The well-being of the fetus depends both on the composition of the mother’s blood and the condition of the placenta, as well as on its own blood circulation.

In order to understand changes in circulatory system after birth, it is necessary to clearly imagine how preparation for them is carried out during intrauterine life. Fetal circulation is radically different from postnatal circulation. Birth is accompanied by sudden changes in the cardiovascular system, and the body no longer encounters such changes until death.

From the section on heart development, remember that the atria are never completely separated from each other. Appear sequentially trimorphologically different interatrial foramina: the first - under the septum primum, the second - in the septum primum and, finally, the third - in the septum secundum. This results in the left atrium receiving some blood directly from the inferior vena cava through the right atrium throughout the prenatal period. The influx of this blood compensates for the small amount of blood entering the left atrium from the pulmonary circulation and maintains an approximate balance of blood volumes in the right and left halves of the heart.

In the early stage of intrauterine life, the embryo feeds in a histiotrophic manner, receiving the substances necessary for development from the tissues of the mother’s body. From the end of the 2nd month, placental blood circulation and gas exchange are established, the fetus is provided with nutrients, and metabolic products are removed through the placenta.

There is no direct communication between the fetal blood circulating in the vessels of the villi and the intervillous space, therefore the blood of the fetus and mother do not mix . Metabolism, including gas, occurs through the wall of the capillaries of the villi and their covering epithelium. In this case, nutrients enter the fetal blood not only through diffusion, but also due to the active cellular activity of the villous epithelium.

In the intervillous spaces of the placenta, the speed of blood flow slows down, while in the villi themselves, blood circulates in accordance with the rate of the fetal heart. This feature allows the fetus to most effectively obtain the maximum amount of substances it needs.

Blood enriched with oxygen and nutrients in the placenta reaches the fetus through the umbilical vein. Blood saturation oxygen in the umbilical vein is approximately 80%. This is significantly lower than in extrauterine life.

Umbilical vein on the surface of the liver is divided into two parts: one of them in the form of several branches goes to the lower surface of the liver, penetrates its parenchyma, partially anastomosing with the branches of the portal vein, and supplies the left two-thirds of the liver(the right third of the liver receives blood from the portal vein).

Another part of the umbilical vein in the form venous(obsolete name - arantsieva) duct drains into the inferior vena cava where it combines with venous blood from lower limbs and organs abdominal cavity. From the liver itself, blood flows through the hepatic veins, which flow into the inferior vena cava.

The blood flowing from the inferior vena cava into the right atrium is saturated with oxygen by approximately only 67%, since it is a mixture consisting of the blood of the umbilical vein (80% oxygenated) and the blood of the hepatic and caval veins (26% oxygenated). Thus, fetal liver only receives the most oxygen-rich blood.

However, everything is not so mechanical . The oxygen content of the blood delivered by the inferior vena cava to the right atrium varies significantly over time. It turned out that in the place where the umbilical vein connects within the liver with the portal vein there is a kind of sphincter. If this sphincter delays the movement of the “umbilical” blood, the most depleted blood enters the right atrium. When the sphincter relaxes, placental blood will rush into the ductus venosus under high blood pressure, created while the sphincter was closed. Since venous pressure is generally relatively low, even with a slight increase in pressure in the umbilical vein, the blood from it tends to displace purely venous blood rising through the portal and inferior vena cava. As a result, there are periods when the oxygen content of the blood entering the right atrium through the inferior vena cava will be almost as high as in the umbilical vein. During such periods, the blood passing through the foramen ovale into the left side of the heart and into the systemic circulation will contain sufficient oxygen.

It is also believed that the contractile activity of the uterus leads to periodic squeezing of blood from the spongy placenta and plays a role in changes in the volume and pressure of blood in the umbilical vein.

These periodic changes in the state of the blood passing through the umbilical vein explain the apparent inconsistency of data on oxygen content obtained by various researchers. From a physiological point of view, it is interesting that in the systemic circulation of the embryo, the oxygen content is always maintained at a level that is quite consistent with the degree of metabolism and growth of the embryo.

So, from the inferior vena cava mixed blood enters the right atrium. The superior vena cava also flows here, carrying venous blood from the upper half of the body.

Blood from the inferior vena cava is divided into two directions by the crista dividens. The entrance to the heart of the inferior vena cava is directed in relation to the foramen ovale in such a way that most of the blood coming from the inferior vena cava passes directly into the left atrium.

Careful measurements have also shown that the interatrial foramen ovale in the fetus, even before birth, is significantly smaller than the opening of the inferior vena cava. This means that some of the blood from the inferior vena cava that cannot pass into the left atrium will still have to return back and mix with the blood in the right atrium. It was found (by radioisotope method) that about 1/4 of the blood of each of the flows of the vena cava is mixed.

The blood, after mixing, enters the right ventricle, which pumps it into pulmonary artery(pulmonary trunk). However, only a small amount of blood flows from the right ventricle to the lungs, since they are in a collapsed state and offer very great resistance to blood flow. The left atrium receives this small amount of blood from the pulmonary veins of non-functioning lungs. However, such a slight mixing does not have a significant effect on the gas composition of the blood in the left ventricle.

Most of the mixed blood from the pulmonary artery enters through the open arterial ( outdated name botalls) duct - ductus arteriosus - into the aorta, since the pressure in the aorta in the fetus is lower than in the pulmonary artery.

The duct opens into the descending aorta, necessarily bottom e the origin of large vessels supplying the brain, heart and upper limbs.

The left ventricle itself pushes out blood saturated with oxygen by 60-65%. Most of this blood is used to supply the heart and head. Slightly less oxygenated blood, which is a mixture of blood from the right and left ventricles, enters the descending aorta, and from it into internal organs, limbs and finally into the placenta through the two umbilical arteries. The blood of the umbilical capillaries in the placenta is again saturated with oxygen.

Both ventricles of the fetal heart are connected in parallel, rather than in series, as in adults, and the pressure in the pulmonary artery is higher than in the aorta. The same amount of blood in both halves of the heart is not of such great importance as in adults and in the fetus, the left ventricle expels approximately 20% more blood than the right. Of the total amount of blood expelled by both ventricles, 50% enters the placenta, 30-35% enters the fetal body, and the lungs receive about 15% of the blood. It is clear that the resistance in the blood vessels of the placenta is small, but the lungs provide great resistance.

In the vessels closely connected with the heart, there is a mechanism that ensures the appropriate exit of blood from the right ventricle during the development of the pulmonary circulation.

With the development of the pulmonary arteries from the sixth pair of aortic arches, the right sixth arch soon loses its connection with the dorsal aorta. However, on the left, part of the sixth arch is preserved in the form of a large vessel connecting the pulmonary artery with the dorsal aorta. This vessel is ductus arteriosus ductus arteriosus (botallian duct) - remains open throughout intrauterine life and acts as a reserve passage, allowing any excess blood from the pulmonary vessels to pass into the aorta.

Ductus arteriosus may be called the "training vessel" of the right ventricle, since it allows the right ventricle to do its full workload throughout development and thereby prepare to push all the blood into the lungs after birth.

Before birth, between the origin of the left subclavian artery
and the confluence of the ductus arteriosus is a narrowed part of the arch. This narrowed area is called the isthmus (istmus). Closure of the ductus arteriosus entails a gradual change in the configuration of the aortic arch. Once it closes, all blood entering the descending aorta must travel through the aortic arch. As a result, the isthmus slowly expands.

All traces of narrowing of the fetal aortic arch usually completely disappear 3-4 months after birth.

Consequently, none of the fetal organs, with the exception of the liver, is supplied with blood saturated with oxygen by more than 60-65%. It should be remembered what low pO is 2 in arterial blood is necessarily accompanied by an increase in pCO 2 and a decrease in arterial blood pH. A large degree of hypoxia, as a result of which the blood is less than 15% saturated with oxygen, causes a decrease in heart rate- bradycardia. This hypoxia has long been considered a symptom that the fetus is in danger. During hypoxia, the fetus develops a “diving reflex” and the reduced minute volume of blood is directed mainly to the central nervous system and to the myocardium with significant constriction of the muscles and skin vessels.

During pregnancy, a woman's body experiences significant stress. The volume of circulating blood increases, conditions for venous stagnation appear.

The growing uterus squeezes blood vessels and surrounding organs, causing disruption of blood supply. One result of these changes is inferior vena cava syndrome. Its hidden manifestations are present in more than half of women, and clinically it manifests itself in every tenth pregnant woman. Severe cases of this disease occur in one in a hundred pregnant women.

Synonyms for this condition:

• hypotensive syndrome on the back;
• aortocaval compression syndrome;
• postural hypotensive syndrome;
• hypotensive syndrome of pregnant women in the supine position.

Why does this condition occur?

Inferior vena cava compression syndrome usually occurs when the pregnant woman is lying on her back.

The inferior vena cava is a large diameter vessel that drains blood from the legs and internal organs. venous blood. It is located along the spine. Its walls are soft, the pressure in the venous system is low, so the vein is easily compressed by the enlarged uterus.

Signs of such compression begin to occur periodically in the third trimester of pregnancy if the woman is in a supine position.

When this large vein is compressed, the outflow of blood through it to the heart is hampered, that is, venous return is reduced. As a result, the volume of blood passing through the lungs through the pulmonary circulation decreases. Blood oxygen saturation decreases, hypoxemia occurs.

Cardiac output decreases - the amount of blood ejected by the heart into the aorta. As a result of a small amount of blood and a reduced oxygen content in it, a lack of this gas occurs in all tissues - hypoxia. All organs of the woman and fetus suffer.

Suddenly falls quickly blood pressure, in some cases up to 50/0 mmHg. Art.

On the other hand, a compressed inferior vena cava cannot pass the entire volume of venous blood from the legs and lower torso to the right atrium. Therefore, venous congestion develops in the veins of the lower extremities.

In the development of inferior vena cava syndrome, an increase in intra-abdominal pressure due to the growing uterus, elevation of the diaphragm and compression of all major vessels of the abdominal cavity and retroperitoneal space are important. Many pregnant women develop a network of collaterals - bypass routes of venous outflow, as a result of which the syndrome in question does not occur in them.

How does the condition manifest?

The inferior vena cava is compressed by the enlarged uterus when the woman is lying on her back. At long gestation periods or with polyhydramnios, this can also occur in an upright position of the body.

The first symptoms appear at about 25 weeks. It becomes difficult for a woman to lie on her back, and she may experience dizziness, shortness of breath, and weakness. Blood pressure decreases. In some cases, even collapse with fainting occurs.

In severe cases, a woman quickly turns pale 2 to 3 minutes after turning on her back, complains of dizziness and darkening of the eyes, nausea and cold sweat. More rare signs are ringing in the ears, heaviness behind the sternum, a feeling of strong fetal movement.

Suddenly developing pallor and hypotension are very similar to signs of internal bleeding, so the doctor may mistakenly suspect placental abruption, uterine rupture, or myocardial infarction in such a pregnant woman.

The appearance of a vascular pattern and varicose veins in the legs is also associated with the described syndrome. One of the common manifestations of this condition is hemorrhoids.

Described pathological condition leads to fetal hypoxia and disturbance of its heartbeat. The development of organs and systems of the unborn child suffers. If it occurs during childbirth, it can cause fetal asphyxia. The connection of this disease with premature detachment of a normally located placenta has been proven.

What to do in this condition

The optimal position for a pregnant woman during sleep is lying on her left side.

What not to do in the third trimester of pregnancy:

• A pregnant woman over 25 weeks should not sleep on her back;
• prohibited from practicing physical exercise performed lying on your back, including with tension in the abdominal muscles.

• It is recommended to rest lying on your left side or in a semi-sitting position;
• It is useful to use special pillows for pregnant women, which are placed under the back or between the legs when lying on your side. Changing body position helps prevent compression of the abdominal vessels by the uterus;
• To normalize venous outflow and improve hemodynamics, rational physical activity, especially walking. While walking, the muscles of the legs actively contract, which helps move venous blood upward;
• Exercises in water are useful. Water has a compression effect, squeezing blood out of the veins of the lower extremities;
• During childbirth, the preferred position is lying on the left side or with the head end of the bed raised high.

Diseases and treatment methods of the vein of Galen

Human veins in the brain are deep and superficial. Superficial - located in the pia mater of the brain and absorb blood from the cortex and white matter, and the deep veins are from the subcortical nodes, white matter of the hemispheres, ventricular walls and vascular plexuses. The vein of Galen is one of the veins of the head. The veins of the brain of the head, as a rule, are not accompanied by arteries.

• What is an aneurysm
• Prognosis and treatment
• Research methods
• Deep vein thrombosis of the brain
• Venous cerebral dystonia

Deep vessels pass deep into the brain, and superficial vessels pass along its surface. So, the deep vessels pass through the entire brain and then unite into one large vein - the vein of Galen. It is also commonly called the cisterns of Galen, which are combined with the inferior sagittal sinus, pass along the edge of the falx cerebri from below, uniting into the straight sinus.

The normal speed of blood flow in children under 1 year of age in the vein of Galen is 4–18 cm/s. There can be two veins of Galen various forms: mainline and loose. The first of them has a trunk length of 1.5-3 cm, and at least seven ducts. Vessels of this type of structure are most often found in individuals with a dolichocephalic skull. And the loose form of the trunk is much shorter (up to 0.2-0.3 cm), and has a larger number of ducts (up to 15).

This type of structure is quite often observed in brachycephalics. This vessel is located at a distance of 3-4 mm from the cerebral aqueduct. The vein of Galen has tributaries called:

• epiphysis vein;
• anterior superior vein passing through the cerebellum;
• internal vessels of the brain;
• posterior vein of the corpus callosum;
• Rosenthal vessels;
• medial vessels of the occipital region.

The vein of Galen has a length that varies depending on the shape of the head, and the frequency of occurrence of the tributaries of the vessel does not depend on this.

What is an aneurysm

The unborn child is still at the stage embryonic development There may be a failure in the development or underdevelopment of brain vessels, which is combined into a group of various congenital diseases. These include an aneurysm of the vein of Galen, which is presented in the form of various vascular malformations.

Arteriovenous malformations are “glomeruli” of various shapes and sizes that can form due to the interweaving of pathological vessels. Such vessels have different diameters, thin walls without certain layers. They consist of hyaline and collagen fibers.

Aneurysm of the vessels of the head

This pathology is quite rare and unique from huge size to multiple foci between the vein system and the cerebral vessels of the vertebrobasilar and carotid arteries. After describing a large number of clinical observations of this pathology, half of them were diagnosed in the prenatal period in the third trimester.

At the time of ultrasound examination, the pathology of the vessel is detected in the form of a median hypoechoic formation, which is localized above the tentorium of the cerebellum. If arterial turbulent and venous blood flow is detected in it, then this is considered the main criterion for making a diagnosis.

To fully clarify it, after the birth of the child, an MRI of his brain is performed, which makes it possible to determine the structure of the vascular bed and detect venous drainages.

In modified vessels there is no capillary network. Therefore, blood is pumped directly from the arteries to the system of superficial and deep veins. Thus, the blood passing into the hemispheres does not participate in the blood supply to the brain tissue, but occurs through arteriovenous malformations. This is the cause of the vein of Galen aneurysm.

Prognosis and treatment

An aneurysm is unfavorable diagnosis and death occurs in infancy during the neonatal period in more than 90% of cases. Most often observed in male fetuses. Treatment of such Galenic pathology is not easy, and is performed by embolization of the arteriovenous malformation.

Embolization is arterial and venous occlusion of a malformation. Even despite the successful operation, the risk of death is still at least 80%.

For precise setting diagnosis, it is very important to conduct prenatal diagnosis, which will certainly confirm or exclude an aneurysm. Children born with this diagnosis have symptoms of heart failure, but in some cases there may be no symptoms. Associated conditions may be:

• intracranial hemorrhage;
• cerebrovascular accident;
• epileptic syndrome;
• ischemia;
• delayed psychomotor development.

Research methods

The diagnosis occurs in the last three months of pregnancy after magnetic resonance imaging and ultrasound to determine the state of the fetal brain. In order to distinguish an aneurysm from a subarachnoid cyst and porencephaly, color Doppler mapping is performed. The blood flow through the vein of Galen normally has a pulsating-wavy character.

Deep vein thrombosis of the brain

The clinical picture of thrombus formation in the vein of Galen is particularly severe. The patient, as a rule, is in a state of coma with clearly expressed cerebral phenomena, signs of dysfunction of the trunks and subcortical structures. Symptoms of thrombosis:

• headaches;
• meningeal signs;
• nausea, vomiting;
• swelling of the tissue of the face and head;
• high temperature;
• increase in leukocytes in the blood;
• change of consciousness.

The severe course of the disease with damage to the vessel contributes to its hemorrhagic softening, therefore thrombosis is accompanied by extensive necrosis of the mediabasal parts of the brain in a state of coma. Vein thrombosis, as well as thrombophlebitis, can be complicated by encephalitis, meningitis with the addition of pus and abscess of the brain of the head.

Venous cerebral dystonia

The most pressing problem today is pathologies associated with cerebral vascular diseases. Recognition and timely treatment of perinatal cerebral disorders is relevant today. Thus, due to insufficient maturity of the newborn’s brain, errors in the diagnosis and interpretation of arterial and venous cerebrovascular accidents are possible.

During the neonatal period and the first year of life, active maturation and development of the brain occurs. But there is still no uniform method for early diagnosis brain disorders, treatment and subsequent rehabilitation of newborns. The study of changes in hemodynamics in the brain in children in the first year of life and newborns does not lose relevance and is very important for timely diagnosis, complications in the central nervous system and planning preventive measures and treatment.

The reasons that lead to disruption of the cerebral blood supply to the venous vessels in newborns and children under one year of age are intracerebral factors, including venous dystonia along with disorders of vascular autoregulation.

The vein of Galen may have increased or decreased blood flow with an altered nature of the venous curve, which indicates the presence of discirculation in the vessels. The pulsating nature of blood flow in a vein is a sign of a change in venous outflow.

Slowdown normal speed blood flow in the vein of Galen in combination with increased intracranial pressure up to 300 mmHg. and above is considered a poor prognosis for serious brain damage and the development of brain edema in patients with neurological complications.

By leaving a comment, you accept the User Agreement

• Arrhythmia
• Atherosclerosis
• Varicose veins
• Varicocele
• Haemorrhoids
• Hypertension
• Hypotension
• Diagnostics
• Dystonia
• Stroke
• Heart attack
• Ischemia
• Blood
• Operations
• Heart
• Vessels
• Angina pectoris
• Tachycardia
• Thrombosis and thrombophlebitis

• Heart tea
• Hypertension
• Pressure bracelet
• Normalife
• Allapinin
• Asparkam
• Detralex

Umbilical cord, or umbilical cord (funiculus umbilicalis), occurs when the ventral wall of the embryo closes and its body separates from the amnion and yolk sac. In this process, already described in previous chapters, the umbilical duct, the allantois outlet (urachus), the vessels formed in the allantois mesoderm (umbilical vessels), and the mesoderm of the embryonic trunk are compressed into an increasingly thinner cord, the surface of which is finally covered ectodermal epithelium of the amnion.

Thus, umbilical cord appears, cord connecting the placenta to the ventral wall of the fetal body; The umbilical cord contains umbilical cord vessels, which provide a connection between the fetal blood circulation and the capillary network of the placenta (chorion).

Umbilical duct and the urinary tract of the embryo in the second month of pregnancy becomes obliterated and then completely disappears, and therefore not a trace of them remains in the developed umbilical cord. In a similar way, at an early stage, the reverse development of the umbilical-mesenteric vessels occurs - the yolk vessels (vasa omphalomesenterica), which were first located in the area of ​​the yolk sac. Finally, the remainder of the yolk sac (vesicula umbilicalis) also disappears, which first remains for some time between the chorion in the area where the umbilical cord attaches to the placenta, and then also disappears.

Full-term human fetal umbilical cord It is a cord, 40-50 cm long with a diameter of approximately 1.5 cm. It lies between the inner (fetal) side of the placenta and the ventral wall of the fetal body. The surface of the umbilical cord is covered with the ectodermal epithelium of the amnion, which in the placenta imperceptibly passes into the amniotic ectoderm covering the inner surface of the placenta, and towards the fetus passes directly into the skin (epidermis) of the surface of the fetus or, rather, the newborn.

Place of attachment umbilical cord towards the ventral wall of the fetal body it has a ring-shaped shape (umbilicus, umbilicus). The basis of the umbilical cord stroma is formed by embryonic jelly-like tissue containing a relatively small number of cells, some fibrils and a significant amount of gelatinous ground substance (Wharton's jelly). Rudiments of the umbilical duct and urinary tract of the embryo in the full-term umbilical cord are usually absent.

In the stroma of the umbilical cord umbilical vessels pass through, namely one umbilical vein, initially laid in pairs, and two umbilical arteries. The umbilical vein (vena umbilicalis) carries oxygenated fetal blood from the capillary network of the chorionic villi of the placenta into the fetal body, while the two umbilical arteries drain oxygen-deprived blood into the placenta. At the site of attachment of the umbilical cord to the placenta, the umbilical vessels first branch in the chorionic membrane into fairly large branches that are visible through the amniotic membrane of the placenta.
Smaller branches of these branches then pass into the chorionic villi, forming a capillary network in them.

Return to the contents of the section " "

3. Immediate, main, background causes of perinatal mortality.

4. Maternal mortality: definition of the concept, structure, coefficient.

5. Organizational measures to reduce perinatal and maternal morbidity and mortality.

6. Critical periods in the development of the embryo and fetus.

7. The influence of unfavorable environmental factors and medications on the development of the embryo and fetus.

1. Medicines.

2. Ionizing radiation.

3. Bad habits in a pregnant woman.

8. Prenatal diagnosis of fetal malformations.

9. Intrauterine infection of the fetus: the effect on the fetus of viral and bacterial infections (influenza, measles, rubella, cytomegalovirus, herpes, chlamydia, mycoplasmosis, listeriosis, toxoplasmosis).

10. Fetoplacental insufficiency: diagnosis, correction methods, prevention.

11. Fetal hypoxia and asphyxia of the newborn: diagnosis, treatment, prevention, methods of resuscitation of newborns.

12. Fetal growth retardation syndrome: diagnosis, treatment, prevention.

13. Hemolytic disease of the fetus and newborn.

14. Special conditions of newborns.

15. Respiratory distress syndrome in newborns.

16. Birth trauma in newborns.

2. Birth injuries of the scalp.

3. Birth injuries to the skeleton.

5. Birth injuries of the peripheral and central nervous system.

17. Purulent-septic diseases of newborns.

18. Anatomical and physiological characteristics of full-term, premature and post-term newborns.

1. Afo of full-term children.

2. Afo of premature and post-term infants.

1. Fertilization. Early embryogenesis.

2. Development and functions of the placenta and amniotic fluid. The structure of the umbilical cord and placenta.

3. The fetus during certain periods of intrauterine development. Blood circulation of the intrauterine fetus and newborn.

4. The fetus as an object of birth.

5. The female pelvis from an obstetric point of view: structure, planes and dimensions.

6. Physiological changes in a woman’s body during pregnancy.

7. Hygiene and nutrition of pregnant women.

8. Physiopsychoprophylactic preparation of pregnant women for childbirth.

9. Determination of pregnancy and childbirth. Rules for registration of maternity leave.

10. Ultrasound examination.

11. Amniocentesis.

12. Amnioscopy.

13. Determination of α-fetoprotein.

14. Biophysical profile of the fetus and its assessment.

15. Electrocardiography and phonography of the fetus.

16. Cardiotocography.

18. Dopplerometry.

19. Diagnosis of early and late pregnancy.

20. Methods of examination of pregnant women, women in labor and postpartum women. Speculum and vaginal examination.

21. Reasons for the onset of labor.

22. Harbingers of childbirth.

23. Preliminary period.

24. Assessing the readiness of a woman’s body for childbirth.

2. Oxytocin test.

25. Induced labor.

26. Physiological course and management of labor by periods.

4. Postpartum period.

27. Biomechanism of labor in anterior and posterior occipital presentation.

28. Modern methods of labor pain relief.

29. Primary treatment of a newborn.

30. Assessment of the newborn using the Apgar scale.

31. Acceptable blood loss during childbirth: definition, diagnostic methods and prevention of bleeding during childbirth.

32. Principles of breastfeeding.

1. Optimal and balanced nutritional value.

2. High digestibility of nutrients.

3. The protective role of breast milk.

4. Influence on the formation of intestinal microbiocenosis.

5. Sterility and optimal temperature of breast milk.

6. Regulatory role.

7. Influence on the formation of the child’s maxillofacial skeleton.

Pathological obstetrics

1. Buttock presentation (flexion):

2. Leg presentation (extensor):

2. Transverse and oblique position of the fetus.

3. Extensor presentation of the fetal head: anterocephalic, frontal, facial.

4. Multiple pregnancy: clinical picture and diagnosis, management of pregnancy and childbirth.

5. Polyhydramnios and oligohydramnios: definition, etiology, diagnosis, treatment methods, complications, management of pregnancy and childbirth.

6. Large fetus in modern obstetrics: etiology, diagnosis, features of delivery.

7. Miscarriage. Spontaneous miscarriage: classification, diagnosis, obstetric tactics. Premature birth: features of the course and management.

8. Post-term and prolonged pregnancy: clinical picture, diagnostic methods, pregnancy management, course and management of labor, complications for the mother and fetus.

9. Diseases of the cardiovascular system: heart defects, hypertension. The course and management of pregnancy, timing and methods of delivery. Indications for termination of pregnancy.

10. Blood diseases and pregnancy (anemia, leukemia, thrombocytopenic purpura). Features of the course and management of pregnancy and childbirth.

11. Diabetes mellitus and pregnancy. The course and management of pregnancy, timing and methods of delivery. Indications for termination of pregnancy. Effect on the fetus and newborn.

13. High-risk pregnancy with diseases of the nervous system, respiratory system, myopia. Features of childbirth. Prevention of possible complications in mother and fetus.

14. Sexually transmitted diseases: herpes, chlamydia, bacterial vaginosis, cytomegalovirus, candidiasis, gonorrhea, trichomoniasis.

15. Infectious diseases: viral hepatitis, influenza, measles, rubella, toxoplasmosis, syphilis.

16. Acute surgical pathology: acute appendicitis, intestinal obstruction, cholecystitis, pancreatitis.

17. Pathology of the reproductive system: uterine fibroids, ovarian tumors.

18. Features of pregnancy and childbirth in women over 30 years of age.

19. Pregnancy and childbirth in women with an operated uterus.

20. Early and late gestosis. Etiology. Pathogenesis. Clinical picture and diagnosis. Treatment. Methods of delivery, features of labor management. Prevention of severe forms of gestosis.

21. Atypical forms of gestosis - non-llp syndrome, acute yellow liver dystrophy, cholestatic hepatosis of pregnant women.

23. Anomalies of labor: etiology, classification, diagnostic methods, management of labor, prevention of anomalies of labor.

I. Bleeding not associated with the pathology of the ovum.

II. Bleeding associated with pathology of the ovum.

1. Hypo- and atonic bleeding.

Stage I:

Stage II:

4. Placenta accreta.

25. Birth trauma in obstetrics: ruptures of the uterus, perineum, vagina, cervix, pubic symphysis, hematoma. Etiology, classification, clinic, diagnostic methods, obstetric tactics.

26. Disorders of the hemostasis system in pregnant women: hemorrhagic shock, disseminated intravascular coagulation syndrome, amniotic fluid embolism.

Stage I:

Stage II:

Stage III:

27. Caesarean section: indications, contraindications, conditions, surgical technique, complications.

28. Obstetric forceps: indications, contraindications, conditions, surgical technique, complications.

29. Vacuum extraction of the fetus: indications, contraindications, conditions, surgical technique, complications.

30. Fruit-destroying operations: indications, contraindications, conditions, surgical technique, complications.

31. Termination of pregnancy in early and late stages: indications and contraindications, methods of termination, complications. Infected abortion.

2. Ovarian dysfunction with menstrual irregularities

32. Postpartum purulent-septic diseases: chorioamnionitis, postpartum ulcer, postpartum endometritis, postpartum mastitis, sepsis, infectious-toxic shock, obstetric peritonitis.

1. Periods of a woman’s life, fertile age.

2. Anatomical and physiological features of the female reproductive system.

3. Biological protective function of the vagina. The importance of determining the degree of vaginal cleanliness.

4. Menstrual cycle and its regulation.

5. General and special methods of objective research. Main symptoms of gynecological diseases.

3. Gynecological examination: external, using vaginal speculum, two-handed (vaginal and rectal).

4.1. Cervical biopsy: targeted, cone-shaped. Indications, technique.

4.2. Puncture of the abdominal cavity through the posterior vaginal fornix: indications, technique.

4.3. Separate diagnostic curettage of the cervical canal and uterine cavity: indications, technique.

5. X-ray methods: metrosalpingography, bicontrast genicography. Indications. Contraindications. Technique.

6. Hormonal studies: (functional diagnostic tests, determination of hormone levels in the blood and urine, hormonal tests).

7. Endoscopic methods: hysteroscopy, laparoscopy, colposcopy.

7.1. Colposcopy: simple and extended. Microcolposcopy.

8. Ultrasound diagnostics

6. Main symptoms of gynecological diseases:

7. Features of gynecological examination of girls.

8. Basic physiotherapeutic methods in the treatment of gynecological patients. Indications and contraindications for their use.

9. Amenorrhea.

1. Primary amenorrhea: etiology, classification, diagnosis and treatment.

2. Secondary amenorrhea: etiology, classification, diagnosis and treatment.

3. Ovarian:

3. Hypothalamic-pituitary form of amenorrhea. Diagnosis and treatment.

4. Ovarian and uterine forms of amenorrhea: diagnosis and treatment.

10. Algodysmenorrhea: etiopathogenesis, clinical picture, diagnosis and treatment.

11. Dysfunctional uterine bleeding at different age periods of a woman’s life

1. Juvenile bleeding.

2. Dysfunctional uterine bleeding during the reproductive period.

3. Dysfunctional uterine bleeding during menopause.

4. Ovulatory dysfunctional uterine bleeding.

I. Irregular menstruation

II. Violation of the amount of lost menstrual blood:

III. Irregular menstruation

IV. Intermenstrual DMC

5. Anovulatory dysfunctional uterine bleeding.

12. Premenstrual syndrome: etiopathogenesis, clinical picture, diagnosis and treatment.

13. Menopausal syndrome: risk factors, classification, clinical picture and diagnosis. Principles of hormone replacement therapy.

14. Post-castration syndrome (post-variectomy). Principles of correction.

15. Polycystic ovary syndrome (Stein-Leventhal syndrome). Classification. Etiology and pathogenesis. Clinic, treatment and prevention.

16. Hypomenstrual syndrome.

17. Endometritis.

18. Salpingo-oophoritis.

19. Pelvioperitonitis: etiopathogenesis, clinical course, basics of diagnosis and treatment.

20. Infectious-toxic shock: etiopathogenesis, clinical course. Principles of diagnosis and treatment.

21. Features of the treatment of inflammatory diseases of the pelvic organs in the chronic stage.

22. Trichomoniasis: clinical course, diagnosis and treatment. Criteria for cure.

23. Chlamydial infection: clinical picture, diagnosis and treatment.

24. Bacterial vaginosis: etiology, clinical picture, diagnosis and treatment.

25. Myco- and ureaplasmosis: clinical picture, diagnosis, treatment.

26. Genital herpes: clinical picture, diagnosis, treatment. Basics of prevention.

27. Human papillomavirus infection: clinical picture, diagnosis, treatment. Basics of prevention.

28. HIV infection. Routes of transmission, diagnosis of AIDS. Prevention methods. Effect on the reproductive system.

2. Asymptomatic stage of HIV infection

29. Gonorrhea – clinical picture, diagnostic methods, treatment, cure criteria, prevention.

1. Gonorrhea of ​​the lower genital tract

30. Tuberculosis of the female genital organs - clinical picture, diagnostic methods, treatment, prevention, impact on the reproductive system.

31. Background and precancerous diseases of the female genital organs: classification, etiology, diagnostic methods, clinical picture, treatment, prevention.

32. Endometriosis: etiology, classification, diagnostic methods, clinical symptoms, principles of treatment, prevention.

33. Uterine fibroids.

1. Conservative treatment of uterine fibroids.

2. Surgical treatment.

34. Tumors and tumor-like formations of the ovaries.

1. Benign tumors and tumor-like formations of the ovaries.

2. Metastatic ovarian tumors.

35. Hormone-dependent diseases of the mammary glands.

I) diffuse fcm:

II) nodal fcm.

36. Trophoblastic disease (hydatidiform mole, choriocarcinoma).

37. Cervical cancer.

38. Cancer of the uterine body.

39. Ovarian cancer.

40. Ovarian apoplexy.

41. Torsion of the pedicle of an ovarian tumor.

42. Malnutrition of the subserous node with uterine fibroids, birth of a submucosal node (see Question 17 in the “Pathological Obstetrics” section and Question 33 in the “Gynecology” section).

43. Differential diagnosis of acute surgical and gynecological pathology.

1) Questioning:

2) Examination of the patient and objective examination

4) Laboratory research methods:

44. Causes of intra-abdominal bleeding in gynecology.

45. Ectopic pregnancy: etiology, classification, diagnosis, treatment, prevention.

1. Ectopic

2. Abnormal variants of the uterine

46. ​​Infertility: types of infertility, causes, examination methods, modern treatment methods.

47. Family planning: birth control, means and methods of contraception, abortion prevention.

2. Hormonal agents

48. Infertile marriage. Algorithm for examining a married couple with infertility.

49. Preoperative preparation of gynecological patients.

50. Postoperative management of gynecological patients.

51. Complications in the postoperative period and their prevention.

52. Typical gynecological operations for prolapse and prolapse of the genital organs

53. Typical gynecological operations on the vaginal part of the cervix, on the uterus and uterine appendages.

3. Organ-preserving (plastic surgery on the appendages).

4. Plastic surgery on pipes.

I. Organ-preserving operations.

2. Removal of submucous uterine myomatous nodes transvaginally.

1. Supravaginal amputation of the uterus without appendages:

3. Extirpation of the uterus without appendages:

54. Prevention of thromboembolic complications in risk groups.

55. Infusion-transfusion therapy for acute blood loss. Indications for blood transfusion.

56. Hyperplastic processes of the endometrium.

1. Assessment of the physical and sexual development of children and adolescents (morphogram, sex formula).

2. Anomalies in the development of the genital organs. Incorrect positions of the genital organs.

3. Premature and early puberty. Delay and lack of sexual development.

4. Genital infantilism.

8. Inflammatory diseases of the reproductive system in girls and adolescent girls: etiology, predisposing factors, localization features, diagnosis, clinic, principles of treatment, prevention.

9. Ovarian tumors in childhood and adolescence.

10. Injuries to the genital organs: medical care, forensic medical examination.

2. Development and functions of the placenta and amniotic fluid. The structure of the umbilical cord and placenta.

Placenta.

The human placenta has a hemochorial type of structure - the presence of direct contact of maternal blood with the chorion due to a violation of the integrity of the decidua of the uterus with the opening of its vessels.

Development of the placenta. The main part of the placenta is chorionic villi - derivatives of trophoblast. At the early stages of ontogenesis, the trophoblast forms protoplasmic outgrowths consisting of cytotrophoblast cells - primary villi. Primary villi do not have blood vessels, and the supply of nutrients and oxygen to the fetal body from the surrounding maternal blood occurs according to the laws of osmosis and diffusion. By the end of the 2nd week of pregnancy, connective tissue grows into the primary villi and secondary villi are formed. Their basis is connective tissue, and the outer cover is represented by epithelium - trophoblast. Primary and secondary villi are evenly distributed over the surface of the fertilized egg.

The epithelium of secondary villi consists of two layers:

a) cytotrophoblast (Langhans layer)- consists of round-shaped cells with light cytoplasm, large cell nuclei.

b) syncytium (symplast)- cell boundaries are practically indistinguishable, the cytoplasm is dark, granular, with a brush border. The kernels are relatively small in size, spherical or oval.

From the 3rd week of embryo development, a very important process of placental development begins, which consists of vascularization of the villi and their transformation into tertiary ones containing vessels. The formation of placental vessels occurs both from the angioblasts of the embryo and from the umbilical vessels growing from the allantois.

The vessels of the allantois grow into the secondary villi, as a result of which each secondary villi receives vascularization. The establishment of allantoic blood circulation ensures intensive exchange between the organisms of the fetus and mother.

On early stages During intrauterine development, chorionic villi evenly cover the entire surface of the fetal egg. However, starting from the 2nd month of ontogenesis, the villi on the larger surface of the fetal egg atrophy, while at the same time villi develop, facing the basal part of the decidua membrane. This is how a smooth and branched chorion is formed.

At a gestational age of 5-6 weeks, the thickness of the syncytiotrophoblast exceeds the thickness of the Langhans layer, and, starting from a period of 9-10 weeks, the syncytiotrophoblast gradually becomes thinner and the number of nuclei in it increases. On the free surface of the syncytiotrophoblast, facing the intervillous space, long thin cytoplasmic projections (microvilli) become clearly visible, which significantly increase the resorption surface of the placenta. At the beginning of the second trimester of pregnancy, an intensive transformation of cytotrophoblast into syncytium occurs, as a result of which Langhans’ layer completely disappears in many areas.

At the end of pregnancy, involution-dystrophic processes begin in the placenta, which are sometimes called placental aging. Fibrin (fibrinoid) begins to fall out of the blood circulating in the intervillous space, which is deposited mainly on the surface of the villi. The loss of this substance promotes the processes of microthrombosis and the death of individual sections of the epithelial cover of the villi. Villi coated with fibrinoid are largely excluded from the active exchange between the organisms of the mother and fetus.

There is a pronounced thinning of the placental membrane. The villous stroma becomes more fibrous and homogeneous. Some thickening of the capillary endothelium is observed. Lime salts are often deposited in areas of dystrophy. All these changes affect the functions of the placenta.

However, along with the processes of involution, there is an increase in young villi, which largely compensate for the function of the lost ones, but they only partially improve the function of the placenta as a whole. As a result, at the end of pregnancy there is a decrease in placental function.

The structure of the mature placenta. Macroscopically, the mature placenta closely resembles a thick, soft cake. The weight of the placenta is 500-600 g, the diameter is 15-18 cm, the thickness is 2-3 cm. The placenta has two surfaces:

a) maternal - facing the wall of the uterus - the placenta is grayish-red in color and represents the remains of the basal part of the decidua.

b) fruit - facing the fetus - covered with a shiny amniotic membrane, under which the vessels coming from the place of attachment of the umbilical cord to the periphery of the placenta approach the chorion.

The main part of the fetal placenta is represented by numerous chorionic villi, which are combined into lobular formations - cotyledons, or lobules– the main structural and functional unit of the formed placenta. Their number reaches 15-20. Placental lobules are formed as a result of the division of chorionic villi by partitions (septa) emanating from the basal plate. Each of these lobules has its own large vessel.

Microscopic structure of mature villi. Distinguish two types of lint:

a) free - immersed in the intervillous space of the decidua and “float” in the maternal blood.

b) securing (anchor) - attached to the basal decidua and ensure fixation of the placenta to the wall of the uterus. In the third stage of labor, the connection of such villi with the decidua is disrupted and, under the influence of uterine contractions, the placenta is separated from the uterine wall.

When studying the structure of mature villi microscopically, the following formations are differentiated:

Syncytium without clear cellular boundaries;

Layer (or remains) of cytotrophoblast;

Villous stroma;

The endothelium of the capillary, in the lumen of which elements of fetal blood are clearly visible.

Uteroplacental circulation. The blood flow of both mother and fetus is separated by the following structural units of chorionic villi:

Epithelial layer (syncytium, cytotrophoblast);

Villous stroma;

Endothelium of capillaries.

Blood flow in the uterus is carried out with the help of 150-200 maternal spiral arteries, which open into the vast intervillous space. The walls of the arteries are devoid of muscle layer, and the mouths are not able to contract and expand. They have low vascular resistance to blood flow. All these hemodynamic features are of great importance in ensuring uninterrupted transport of arterial blood from the mother’s body to the fetus. The overflowing arterial blood washes the chorionic villi, releasing oxygen, essential nutrients, many hormones, vitamins, electrolytes and other chemicals, as well as microelements necessary for the fetus for its proper growth and development, into the fetal blood. Blood containing CO 2 and other products of fetal metabolism is poured into the venous openings of the maternal veins, total number which exceeds 180. Blood flow in the intervillous space at the end of pregnancy is quite intense and averages 500-700 ml of blood per minute.

Features of blood circulation in the maternal system- placenta- fetus. The arterial vessels of the placenta, after leaving the umbilical cord, are divided radially in accordance with the number of placental lobes (cotyledons). As a result of further branching of the arterial vessels in the terminal villi, a network of capillaries is formed, the blood from which collects in the venous system. The veins in which arterial blood flows collect into larger venous trunks and flow into the umbilical cord vein.

Blood circulation in the placenta is maintained by the heartbeats of the mother and fetus. An important role in the stability of this blood circulation also belongs to the mechanisms of self-regulation of the uteroplacental circulation.

Basic functions of the placenta. The placenta performs the following main functions: respiratory, excretory, trophic, protective and incretory. It also performs the functions of antigen production and immune protection. The membranes and amniotic fluid play a major role in the implementation of these functions.

1. Respiratory function. Gas exchange in the placenta is carried out by the penetration of oxygen to the fetus and the removal of CO 2 from its body. These processes are carried out according to the laws of simple diffusion. The placenta does not have the ability to accumulate oxygen and CO 2, so their transport occurs continuously. The exchange of gases in the placenta is similar to that in the lungs. Amniotic fluid and paraplacental exchange play a significant role in the removal of CO 2 from the fetal body.

2. Trophic function. Fetal nutrition is carried out by transporting metabolic products through the placenta.

Squirrels. The state of protein metabolism in the mother-fetus system is determined by the protein composition of the mother’s blood, the state of the protein-synthesizing system of the placenta, enzyme activity, hormone levels and a number of other factors. The content of amino acids in the blood of the fetus is slightly higher than their concentration in the blood of the mother.

Lipids. Transport of lipids (phospholipids, neutral fats, etc.) to the fetus occurs after their preliminary enzymatic breakdown in the placenta. Lipids penetrate to the fetus in the form of triglycerides and fatty acids.

Glucose. It passes through the placenta according to the mechanism of facilitated diffusion, so its concentration in the fetal blood may be higher than in the mother. The fetus also uses liver glycogen to produce glucose. Glucose is the main nutrient for the fetus. It also plays a very important role in the processes of anaerobic glycolysis.

Water. A large amount of water passes through the placenta to replenish the extracellular space and the volume of amniotic fluid. Water accumulates in the uterus, tissues and organs of the fetus, placenta and amniotic fluid. During physiological pregnancy, the amount of amniotic fluid increases daily by 30-40 ml. Water is necessary for proper metabolism in the uterus, placenta and in the fetus. Water transport can occur against a concentration gradient.

Electrolytes. Electrolyte exchange occurs transplacentally and through the amniotic fluid (paraplacental). Potassium, sodium, chlorides, bicarbonates freely penetrate from mother to fetus and in the opposite direction. Calcium, phosphorus, iron and some other trace elements can be deposited in the placenta.

Vitamins. Vitamin A and carotene are deposited in the placenta in significant quantities. In the fetal liver, carotene is converted into vitamin A. B vitamins accumulate in the placenta and then, binding to phosphoric acid, pass to the fetus. The placenta contains a significant amount of vitamin C. In the fetus, this vitamin accumulates in excess in the liver and adrenal glands. The content of vitamin D in the placenta and its transport to the fetus depend on the content of the vitamin in the mother’s blood. This vitamin regulates the metabolism and transport of calcium in the mother-fetus system. Vitamin E, like vitamin K, does not cross the placenta.

3. Endocrine function. During the physiological course of pregnancy, there is a close connection between the hormonal status of the maternal body, the placenta and the fetus. The placenta has a selective ability to transfer maternal hormones. Hormones with a complex protein structure (somatotropin, thyroid-stimulating hormone, ACTH, etc.) practically do not cross the placenta. The penetration of oxytocin through the placental barrier is prevented by the high activity of the enzyme oxytocinase in the placenta. Steroid hormones have the ability to cross the placenta (estrogens, progesterone, androgens, glucocorticoids). Maternal thyroid hormones also penetrate the placenta, but the transplacental transition of thyroxine occurs more slowly than triiodothyronine.

Along with its function of transforming maternal hormones, the placenta itself transforms during pregnancy into a powerful endocrine organ that ensures optimal hormonal homeostasis in both mother and fetus.

One of the most important placental hormones of protein nature is placental lactogen (PL). In its structure, PL is close to the growth hormone of the adenohypophysis. The hormone enters almost entirely into the maternal bloodstream and takes an active part in carbohydrate and lipid metabolism. In the blood of a pregnant woman, PL begins to be detected very early - from the 5th week, and its concentration progressively increases, reaching a maximum at the end of gestation. PL practically does not penetrate to the fetus, and is contained in amniotic fluid in low concentrations. This hormone plays an important role in the diagnosis of placental insufficiency.

Another placental hormone of protein origin is human chorionic gonadotropin (XG). HCG in the mother's blood is detected in the early stages of pregnancy, the maximum concentrations of this hormone are observed in 8-10 weeks of pregnancy. Passes to the fetus in limited quantities. Hormonal pregnancy tests are based on the determination of hCG in the blood and urine: immunological reaction, Aschheim-Tsondeka reaction, hormonal reaction in male frogs .

The placenta, along with the pituitary gland of the mother and fetus, produces prolactin. The physiological role of placental prolactin is similar to that of the pituitary gland.

Estrogens (estradiol, estrone, estriol) are produced by the placenta in increasing quantities, with the highest concentrations of these hormones observed before childbirth. About 90% of placental estrogens are estriol. Its content reflects not only the function of the placenta, but also the condition of the fetus.

An important place in the endocrine function of the placenta belongs to the synthesis progesterone. The production of this hormone begins in the early stages of pregnancy, but during the first 3 months the main role in the synthesis of progesterone belongs to the corpus luteum and only then does the placenta take on this role. From the placenta, progesterone enters mainly into the maternal bloodstream and to a much lesser extent into the fetal bloodstream.

The placenta produces a glucocorticoid steroid cortisol This hormone is also produced in the fetal adrenal glands, so the concentration of cortisol in the mother's blood reflects the condition of both the fetus and the placenta (fetoplacental system).

4. Barrier function of the placenta. The concept of “placental barrier” includes the following histological formations: syncytiotrophoblast, cytotrophoblast, layer of mesenchymal cells (villous stroma) and fetal capillary endothelium. Characterized by the transition of various substances in two directions. The permeability of the placenta is variable. During physiological pregnancy, the permeability of the placental barrier progressively increases until the 32-35th week of pregnancy, and then decreases slightly. This is due to the structural features of the placenta at different stages of pregnancy, as well as the needs of the fetus for certain chemical compounds. The limited barrier functions of the placenta in relation to chemicals that accidentally enter the mother’s body are manifested in the fact that toxic chemical products, most medications, nicotine, alcohol, pesticides, infectious agents, etc. pass through the placenta relatively easily. The barrier functions of the placenta are most fully manifested only under physiological conditions, i.e. during uncomplicated pregnancy. Under the influence of pathogenic factors (microorganisms and their toxins, sensitization of the mother’s body, the effects of alcohol, nicotine, drugs), the barrier function of the placenta is disrupted, and it becomes permeable even to substances that, under normal physiological conditions, pass through it in limited quantities.

Amniotic fluid.

Amniotic fluid, or amniotic fluid, is a biologically active medium surrounding the fetus. The amniotic sac appears in the 8th week of pregnancy as a derivative of the embryoblast. Subsequently, as the fetus grows and develops, there is a progressive increase in the volume of the amniotic cavity due to the accumulation of amniotic fluid in it.

Amniotic fluid is mainly a filtrate of the mother's blood plasma. The secretion of the amniotic epithelium also plays an important role in its formation. At later stages of intrauterine development, the kidneys and lung tissue of the fetus take part in the production of amniotic fluid.

The volume of amniotic fluid depends on the stage of pregnancy. The increase in volume occurs unevenly. At 10 weeks of pregnancy, the volume of amniotic fluid averages 30 ml, at 13-14 weeks - 100 ml, at 18 weeks - 400 ml, etc. The maximum volume is observed at 37-38 weeks of pregnancy, averaging 1000-1500 ml. By the end of pregnancy, the amount of water may decrease to 800 ml. During postterm pregnancy (41-42 weeks), a decrease in the volume of amniotic fluid is observed (less than 800 ml).

Amniotic fluid is characterized by a high rate of exchange. During a full-term pregnancy, about 500 ml of water is exchanged within 1 hour. A complete exchange of amniotic fluid occurs on average in 3 hours. During the exchange process, 1/3 of the amniotic fluid passes through the fetus, which swallows approximately 20 ml of water in 1 hour. In the third trimester of pregnancy, as a result of the respiratory movements of the fetus, 600-800 diffuses through its lungs ml of liquid per day. Until 24 weeks of pregnancy, the exchange of amniotic fluid also occurs through the skin of the fetus, and later, when keratinization of the epidermis occurs, the fetal skin becomes almost impermeable to the liquid medium.

The fetus not only absorbs the liquid environment around it, but is itself the source of its formation. At the end of pregnancy, the fetus produces about 600-800 ml of urine per day. Fetal urine is an important component of amniotic fluid.

The exchange of amniotic fluid occurs through the amnion and chorion. An important role in water exchange belongs to the so-called paraplacental pathway, i.e. through the extraplacental part of the membranes.

At the beginning of pregnancy, amniotic fluid is a colorless transparent liquid, which subsequently changes its appearance and properties. From transparent, it becomes cloudy due to the ingress of secretions from the sebaceous glands of the fetal skin, vellus hairs, scales of desquamated epithelium, droplets of fat and some other substances.

From a chemical point of view, amniotic fluid is a colloidal solution of a complex chemical composition. The acid-base composition of amniotic fluid changes during pregnancy. It should be noted that the pH of the amniotic fluid correlates with the pH of the fetal blood.

Amniotic fluid contains oxygen and CO 2 in dissolved form; it contains all the electrolytes that are present in the blood of the mother and fetus. Proteins, lipids, carbohydrates, hormones, enzymes, various biologically active substances, and vitamins are also found in amniotic fluid. The detection of phospholipids in the amniotic fluid, which are part of the surfactant, is of important diagnostic importance. For a physiologically occurring full-term pregnancy, the optimal ratio between the concentration of lecithin and sphingomyelin in water is 2 (the lecithin concentration is 2 times higher than the sphingomyelin concentration). This ratio of these chemical agents is typical for a fetus with mature lungs. Under these conditions, they easily straighten during the first extrauterine breath, thereby ensuring the establishment of pulmonary respiration.

Determining the concentration of a-fetoprotein in the amniotic fluid is also important diagnostic value. This protein is produced in the fetal liver and then enters the amniotic fluid along with urine. A high concentration of this protein indicates fetal developmental abnormalities, mainly in the nervous system.

Along with this, the determination of creatinine content in amniotic fluid, which reflects the degree of maturity of the fetal kidneys, has a known diagnostic value.

Amniotic fluid contains factors that affect the blood coagulation system. These include thromboplastin, fibrinolysis, and factors X and XIII. In general, amniotic fluid has relatively high coagulating properties.

Amniotic fluid also performs an important mechanical function. They create conditions for free movements of the fetus, protect the fetal body from adverse external influences, and protect the umbilical cord from compression between the fetal body and the walls of the uterus. The amniotic sac contributes to the physiological course of the first stage of labor.

Umbilical cord.

Umbilical cord(umbilical cord). It is formed from the amniotic leg, which connects the embryo with the amnion and chorion. The allantois, which carries fetal vessels, grows into the amniotic leg from the endoderm of the hindgut of the embryo. The umbilical cord rudiment includes remnants of the vitelline duct and yolk sac. In the third month of intrauterine development, the yolk sac ceases to function as a hematopoietic and circulatory organ, is reduced and remains in the form of a small cystic formation at the base of the umbilical cord. The allantois completely disappears in the fifth month of intrauterine life.

In the early stages of ontogenesis, the umbilical cord contains 2 arteries and 2 veins. Subsequently, both veins merge into one. The umbilical cord vein carries arterial blood from the placenta to the fetus, and the arteries carry venous blood from the fetus to the placenta. The vessels of the umbilical cord have a tortuous course, so the umbilical cord seems to be twisted along its length.

The vessels of the umbilical cord are surrounded by a gelatinous substance (Wharton's jelly), which contains large amounts of hyaluronic acid. Cellular elements are represented by fibroblasts, mast cells, histiocytes, etc. The walls of the arteries and veins of the umbilical cord have different permeability, which ensures the peculiarities of metabolism. Wharton's jelly provides elasticity to the umbilical cord. It not only fixes the vessels of the umbilical cord and protects them from compression and injury, but also plays the role of vasa vasorum, providing nutrition to the vascular wall, and also carries out the exchange of substances between fetal blood and amniotic fluid. Nerve trunks and nerve cells are located along the vessels of the umbilical cord, so compression of the umbilical cord is dangerous not only from the point of view of disrupting the hemodynamics of the fetus, but also in terms of the occurrence of negative neurogenic reactions.

There are several options for attaching the umbilical cord to the placenta. In some cases it is attached in the center of the placenta - central attachment, in others - on the side - side attachment. Sometimes the umbilical cord is attached to the membranes without reaching the placenta itself - umbilical cord attachment. In these cases, the umbilical cord vessels approach the placenta between the membranes.

The length and thickness of the umbilical cord change during intrauterine development. In a full-term pregnancy, the length of the umbilical cord on average corresponds to the length of the fetus (50 cm). An excessively short (3540 cm) and very long umbilical cord can pose a danger to the fetus.

Afterbirth.

The placenta consists of the placenta, membranes and umbilical cord. The placenta is expelled in the third stage of labor after the birth of the child.

The site provides background information for informational purposes only. Diagnosis and treatment of diseases must be carried out under the supervision of a specialist. All drugs have contraindications. Consultation with a specialist is required!

Umbilical cord- This is an organ in the form of a long thin tube that connects the fetus with the mother’s body.

Functions, structure, blood circulation

The formation of the organ begins in the second week of gestation; as the fetus grows, the umbilical cord also increases.
The length of this organ can reach 60 centimeters, diameter 2 centimeters. The surface is covered with special membranes. This tube is quite dense, it feels like a dense hose.

Since the main function of the organ is to supply the fetus with nutrients and remove metabolic products, its basis is blood vessels: 2 arteries and a vein. Initially, 2 veins are formed, but during fetal development one of them closes. The vessels are very well protected from pinching and rupture. They are enveloped in a shell of a thick jelly-like substance called Wharton's jelly. The same substance has the function of transferring certain substances from the fetal blood into the amniotic fluid.

Arterial blood, rich in nutrients and oxygen, flows through the vein to the fetus; through the arteries, already used venous blood is drained from the fetus’s body to the placenta, which performs the purification function ( the fetal liver is not yet able to cope with this work). In the fetus before birth, 240 ml of blood per minute passes through the arteries, in the fetus at the twentieth week - only 35 ml per minute.

In addition to the above elements, the umbilical cord contains:

• Vitelline duct– it carries nutrients from the yolk sac to the embryo,
• Urachus– connecting channel between the placenta and bladder.

Umbilical cord blood test (cordocentesis)

The procedure is carried out under ultrasound control. A thick needle is used to pierce the umbilical cord where it attaches to the placenta and a blood sample is taken.

The procedure is performed for diagnostic purposes if:

• Hereditary neutropenia,
• Chronic granulomatosis,
• Mixed immunodeficiency.

Most often, this analysis is prescribed in cases where an ultrasound examination in late gestation reveals developmental disorders. In such cases, it is necessary to carry out a karyotype analysis ( set of chromosomes) fruit. Using special analysis methods, the result can be obtained within two to three days after blood sampling.

A few years ago, cordocentesis ( fetal cord blood test) was used to determine hemophilia, thalassemia, hemoglobinopathy, Down syndrome. Today, for these purposes, amniotic fluid analysis is used, as well as chorionic villus biopsy ( BVH).

After childbirth

In order for blood to flow normally through the vessels of the umbilical cord, it is necessary to maintain a certain level of hormones in the Wharton jelly. During childbirth, the amount of oxytocin- a hormone that provokes labor. The vessels contract and the blood flow stops - organ atrophy begins, which occurs for several hours after the birth of the child.
Already 15 minutes after the birth of the baby, blood circulation in the umbilical cord stops ( if childbirth takes place without pathology). In this process, the temperature of the medium also plays a certain role - when cooling, the vessels also contract.

How and when is it cut?

After the baby is born, the umbilical cord is clamped on both sides with special clamps, after which it is cut.
Today there is a lot of debate about how quickly a baby’s umbilical cord should be cut: immediately after birth or after it stops pulsating.
In America and Europe, this procedure is carried out within 30 - 60 seconds after the birth of the baby. There is an opinion that the baby does not receive cord blood, which is very useful for him, and may develop anemia.

American scientists conducted a study that proves that cutting done a little later reduces the likelihood of developing sepsis. respiratory diseases, respiratory diseases, anemia, cerebral hemorrhage, and visual impairment.

According to research by specialists from the World Health Organization, within 60 seconds after birth, 80 ml of blood from the placenta enters the baby’s body, and after another 2 minutes – 100 ml. This is an additional source of iron for a newborn, sufficient to provide the baby with this element for a whole year!
The term “late” cutting by specialists means cutting 2 to 3 minutes after birth. This should not be confused with some practices of savage tribes that leave the umbilical cord uncut at all ( after a few days it dries up on its own). As for cutting after the complete cessation of pulsation or 5 minutes after birth, such babies often experience functional jaundice. Therefore, everything is good in moderation.

In newborns

The remainder of the cut umbilical cord dries out quite quickly and falls off on its own after a few days.
A small wound remains at the site of its attachment. You need to take special care of it and then the wound will heal without problems.

Usually, daily treatment of the navel area with brilliant green, hydrogen peroxide, and do not wet it until the remainder of the umbilical cord falls off is enough. You should also let your navel “breathe” for a minute while changing the diaper.

But sometimes wound healing is complicated. Doctor's help required:

• If the body around the wound is swollen and red,
• If a foul-smelling, pus-like liquid leaks from the wound.

It is normal if a little ichor is released from the wound before complete healing.

Ultrasound

During an ultrasound examination, parameters such as:

• The junction of the placenta and the umbilical cord,
• The junction of the umbilical cord and the abdominal wall of the fetus,
• The presence of a normal number of arteries and veins.

The study allows you to detect expansion of the umbilical ring, single artery syndrome ( often combined with congenital heart defects and other genetic disorders), entanglement around the neck, cysts.

Doppler measurements can detect circulatory disorders in the vessels of the placenta and in the fetal body.

entwinement

Causes of pathology:

• Periodic stress,
• Lack of oxygen.

In the first case, an increased amount of adrenaline enters the fetus’s body, causing it to actively move.
In the second case, the lack of oxygen causes discomfort to the fetus, which also forces it to move more, increasing blood circulation and thereby receiving more oxygen.
The child may become entangled in the umbilical cord and unravel after a while. That's why this state is not always dangerous.
Entanglement can be detected using ultrasound from the fifteenth week of gestation. In order to determine how much the baby’s body is being compressed, Doppler testing is done. In the event that there is a possibility oxygen starvation, the examination is carried out more than once.

How to prevent entanglement?

• Spend more time in the fresh air, walk, do light exercises,
• Avoid stress
• Do special breathing exercises,
• Visit a gynecologist on time and undergo all necessary examinations.

Long or short

Violation of the length of the umbilical cord is the most common anomaly of the organ. The norm is 50 centimeters, that is, approximately the body length of a newborn baby.
More often, the umbilical cord is too long - 70 or even 80 centimeters. With such a length, there is a possibility of part of the umbilical cord falling out during the outpouring of water ( if breech presentation is observed). Also, an umbilical cord that is too long can cause it to become wrapped around the neck. But there is no evidence that length affects the likelihood of entanglement. If the loops are not wrapped tightly, then the birth can proceed normally, and there is no danger to the baby’s life.

If the length of the umbilical cord is less than 40 centimeters, and sometimes even up to 10 centimeters, they speak of shortening. With such a short umbilical cord, there is a high probability of fetal malposition. A short umbilical cord can create tight loops around your baby's neck. In addition, during childbirth it is more difficult for the baby to roll over and pass through the birth canal. With strong tension, there is a possibility of placental abruption.

False and true nodes

True node is formed in the first weeks of gestation. During this period, the fetus is still very small and its active movement causes “tangling” of the umbilical cord.
Such a knot poses a danger during childbirth, since as the fetus passes through the birth canal, the knot may tighten and the fetus will begin to suffocate. If the baby is not born very quickly, it may die. This happens ten percent of the time.

False knot– this is an increase in the diameter of the umbilical cord.

Reasons:

• Varicose veins,
• Tortuosity of blood vessels,
• Displacement of Wharton's jelly.

This is a harmless condition that does not in any way interfere with the normal development of the fetus and childbirth.

Hernia

This is a fairly rare disorder of fetal development. With a hernia, some internal organs of the fetus develop under the umbilical cord membrane. More often this happens with the intestines. This disorder is usually detected by ultrasound examination. However, sometimes it is very minor. In such cases, there is a danger of organ injury during cutting of the umbilical cord. Therefore, before cutting, the obstetrician must very carefully examine the navel area and the part of the umbilical cord located in close proximity to the baby’s body.
Very often, such a disorder is combined with other developmental defects. A hernia can only be treated surgically.

Umbilical cord prolapse

One of the first stages of labor is the breaking of amniotic fluid. Sometimes the flow of water captures the umbilical cord, which penetrates the cervix or even the vagina. This is exactly the situation that is called loss.
This phenomenon is dangerous because the fetus moves along the cervix and can compress the umbilical cord, that is, the movement of blood and oxygen into its body is blocked.
Prolapse is more common during early labor and during breech presentation.
The prolapse is detected after the water comes out. A woman in labor may feel “something foreign” in the vagina. If at this moment the woman is not in the maternity hospital, she should get on all fours, lean on her elbows and urgently call an ambulance.
In some cases, the umbilical cord is inserted into place. Sometimes surgical delivery is prescribed.

Cyst

This is a fairly rare pathology, and it is usually possible to determine the cyst with accuracy only after the birth of the child.
This formation may be in a single copy or there may be several of them. Most often they are formed in Wharton jelly.
Cysts are noticeable during ultrasound examination. They do not in any way affect the blood circulation between the fetus and the placenta.
In most cases, cysts are combined with fetal malformations, so if cysts are present, it is recommended to undergo genetic analysis.
Cysts are divided into false and true.

False– without capsule, located in Wharton’s jelly tissue. They are quite small and are found in all segments of the umbilical cord. The reasons for the appearance of such cysts often remain unknown. Sometimes they appear at the site of hematoma or edema.

True cysts are formed from particles of the vitelline duct. Such cysts have a capsule and can be quite large - up to one centimeter in diameter. They are always formed near the fetal body. It is not always possible to distinguish a false cyst from a true one.

The rarest type of umbilical cord cysts are umbilical mesenteric cysts. Such formations appear if the formation of the fetus is disrupted in the early stages of pregnancy. In this case, between the bladder and urachus ( umbilical cord component) a cavity is formed in which fetal urine accumulates. Only ten similar cases have been described in medicine.