubes and the resulting inferiority of the egg.

The Pearl index when using neutral IUDs is 4.

2) medicated IUDs - contain copper and gestagens. Mechanism of action of medicated IUDs:

Copper has a bactericidal and spermicidal effect;

Gestagens change the properties of cervical mucus, which leads to difficulty in the penetration of sperm into the uterine cavity, and also causes the inability of the endometrium to implant an egg.

The Pearl index when using medicated IUDs is 1-2.

Contraindications to the use of IUDs:

Acute and subacute inflammatory diseases of the genital organs;

Chronic inflammatory processes with frequent exacerbations;

Infectious and septic diseases and fever of any etiology;

Isthmic-cervical insufficiency;

Benign and malignant tumors of the genital organs;

Polyps of the cervical canal;

Erythroplakia and leioplakia of the endometrium;

Polyposis and endometrial hyperplasia;

Tuberculosis of the genital organs;

Malformations of the uterus;

Intrauterine synechiae;

Menstrual irregularities such as menorrhagia or metrorrhagia;

Disorders of the blood coagulation system, accompanied by increased bleeding.

The IUD is inserted by the doctor, observing the rules of asepsis, on the 5th-7th day of the menstrual cycle, after an induced abortion - immediately (or after the next menstruation), after childbirth - 3 months later. Necessary conditions are: normal blood picture, 1-2 degree vaginal frequency.

After inserting the IUD, the doctor should examine the woman a week after the first menstruation, then after 3 months, subsequent examinations are carried out once every 6 months. The duration of stay of the IUD in the uterine cavity is 3-5 years.

Complications of intrauterine contraception:

Lower abdominal pain;

Uterine bleeding;

Ectopic pregnancy;

Intrauterine pregnancy, often ending in spontaneous abortion;

Perforation of the uterus (partial - when the IUD is inserted into the muscle of the uterus in the area of the fundus or side walls; complete - with the movement of part or all of the IUD into the abdominal cavity).

2. Hormonal contraception.

Classification of hormonal contraceptives:

1) according to method of application:

Tablets (oral);

Injected intramuscularly (medroxyprogesterone);

Implanted under the skin (levonoreggrel);

2) by composition:

a) combined estrogen-gestagen hormonal contraceptives:

Single-phase - tablets with a constant content of estrogens and gestogens (non-ovlon, bisecurin, ovulene, rigevidon). The Pearl index when using single-phase hormonal oral contraceptives is less than 1.

Biphasic - includes 2 types of tablets, intended respectively for use in the first and second phases of the menstrual cycle. The estrogen content in them is the same, but tablets taken in the second phase of the menstrual cycle contain more gestogens;

Three-phase - contain gestagens and estrogens in various combinations (trisiston, tirkvilar). In tablets of the first type, the content of estrogens and gestagens is the lowest (ratio 1: 1.2), in tablets of the second type, the dose of estrogens and especially gestagens increases (ratio 1: 1.5), in tablets of the third type, the content of estrogens is reduced to the original level, and the dose of gestagens increases (ratio 1:4). Three-phase administration of sex steroids allows for the same change in the content of estrogens and gestagens in the blood as during a normal menstrual cycle. The Pearl index when using three-phase combined oral contraceptives is less than 1.

The contraceptive effect of combined estrogen-gestagen oral contraceptives is the inhibition of ovulation due to suppression of the ovulatory release of gonadotropins of the anterior pituitary gland, disruption of implantation as a result of inhibition of secretory changes in the endometrium and disruption of sperm movement due to thickening of the mucus in the cervical canal;

b) gestagen-containing hormonal contraceptives:

Mini-pills (continuin, fermulen) - contain 500-300 mcg per tablet. The contraceptive effect is based on inhibition of contractile activity of the fallopian tubes, increased viscosity of mucus in the cervical canal, disruption of cyclic processes in the endometrium, Pearl Index - 1.5-2.

Postcoital oral contraceptives (postinor) - for women with irregular sex life. The contraceptive effect is based on the prevention of implantation of a fertilized egg due to changes in the endometrium and its rejection in response to a decrease in hormone levels after taking the drug;

Long-acting agents (medroxy-progesterone acetate - administered intramuscularly, norplant - implanted subcutaneously in a capsule). The contraceptive effect of these drugs is associated with a decrease in the permeability (increase in viscosity) of cervical mucus for sperm, suppression of the ovulatory release of gonadotropins, and atrophic changes in the endometrium. Pearl index – 1.

Also among hormonal contraceptives there are:

The closest to cyclical changes in a woman’s body (three-phase oral contraceptives);

Least close to cyclical changes in a woman’s body (single-phase oral contraceptives);

With a minimal content of hormones (used for hypoestrogenemia, hypogonadotropinemia);

High in hormones;

With a therapeutic effect (single-phase oral contraceptives - help regulate the menstrual cycle, reduce blood loss during menstruation, disappearance of pain and other painful symptoms during menstruation, have a pronounced therapeutic effect for endometriosis of any localization, fibrocystic mastopathy, hyperplasia, endometrial polyposis, follicular ovarian cysts ; three-phase oral contraceptives - reduce the content of low-density lipoproteins in the blood, have a therapeutic effect in various progesterone-deficient conditions, namely: mastopathy, some forms of premenstrual syndrome, anovular menstrual cycles).

14.1 Endoscopic research methods– examination of internal organs using special optical instruments and devices. Using these methods, targeted biopsies can be performed.

The following main endoscopic methods are used in gynecological practice:

1) Colposcopy - examination of the vagina and vaginal part of the cervix using a binocular or monocular magnifying glass equipped with a lighting device (magnification of the area under study by 30 times or more);

2) Microscopic colposcopy (colpomicroscopy) - colposcopy under high magnification (80-90 times) using a contact lens and with preliminary staining of the study area;

3) Cervicoscopy – examination of the mucous membrane of the cervix using a cervicoscope;

4) Hysteroscopy - examination of the inner surface of the uterus to identify pathological changes in the endometrium;

5) Peritoneoscopy (laparoscopy) is a research method by which the pelvic and abdominal organs are examined with an optical instrument inserted into the abdominal cavity through an opening in the anterior abdominal wall.

Using laparoscopy, you can perform a number of gynecological surgical interventions - sterilization (coagulation of the fallopian tubes, application of a tantalum staple or suture), dissection and coagulation of adhesions in the pelvis, coagulation of endometrioid nodes, puncture of ovarian retention formations, coagulation of ovarian tissue in patients with ovarian apoplexy;

37.3 CHORIONEPITHELIOMA.

II. Chorionepithelioma is a malignant tumor arising from the epithelial cells of the chorionic villi.

Classification of chorionepithelioma:

1. Non-metastatic - the process is limited to the uterus.

2. Metastatic - the process spreads beyond the uterus (to the gastrointestinal tract, genitourinary system, liver, lungs, brain):

With a favorable prognosis (low risk) - with a short duration of the disease (less than 4 months), the titer of human chorionic gonadotropin before treatment is less than 40,000 mIU/ml, and there is no need for chemotherapy;

With an unfavorable prognosis (high risk) - with a disease duration of more than 4 months, the titer of human chorionic gonadotropin before treatment is more than 40,000 mIU/ml, metastases to the liver and brain, no effect from previously administered chemotherapy, the onset of the disease after full-term pregnancy.

The clinical picture of chorionepithelioma is manifested primarily by blood discharge caused by the destruction of blood vessels by the tumor. At first, the discharge is moderate, but it intensifies. When the tumor is located deep in the uterine wall and the serous covering of the organ is destroyed, profuse intraorgan bleeding occurs. Bleeding can occur in the abdominal cavity and from metastatic nodes in the liver and intestines. External bleeding may have its source in metastases of chorionepithelioma in the vagina.

The second important symptom is anemia, which progresses rapidly. It is the result of both uterine bleeding and intoxication caused by the absorption of tumor decay products.

Due to necrosis and infection of chorionepithelioma nodes, a febrile state may develop.

When affected by metastases of pulmonary chorionepithelioma, a cough with sputum and chest pain appear. Brain metastases cause pain and other neurological symptoms associated with the location of the metastatic nodes. Metastases in the digestive organs cause bleeding, pain, and dyspeptic symptoms.

The walls of the vagina and cervix are cyanotic, the uterus is enlarged, and thecal lutein cells appear in the ovaries. The mammary glands may be enlarged, colostrum is released from them, and the areolas are pigmented.

Chorionepithelioma cells have a pronounced ability to produce human chorionic gonadotropin, which circulates in the blood and is excreted in the urine, and trophoblastic beta globulin, secreted into the blood.

Diagnostics:

Anamnesis - an indication of the appearance of bleeding from the genital organs after a previous pregnancy and especially after a hydatidiform mole;

Examination in the mirrors - tumor metastases in the form of dark red elevations and nodules;

Positive immunological test for trophoblastic beta globulin;

Histological examination of a scraping from the uterus reveals elements of a tumor;

Pelvic angiography - abundant vascularization and the formation of lacunar accumulations of contrast material in the affected area;

Hysterography - detection of chorionepithelioma nodes in their submucosal location;

Ultrasound examination – detection of chorionepithelioma nodes.

1. Use of antitumor drugs: antimetabolites (methotrexate, 6-mercaptopurine), antibiotics (rubomycin, lactinomycin), herbal drugs (vinblastine, vincristine) and others:

Treatment with one antitumor drug is carried out when the tumor is localized only within the uterus, the duration of the disease is less than six months, the size of the uterus is small (not exceeding that of 8 weeks of pregnancy);

Various combinations of drugs are used when the symptoms of the disease last for more than six months, the occurrence of chorionepithelioma after childbirth, the ineffectiveness of treatment with one drug, and in the presence of metastases.

2. Surgical treatment (extirpation of the uterus with or without appendages) - in case of uterine bleeding that is life-threatening for the patient, the threat of destruction of the uterine wall by a tumor, the ineffectiveness of drug antitumor therapy;

3. Radiation therapy is an additional treatment method for metastases in parametric tissue (external gamma therapy) and in the vagina (intracavitary irradiation).

The criteria for cure are restoration of menstrual function, reduction in the size of the uterus to normal, normalization of the levels of human chorionic gonadotropin and trophoblastic beta globulin in the blood serum.

After treatment, the woman is regularly monitored for 2 years with a general examination, gynecological examination, chest X-ray, and a blood test to determine human chorionic gonadotropin.

Prevention of chorionepithelioma consists of rational treatment of hydatidiform mole using as indicated.

5.1.Uterine amenorrhea:

1. Primary form - caused by changes in the endometrium, the degree of which can be expressed differently: from a decrease in the sensitivity of its receptors to the effects of sex hormones to the complete destruction of the entire endometrium (most often due to the tuberculosis process).

2. Secondary form:

1) Intrauterine synechiae (Asherman syndrome) - Intrauterine synechiae - are formed after traumatic curettage due to abortion, uterine bleeding, rough separation of the placenta. Synechiae are avascular cords in the uterine cavity, running between its walls, often in the fundus, and deforming the uterine cavity. The clinical manifestation of this pathology, called Asherman's syndrome, is amenorrhea or hypomenorrhea in combination with ovulatory infertility.

Based on the hysteroscopic picture, the following forms of intrauterine synechiae are distinguished:

Mild form - synechiae are thin, thread-like, occupy less than a quarter of the uterine cavity, the tubal angles are free or obliterated;

Moderate form - synechiae occupy more than a quarter of the uterine cavity, the fundus of the uterus is partially obliterated, the tubal angles are obliterated;

Severe form - synechiae occupy more than a quarter of the uterine cavity, the uterine fundus is obliterated, the tubal angles are obliterated.

The cause of intrauterine synechiae can also be tuberculosis of the endometrium.

Diagnosis is based on a typical history; Hysteroscopy is of decisive importance in diagnosis, in which the extent of the process is determined.

Treatment: sharp separation of adhesions under hysteroscopy control and introduction of a special protector, which is a polyethylene frame with a catheter. A mixture containing 64 units of lidase, a 0.1% solution of estrodiol dipropionate and 125 mg of a suspension of hydrocortisone acetate is administered through a catheter for a week. The frame is removed on the 7-8th day and a Lips loop is inserted into the uterine cavity for a period of 2 years. Within 6 months. After separation of adhesions, cyclic hormone therapy is recommended.

The prognosis for restoring menstrual function is favorable, but for reproductive function it is less encouraging. The resulting pregnancy is often complicated by miscarriage, and childbirth is often complicated by tight attachment of the placenta.

2) Specific (tuberculous) endometritis – Pr

Tuberculous endometritis most often does not have characteristic symptoms. The main complaint is infertility, often primary, less often secondary. Pain in the lower abdomen and lower back is not associated with the menstrual cycle, is permanent and is caused by adhesive changes in the pelvis. There are symptoms of tuberculosis intoxication, menstrual irregularities (hypomenorrhea, primary and secondary amenorrhea, algomenorrhea, oligomenorrhea).

Tuberculosis of the genital organs is often combined with other gynecological diseases, which can predominate in the clinical picture and determine the doctor’s further treatment tactics.

The most common are small and latent forms of the disease with minor anatomical and functional changes that are difficult to recognize. The bimanual examination data is uninformative: either there are no deviations from the norm, or there are small adhesive changes in the area of non-enlarged uterine appendages. With this form, the only complaint is infertility. Tuberculosis intoxication and bacilli excretion rarely occur; menstrual irregularities are somewhat more common.

In the form with pronounced anatomical and functional changes, pain, bacilli discharge, tuberculosis intoxication, and menstrual irregularities are more often observed. The uterine appendages are tubo-ovarian inflammatory formations. Very often the peritoneum is involved in the process.

Tuberculomas in the area of the uterine appendages (determined x-ray) require surgical removal, since they are a depot of Mycobacterium tuberculosis and pose a constant threat of exacerbation of the process. The clinical picture of the disease depends on the severity of the inflammatory reaction around the caseous lesion.

8.1.Induced abortion (from obstetrics) is a deliberate interruption pregnancy performed in medical institutions.

There are induced abortions:

Early terms (up to 12 weeks)

Late terms (from 13 to 27 weeks)

Artificial termination of pregnancy is permitted only in medical institutions. Artificial abortion in the early stages of pregnancy (up to 12 weeks) is performed:

If a woman wishes to terminate her pregnancy

For medical reasons:

Neoplasms

Diseases of the endocrine system, blood, hematopoietic organs

Mental disorders

Diseases of the nervous system and sensory organs

Diseases of the circulatory, respiratory, digestive, and genitourinary systems.

Complications of pregnancy, childbirth and the postpartum period

Diseases of the skin and subcutaneous tissue

Diseases of the musculoskeletal system and connective tissue

Congenital anomalies

Hereditary diseases

Methods for early termination of pregnancy:

1. mini-abortion - the method can be used when menstruation is delayed from 2-3 days to 25 days. Before performing a mini-abortion, it is necessary to accurately determine the presence and duration of pregnancy, for which it is recommended to use a vaginal examination, measurement of basal temperature, immunological reactions to pregnancy, and ultrasound.

Mini-abortion is performed using a vacuum device and flexible polyvinyl chloride plastic cannulas with a diameter of 4.5-6 mm with two holes at the end. Cannulas are inserted into the uterine cavity without first dilating the cervical canal after probing the uterine cavity. A negative pressure of 0.6-.0.8 atmospheres is created and the contents of the uterine cavity are aspirated. The manipulation is considered complete if the contents do not enter the tank. No anesthesia is required. Mini-abortion can be performed both in a hospital and on an outpatient basis.

2. Artificial abortion by curettage of the uterus - one-step surgical removal of the fertilized egg by curettage with mandatory anesthesia. The operation of uterine curettage is reduced to expanding the cervical canal with a Hegar dilator (up to No. 12-14, depending on the stage of pregnancy), removing large parts of the fetus with a blunt curette or abortion forceps, scraping out the remnants of the fertilized egg and the decidua of the uterus with a sharp curette.

Complications:

Immediate (occurs at the time of surgery or shortly after it)

Perforation of the uterus

Bleeding

Leaving parts of the fertilized egg

Acute hematometra

Remote:

Inflammatory processes inside the genital organs

Ovarian dysfunction with menstrual irregularities

Infertility

Ectopic pregnancy

Isthmic-cervical insufficiency (ICI)

Anomaly of labor during subsequent births.

Bleeding in the placenta or early postpartum period

For a more gentle dilatation of the cervix (prevention of ICI), you can insert a suppository with prostaglandin F2 and E2 into the cervical canal the night before the operation.

3.Artificial abortion using vacuum aspiration – one-step surgical removal of the fertilized egg by vacuum aspiration with mandatory anesthesia. Main parts of the vacuum aspirator:

 set of tips

 electric suction device

 tubes connecting the electric suction device to the handpiece.

After anesthesia, the cervical canal is expanded using a Hegar dilator or vibrodilator.

After expanding the cervical canal to the required diameter, the tip of a vacuum aspirator is inserted into the uterine cavity and the electric suction device is turned on, creating negative pressure. During aspiration, the tip is turned into the side hole towards the wall of the uterus and a movement (non-scraping) is made from the fundus to the internal pharynx and in a circle of 360 degrees. The tip should be periodically removed from the uterine cavity so that the air thus sucked in will help move parts of the fertilized egg along the hose. The operation is considered completed if the contents from the uterine cavity no longer enter the reservoir, and the operating hand feels the walls of the contracted uterus through the tip. After artificial termination of the first pregnancy, women with Rh-negative blood are immunized with human anti-Rhesus Rh (D) immunoglobulin.

Physiological amenorrhea is the absence of menstruation during puberty, during pregnancy, during breastfeeding (lactation) and in old age;

Pathological amenorrhea - occurs in various diseases of the female reproductive system: lesions of the central nervous system and hormonal disorders (hypothalamus, ovaries, pituitary gland and adrenal glands), acute and chronic infectious diseases (tuberculosis, adenoviral infection, septic conditions), severe intoxications (poisoning with heavy metals, alcohol, household poisons), metabolic disorders (malnutrition, anemia, intense physical activity); in turn, pathological amenorrhea can be primary and secondary:

Primary pathological amenorrhea is the absence of menstruation in a woman who has reached the age of 16, or in a woman who has never had one;

Secondary pathological amenorrhea is the absence of menstruation for 3 or more periods of the normal menstrual cycle in a woman who previously menstruated;

FALSE is a condition in which cyclic processes in a woman’s reproductive system occur, however, there is no external bleeding due to psychogenic causes (false or imaginary pregnancy, emotional stress), mechanical obstacles (fusion of the hymen, vagina; fusion of the cervical canal (cervical canal); septum and adhesions in the uterine cavity); false amenorrhea occurs as a result of impaired development of the female genital organs and after reactive changes in the mucous membrane of the uterine cavity (endometritis, endocervicitis, frequent curettage of the walls of the uterine cavity, including during medical abortions).

I degree (mild) - duration no more than 1 year, no complaints, the uterus is slightly enlarged, according to the probe - from 5 to 7.5 cm;

II degree (moderate) - duration of amenorrhea from 1 to 3 years. Vegetative-vascular disorders appear (in 50% of women). The uterus is enlarged in size, the uterine cavity according to the probe is from 3.5 to 5.5 cm;

III degree (severe) - duration more than 3 years, pronounced clinical manifestations, practically not amenable to therapy;

By time of occurrence: primary amenorrhea (there has never been menstruation); secondary amenorrhea (develops after a period of normal menstruation (as a consequence of abortion, inflammatory, tumor processes, etc.);

Due to the occurrence: amenorrhea of central origin (occurs as a result of changes in the cerebral cortex, hypothalamus, pituitary gland); amenorrhea of peripheral origin (due to changes in the adrenal glands, thyroid gland, ovaries, uterus);

Depending on the level of pathology: hypothalamic; pituitary; ovarian; uterine; adrenal; amenorrhea due to thyroid pathology.

Amenorrhea is a consequence of dysfunction of the cerebral cortex,

Amenorrhea due to damage to subcortical structures (hypothalamic-pituitary amenorrhea); disorders of the hypothalamic-pituitary system can be:

(1) - functional: chronic psychogenic stress, poor diet, chronic infections (frequent tonsillitis) and especially neuroinfections, endocrine diseases, taking drugs that deplete dopamine reserves in the central nervous system (reserpine, opioids, monoamine oxidase inhibitors) and affecting the secretion and metabolism of dopamine ( haloperidol, metoclopramide);

(2) – organic (anatomical);

(3) - a consequence of congenital pathology.

Taking medications (psychotropic drugs, antihypertensives, hormonal drugs, sleeping pills);

Severe somatic or mental pathology;

Aplasia of the endometrium or uterine synechiae (Asherman's syndrome);

Organic neoplasms and pathological changes in the hypothalamic-pituitary region;

Endocrine and metabolic disorders, additionally confirmed by the results of hormonal studies.

Hormonally active pituitary tumors: prolactinoma, mixed prolactin- and ACTH-secreting pituitary adenomas;

Damage to the hypothalamus and pituitary stalk as a result of: tumor (for example, craniopharyngiomas), trauma (trauma to the base of the skull, hemorrhage), basal meningitis, granuloma, reticulosis, surgery, exposure to radiation, infectious-allergic and neuro-reflex damage to the hypothalamic region in chronic tonsillitis ;

Necrosis of pituitary tissue due to thrombosis of pituitary vessels or massive postpartum or post-abortion bleeding.

Central genesis is

L.A. Ulitsky, M.L. Chukhlovina, E.P. Shuvalova, T.V. Belyaeva, St. Petersburg 2001

The so-called habitual or constitutional fever deserves special attention. It really exists, especially in young people (usually young women) with a labile autonomic nervous system and asthenic constitution in situations with high physical or emotional stress. Currently, such temperature disorders are considered as manifestations of cerebral autonomic disorders and are included in the picture of autonomic dystonia syndrome (dysfunction). The latter is interpreted as a psychovegetative syndrome. It should be emphasized that autonomic dysfunction syndrome can develop against the background of clinical signs of hypothalamic dysfunction or without it. In the first case, monotonous low-grade fever in combination with endocrine and autonomic disorders of a permanent or paroxysmal nature is more common. In the second case, thermoregulation disorders occur without signs of damage to the hypothalamus, hyperthermia is characterized by febrile levels. has a long-term persistent nature. However, it has been established that hyperthermia is caused by cerebral autonomic disorders. is possible only after a detailed and persistent examination, excluding other causes of prolonged increase in body temperature.

Currently, low-grade fever is usually defined as an increase in body temperature no higher than 37.9 C, lasting more than 3 weeks.

It is completely unacceptable to suspect a simulation of the disease after the first unsuccessful attempts to discover the cause of low-grade fever. Unfortunately, such unfounded suspicions sometimes arise. Meanwhile, our teachers also argued: simulation cannot be assumed. it must be proven. Currently, low-grade fever of infectious and non-infectious etiology is still distinguished. The cause of the latter may be tumors of various locations, lesions of the diencephalic region of the brain. systemic blood diseases, diffuse connective tissue diseases. If the subfebrile condition is infectious, one should, first of all, exclude certain infectious nosological forms, identify or exclude pulmonary and extrapulmonary tuberculosis, and then direct one’s efforts to search for a focal infection.

And, nevertheless, many therapists, as experience shows, in the absence of obvious pathology from the lungs, lymph glands and with a normal blood picture, make hasty conclusions about this. that the patient has a low-grade fever “due to nervousness” and patients are often assured of this. As a result, a patient with persistent low-grade fever in some cases becomes a permanent patient of a neurologist or psychotherapist.

What diseases of the nervous system can cause long-term low-grade fevers? First of all, these are diseases associated with damage to the hypothalamus, due to its critical role in thermoregulation. It is known that damage to the hypothalamus is polyetiological. Thus, in case of trauma in the case of a fracture of the base of the skull, there may be direct damage to the pituitary stalk; in case of a traumatic extra-, subdural or intracerebral hematoma, the ventral displacement of the hypothalamus leads to local circulatory impairment. The latter may affect the supraoptic nuclei. In this case, transient diabetes insipidus occurs, combined with central fever.

Among tumors that affect the hypothalamus and optic chiasm by compression, the most common are suprasellar meningiomas. Craniopharyngiomas and pituitary tumors. These tumors can also cause diabetes insipidus and mental and emotional disorders. and in some cases - central fever.

If the aneurysm of the circle of Willis vessels is large, it, like a tumor formation, can compress the hypothalamus. In cases of granulomatous basal meningitis (eg tuberculosis or syphilis), the blood vessels may be narrowed due to vasculitis, resulting in the formation of areas of insufficient blood supply in the hypothalamus.

From the above data it follows that there are many reasons for the development of central fever, hyperthermia, low-grade fever - and yet this is rare. Nevertheless, the neurologist must use all modern research methods (including CT, MRI, ultrasound) to exclude damage to the hypothalamic region. If all this has been done and dynamic observation fails to identify symptoms of a primary CNS disease, the neurologist has the right to conclude that it is currently not possible to explain the presence of persistent low-grade fever by a neurological disease.

In order to assess how fully a patient with low-grade fever has been somatically examined, the neurologist must know other, non-neurological causes of persistent low-grade fever.

The diagnostic search should begin with an analysis of infectious causes: conduct an examination aimed at identifying infectious nosological forms, pulmonary and extrapulmonary tuberculosis and the so-called focal infection with and without generalization.

As for infectious nosological forms. then, first of all, brucellosis should be excluded (Wright and Heddelson reactions, immunological methods, intradermal Burnet poisoning).

In the presence of persistent low-grade fever, it is recommended to show the patient to an ophthalmologist, since it is necessary to ensure the absence of chorioretinitis, especially if the patient develops photopsia and metamorphopsia. These symptoms, combined with low-grade fever, make one think about chronic toxoplasmosis. The disease is not as rare as is commonly thought.

The neurologist should remember that in the case of the manifest form of toxoplasmosis, patients present with complaints of an asthenoneurotic nature (general weakness, fatigue, irritability, headaches, memory loss, sleep disturbance, muscle and joint pain). Women often have a history of recurrent miscarriages. Serological tests and intradermal testing with toxoplasmin are carried out. This disease affects people of any age, but more often young cat lovers.

A neurologist must remember the possibilities of HIV infection, especially if he works in the prehospital setting.

It should also be noted that outpatient doctors and therapeutic hospitals do not show proper persistence in diagnosing tuberculosis in febrile patients. At the same time, one must think about the possibility of tuberculosis of the mesenteric nodes and serous membranes in all cases of prolonged low-grade fever. Fever in these localizations of the tuberculosis process is particularly persistent and “dumb.”

It is also known that one of the reasons for prolonged low-grade fever may be helminthiasis (ascariasis, trichocephalosis, diphyllobothriasis), according to the latter, St. Petersburg and the region are endemic. In some cases, persistent low-grade fever is caused by infection of the intra- and extrahepatic biliary tract, as well as pathology of the urinary structures.

Focal infection deserves special attention. Suffice it to say that granulomas of the apices of the roots of the teeth are one of the most common causes of prolonged low-grade fever. Such patients are usually referred to a dentist, and they return to the attending physician with the conclusion: “the oral cavity has been sanitized.” Meanwhile, granulomas and apical abscesses can also affect apparently healthy, filled teeth. In order not to miss the source of infection, an X-ray examination of this area is required, and in the absence of tooth pain during percussion, it is often not performed.

Sometimes chronic purulent sinusitis and frontal sinusitis can occur for a long time without pronounced clinical symptoms, but in some cases they end in a brain abscess. Apparently, a thorough, sometimes repeated x-ray examination is required in order not to miss the cause of low-grade fever and to prevent dangerous complications.

Taking into account the anamnesis, one should also keep in mind the possibility of subdiaphragmatic, subhepatic, perinephric abscesses, which are not easy to recognize. One of the common causes of persistent low-grade fever is the pathology of the female genital organs and, most often, the uterine appendages. Experience shows that in some cases in women, prolonged low-grade fever can be a consequence of various kinds of hormonal disorders. In this regard, it is recommended to refer such patients for consultation to a gynecologist-endocrinologist.

It should be emphasized that no matter in what direction the research into the causes of persistent low-grade fever is conducted, it should not be superficial and fragmented.

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Precocious puberty

Precocious puberty (PPP) refers to the appearance of secondary sexual characteristics (SCH) before age 7 and menstruation before age 10. There are isosexual (VPS correspond to the sex of the child) and heterosexual (VPS are opposite to the sex of the child) forms of PPP. Regardless of the genesis of the disease, a distinction is made between complete and incomplete forms of PPS. Complete is manifested by the development of SFP and menstruation, incomplete – by the presence of at least one of the SFP in the absence of menstruation.

Premature puberty according to the female type (isosexual type of sexual development). The goal of treatment is to eliminate cerebral disorders that have arisen as a result of pathological processes of a predominantly organic or functional nature with simultaneous inhibition of PPS. The principles of management and therapeutic measures for disorders of sexual development depend on the form of the disease and the level of hormonal regulation at which a particular lesion occurs.

Central genesis of the disease

Of great importance in the prevention of this type of PPS is the fight against intranatal and antenatal pathology (fetal hypoxia, asphyxia during childbirth, birth trauma). It has a direct damaging effect and creates a favorable background for the effects of toxic and infectious factors during the neonatal period and early childhood. All measures should be aimed at treating diencephalic pathology: dehydration therapy, vitamins, APT. If a hamartoma is detected (computed tomography), conservative hormonal treatment is performed. With isolated transient thelarche (enlargement of the mammary glands) at the age of 2 to 4 years, the use of any type of therapy in this group of girls is inappropriate. Dispensary observation by a pediatric gynecologist is indicated before the onset of puberty (up to 4 years, once every six months, after 4 years - once a year), prevention of viral diseases, respiratory diseases, abstinence from vaccinations (except for polio) until the manifestations of PPS completely disappear.

Patients with isolated early thelarche should be under the supervision of a pediatric gynecologist (once every six months) until puberty. With true PPS, patients have no disturbances in menstrual function, fertility occurs at an early age, and the timing of menopause corresponds to physiological parameters (i.e., the generative period increases). Upon reaching reproductive age, these patients suffer from short stature (height 130–150 cm).

Pharmacotherapy

Hormonal therapy is aimed at inhibiting PPS, improving the prognosis of the final growth of patients, and improving the social adaptation of patients among peers and adults. The main indication for hormone therapy is the full form of PPS with the manifestation of SPP and menstruation before the age of 3 years. This is the most severe group of patients with PPS: the appearance of SPP and menstruation at an early age, the rapid closure of growth zones, the appearance of feminine features in the figure of a little girl make it impossible for her to remain in a children's group.

For hormonal therapy, progesterone drugs are used (medroxylrogesterone capronate, chlomadinone acetate, 17-OPK); synthetic progestins (Diane-35, Androkur), sigetin; synthetic analogues of luliberin. Medroxyprogesterone capronate is prescribed at a dose of 100–200 mg/day. every 10–14 days. for 2–6 months, sometimes the dose is increased to 200–300 mg/day. (suppresses thelarche, menstruation, but does not inhibit the process of bone maturation). The drugs of choice are antiandrogens - cyproterone acetate (Androcur), Diane-35. Androcur is prescribed orally, the dose is selected individually, it ranges from 25 to 100 mg/day. At doses of 50–75 mg/day. in girls, the SLP begins to regress, the rate of differentiation of the bone skeleton stabilizes, and short stature is prevented.

The withdrawal of the drug should be carried out gradually, as with cortisol drugs. Sigetin is prescribed in age-specific dosages for 2–3 months. The gonadotropin-releasing hormone (GT-RH) agonist buserelin is administered daily at 400–600 mg intranasally for “pituitary desensitization” and suppression of pubertal levels of gonadotropins and sex steroids. Combination therapy with a GT-RH agonist and Androcur is acceptable in the initial stages of treatment. The GT-RH agonist has a stimulating effect at the beginning of therapy, which is neutralized by Androcur. Subsequently, Androkur is canceled.

Monitoring of patients receiving hormones should be carried out in highly specialized institutions at least once every six months until the end of puberty and the establishment of a regular menstrual cycle after discontinuation of therapy, which should last for at least 8 years. For girls with the full form of PPS and the onset of clinical symptoms at a time close to the physiological period of puberty (6–8 years), given the favorable results of long-term observations, hormonal therapy is not indicated. The child is observed once a year by a pediatric gynecologist or neurologist until the end of puberty. Symptomatic therapy is prescribed according to indications.

Ovarian genesis of PPS

In the presence of a hormonally active ovarian tumor, surgical treatment is indicated. The extent of the operation depends on the morphogenesis of the tumor, taking into account the young age of the patient. Usually after tumor removal 2 weeks later. signs of PPS disappear. To prevent recurrence of the tumor in the remaining ovary, the girl must be under constant monitoring. When identifying a follicular ovarian cyst, the gynecologist’s tactics should be wait-and-see due to the functional nature of the disorders and the short-term existence of the cyst. The exception is patients with a long-term increase in ovarian size when it is impossible to exclude a hormonally active tumor. Surgical intervention is indicated no later than after 2 months. careful monitoring of the patient.

Non-drug treatment

To curb the development of SPT, herbal medicine is most often used - freshly prepared potato juice orally (2 tablespoons per day) for 2-3 months.

Premature puberty according to the male type (heterosexual type of sexual development). It is characterized by premature adrenarche (the appearance of pubic hair in girls under the age of 8–9 years), often occurring as a result of congenital adrenal cortex dysfunction (CAD) or adrenogenital syndrome (AGS).

Pharmacotherapy

Cortisol replacement therapy is the treatment of choice. At the same time, adrenal insufficiency is compensated and excess secretion of androgens is suppressed. Treatment is carried out continuously, for life. At the beginning of treatment, a dexamethasone test (large doses of the drug) is required, followed by individual selection of the therapeutic dose of dexamethasone or prednisolone. The level of 17-KS in urine, the bone age of the child, and the degree of virilization at the start of treatment must be taken into account. The dose is considered adequate when the level of 17-KS in daily urine remains within normal limits. The dose is increased with age and with concomitant infectious diseases. Long-term use of prednisolone inhibits virilization, stops rapid growth and development, and feminization occurs in girls. In the salt-wasting form of CADC, prednisolone therapy is supplemented with the oral administration of table salt and DOX.

Surgery

Carry out simultaneously with glucocorticoid therapy in the form of plastic surgery of the external genitalia (amputation of the hypertrophied clitoris - up to 3-5 years; dissection of the urogenital sinus - at 10-12 years).

Amenorrhea of central origin includes dysfunction of both the cerebral cortex and subcortical structures (hypothalamic-pituitary amenorrhea). Disorders of the hypothalamic-pituitary system can be functional, organic, or a consequence of congenital pathology.

Amenorrhea of central origin is more often functional and, as a rule, occurs as a result of exposure to unfavorable environmental factors. The mechanisms of the disorder are realized through neurosecretory structures of the brain that regulate the tonic and cyclic secretion of gonadotropins. Under the influence of stress, there is an excessive release of endogenous opioids, which reduce the formation of dopamine, as well as a decrease in the formation and release of gonadoliberins, which can lead to amenorrhea. With minor disturbances, the number of anovulatory cycles increases, and luteal phase deficiency appears.

Most often, the occurrence of central forms of amenorrhea is preceded by mental trauma, neuroinfections, intoxication, stress, complicated pregnancy and childbirth. Amenorrhea is observed in every 3rd patient with schizophrenia and manic-depressive psychosis, especially during exacerbation. Psychological stress and infectious diseases suffered in childhood are important. Physical overload associated with significant emotional and volitional stress can cause amenorrhea with mental, asthenoneurotic, asthenodepressive or asthenohypochondriacal disorders. Menstruation stops suddenly. Along with amenorrhea, irritability, tearfulness, headache, memory impairment, performance impairment, and sleep disturbance are observed. During the war, as a result of forced starvation, women sharply lost weight, which led to disruption in the hypothalamic-pituitary region and to the so-called wartime amenorrhea. Psycho-emotional stress also contributed to this.

Functional disorders of the hypothalamic-pituitary system lead to the development anorexia nervosa, Itsenko-Cushing's disease, gigantism, functional hyperprolactinemia. Causes of functional disorders of the hypothalamic-pituitary system:

Chronic psychogenic stress;

Chronic infections (frequent sore throats) and especially neuroinfections;

Endocrine diseases;

Taking drugs that deplete dopamine reserves in the central nervous system (reserpine, opioids, monoamine oxidase inhibitors) and affect the secretion and metabolism of dopamine (haloperidol, metoclopramide).

Anatomical disorders of the hypothalamic-pituitary structures, leading to Schiehen's syndrome And hyperprolactinemia, are as follows:

Hormonally active pituitary tumors: prolactinoma, mixed prolactin- and ACTH-secreting pituitary adenomas;

Damage to the pituitary stalk as a result of injury or surgery, exposure to radiation;

Necrosis of pituitary tissue, thrombosis of pituitary vessels.

Congenital pathology of the hypothalamic-pituitary system can lead to adiposogenital dystrophy.

Regardless of the causes of damage to the hypothalamic-pituitary region, the production of hypothalamic GnRH is disrupted, which leads to changes in the secretion of FSH, LH, ACTH, STH, TSH and prolactin. In this case, the cyclicity of their secretion may be disrupted. When the hormone-producing function of the pituitary gland changes, various syndromes arise. A decrease in the secretion of FSH and LH leads to impaired development of follicles and, consequently, insufficient production of estrogen by the ovaries. Secondary hypoestrogenism, as a rule, is accompanied by hyperandrogenism, which, in turn, contributes to the emergence of virile syndrome, moderately expressed in hypothalamic-pituitary disorders.

Since the pituitary gland is also responsible for metabolic processes, when the hypothalamic-pituitary region is affected, patients have a characteristic appearance: obesity, a moon-shaped face, a fat apron, stretch marks on the abdomen and thighs, but excessive thinness with weakly expressed secondary sexual characteristics is also possible. Obesity and severe weight loss as a result of disorders of the hypothalamic-pituitary region aggravate the manifestations of hormonal dysfunction.

To amenorrhea with anorexia nervosa leads to a sharp decrease in the secretion of gonadotropins. This is often observed with a persistent desire to lose weight and a rapid decrease in body weight by 15% or more. This pathology is common among teenage girls who exhaust themselves with diet and physical activity, and can be the onset of mental illness. Lack of menstruation is one of the first signs of the onset of the disease, which brings girls to the gynecologist. Upon examination, a sharp decrease in subcutaneous fatty tissue is noted in women with a female body type. Secondary sexual characteristics are developed normally. A gynecological examination reveals moderate hypoplasia of the external and internal genital organs. Continued weight loss can lead to bradycardia, hypotension, and hypothermia. Subsequently, irritability, aggressiveness, and cachexia appear with complete loss of appetite and aversion to food. The hypoestrogenic state, along with lack of nutrition, predisposes patients to osteoporosis.

Itsenko-Cushing syndrome (disease) characterized by increased production of corticoliberin by the hypothalamus. This causes activation of the adreno-corticotropic function of the anterior pituitary gland due to hyperplasia of basophilic cells and, as a result, hypertrophy and hyperfunction of the adrenal glands, excessive formation of glucocorticosteroids and androgens. The consequence of such hormonal disorders is hypercorticism, which leads to hypokalemic acidosis, increased glyconeogenesis processes, increased blood sugar and ultimately to steroid diabetes. The disease occurs at any age. In children, Itsenko-Cushing's disease is accompanied by virilization of varying severity; in adults, amenorrhea is observed at the beginning of the disease, and later signs of virilization appear. Characterized by disproportionate obesity with the deposition of subcutaneous fat on the face, neck, and upper half of the body. Patients have a round, cyanotic-red face.

The skin is dry, atrophic, with a marbled pattern and areas of pigmentation and acne. There are purplish-red stretch marks on the chest, abdomen, and thighs.

Gigantism also becomes a consequence of hyperplasia of eosinophilic cells of the pituitary gland with increased production of somatotropic and lactogenic hormones. With hyperproduction of GH, growth is excessively high, relatively proportional or disproportionate. Excessive height gain is usually noticed during the prepubertal and pubertal periods, over a period of years. Over time, acromegaloid enlargement of facial features may develop. From the very beginning of the disease, hypogonadism, primary amenorrhea, or early cessation of menstruation are observed.

TO Schiehen's syndrome lead to structural changes in the pituitary gland due to massive postpartum or post-abortion bleeding. In this case, necrotic changes and intravascular thrombosis in the pituitary gland are detected. Pituitary ischemia is also facilitated by a physiological decrease in ACTH release in the postpartum period. Intravascular thrombosis also leads to changes in the liver, kidneys, and brain structures. The severity of the clinical manifestations of Sheen's syndrome depends on the size and location of the pituitary gland lesion and, accordingly, the insufficiency of its gonadotropic, thyroid-tropic, and adrenocorticotropic functions. The disease is often accompanied by a clinical picture of hypofunction of the thyroid gland or vegetative-vascular dystonia of the hypotonic type (headache, increased fatigue, chilliness). A decrease in ovarian hormonal function is manifested by oligomenorrhea and anovulatory infertility. Symptoms of total hypofunction of the pituitary gland are caused by severe insufficiency of gonadotropic, thyrotropic and adrenocorticotropic functions: persistent amenorrhea, hypotrophy of the genital organs and mammary glands, baldness, memory loss, weakness, adynamia, weight loss.

When collecting anamnesis, the connection between the onset of the disease and complicated childbirth or abortion is clarified. The diagnosis can be clarified by a decrease in the blood levels of gonadotropins, TSH, ACTH, as well as estradiol, cortisol, T 3 and T 4.

Hyperprolactinemia. The occurrence of amenorrhea of hypothalamic-pituitary origin is often accompanied by excessive secretion of prolactin - hyperprolactinemia. Prolactin is the only hormone of the anterior pituitary gland, the secretion of which is constantly suppressed by the hypothalamus and increases sharply after the pituitary gland is released from hypothalamic control. Physiological hyperprolactinemia is observed during pregnancy and lactation, in practically healthy women during sleep, after exercise, and also during stress. Hyperprolactinemia is possible due to damage to intrauterine receptors with frequent curettage of the mucous membrane of the uterine body, manual examination of the walls of the uterus after childbirth.

Etiology and pathogenesis. The cause of hyperprolactinemia can be both anatomical and functional disorders in the hypothalamic-pituitary system. In addition, prolactin production is affected by:

Estrogens, estrogen-containing oral contraceptives;

Drugs that affect the secretion and metabolism of dopamine (haloperidol, metoclopramide, sulpiride);

Drugs that deplete dopamine reserves in the central nervous system (reserpine, opioids, monoamine oxidase inhibitors);

Stimulants of the serotonergic system (hallucinogens, amphetamines);

Hypofunction of the thyroid gland.

The pathogenesis of hyperprolactinemia is a violation of the tonic dopaminergic inhibitory control of prolactin secretion caused by dysfunction of the hypothalamus. Of the endogenous prolactin-inhibiting substances, dopamine is the most important. A decrease in its content in the hypothalamus leads to a decrease in the level of prolactin-inhibiting factor and an increase in the amount of circulating prolactin. Continuous stimulation of prolactin secretion leads to hyperplasia of prolactotrophs, and then micro- and macroadenoma of the pituitary gland can form.

30-40% of women with hyperprolactinemia have increased levels of adrenal androgens - DHEA and DHEA-S. Hyperandrogenism in hyperprolactinemia is explained by the commonality of the hypothalamic regulation of prolactin- and ACTH-secreting functions of the pituitary gland. In addition, receptors for prolactin were found in the zona reticularis of the adrenal cortex.

The mechanism of reproductive dysfunction due to hyperprolactinemia is as follows. In the hypothalamus, under the influence of prolactin, the synthesis and release of GnRH and, accordingly, LH and FSH decrease. In the ovaries, prolactin inhibits gonadotropin-dependent synthesis of steroids and reduces the sensitivity of the ovaries to exogenous gonadotropins.

Clinical symptoms. Hyperprolactinemia is manifested by menstrual cycle disorders such as hypo-, oligo-, opso- and amenorrhea, as well as infertility.

Women with hyperprolactinemia often experience galactorrhea, and it does not always correlate with prolactin levels. Thus, galactorrhea is possible even when its level is normal, which is associated with hypersensitivity of prolactin receptors in the mammary gland.

There is so-called asymptomatic hyperprolactinemia, in which the level of biologically active prolactin is increased. About 50% of women with hyperprolactinemia report headache and dizziness, and a transient increase in blood pressure.

Diagnostics hyperprolactinemia includes a study of general and gynecological history, a detailed general therapeutic examination. The state of the endocrine system, mainly the thyroid gland and adrenal cortex, deserves special attention.

An increase in the level of prolactin in peripheral blood plasma is one of the confirmations of hyperprolactinemia. The ratio of the content of gonadotropic and sex hormones is also important. For differential diagnosis of hyperprolactinemia, and in particular its transient form, it is necessary to repeatedly determine prolactin over time. The most informative are functional tests with the dopamine agonist bromocriptine (Parlodel ♠) and the dopamine antagonist metoclopramide (Cerucal ♠). Functional hyperprolactinemia is not accompanied by

changes in the sella turcica on an x-ray, CT and MRI in case of an increase in prolactin levels to 2000 mIU/l.

To exclude anatomical changes in the pituitary gland, an X-ray examination of the skull is performed to identify changes in the area of the sella turcica. With pituitary macroadenoma, the size of the sella turcica is increased, its bottom is 2-3-contour, and there are signs of sclerosis of the sella turcica. The level of prolactin in macroadenoma exceeds 5000 mIU/l. With pituitary macroadenoma, amenorrhea and galactorrhea are observed. Diagnosis of pituitary microadenoma is possible using CT or MRI. Prolactin levels in microadenoma range from 2500 to 10,000 mIU/l.

Treatment hyperprolactinemia is carried out taking into account its form. Dopamine agonists are widely used to treat functional hyperprolactinemia. Treatment begins with the appointment of 1/2 tablet of bromocriptine per day with meals, then the dose is increased every two days by 1/2 tablet, bringing to 3-4 tablets per day under the control of blood prolactin levels and basal temperature. When ovulatory menstrual cycles are restored, the dose is reduced to 1 tablet per day; This treatment is carried out for 6-8 months. Fertility is restored in 75-90% of cases. If the 2nd phase of the cycle is insufficient, you can additionally prescribe clomiphene from the 5th to the 9th day of the menstrual cycle, which stimulates ovulation. The latest generation of drugs in the treatment of hyperprolactinemia include quinagolide (norprolac ♠) and cabergoline (dostinex ♠) (1 mg per week for 3-4 weeks). These are long-acting drugs with minimal side effects.

For pituitary microadenoma, therapy is also carried out with bromocriptine or its analogues. With long-term treatment, dystrophic changes in the tumor develop; it decreases until it disappears completely. Pregnancy during treatment in patients with pituitary microadenoma proceeds safely. During pregnancy, observation by a neurologist and ophthalmologist is mandatory.

Pituitary macroadenoma is an indication for surgical treatment performed by a neurosurgeon or for radiation therapy.

Adiposogenital dystrophy is a consequence of congenital pathology of the hypothalamic-pituitary region. The disease is accompanied by progressive obesity as a result of disruption of the central regulation of the feeling of satiety due to damage to the paraventricular nuclei of the hypothalamus. A decrease in the gonadotropic function of the pituitary gland causes underdevelopment of the reproductive system (hypogonadism). Infectious processes in the pituitary region and pituitary adenoma with hyperplasia of eosinophilic pituitary cells can lead to hyperproduction of GH and excessively high growth (relatively proportional or disproportionate gigantism).

Ovarian amenorrhea

Ovarian forms of amenorrhea are caused by functional, organic changes and congenital pathology of the ovaries. The most common cause of functional and morphological disorders in

the ovarian level of regulation of the menstrual cycle is polycystic ovary syndrome(PCOS). A decrease or depletion of ovarian hormonal function is observed when resistant ovarian syndrome(SRY) and ovarian wasting syndrome(SIYA). Organic changes in the ovaries, accompanied by menstrual dysfunction, are caused by hormonally active ovarian tumors(see "Ovarian tumors").

PCOS - pathology of the structure and function of the ovaries with a very diverse clinical picture, the most constant component of which is anovulation. PCOS consists of significant morphological changes in the ovaries. This is a smooth and dense tunica albuginea, proliferation of connective tissue, an increase in the number of cystic follicles in the absence of a dominant follicle. Polycystic ovaries are enlarged in volume (>9 cm 3) as a result of the proliferation of connective tissue, the tunica albuginea is pearly white. When cut through, the cortex resembles a honeycomb, since the follicles are of different diameters.

PCOS is accompanied by chronic anovulation, infertility, often metabolic disorders, decreased glucose tolerance, as well as hyperandrogenism and, consequently, virilization. Excessively high production of androgens is promoted by the proliferation of interstitial tissue

with PCOS.

Based on the results of numerous hormonal and clinical studies, primary (Stein-Leventhal syndrome, described in 1935) and secondary polycystic ovaries are distinguished, the latter developing with adrenal hyperandrogenism, hyperprolactinemia, and neurometabolic-endocrine syndromes.

The most convenient for use in clinical practice is the one proposed by M.L. Crimean classification, including three forms:

A typical form, accompanied predominantly by ovarian hyperandrogenism, is primary polycystic ovaries;

Combined or mixed form with both ovarian and adrenal hyperandrogenism;

Central form with hyperandrogenism and severe dysfunction of the central parts of the reproductive system with a predominance of secondary polycystic ovaries.

Etiology and pathogenesis. The etiology and pathogenesis depend on the form of PCOS. In the 60s of the twentieth century, the pathogenesis typical shape PCOS (Stein-Leventhal syndrome) has been associated with a genetically determined deficiency of ovarian enzymes that blocks the conversion of androgens to estrogens. However, it was subsequently shown that the activity of granulosa cells depends on FSH. Disruption of the process of aromatization of androgens into estrogens leads to the accumulation of testosterone (active androgen) and a decrease in estrogen levels in the ovaries. As a result, the cyclic secretion of gonadotropins is disrupted by a feedback mechanism, which, in turn, leads to hyperplasia of the ovarian stroma and theca cells, excessive or increased production of androgens. Androgens are partially converted to estrone, and part of the estrone is converted to estradiol. However, this is not enough for

the occurrence of preovulatory and luteal peaks. The menstrual cycle becomes monophasic.

In pathogenesis mixed (forms PCOS can be triggered by primary dysfunction of the adrenal cortex or transient excess of adrenal androgens during the period of adrenarche. In peripheral tissues, androgens are partially converted to estrogens. When a critical body weight is reached, the peripheral conversion of androgens in adipose tissue increases. This is accompanied by an increase in LH synthesis in the pituitary gland and a violation of the LH/FSH ratio, which leads to hyperplasia of theca cells and ovarian stroma. The listed structures synthesize androgens in excess quantities. Hyperandrogenism prevents follicular maturation, leads to anovulation and further suppresses FSH secretion. This closes a vicious circle.

Participation of brain structures in development central shape PCOS is confirmed by the chronological connection between the onset of the disease and a stressful state (onset of sexual activity, mental trauma, childbirth, abortion). Dysfunction of the central nervous system may be a consequence of acute or chronic infection or intoxication. At the same time, the synthesis and release of endogenous opioids increases, which disrupts the dopaminergic regulation of GnRH secretion, leading to an increase in the basal level of LH secretion, a relative decrease in FSH production and impaired folliculogenesis. An increase in LH secretion in PCOS is due to both a primary impairment of GnRH synthesis and chronic anovulation; these effects are mutually potentiated.

The modern understanding of the pathogenesis of PCOS, in addition to disorders of the hypothalamic-pituitary complex, ovaries and adrenal glands, includes metabolic disorders and autoparacrine factors regulating steroidogenesis in the ovaries. Metabolic disorders are associated with the insulin-glucose system, since insulin is involved in the production of ovarian androgens. Obesity does not play a decisive role in the pathogenesis of PCOS, however, as a result of hyperinsulinemia and insulin resistance, existing endocrine disorders are aggravated. In obese patients with insulin resistance, chronic hyperinsulinemia stimulates the formation of insulin-like growth factor-1 (IGF-1). The latter, through specific receptors, increases the formation of androgens in the cells and interstitial tissue of the ovaries. In addition, insulin is able to inhibit the formation of globulins in the liver that bind sex hormones, resulting in an increase in the free biologically active fraction of testosterone in the blood.

According to the existing hypothesis, the stimulating effect of insulin on the synthesis of androgens in the ovary is due to a genetic predisposition.

PCOS develops in women with normal body weight. In their blood, the level of growth hormone is increased, which causes the formation of IGF-1 in granulosa cells and enhances the formation of ovarian androgens. The study of hormone biosynthesis in granulosa cells of polycystic ovaries has so far

It turned out that luteinized cells lose the ability to synthesize progesterone. This is one of the possible mechanisms of anovulation in patients

Clinical symptoms. The clinical manifestations of PCOS are very different, but the main ones in all forms of PCOS are hypo-, opso-, oligo- and amenorrhea. Violations of folliculogenesis lead to the development of anovulatory primary and secondary infertility.

In the typical form of PCOS, menstrual irregularities begin at menarche. In the mixed form of PCOS, late menarche is combined with later menstrual irregularities such as secondary amenorrhea. During reproductive age, chronic anovulation and infertility, often primary, are observed. In the central form of PCOS, menarche is normal, but the menstrual cycle is unstable. This subsequently leads to hypo-, opso-, oligo- or amenorrhea. Reproductive function disorders include short-term miscarriage and secondary infertility. In addition to menstrual dysfunction, dysfunction of the hypothalamic-pituitary system is noted. The onset of the disease may be associated with stress, adenoviral infection, or brain injury.

The main reason for young patients to see a doctor is excessive hair growth, the frequency of which in PCOS, according to various authors, ranges from 50 to 100%. Hirsutism in the typical form of PCOS develops gradually from the period of menarche. Excessive hair growth is noted on the upper lip, chin, and along the white line of the abdomen. Severe hirsutism and hypertrichosis are not typical for this form of PCOS, but in the mixed form, hirsutism is observed in all patients. Areas of excess hair growth are the inner and outer surfaces of the thighs, the white line of the abdomen, the upper lip, and the lower legs. Hair growth begins at menarche or earlier. In the central form of PCOS, hirsutism is detected in 90% of patients, occurs 3-5 years after menstrual dysfunction, already against the background of obesity, and is more pronounced during reproductive age. In these patients, degenerative changes can be noticed: stretch marks on the chest, abdomen, hips, brittle nails and hair.

The clinical picture of PCOS is largely determined by general metabolic disorders - such as dyslipidemia, carbohydrate metabolism disorders, and an increased risk of developing genital hyperplastic processes. These disorders can cause the early development of atherosclerotic changes in blood vessels, hypertension, and coronary heart disease. In 50% of patients with a typical form of PCOS, increased body weight with an even distribution of subcutaneous fat occurs from adolescence. In mixed forms of PCOS, obesity is rare. In the central form, the leading complaint is about excess body weight. Obesity reaches II-III degree; adipose tissue is localized mainly on the shoulder girdle, lower abdomen and thighs.

Diagnostics PCOS must begin with a careful examination of the medical history and physical findings. The formation of PCOS begins with puberty

long period and is accompanied by disruption of the formation of menstrual function. Primary polycystic ovaries cause irregular menstruation from puberty, which distinguishes them from secondary polycystic ovaries.

The clinical criterion for diagnosing PCOS is hirsutism (in 69% of patients), which appears simultaneously with the onset of puberty. The severity of other clinical manifestations of hyperandrogenism varies. With the progression of virilization symptoms (clitoral hypertrophy, defeminization of the figure, decreased voice), it is necessary to exclude hormonally active tumors of the ovaries and adrenal glands; This is usually not typical for PCOS.

The main methods for diagnosing PCOS include echography of the pelvic organs, study of blood plasma hormones, laparoscopy with biopsy and histological examination of ovarian tissue.

Bilateral enlargement of the ovaries is pathognomonic for PCOS, often with a hypoplastic uterus, which is clearly determined by echography. An echoscopic picture of the ovaries with transvaginal ultrasound (Fig. 9.1) shows an increase in the volume of the ovaries by more than 9 cm 3 (on average 16-20 cm 3), hyperplastic stroma, more than 10 atretic follicles located along the periphery under a thickened capsule.

The hormonal criteria for diagnosing PCOS include an LH/FSH ratio of more than 2.5-3. However, in recent years it has been shown that normal levels of gonadotropic hormones do not exclude the diagnosis of PCOS. Thus, the level of DHEA and DHEA-S is normal in the typical form and increased in the presence of the adrenal component (mixed form of PCOS). In the central form of PCOS, the LH/FSH ratio is the same as in the typical form, but an appropriate history and clinical symptoms allow the diagnosis to be verified.

Rice. 9.1. Polycystic ovary syndrome. Ultrasound

An obligatory stage in the examination of patients with PCOS is the diagnosis of metabolic disorders: hyperinsulinemia and insulin resistance. A BMI of more than 25 kg/m2 and dyslipidemia indicate hyperinsulinemia and insulin resistance.

Typical laparoscopic picture of the ovaries in PCOS: increased size (up to 5-6 cm in length and 4 cm in width), smoothed, thickened, pearly-whitish capsule. The absence of translucent small follicular cysts and ovulation stigmas indicates a pronounced thickness of the ovarian capsule, which sometimes complicates biopsy (Fig. 9.2).

Treatment. The sequence of treatment measures in patients with PCOS depends on the complaints, clinical manifestations and age of the patient. Since the main reason for seeing a doctor in patients of reproductive age is infertility, the goals of treatment are restoration of menstrual and at the same time reproductive function, prevention of hyperplastic processes in target organs and correction of the prevailing symptom complex. For this purpose, conservative and surgical treatment methods are used.

For obesity, the first stage of treatment (regardless of the form of the disease) is normalization of body weight. However, therapeutic fasting is contraindicated; The greatest therapeutic effect is obtained by combining diet therapy with physiotherapeutic measures - massage, physical therapy, acupuncture. Losing body weight leads to the normalization of the endocrine blood profile, a decrease in insulin and androgen levels, and the restoration of regular menstruation. In PCOS of central origin, the use of drugs that correct neurotransmitter metabolism (phenytoin - diphenin *, beclamide - chloracon *) is pathogenetically justified. It is possible to prescribe orlistat, which selectively inhibits lipid metabolism, or subitramine, which blocks the saturation center.

The next stage of treatment is stimulation of ovulation. Stimulation begins with the use of clomiphene, which gives an antiestrogenic effect by blocking estradiol receptors. After discontinuation of the drug, gonadotropic function normalizes. Clomiphene does not directly stimulate

Rice. 9.2. Ovarian biopsy. Laparoscopy

specifically the ovaries, but causes ovulation due to short-term normalization of the hypothalamic-pituitary-ovarian system. The drug is prescribed 100 mg from the 5th to the 10th day of the menstrual cycle. Treatment with clomiphene restores ovulation in 48-80% of patients, pregnancy occurs in 20-46%. In case of resistance to clomiphene, ovulation stimulation can be carried out with gonadotropic drugs (pergonal ♠, humegon ♠) according to individual schemes. However, stimulation of ovulation, especially with elevated insulin levels and obesity, increases the risk of developing hyperstimulation syndrome or may lead to ovarian unresponsiveness.

Treatment of women who are not planning a pregnancy is aimed at restoring the menstrual cycle, treating hirsutism and preventing the long-term consequences of PCOS, which worsen the quality of life. For this purpose, combined oral contraceptives (COCs) are used, which reduce the level of androgens, normalize the menstrual cycle and help prevent endometrial hyperplastic processes. In patients with PCOS and lipid metabolism disorders, it is advisable to combine COCs with drug therapy for insulin resistance. The combination of COCs with antiandrogens potentiates a decrease in androgen secretion. Antiandrogens block androgen receptors in target tissue and suppress gonadotropic secretion. The use of drugs with antiandrogenic properties (Diane-35*) has significantly expanded the therapeutic options for PCOS. The antiandrogenic effect of Diane-35 ♠ can be enhanced by additional administration of cyproterone (androcur ♠) 25-50 mg from the 5th to the 15th day of the menstrual cycle. The duration of treatment is from 6 months to 2 years or more.

Spironolactone (veroshpiron ♠) has an antiandrogenic effect, blocking peripheral receptors and androgen synthesis in the adrenal glands and ovaries. Its long-term use at a dose of 100 mg/day reduces hirsutism. However, drug treatment for hirsutism is not always effective.

Surgical methods for treating PCOS are often performed using an endoscopic approach. Surgical treatment normalizes gonadotropic secretion by reducing the volume of androgen-secreting tissues of polycystic ovaries. As a result, the level of extragonadal estrogens, which increases the sensitivity of the pituitary gland to GnRH, decreases. Surgical methods for correcting PCOS include wedge resection, thermal cauterization (Fig. 9.3), thermal vaporization and decapsulation of polycystic ovaries. Surgical treatment is most effective for the typical form of PCOS.

The ineffectiveness of wedge resection of the ovaries in some patients indicates combined adrenal-ovarian hyperandrogenism.

The frequency of development of endometrial hyperplastic processes and the risk of endometrial cancer in patients with PCOS, especially with typical and central forms, determine active management tactics (hysteroscopy with separate diagnostic curettage) even in the absence of complaints. Timely diagnosis and treatment of such patients are measures to prevent endometrial cancer.

Rice. 9.3. Ovary after cautery. Laparoscopy

Resistant ovarian syndrome. In rare cases, ovarian failure may be caused by resistant ovarian syndrome (ROS; Savage syndrome). In women under 35 years of age, amenorrhea, infertility, micro- and macroscopically unchanged ovaries with high levels of gonadotropins are observed. Secondary sexual characteristics are developed normally. The causes of ROS have not been studied; the autoimmune nature of this pathology is assumed. It is known that hypergonadotropic amenorrhea can be combined with autoimmune diseases: Hashimoto's disease, myasthenia gravis, alopecia, thrombocytopenic purpura, autoimmune hemolytic anemia. Ovarian resistance to high levels of gonadotropins may be due to an abnormality of the FSH molecule or the lack of biological activity of the hormone. A large role is given to intraovarian factors involved in the regulation of ovarian function. There is data on the influence of iatrogenic factors - radiotherapy, cytotoxic drugs, immunosuppressants, surgical interventions on the ovaries. The development of resistant ovaries can be facilitated by damage to ovarian tissue due to tuberculosis, mumps, and sarcoidosis.

Clinical symptoms and diagnosis. Most patients associate the onset of the disease with stress and severe viral infections. The first menstruation, as a rule, occurs in a timely manner, and after 5-10 years amenorrhea develops, but 84% of patients subsequently have menstruation sporadically. Pregnancy and childbirth occur in 5% of patients. Patients with SRS have a correct physique, satisfactory nutrition, and well-developed secondary sexual characteristics. Periodically, they feel hot flashes of heat to the head. When examined using functional diagnostic tests, they reveal signs of ovarian hypofunction: thinning of the mucous membranes of the vulva and vagina, a weakly positive “pupil” phenomenon, low CPI values (from 0 to 25%).

During gynecological examination, echography, and laparoscopy, the uterus and ovaries were slightly reduced. Most authors believe that the diagnosis of EOC can only be made after laparoscopy and ovarian biopsy followed by histological examination, which reveals

There are primordial and preantral follicles. During laparoscopy, translucent follicles are visible in the ovaries.

Hormonal studies indicate high levels of FSH and LH in the blood plasma. Prolactin levels are normal.

Hormonal tests have great diagnostic value. A decrease in the level of FSH with the introduction of estrogen and an increase in the level of FSH and LH in response to the administration of luliberin indicate the preservation of the feedback mechanism between the hypothalamic-pituitary system and sex steroids.

Treatment. Treatment of SOC presents great difficulties. Conflicting data have been obtained with treatment with gonadotropins. Some authors noted an increase in follicles and menstrual-like discharge during the administration of FSH and LH, while others noted only the growth of follicles (empty follicles) without an increase in the level of blood estrogen.

The prescription of estrogens is based on the blockade of endogenous gonadotropins and the subsequent rebound effect (reflection effect). In addition, estrogens increase the number of gonadotropic receptors in the ovaries and, possibly, thus enhance the response of follicles to endogenous gonadotropins. Restoring generative function is possible only with the help of assisted reproductive technologies (IVF of a donor egg).

Amenorrhea of central origin (origin) can manifest itself in different ways, depending on which brain structures are affected and how severely they are affected. This group of amenorrhea includes all its types caused by disturbances in the functioning of the central nervous system.

What is amenorrhea of central origin

This type of amenorrhea is also called hypothalamic-pituitary, that is, occurring with any pathology in the area of the hypothalamus or pituitary gland. As is known, a woman’s neurohormonal system consists of the following structures that mutually influence each other: cerebral cortex – hypothalamus – pituitary gland – ovaries – uterus. Failure at any of these levels can cause amenorrhea. A malfunction at the level of the cerebral cortex - hypothalamus - pituitary gland causes amenorrhea of central origin.

All types of amenorrhea of central origin can be divided into two large groups - functional and organic. Functional changes occur without visible changes in brain structure. But changes occur at the biochemical level under the influence of various factors: starvation, mental trauma, various diseases (acute infections, frequent exacerbations of chronic diseases), intoxication, and so on.

Organic types of amenorrhea of central origin include those caused by diseases and tumors in the hypothalamus and pituitary gland. At the same time, structural disorders occur in the brain tissue, which lead to the appearance of a number of symptoms, including amenorrhea.

Functional amenorrhea of central origin

With stress, intoxication, fasting and any other general effects on the cerebral cortex, functional changes also occur in the subcortical structures - the hypothalamus and pituitary gland. It all starts with the fact that, at the command of the cerebral cortex, the production of endogenous opioids increases - substances whose main task is to smooth out the unpleasant consequences of their effects on the brain.

This starts a real chain reaction: under the influence of opioids, the amount of the neurotransmitter dopamine and the secretion of hypothalamic hormones, which regulate the secretion of pituitary hormones, are reduced. In particular, the production of gonadotropin-Riesling hormone of the hypothalamus, which regulates the amount and cyclicity of secretion of gonadotropic hormones of the pituitary gland - follicle-stimulating hormone (FSH - the hormone of the first half of the menstrual cycle) and luteinizing hormone (LH - the hormone of the second half of the menstrual cycle), may decrease.

And since, under the influence of FSH and LH, the egg first matures and then leaves the ovary (ovulation), as well as the secretion of female sex hormones that prepare the uterus for pregnancy, the menstrual cycle is disrupted . The mucous membrane of the uterus does not grow, does not begin to secrete and then is not rejected - there is no menstruation.

As a rule, functional amenorrhea of central origin disappears after the cause of the disease is eliminated. But if it lasts for a long time, irreversible changes can occur in the hormonal system (usually in the ovaries). Therefore, any amenorrhea should be treated promptly.

Organic amenorrhea of central origin

Organic amenorrhea of central origin is caused by diseases and tumors of the hypothalamic-pituitary system. In this case, the pituitary gland is most often affected. And since the pituitary gland, with the help of its hormones, regulates the function of all other endocrine glands, depending on the location of the lesion and its degree, certain symptoms of the disease may appear, which also include amenorrhea. The most common syndromes are Sheehan's, Itsenko-Cushing's and gigantism.

With Sheehan's syndrome, changes in pituitary tissue occur against the background of significant bleeding during childbirth, induced abortion or miscarriage. Due to lack of blood supply (ischemia), necrosis (tissue death) can occur in the pituitary tissue. A thrombus in the blood vessels in the pituitary gland can cause the same disturbances. This is what causes the various symptoms of the disease, which manifest themselves to varying degrees depending on the size and location of the pituitary gland lesion. Structures responsible for control of the gonads, thyroid gland, and adrenal glands may be affected. Therefore, amenorrhea can occur against the background of other symptoms, for example, underactive thyroid gland (weakness, decreased performance, low blood pressure). There may be a complete defeat of all functions of the pituitary gland, resulting in persistent amenorrhea, a decrease in the volume of the genital organs and mammary glands, baldness, memory impairment, weakness, lethargy, and weight loss.

With some organic lesions of the hypothalamus, the secretion of the hypothalamic hormones increases, regulating the formation by the pituitary gland of hormones responsible for the function of the adrenal glands. This causes excessive production of glucocorticoid and male sex hormones. The result is amenorrhea, male-type changes (including increased hair growth), disproportionate obesity with the deposition of subcutaneous fat in the face, neck, and upper half of the torso.

Let's consider the definition of “amenorrhea” and the possible causes of its occurrence.

TRUE - these are disorders in which there are no cyclic processes in the woman’s reproductive system; true amenorrhea is divided into physiological and pathological: