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Table of contents

1. History of domestic pediatrics, organization of maternity protection. Childhood periods
2. Feeding children. Prevention of hypogalactia. Characteristics of milk mixtures
3. Constitutional anomalies in children. Diathesis options (Allergic diathesis. Exudative-catarrhal diathesis. Lymphatic diathesis. Neuro-arthritic diathesis)
4. Chronic eating disorders, hypovitaminosis in children (Hypotrophy. Hypovitaminosis. Vitamin A deficiency. Vitamin B1 deficiency (thiamine). Vitamin B2 deficiency (riboflavin). Nicotinic acid deficiency (vitamins PP, B3, etc.). Vitamin B6 deficiency (pyridoxine). Vitamin C deficiency (ascorbic acid) . Vitamin D deficiency. Vitamin K deficiency)
5. Vaccination (Live vaccines. Killed vaccines. Recombinant vaccines and toxoids. Formation of an immune response. Vaccination calendar and rules for administering vaccines for certain types of vaccinations)
6. Rickets, rickets-like diseases
7. Respiratory diseases. Classification, clinic, diagnosis, treatment (Acute bronchitis. Chronic bronchitis. Pneumonia. Bronchial asthma. Asthmatic condition)
8. Diseases of the digestive system in children. Chronic gastroduodenitis. Stomach ulcer (Chronic gastroduodenitis. Peptic ulcer of the stomach or duodenum)
9. Diseases of the biliary system in children (Classification of pathological conditions of the biliary tract in childhood. Biliary dyskinesia. Chronic cholecystitis)
10. Acute and chronic viral hepatitis in children (Acute hepatitis. Chronic hepatitis)
11. Kidney diseases in children. Classification (Classification of kidney diseases in children. Pyelonephritis. Chronic pyelonephritis. Glomerulonephritis. Acute glomerulonephritis. Subacute diffuse glomerulonephritis. Chronic diffuse glomerulonephritis)
12. Kidney diseases in children. Acute renal failure (ARF). Chronic renal failure (CRF) (Kidney failure. Prerenal acute renal failure. Renal acute renal failure. Partial chronic renal failure)
13. Diffuse connective tissue diseases. Systemic lupus erythematosus. Dermatomyositis. Systemic scleroderma (Systemic lupus erythematosus. Localized scleroderma. Dermatomyositis)
14. Hemorrhagic diseases in children, hemorrhagic diathesis, thrombocytopenic purpura, hemorrhagic vasculitis. Hemophilia, emergency treatment for bleeding (Hemorrhagic diathesis and syndromes. Types of bleeding. Thrombocytopenic purpura. Hemorrhagic vasculitis (Schönlein-Henoch disease). Hemophilia A and B)
15. Anemia and leukemia in children (Anemia. Leukemia)
16. Pathology of the neonatal period. Perinatal pathology of the central nervous system. Hemolytic disease of the newborn. Intrauterine infection. Sepsis (Perinatal pathology of the central nervous system. Hemolytic disease of the newborn. Bacterial sepsis of the newborn)
17. Parasitic diseases in children (Helminthiasis. Alveococcosis. Hookworm disease (hookworm and necatoriasis). Diphyllobothriasis. Opisthorchiasis. Teniosis. Trichocephalosis. Fascioliasis. Echinococcosis. Enterobiasis)
18. Rheumatism in children and adolescents

LECTURE No. 1. History of domestic pediatrics, organization of maternity care. Childhood periods

Pediatrics became an independent medical discipline in Russia in the 1802th century. The world's first children's hospital was opened in Paris (1834), the first children's hospital in Russia was opened in St. Petersburg (1842) - the Nikolaev Hospital, later the N. F. Filatov Children's Hospital, the second children's hospital was established in Moscow (1844), the third children's hospital in Russia was established in St. Petersburg in XNUMX.

Before the revolution, polyclinic care for children was provided on an outpatient basis at hospitals and clinics. After the October Revolution, the protection of motherhood and childhood was declared a state task. A wide network of nurseries, mother and child homes, dairy kitchens, consultations for infants and young children, children's preventive outpatient clinics and polyclinics has been developed. After the Great Patriotic War, consultations for infants and polyclinics were merged into children's polyclinics. In 1998, there were 491 children's polyclinics in Russia.

The child is constantly growing and developing. At each age stage of his life, he appears in his morphological, physical and psychological quality. In the process of human ontogenesis, a number of periods of development are distinguished.

1. Antenatal period development includes:

1) embryonic period (1-6th week) - the laying and formation of organs occurs;

2) embryofetal period (7-8th week) - the placenta is formed;

3) the fetal period (from the 9th week to birth) there is a growth of the fetus and tissue differentiation of organs.

2. Intranatal period - from the onset of labor pains to the moment of clamping the umbilical cord and the birth of the fetus.

3. postnatal period development includes:

1) neonatal period (up to 3-4 weeks). Highlight:

a) early neonatal period - the first 7 days (intrauterine dynamics stops, pulmonary respiration appears, the pulmonary circulation begins to function, enteral nutrition begins, energy and water metabolism changes;

b) late neonatal period (from the 8th day of life to the end of the 1st month). During this period, the development of analyzers takes place, coordination of movements and conditioned reflexes begin to form. There is an adaptation to the conditions of life;

2) the period of infancy (from 3-4 weeks to 12 months): the completion of the main processes of adaptation to extrauterine life, intensive physical, neuropsychic, motor and intellectual development, there is insufficient morphological and functional maturity of all organs and systems;

3) the period of early childhood (from 1 year to 3 years): improvement in coordination of movements, rapid development of motor speech and mental functions, a significant increase in motor activity;

4) preschool period (from 3 to 6 years): a slower increase in body weight, the beginning of the replacement of milk teeth with permanent ones, a significant improvement in memory, improvement of speech, the correct construction of phrases and pronunciation of sounds, the emergence of complex relationships with different children and adults, the formation of pride ;

5) junior school period (from 7 to 11 years): the process of the appearance of permanent teeth continues, all body systems are improved;

6) senior school period (from 12 to 17-18 years).

Physical and neuropsychic development of early childhood is one of the most important indicators of a child's health.

From 10 to 20 days, the child keeps an object in sight.

At 1 month old, he fixes his gaze on a fixed object. Listens to sounds, voice, starts to smile. Lying on his stomach, he tries to raise and hold his head.

At 2 months, it fixes the gaze for a long time. Makes seeking turns of the head to the sound. He rises and holds his head for a short time.

At 3 months, being in an upright position, he is able to hold his gaze. Keeps head upright. With the support of the armpits, it firmly rests with the legs with a maximum load in the hip joints. Pronounces the first sounds.

At 4 months, he recognizes his mother, examines his hands, laughs, is able to grab toys with his hands.

At 5 months old, he recognizes his mother's voice, distinguishes between strict and affectionate intonations. He begins to lie on his stomach for a long time, leaning on the palms of straightened arms.

At 6 months, he is able to distinguish between his own and someone else's name, takes a toy. Can roll over from stomach to back and move around. Produces individual sounds.

At 7 months he is actively engaged with a toy, crawling. To the question "where?" able to look for an object.

At 8 months old, he plays with toys for a long time, sits, sits, lies down, gets up and steps on his own, holding on to the barrier. He himself holds and eats a piece of bread.

At 9 months, he makes dance movements to the sound of music. Listens to music intently. Moves from object to object, holding on to them with his hands. He drinks from a cup, holding it lightly with his hands.

At 10 months, at the request of an adult, he performs various actions (opens, closes), at the request of "give" he finds and gives familiar objects.

At 11 months, he is able to stand on his own, take the first steps. Pronounces the first words. Holds a spoon while feeding.

At 12 months, he recognizes familiar people in photographs, looks at pictures. Sits independently without support. Distinguishes the meanings of the words "can" and "impossible", independently drinks from a cup. Knows a few words.

At the age of 1 year and 3 months, he walks independently, squats, bends over. Eats solid food on its own.

At 1 year and 6 months, he steps over obstacles with a side step. Able to select objects similar in appearance from objects of different shapes according to the proposed pattern or word.

At 1 year and 9 months, he begins to assemble primitive structures. Overcomes obstacles by alternating pace. Makes independent attempts to dress and undress.

At 2 years old, builds sentences of 3 or more words. He dresses independently, but does not know how to fasten buttons. Understands short stories.

At 3 years old, questions “when”, “why”, names 4 primary colors appear. Able to perform a specific role in the game (for example, playing with a doll, acts on behalf of the mother or doctor).

LECTURE No. 2. Feeding children. Prevention of hypogalactia. Characteristics of milk mixtures

Feeding a child in the first year of life with human milk is called natural. In the process of sucking, the jaw apparatus, muscles of the mouth and tongue develop, and the correct bite is formed. Breastfeeding of the child by the mother has a beneficial effect on the development of the central nervous system of the child and his mental activity.

Quantitative differences between women's milk and animal milk: the total amount of protein is approximately 2 times less than in cow's milk, and the amount of carbohydrates is 2 times more. It is generally accepted that on average 100 ml of human milk contains 1,2 g of protein, 3,5 g of fat, 7,5 g of carbohydrates. The energy value of 100 ml of human milk is 70 kcal.

Qualitative differences between women's milk and animal milk: in women's milk, the content of lactoalbumin, lactoglobulin, immunoglobulins is much higher than casein. The content of amino acids in women's milk is less than in cow's milk, but their ratio is more consistent with the needs of a child in the first year of life. Hydrolytic enzymes contained in human milk and involved in the breakdown of protein are of great importance.

Triglycerides are the main component of fat in human milk. The amount of milk sugar - lactose - in women's milk is greater. Qualitative differences lie in the different isomeric structure of milk sugar: human milk contains β-lactose, and cow's milk contains L-lactose. α-lactose is absorbed more slowly in the small intestine than β-lactose, and has time to reach the large intestine and stimulates the growth of gram-positive bacterial flora. β-lactose stimulates the synthesis of B vitamins and affects the composition of lipids, reducing the content of neutral fats and increasing the content of lecithin. Human milk contains oligoamino sugars, which stimulate the growth of bifidobacteria. The total amount of mineral salts in women's milk is less than in cow's milk, which makes it possible to avoid the retention of osmotically active ions in the body of a child in the first months of life, which has a low excretory function of the kidneys.

In human milk the ratio between phosphorus and calcium is 1:2, and in cow's milk it is 1:1. The amount of vitamins in human milk depends on the time of year and on the vitamin value of the nursing mother’s food. On average, human milk contains significantly more fat-soluble vitamins (A, D, E) than cow's milk.

The first breastfeeding should take place in the delivery room 20-30 minutes after birth. During the first application, skin-to-skin contact is very important. The duration of the first contact should be at least an hour. Early breastfeeding also contributes to good uterine contractions in the postpartum period.

Preparing women for successful breastfeeding: in the first half of pregnancy, nutrition does not require special correction, it is only important to provide sufficient vitamins and minerals, rich sources of which are vegetables and fruits.

In the second half of pregnancy, when the weight of the fetus begins to increase rapidly, the woman’s need for basic nutrients (protein, minerals) increases. It is advisable that the diet include about 500-600 ml of milk or fermented milk products, 100-150 g of cottage cheese, 100-200 g of meat or fish, 500-600 g of vegetables, 200-300 g of fruits or berries.

By the end of pregnancy, in order to avoid too much weight gain, it is advisable to somewhat limit the amount of carbohydrates in the diet by reducing the consumption of bread, confectionery, and sugar.

For sufficient provision of the body with vitamins during pregnancy, it is recommended to take B vitamins and ascorbic acid.

Contraindications for early attachment of the child to the mother's breast: on the part of the mother, these include moderate and severe nephropathy, operative delivery, large blood loss during childbirth, perineal ruptures of I-II degree, purulent-inflammatory diseases of the mother, Rh-negative blood, as well as severe extragenital diseases; on the part of the child, these include an Apgar score below 7 points, asphyxia, birth trauma, hemolytic disease of the newborn, malformations, prematurity, respiratory distress syndrome.

Contraindications to feeding with mother's milk: metabolic disease (galactosemia, phenylketonuria), mother taking cytostatics, radioactive drugs.

Despite a sufficient amount of milk from the mother, the baby needs to be introduced to complementary foods at 5-6 months.

Lure - This is an additional type of food of animal or plant origin. Rules for introducing complementary foods: complementary foods are introduced only to a healthy child, after doubling body weight; Complementary foods should be given before breastfeeding, starting with 5-10 g, gradually increasing to 150 g.

In the second half of the child’s life, the volume of complementary foods should not exceed 180 g. A new type of complementary food is introduced after complete adaptation to the previous one. Complementary feeding dishes should be homogeneous in consistency and should not cause difficulty in swallowing. As you age, you need to move on to thicker and then denser foods. Complementary foods are given warm with a spoon in a sitting position. When introducing complementary foods, you should monitor the baby's skin and stool: if it remains normal, then the next day the amount of complementary foods should be increased. You cannot combine the introduction of complementary foods with preventive vaccinations.

The first nutritional supplement is administered in the form of fruit juice at 3-3,5 months, starting with 1-2 tsp, increasing the amount to 20-30 ml. Fruit puree is administered 3-4 weeks after juice (from 3,5-4 months), starting with 3-5 g, increasing to 10-12 ml by 80-100 months.

At 5 months, the first complementary meal is introduced, replacing one feeding - vegetable puree from zucchini, carrots, potatoes. You can not add onions, garlic, spices.

At 6 months, porridge from rice, buckwheat, corn is introduced, starting with 50 g, increasing to 150 g (you cannot start complementary feeding with semolina porridge!), cottage cheese in the amount of 3-5 g/kg, and cookies.

From 7 months, ripe fruits, minced meat, and yolk (1/4-1/2 part) are introduced.

From 8 months they introduce kefir, bread.

From 9 months, the child is given fish instead of meat 1-2 times a week. By the year steam cutlets.

Artificial feeding - this is feeding, in which the child in the first half of life receives not breast milk, but milk mixtures as the main food. Currently, numerous dry formulas used for artificial feeding of healthy children can be divided into four groups.

Group I - adapted mixtures (cow's milk is used for production, and adaptation is reduced to a decrease in the content of protein and calcium salts in it). These include "Nan", "Nutrilon", "Heinz", "Enfamil".

Group II - partially adapted mixtures (they are partially close to the composition of human milk). These include "Baby", "Baby", "Milumil".

Group III - subsequent formulas, i.e. milk mixtures intended for nutrition at a subsequent age stage. These include "Hipp-2", "Enfamil-2".

Group IV - non-adapted mixes "Krepysh", "Health".

Mixed feeding - this is feeding, in which the child in the first half of life receives mother's breast milk and supplementary feeding, i.e., milk formula, since complementary foods cannot be prescribed to the child by age. The reasons for transferring children to mixed feeding are hypogalactia in the mother and social factors (for example, when the mother goes to work).

Hypogalactia is a decrease in the secretory ability of the mammary glands. There are early hypogalactia, developing in the first 10-14 days; late - at a later date; primary of neuroendocrine origin and secondary, caused by poor nutrition, violation of the daily routine, somatic and infectious diseases of the mother.

Lactation crises are a decrease in the amount of milk without external reasons. They are observed in the first 3 months of lactation, sometimes after 6-8 months, the duration of transient hypogalactia is 3-4 days, rarely - 6-8 days.

Prevention. Put the baby to the breast as often as possible, avoid nervous stress and mental stress, take medications that enhance lactation, ensure good nutrition by drinking carrot juice, infusion of dill, anise and infusion of walnuts (1/2 cup of walnuts, brew 1/2 liter boiling milk in a thermos and infuse for 3-4 hours, take the infusion 1/3 cup 20 minutes before breastfeeding).

LECTURE No. 3. Anomalies of the constitution in children. Diathesis options

Constitution - this is a set of relatively stable morphological and functional properties of a person, due to heredity, age and long-term intensive influence of the environment, which determines the functional abilities and reactivity of the body.

Diathesis - this is a genetically determined feature of the body, which determines the originality of its adaptive reactions and predisposes to a certain group of diseases. Diathesis is not a disease, but a predisposition that, under certain environmental conditions, can transform into a disease.

1. Allergic diathesis

Allergic diathesis is a constitutional anomaly characterized by the body's predisposition to allergic and inflammatory diseases. This constitutional anomaly is quite common. It is usually detected at the age of 3-6 months and lasts for 1-2 years; in most children it subsequently disappears. Atopic diathesis is distinguished, associated with an allergic reaction to food and non-infectious antigens in contact with the mucous membrane of the respiratory tract. Autoimmune diathesis, where there is increased sensitivity of the skin to UV irradiation, a significant increase in the level of γ-globulins in the blood, frequent detection of LE cells, antinuclear factors in a state of complete clinical well-being, polyclonal activation of B lymphocytes, as well as T helper cells with decreased activity T-suppressors, increased blood levels of immunoglobulins M. Infectious-allergic diathesis, where there are long periods of increased ESR and low-grade temperature, after acute respiratory viral infections and diseases of the nasopharynx.

Etiology, pathogenesis, clinic, treatment similar to exudative-catarrhal diathesis.

2. Exudative catarrhal diathesis

Exudative-catarrhal diathesis is a peculiar state of reactivity in young children, characterized by a tendency to recurrent infiltrative-desquamous lesions of the skin and mucous membranes, the development of pseudo-allergic reactions and a protracted course of inflammatory processes, with lymphoid hyperplasia, lability of water-salt metabolism.

Etiology and pathogenesis are not fully understood, but hereditary predisposition, as well as the influence of environmental factors, play an important role. A positive family “allergic history” is detected in 2/3-3/4 of children with allergic diathesis. In such children, a high level of immunodepth E in the blood or excessive secretion and release of histamine from mast cells, its insufficient inactivation, which determines the tendency to allergic reactions, is determined. Provoking factors may be toxicosis of the first and second half of pregnancy, infectious diseases, use of medications during pregnancy, violation of the pregnant woman’s diet, especially in the last months of pregnancy (monotonous diet with excessive consumption of one of the obligate allergens - eggs, honey, confectionery, milk, tangerines), as well as during breastfeeding.

Even in the prenatal period, a child can become diaplacentally sensitized to allergens circulating in the mother’s body. In the extrauterine period, allergens are transmitted with breast milk and food through the intestinal wall, which has increased permeability, especially in infants, especially after gastrointestinal diseases, as well as during the period of recovery from various diseases, with weight loss and exhaustion. A potential sensitizing agent can be food that has not been subjected to heat treatment (egnog, berries whipped with protein, etc.), as well as products such as fish, nuts and some others that do not reduce their allergenic properties when cooked. Allergization can also be caused by ordinary foods if the child receives them in excess (overfeeding), especially with a monotonous set of nutrients. Foods that are consumed in a particular season or infrequently become allergens when they are included in the diet in large quantities (berries, vegetables, nuts, etc.), as well as when foods that are not age-appropriate are introduced into the diet (caviar, shrimp, chocolate and etc.). Disordered eating, abuse of sweets, spicy, salty foods, and the introduction of many new foods into the child’s diet in a short period of time are important. A child with allergic diathesis easily becomes hypersensitive not only to nutrients, but also to external allergens such as wool and house dust.

Allergens can enter the child's body through the skin and mucous membranes (conjunctiva, etc.), as well as during numerous injections and vaccinations. In children with allergic diathesis, disturbances in cortical-subcortical relationships are found, parasympathetic mood or dystonia of the autonomic nervous system is detected, functional changes in the liver in the form of metabolic disorders (fat, carbohydrate, protein, water, salt, vitamin, acid-base balance), which is not indifferent to the body in the process of its adaptation to the external environment and nutrition.

The development of an allergic reaction is accompanied by an increase in the blood of a number of biologically active substances: histamine, serotonin, leukotrienes, etc. In the pathogenesis, autoallergic processes play a certain role, which most likely occur secondarily in the course of the disease. The development of autoallergization processes with a constant intake of autoallergens into the blood contributes to a more torpid course of allergic diathesis.

Clinic. Such children are characterized by high birth weight, especially if this is the first child in the family; Diaper rash that appears early and persists for a long time under conditions of proper care; disappearing and reappearing seborrhea of ​​the scalp; significantly exceeding the age norm of body weight gain and its large fluctuations under the influence of unfavorable conditions; positive skin tests for exogenous allergens in the absence of any clinical manifestations of allergic diathesis.

On examination, attention is drawn to a puffy pale face, excessive body weight, decreased tissue turgor (pastose type) or thinness, geographical tongue, abdominal pain, flatulence.

In the first year of life, children with increased nervous excitability, irritability, sleep disorders, reduced appetite are capricious, nervous. Children do not tolerate heavy physical exertion. Often, children with immunoglobulin A deficiency develop chronic foci of infection, enlarged peripheral lymph nodes, spleens, prolonged subfebrile conditions, and a protracted course of infectious diseases.

Gneiss occurs only in infants: dirty gray or brown seborrheic scales in the form of a cap or shell on the scalp, mainly on the crown and crown. The course of gneiss is usually favorable, but in some children it transforms into seborrheic eczema (swelling, redness, weeping, increased crusting), which often spreads to the auricles, forehead, cheeks.

The most common symptom of allergic diathesis, especially in children of the first year of life, is a milk scab (or crust): on the skin of the cheeks, often near the auricles, redness, swelling, sharply separated from healthy skin, is formed, often with signs of peeling. In some children, the milk scab is accompanied by itching, sometimes it can transform into eczema.

The persistent form of diaper rash - intertrigo - is one of the important symptoms of allergic diathesis. The diaper rash may be dry, in other cases there is maceration of the skin (usually in obese, pasty infants). The most severe form of allergic diathesis should be considered childhood eczema, which occurs in older children. In older children, it can transform into neurodermatitis.

Diagnosis established on the basis of anamnesis and clinical findings.

Differential diagnosis carried out with true eczema, erythroderma, dermatitis, immunodeficiency, psoriasis, and the syndrome of impaired intestinal absorption.

Treatment. There is no standard diet. A balanced diet and breastfeeding are necessary, although the presence of allergens is possible. The mother's diet should be low in carbohydrates, fats, table salt and possible allergens. In some cases (fat breast milk), expressed breast milk is pasteurized (for 30 minutes at a temperature of 65 ° C) and the top film is removed or the milk is placed in the refrigerator for 3-4 hours, and then the cream is skimmed, after which it is pasteurized. Older children are advised to exclude jelly, mousse, pork, beef broth, fish, eggs in any form, legumes, nuts, spices, seasonings (moderately limit fats and proteins, liquid). Among porridges, preference is given to buckwheat; in the evening, vegetables, salads, and casseroles are recommended. If eczema is the result of consuming an allergen, then it can subside within 24 hours with the following diet: dishes of rice water, 1 dish of fruit (not yellow), 1 dish of vegetables (potatoes), 1 dish of rice with fruit juice (not yellow color). On each subsequent day, a new dish is added to this basic diet under the control of the dynamics of the disease. If dysbiosis is diagnosed against the background of allergic diathesis, then 10-day courses of Lactobacterin and Bifidumbacterin may be effective. Prescribed medications that help reduce itching and permeability of the vascular wall, sedatives: 3-5% sodium bromide solution, diphenhydramine or antihistamines in age-appropriate dosages. B vitamins are also prescribed₅, AT₆, AT₁₂, AT₁₅, A, C (ascorbic acid can increase itching) in therapeutic doses for at least 3-4 weeks. Local treatment: first lotions, after swelling and weeping disappear - ointment therapy. In addition, moderately warm baths (not higher than 38 ° C) are prescribed for 10-15 minutes with wheat bran or potato flour (400-600 g per bath), with oak bark, string, celandine, with the addition of lagochilus, potassium permanganate (up to light pink color). Apply general ultraviolet irradiation from 1/4 to 1 erythemal dose 15-20 times (daily or every other day). Elimination of foci of secondary infection also improves the general condition of the patient.

Prevention. Rational nutrition for pregnant and nursing mothers, especially if they have allergies, with the consumption of moderate amounts of varied, well-cooked foods, excluding eggs from the diet, limiting milk (up to 1-2 glasses per day), sugar, honey, chocolate, sweets, nuts, as well as sausages, sausages, canned fish. Organization of child nutrition in accordance with age.

During illness and during convalescence, it is recommended to give the child well-processed food in moderation, avoiding the introduction of new foods. It is necessary to comply with the rules of vaccination, which is desirable to be carried out only during the period of remission and after appropriate preparation. Need hygienic care for an infant. It is better to avoid the use of perfumes, shampoos, toilet water. The prognosis, subject to all preventive and treatment measures, is favorable.

3. Lymphatic diathesis

Lymphatic diathesis (lymphatic-hypoplastic) is a hereditary insufficiency of the lymphatic system associated with a reduced function of the thymus gland as the main organ that controls the maturation of lymphocytes; characterized by a generalized persistent enlargement of the lymph nodes, dysfunction of the endocrine system (hypofunction of the adrenal glands, sympathoadrenal system, etc.), a tendency to allergic and hyperergic reactions and infectious diseases. One of the manifestations of lymphatic diathesis may be the pathology of local immunity of the mucous membranes, the insufficiency of the synthesis of secretory immunoglobulins.

Clinic. Dysplastic physique - often a short body, somewhat elongated limbs. The skin is pale, the skin fold is flabby, the muscles are poorly developed, its tone is reduced, the tissues are pasty. The lymph nodes are enlarged, the tonsils and adenoids are hyperplastic and loose. Adenoids after adenotomy are prone to re-growth. X-rays show enlargement of the thymus gland in 70% of cases, which can cause obstruction of bronchial obstruction. There is a tendency to arterial hypotension. In the blood - slight leukocytosis, lymphocytosis, monocytosis, anemia, neutropenia.

Diagnosis is established on the basis of the anamnesis, the characteristic appearance of the child, the detection of hyperplasia of the lymph nodes and the thymus gland.

Differential diagnosis carried out with immunodeficiency states.

Treatment. Maintaining a daily routine, sufficient time in the fresh air, hardening procedures, massage, gymnastics, physiotherapy, vitamin therapy. Prescription of adaptogens and agents that stimulate the body's defenses and adrenal function (dibazole, metacil, aloe, eleutherococcus, ginseng). In case of persistent viral infection and the presence of chronic foci of infection, a course of Viferon is prescribed.

Prevention. Rational nutrition for pregnant women and proper feeding of the child in accordance with age. Maintaining a daily routine, walks, hardening, massage and gymnastics. Constant use of adaptogen plants (Eleutherococcus, etc.) in combination with vitamins (separate courses of 2 weeks).

Forecast at observance of treatment-and-prophylactic measures favorable.

4. Nervous-arthritic diathesis

Nervous-arthritic diathesis is characterized by increased nervous excitability, a tendency to ketoacidosis, and in the future - a predisposition to the development of obesity, interstitial nephritis, urolithiasis, atherosclerosis, diabetes mellitus, gout. Violation of uric acid metabolism is the leading, but not the only laboratory marker.

Etiology. On the one hand, the formation of inheritance of pathological properties of metabolism, on the other hand, disturbances in nutrition in the family, work and rest regime, and environment.

Pathogenesis. Of particular importance are the high level of excitability at any level of reception, impaired purine metabolism with an increase in their content in the blood and urine, low acetylating ability of the liver and other undeciphered mitochondrial defects.

Clinic. Already in infancy, increased nervous excitability is noted; with age, children become even more excitable. Mental development is ahead of age norms: they are inquisitive, animated, remember what they hear or read. Sometimes such children have night terrors, tics, choreo-like attacks, and emotional lability. Periodically or suddenly, after a short period of illness, attacks of headache, nausea, vomiting, abdominal pain, and the smell of acetone from the mouth may occur, which indicates the development of an acetonemic crisis. During a crisis, the level of ketone bodies, ammonia, and uric acid in the blood increases, and the pH decreases.

Diagnosis established on the basis of anamnesis, clinical and laboratory data.

Differential diagnostics performed with neurosis, rheumatism, diabetes, etc.

Treatment. Rational regime and diet, hardening, walks, physical education. Avoid mental stress, limit TV viewing. At the initial symptoms of an acetonemic crisis or its precursors, give sweet tea, fruit juices, and alkaline mineral water to drink. It is advisable to hospitalize the child in a hospital. They do a cleansing enema and gastric lavage to improve the removal of ketone bodies from the intestines. Prescribe Essentiale or vitamin B₁₂, with acetonemic vomiting, treatment is aimed at combating acytosis and enhancing the excretion and utilization of ketone bodies: a 5% glucose solution, a 0,9% sodium chloride solution are injected. Prevention: observance of the child's day regimen, rational nutrition, protecting the child from mental stress.

LECTURE No. 4. Chronic eating disorders, hypovitaminosis in children

1. Hypotrophy

Hypotrophy is a chronic eating disorder that manifests itself in varying degrees of weight loss.

Etiology, pathogenesis. The disease is polyetiological. There are congenital (prenatal) and acquired (postnatal) malnutrition. Congenital malnutrition is primarily caused by maternal diseases or is associated with intrauterine hypoxia, fetal infection, genomic and chromosomal mutations. Among the causes of acquired malnutrition, exogenous and endogenous are distinguished.

Exogenous causes include nutritional factors (quantitative underfeeding in hypogalactia, pyloric stenosis and pylorospasm or qualitative underfeeding when using age-inappropriate mixtures, late introduction of complementary foods, etc.), infectious factors, intrauterine generalized infections, infections of the gastrointestinal tract, toxic factors, drug poisoning (hypervitaminosis D, etc.), anorexia due to psychogenic and other deprivation, when the child does not receive enough attention, affection, walks, massage, lack of care, regimen, education, etc. Prenatal encephalopathies can be attributed to endogenous causes of malnutrition of various origins, bronchopulmonary dysplasia, hereditary metabolic anomalies and immunodeficiency states, malformations of the gastrointestinal tract and other organs, CNS lesions, endocrine diseases, psychopathy, neurosis, etc.

The pathogenesis of malnutrition is based on a decrease in the utilization of nutrients with a violation of the processes of digestion, absorption and assimilation under the influence of various factors. There are I, II and III degrees of severity of malnutrition.

Clinic. Hypotrophy of the first degree is manifested by a loss of body weight of no more than 20% of that required by age. Paleness of the skin and mucous membranes. The subcutaneous fat layer on the abdomen becomes thinner, tissue turgor and elasticity decrease.

The weight gain curve is flattened. The growth of the child does not lag behind the norm. Other indicators are usually within the normal range or slightly reduced.

With II degree malnutrition, the loss of body weight is 25-30% compared to the age norm. The subcutaneous layer is preserved only on the face, and is especially thin on the abdomen and limbs. The skin is dry, pale, flabby, the skin easily gathers into folds, hangs down in some places, tissue turgor is reduced. Growth retardation is observed, appetite decreases, the child becomes weak, irritable, noisy, whiny, loses previously acquired skills, thermoregulation is disrupted, the child quickly cools down or overheats. The curve of body weight increase is flat.

The Chulitsky body condition index is 1-10. The stool is unstable: “hungry” stool (scanty, dry, discolored, with a sharp and unpleasant odor) is replaced by dyspeptic stool (green with undigested food particles, with mucus).

With malnutrition of the III degree, the loss of body weight is more than 30% of the due to age. There is no increase in body weight, the child is significantly behind in growth. Outwardly - an extreme degree of exhaustion, the child resembles a skeleton covered with skin. The skin is pale gray, dry, the limbs are cold, the subcutaneous fat layer is completely absent. The skin fold does not straighten, there is no elasticity. The mucous membranes are pale, dry, in the mouth - elements of candidal stomatitis (thrush).

Fatness index Chulitsky negative. Breathing is shallow, heart sounds are muffled, blood pressure is reduced.

The body temperature is lowered, there are periodic rises to subfebrile numbers, there is no difference between the axillary and rectal temperatures. Infectious processes are asymptomatic. Often there are signs of subacute rickets.

The abdomen is distended, distended, or bowel loops are contoured. The chair is unstable, often constipation, alternating with soapy-calcareous stools. The child is severely retarded.

Diagnosis malnutrition is usually not difficult. It is much more difficult to find out the causes of malnutrition.

Treatment patients should be comprehensive and include measures aimed at eliminating or correcting causally significant factors, diet therapy, the appointment of restorative procedures, enzymes and symptomatic agents, the elimination of foci of infection, vitamin therapy. In all cases, when prescribing a diet, it is necessary to ascertain food tolerance. During the period of increased food load, scatological control is needed.

With hypotrophy of the I degree, the amount of proteins and carbohydrates is usually calculated per 1 kg of body weight due to age, and fats - per 1 kg of existing body weight.

In case of II degree malnutrition, food tolerance is established within 3-5 days. As a rule, breast milk or acidic mixtures are prescribed (kefir, acidophilic mixture “Malyutka”, biolact, etc.).

The calculation is first carried out on the child’s existing body weight, then on approximately the expected one (existing + 20) and only then on the expected one. After 3-4 days, the protein load is gradually increased, then the carbohydrate load and, lastly, the fat load.

For grade III malnutrition, it is preferable to start diet therapy with the introduction of breast milk every 2 hours, 20-30 ml. Having brought the amount of food to 50 ml, reduce the number of feedings. The order of increasing the load with proteins, carbohydrates and fats is the same as with degree II malnutrition, but more gradual. Food tolerance is determined within 2 weeks.

In case of malnutrition of the II and III degrees, the missing amount of fluid, nutrients and electrolytes is administered intravenously: 5-10% glucose solution, isotonic sodium chloride solution, Ringer's solution, protein hydrolysates, albumin, protein (albumin 3-5 ml/ kg; hemodez up to 15 ml/kg, but not more than 200 ml; rheopolyglucin 3 - 8 ml/kg, etc.). Insulin glucose therapy is indicated (s.c. 1 unit of insulin per 5 g of administered glucose).

Treatment of malnutrition II - III degree must be carried out in a hospital. In the presence of foci of infection, antibiotic therapy is prescribed (avoid nephro-, hepato- and ototoxic drugs), if necessary, surgical intervention is performed. Enzyme therapy, vitamin therapy are widely used.

Stimulants prescribed include apilak, γ-globulin, albumin, plasma, and blood transfusions. In some cases, it is advisable to use anabolic hormones (retabolil-1 mg/kg once every 1 weeks, etc.). Massage and exercise therapy, spending time in the fresh air are recommended. The prognosis depends on the cause that led to malnutrition and the possibilities of eliminating it. With primary malnutrition of the third degree, the prognosis is always serious; mortality rate is up to 2%.

Prevention. If possible, ensure natural feeding, treatment of hypogalactia, rational feeding, early diagnosis of diseases in newborns and infants.

2. Hypovitaminosis

Hypovitaminosis is a group of diseases caused by a deficiency in the body of one or more vitamins.

Vitamins - these are irreplaceable biologically active substances that act as catalysts for various enzyme systems or are part of many enzymes.

Vitamins are necessary for normal metabolism, growth and renewal of tissues, biochemical support of all body functions. Insufficient intake of vitamins leads to disruption of enzymatic reactions, hypo- and beriberi with a corresponding picture of the disease.

Etiology, pathogenesis. Hypovitaminosis is distinguished between primary (exogenous, caused by a deficiency of vitamins in the body with food) and secondary (endogenous, associated with impaired absorption of vitamins in the gastrointestinal tract or their assimilation, with an excessive need for vitamins during treatment with certain antibiotics). Also contributing to the occurrence of vitamin deficiency are excessively low or high ambient temperatures, prolonged physical or mental stress, diseases of the endocrine glands, some occupational hazards and other factors. Of particular importance are limited diet (with insufficient vitamin content in food), helminthiasis (consumption of large amounts of vitamins by helminths), pregnancy and lactation in women (increased need for vitamins for the fetus and infant).

Polyhypovitaminosis was often observed in various countries during social and natural disasters (wars, crop failures), with irrational (unbalanced) nutrition of both groups of people (during long hikes, travels, etc.) and individuals (food canned food, dried products, long monotonous food). In some developing countries, vitamin deficiency diseases are still very common.

Many diseases of the gastrointestinal tract, accompanied by syndromes of insufficiency of digestion and insufficiency of absorption, lead to vitamin deficiency.

3. Vitamin A deficiency

Vitamin A deficiency (retinol deficiency) occurs when there is a lack of vitamin A and carotene in food, a violation of its absorption in the intestine and the synthesis of vitamin A from carotene in the body.

Vitamin A is found in many products of animal origin (butter, egg yolk, liver of some fish and marine animals); Plant foods contain carotene, which is provitamin A, from which this vitamin is synthesized in the human body. Vitamin A is fat soluble. The daily requirement for an adult is 1,5 mg (5000 IU).

Vitamin promotes normal metabolism, growth and development of the body, provides physiological functions of the epithelium of the skin and mucous membranes, sweat, sebaceous and lacrimal glands, the organ of vision.

Clinic. Hemeralopia (night or night blindness due to dystrophic changes in the retina and optic nerves), xerophthalmia (dryness of the conjunctiva, the formation of whitish opaque plaques on it), keratomalacia (ulceration of the cornea), hyperkeratosis (dystrophic changes in the epithelium of the skin, mucous membranes and skin glands) appear - dryness, flaking and pallor of the skin, keratinization of hair follicles, atrophy of the sweat and sebaceous glands, etc.), a tendency to pustular skin diseases, infectious lesions of the respiratory system, urination, digestive tract, general malaise, weakness; in children - delayed growth and development, neurological disorders.

Diagnosis established on the basis of anamnesis, clinical and laboratory data. In a biochemical study of blood serum, the content of retinol in case of vitamin A deficiency is below 100 μg / l, carotene - below 200 μg / l. Ophthalmological examination allows to determine the time of dark adaptation.

Treatment. A nutritious diet including foods rich in retinol and carotene (liver, eggs, cow's milk, fish oil, rose hips, carrots, peas, sea buckthorn, green onions), retinol preparations in a daily dose for adults from 10 to 000 IU/day, depending depending on the severity of vitamin deficiency for 100-000 weeks under close medical supervision (large doses and uncontrolled treatment can cause hypervitaminosis A). For hemeralopia, xerophthalmia and retinitis pigmentosa, riboflavin is prescribed simultaneously.

Prevention. A varied diet with the inclusion of foods rich in retinol and carotene, in conditions of a forced monotonous diet - additional prescription of retinol, 1-2 tablets (3300-6600 IU).

4. Vitamin B deficiency₁ (thiamine)

Vitamin B deficiency₁ (thiamine) occurs when there is a lack of this vitamin in food (primarily eating polished rice in the countries of East and Southeast Asia), a violation of its absorption in the intestines and assimilation (with severe intestinal lesions that occur with malabsorption, persistent vomiting, prolonged diarrhea, etc.). d.).

Predispose to the development of the disease pregnancy and lactation, hard physical labor, febrile illness, thyrotoxicosis, diabetes mellitus. The daily requirement of an adult for vitamin B is about 2 mg. Vitamin B is part of a number of enzymes involved in carbohydrate metabolism, in the body it turns into cocarboxylase, which is a prosthetic group of enzymes involved in carbohydrate metabolism. In the development of a complete clinical picture of avitaminosis B₁ concomitant deficiency of other B vitamins is also important.

Clinic. It manifests itself as widespread damage to peripheral nerves (polyneuritis), the cardiovascular system and edema. Complaints include general weakness, fatigue, headache, shortness of breath and palpitations during physical activity. Then the phenomena of polyneuritis are added: paresthesia and decreased skin sensitivity of the lower extremities, and later other parts of the body, a feeling of heaviness and weakness in the legs, lameness, and fatigue when walking. The calf muscles become hard and painful on palpation. The characteristic gait of beriberi patients is that they step on the heel and then the outer edge of the foot, sparing the toes. Next, tendon reflexes fade and muscle atrophy occurs.

Violation of the activity of the cardiovascular system is manifested by tachycardia, degenerative changes in the heart muscle with circulatory failure, a decrease in blood pressure, mainly diastolic. There are symptoms of dystrophic lesions and dysfunctions of the digestive system, visual disturbances, mental disorders.

According to the prevailing symptoms, there are edematous form (with more pronounced lesions of the cardiovascular system and edema) and dry (with predominant damage to the nervous system), as well as an acute, malignant, fulminant form, often ending in death. It is difficult to recognize beriberi in young children.

Diagnosis established on the basis of anamnesis (nature of nutrition, the presence of diseases that contribute to the manifestation of thiamine deficiency), characteristic changes in the cardiovascular and nervous systems, laboratory data from a biochemical blood test: when the thiamine content in daily urine decreases below 100 mcg, hourly (on an empty stomach) - below 10 mcg, cocarboxylase content in erythrocytes below 20-40 mcg/l. Characterized by an increase in the content of pyruvic acid in plasma (above 0,01 g/l) and increased excretion in the urine (more than 25 mg per day). Recently, a number of more complex modern methods have also been used for this purpose.

Differential diagnosis with infectious (poliomyelitis, diphtheria, etc.) and toxic polyneuritis (poisoning with mercury, methyl alcohol, etc.) is based on taking into account the epidemic situation, the history of the disease, as well as on the results of biochemical studies of thiamine metabolism. The differential diagnosis of the edematous form of beriberi with myocarditis, myocardial dystrophies is facilitated by the presence of symptoms of polyneuritis.

Treatment. Complete food rich in vitamin B (cereals, dried brewer's yeast, cookies, egg yolk, nuts, legumes, pork, black bread). In severe and moderate cases, treatment in a hospital. Bed rest. Vitamin B is prescribed₁ 30-50 mg IM or SC followed by switching to oral administration; simultaneously prescribed nicotinic acid (25 mg), riboflavin (10-20 mg), vitamin B₆.

Symptomatic therapy: cardiovascular drugs, diuretics, to increase the tone of the nervous system - injections of strychnine (1: 1000, 1-1,5 mg each). With endogenous vitamin B deficiency₁ caused by chronic bowel diseases - their treatment.

Prevention. Eat a varied diet including foods rich in thiamine.

5. Vitamin B deficiency₂ (riboflavin)

Vitamin B deficiency₂ (riboflavin) occurs when there is a lack of vitamin B₂ in food, disruption of its absorption in the intestines, assimilation, or with increased destruction in the body. Riboflavin is found in many foods of animal and plant origin. The daily requirement of an adult is 2-3 mg.

In the body, riboflavin, interacting with ATP, forms flavin mono- and flavin dinucleotides, which are involved in the regulation of redox processes. With aribof lavinosis, cellular hypoxia occurs. Riboflavin is involved in the implementation of the visual function of the eye and the synthesis of hemoglobin. In the pathogenesis of ariboflavinosis, the lack of other B vitamins is also important.

Clinic. Manifested by decreased appetite, weight loss, headache, weakness, impaired twilight vision, dystrophic changes in the skin and mucous membranes, burning sensation of the skin, pain in the eyes, the appearance of conjunctivitis, angular and aphthous stomatitis (cracks and maceration of the epithelium and crusts in the corners of the mouth), seborrheic dermatitis, especially pronounced in the area of ​​the nasolabial folds, on the wings of the nose, ears, dry itchy dermatitis on the hands.

With a long course, disorders of the nervous system are observed: paresthesia, increased tendon reflexes, ataxia and others, as well as hypochromic anemia. The course is chronic, with exacerbations in the spring and summer months.

Diagnosis is established on the basis of anamnesis (nature of nutrition, presence of diseases), clinical and laboratory data in a biochemical study: with a decrease in the content of riboflavin in daily urine below 100 mcg, in hourly urine - below 10 mcg, in blood serum - below 3 mcg / l, erythrocytes - below 100 µg/l). Decrease in dark adaptation matters.

Differential diagnosis carried out with pellagra, beriberi A, multiple sclerosis. In doubtful cases, the results of studies of the content of vitamins in the blood and urine are the most conclusive.

Treatment. A complete diet (yeast, liver, kidneys, egg yolk, peanuts, mackerel, cod, cheese, cottage cheese, meat, leafy vegetables), taking riboflavin 10-30 mg orally for 2-4 weeks. At the same time, other B vitamins are prescribed. In case of endogenous deficiency, treatment of intestinal diseases accompanied by malabsorption.

6. Deficiency of nicotinic acid (vitamins PP, B₃ and etc.)

Deficiency of nicotinic acid (vitamins PP, B₃ etc.) is due to insufficient intake of this vitamin with food, insufficient absorption in the intestines (with various diseases of the stomach and small intestine, accompanied by absorption deficiency syndrome) or an increased need for it (during pregnancy, heavy physical work, etc.).

Clinic. It manifests itself as damage to the digestive, nervous systems and skin. Loss of appetite, dryness and burning in the mouth, vomiting, diarrhea alternating with constipation, and general progressive weakness appear. The tongue is bright red, swollen, with painful ulcerations. Atrophic and erosive changes are also found in other parts of the digestive tract. Damage to the nervous system is manifested by general irritability, symptoms of polyneuritis, and sometimes signs of damage to the spinal cord (usually the posterolateral columns). Skin lesions are manifested by pellagritic erythema, accompanied by skin itching, hyperpigmentation (mainly on open areas of the body and extremities), peeling of the skin, and the appearance of follicular papules. The functions of the endocrine system are disrupted, and hypoproteinemia develops. In severe cases, all the symptoms of pellagra appear, which occurs in some countries in Africa and Asia.

Nicotinic acid and its amide are effective antipellagrimic agents and are involved in cellular respiration. With their deficiency in the body, significant metabolic disorders and functions of many organs, dystrophic and degenerative changes in organs and tissues, most pronounced in the skin, nervous and digestive systems, occur. Typically, with pellagra, there are signs of deficiency of other B vitamins, as well as the amino acid tryptophan, contained in complete proteins. The daily requirement of adults for nicotinic acid and its amide is 20-25 mg.

Diagnosis is established on the basis of anamnesis, clinical and laboratory data in biochemical studies: the content of N1-methylnicotinamide in daily urine is below 4 mg, in hourly urine - below 0,3 mg, the content of nicotinic acid is below 0,2 mg. The content of other B vitamins in the blood and urine decreases.

Treatment in moderate and severe cases, inpatient: full-fledged fractional meals with a gradual increase in calorie content, nicotinic acid or nicotinamide orally 25-100 mg per day for 2-3 weeks in combination with other B vitamins. In endogenous forms - parenteral administration of nicotinic acid and its amide.

Prevention. A varied, balanced diet with sufficient content in the diet of foods rich in nicotinic acid (chicken, meat, legumes, liver, green vegetables, fish). In the endogenous form - timely diagnosis and treatment of intestinal diseases, prophylactic administration of nicotinic acid and its amide, additional administration of vitamin PP to persons with an increased need for it.

7. Vitamin B deficiency₆ (pyridoxine)

Only the endogenous form is observed when the bacterial flora of the intestine, which synthesizes pyridoxine in sufficient quantity for the body, is suppressed by long-term use of antibiotics, sulfanilamide and anti-tuberculosis drugs, especially with a simultaneous increased need for this vitamin (with significant physical exertion, pregnancy, etc.). Vitamin B₆ found in sufficient quantities in many products of plant and animal origin, especially in yeast. In the body, it is converted into pyridoxal-5-phosphate and is part of enzymes involved in the deoxylation and transamination of amino acids, histamine metabolism, and fat metabolism. The daily requirement for pyridoxine in adults is 2-2,5 mg.

Clinic. Manifested by irritability or lethargy, insomnia, polyneuritis of the upper and lower extremities, paresthesia, dyspeptic disorders, anorexia, stomatitis, seborrheic and desquamative dermatitis of the face, scalp, neck, hypochromic anemia, dystrophic changes occur in the cells of various organs, especially the digestive and nervous systems , skin; young children experience growth retardation.

Diagnosis is established on the basis of anamnesis, clinical and laboratory data in a biochemical study (the content of N-pyridoxic acid in daily urine is below 0,5 mg, hourly - below 30 μg, pyridoxine content in whole blood is below 50 μg / l). After taking 10 g of tryptophan, the release of xanthurenic acid exceeds 50 mg.

Treatment. Complete nutrition (liver, yeast, grains and legumes, rice, peanuts). Pyridoxine preparations 10-50-100 mg per day for 2-3 weeks orally, for chronic diseases of the gastrointestinal tract - parenterally, elimination of etiological factors.

Prevention. For long-term treatment with antibiotics, sulfonamides and anti-tuberculosis drugs, as well as for conditions accompanied by an increased need for pyridoxine (during pregnancy, sharply increased physical activity, etc.), prophylactic administration of vitamin B₆.

8. Vitamin C (ascorbic acid) deficiency

Vitamin C plays an important role in redox processes, carbohydrate metabolism, collagen and procollagen synthesis, and normalization of vascular permeability.

Clinic. It manifests itself as general weakness, increased fragility of capillaries with the formation of petechiae, bleeding from the gums, hemorrhagic effusions into the joints and pleura, dystrophic changes in the mucous membranes, anemization, and disorders of the nervous system.

Treatment. Good nutrition (fresh green vegetables, fruits, rose hips, citrus berries, black currants, cranberries) and prescription of medications containing vitamin C.

Prevention. A complete, balanced diet, preventive intake of ascorbic acid in conditions of possible deficiency (during long hikes with a predominant diet of canned and dried foods, women during pregnancy and lactation, etc.), proper preparation of food, preventing significant losses of ascorbic acid during culinary processing of products.

9. Vitamin D deficiency

Vitamin D deficiency is the most important₂ (ergocalciferol) and D₃ (cholecalciferol). The main amount of vitamin D is formed in the skin when it is exposed to light (ultraviolet rays); a smaller part comes from food. Vitamin D is fat-soluble, found in small quantities in butter, milk, egg yolk, especially high levels are found in the liver and adipose tissue of cod, some other fish and marine animals. In the body, it participates in the regulation of calcium and phosphorus metabolism. If there is a lack of foods containing vitamin D in food, as well as insufficient exposure to sunlight on the skin, a clinical picture of deficiency of this vitamin occurs in the form of rickets (see lecture below on Rickets in children). An adult's daily requirement for vitamin D is 100 IU, a child's is 500-1000 IU.

For the diagnosis in adults, data from biochemical laboratory studies are of primary importance (a decrease in the content of inorganic phosphorus in the blood below 30 mg / l, an increase in the activity of alkaline phosphatase).

Treatment. Vitamin D preparations₂ and D₃ in combination with calcium preparations and ultraviolet irradiation. In the future - dispensary observation and repeated courses of treatment (an overdose of vitamin D can cause intoxication). In case of vitamin D deficiency in adults caused by diseases of the digestive tract and impaired bile secretion, in addition to prescribing vitamin D preparations, the underlying disease is treated.

10. Vitamin K deficiency

Vitamin K deficiency is rare in adults. It is caused by the cessation of the flow of bile into the intestine, which is necessary for the absorption of phylloquinones (with obstruction and compression of the biliary tract), as well as chronic intestinal diseases, accompanied by a syndrome of insufficiency of absorption. It is also observed with an overdose of dicoumarin. Vitamin K enters the body with food and is partly formed by the intestinal microflora.

Clinic. Hemorrhagic syndrome (bleeding from the nose, gums, gastrointestinal, intradermal and subcutaneous hemorrhages).

Diagnosis is confirmed by clinical observation data (the presence of diseases that contribute to vitamin K deficiency), as well as laboratory biochemical studies: hypoprothrombinemia below 30-35%, proconvertin deficiency, as well as factors IX and x are characteristic.

Treatment carried out in a hospital with vitamin K (vikasol) under the control of the level of prothrombin and coagulogram.

Hypopolivitaminoses, polyavitaminosis are more common than isolated relative or complete insufficiency of one of the vitamins. In the pathogenesis of hypovitaminosis and polyavitaminosis, one should take into account the mutual influence of certain vitamins, their synergism and antagonism.

The underlying disease leading to the syndrome of malabsorption is treated, vitamin preparations are prescribed, parenteral administration of the vitamin. Prevention: timely diagnosis and treatment of diseases of the gastrointestinal tract, in which the absorption of nutrients and vitamins is disturbed, the inclusion of vitamin therapy in the course of treatment of chronic diseases of the digestive tract.

LECTURE No. 5. Vaccination

The organization of preventive work among the child population includes, first of all, vaccination (that is, specific immunization), as well as a system of measures aimed at early detection of the disease and dispensary observation of sick and recovered children. Preventive vaccinations are the most important means of specific immunoprophylaxis and effective control of many infectious diseases. Thanks to the widespread introduction of vaccination in the world, smallpox was completely eliminated, and the number of cases of tetanus, whooping cough, and measles decreased tenfold.

What is vaccination? This is the creation in the human body of protection against the causative agent of infection. This method has been known for several hundred years. Unfortunately, at present there are no vaccines for all infectious agents, but these methods of protection have been created and successfully applied to many of them - against tuberculosis, hepatitis, whooping cough, diphtheria, tetanus, rabies, poliomyelitis, rubella, chicken pox, mumps , measles, etc. In the process of vaccination, specific immunity to infection is created by simulating the infectious process. For this, various types of vaccines are used. In addition, immunity is acquired after the transfer of an infectious disease. As well as after vaccination, and after illness, immunity can be lifelong, persistent or persist for a certain time.

1. Live vaccines

They consist of living but weakened (attenuated) pathogens. Virus strains are taken as pathogens. Examples of live vaccines: rubella, influenza, polio Sabin, mumps. They contain viruses that, when they enter the human body, cause the production of all parts of the immune response (cellular, humoral, secretory). When using live vaccines, stable, intense, long-term immunity is created, but there are a number of disadvantages:

1) a weakened vaccine virus can acquire virulence, i.e., become the causative agent of the disease (for example, vaccine-associated poliomyelitis);

2) live vaccines are difficult to combine, as this can mix viruses and the vaccine may become ineffective;

3) live vaccines have thermolability, i.e., they can lose their properties when the storage temperature changes. Live vaccines also include vaccines containing cross-reacting components that cause a weakened infection in the human body, protecting it from a more severe one. An example of such a vaccine is BCG containing bovine tuberculosis microbacteria;

4) live vaccines have a number of contraindications: they cannot be administered to patients with immunodeficiency; patients using steroid hormones, immunomodulators (suppressors); people who have undergone radiotherapy; patients with blood diseases (with leukemia), tumors of the lymphoid tissue (lymphomas), as well as pregnant women.

2. Killed vaccines

They contain dead pathogens, are easily dosed and combined with other vaccines, and are thermally stable. Killed vaccines cause the production of several types of antibodies that enhance the phagocytosis of microorganisms. An example is the pertussis vaccine. It also has an adjuvant effect, enhancing the immune response to another antigen that is part of the combined (associated) vaccine - DTP.

Disadvantage: when using these vaccines, only a humoral unstable link of immunity arises, therefore they act only for a certain time, require administration in several doses and re-vaccination throughout life. They are often administered with an adjuvant (an adjuvant that enhances the immune response) which is an aluminum compound. The adjuvant acts as a reservoir in which the antigen is stored for a long time. All killed vaccines also contain a preservative (an organic compound of mercury in an amount safe for humans).

3. Recombinant vaccines and toxoids

An example of such a vaccine is the vaccine against viral hepatitis B. In its preparation, a subunit of the virus gene is inserted into yeast cells. The yeast is then cultured and HBsAg is isolated from them. It is cleaned of yeast inclusions. This method of preparing a vaccine is called recombinant. This vaccine also contains a preservative and adsorbent in the form of aluminum hydroxide.

Toxoids are substances produced by pathogens. When preparing a number of vaccines, it is impossible to use the pathogen itself, therefore, in these cases, their toxin is taken. These are tetanus, diphtheria, staphylococcal and some other toxins.

Anatoxins cause persistent antitoxic immunity, they are easy to combine and dose. They are obtained by treating the toxin with formaldehyde under special temperature conditions. In this case, the toxin is neutralized, but its immune properties are preserved. The immunity produced by toxoids is only antitoxic. When using toxoids, bacteriocarrier and the occurrence of mild forms of the disease are possible.

4. Formation of an immune response

An important feature of children of the first year of life is that they have innate immunity to certain infectious diseases. The origin of this immunity is transplacental. Class G immunoglobulins cross the placenta from the 16th week of pregnancy. Thus, the fetus begins to receive ready-made maternal antibodies, and passive individual immunity is formed even in the prenatal period. Passive immunity is called immunity, in which the body acquires ready-made antibodies, and does not produce them itself during vaccination or the transfer of an infectious disease. After the birth of a child, individual maternal antibodies begin to break down, starting at 2 months of age. By the end of the first year of life, they completely disappear. Thus, the body of a newborn during the first year of life is protected from those infections, antibodies to which were obtained from the mother. These antibodies can interfere with vaccine immunity, and this factor is taken into account when developing a vaccination schedule.

Features of the immune response in the human body to the penetration of the antigen determines the main system of histocompatibility. It is located on chromosome 6 and is designated HLA. HLA are antigens found on peripheral blood leukocytes. The height of the immune response, the level of suppression of the formation of antibodies depends on them. Various cells are involved in the immune response: these are macrophages, T-lymphocytes (effector, helper, suppressor, memory T-cells). Also involved in this complex process are B-lymphocytes (memory B-cells), immunoglobulins of classes M, G, A, produced by plasma cells, cytokines. The components of the injected vaccine are taken up by macrophages, which cleave the antigen inside the cell and present parts of the antigen on their surface. T-lymphocytes recognize them and activate B-lymphocytes. B-lymphocytes become cells that form antibodies.

The primary administration of the vaccine takes place in 3 periods:

1) latent - this is the time between the introduction of the antigen and the appearance of antibodies in the blood. It can last from several days to 2-3 weeks depending on the type of vaccine, dose, and the state of the child’s immune system;

2) growth period - at this time, the number of antibodies increases rapidly. This period lasts from 4 days to 3 weeks (depending on the type of vaccine). The amount of antibodies increases especially rapidly with the introduction of measles and mumps vaccines, which makes it possible to use them for active immunization during emergency prophylaxis. With the introduction of pertussis and diphtheria components of DPT, the level of antibodies increases much more slowly than during the incubation period of the onset of the disease, therefore DTP is not used for emergency prevention;

3) a period of decline. After reaching the maximum level in the blood, the amount of antibodies begins to decrease rapidly, then the process slows down. It can go on for years or decades.

5. Immunization calendar and rules for the introduction of vaccines for certain types of vaccinations

BCG vaccination

Vaccination of newborns is carried out on days 4 - 7 of life directly in the ward after examination by a pediatrician. The anti-tuberculosis vaccine is live mycobacteria dried in a solution of monosodium glutamate. It is available in ampoules containing 1 mg of BCG, which is 20 doses of 0,05 mg of the drug. To obtain the required dose of 0,05 mg of BCG in 0,1 ml of solution, the dry BCG vaccine is diluted in 2 ml of isotonic sodium chloride solution. The vaccine is used no later than 2-3 hours after dilution. The newborn's history indicates the date of vaccination and the vaccine series. The exchange card sent to the children's clinic indicates the date of intradermal vaccination, the series of the vaccine, its expiration date, control number and the name of the manufacturing institute.

The BCG vaccine is administered at the border of the upper and middle third of the outer surface of the left shoulder after pre-treatment of the skin with a 70% solution of ethyl alcohol. The vaccine is administered strictly intradermally in a volume of 0,1 ml. At the injection site, a whitish papule is formed, 6 - 8 mm in diameter. After 15-20 minutes, the papule disappears and the skin acquires a normal color. The injection site should not be treated with disinfectant solutions, and a bandage should not be applied. In those vaccinated during the neonatal period, at the site of intradermal administration of the BCG vaccine, after 6 - 8 weeks, a specific reaction develops in the form of an infiltrate with a diameter of 5-10 mm with a small nodule in the center and the formation of a crust. Reversal of changes at the grafting site occurs within 2-4 months, after which a scar measuring up to 10 mm remains.

A gentle immunization with the BCG-M vaccine preparation has also been introduced, which is used in premature babies, as well as in newborns with purulent-septic diseases, hemolytic disease of the newborn, severe birth injuries, and generalized skin diseases.

Anti-tuberculosis revaccination is carried out in children's polyclinics, outpatient clinics under the guidance of an anti-tuberculosis dispensary. Re-vaccination of children in the absence of a scar can be carried out only according to epidemiological indications with a negative Mantoux test 2TE, not earlier than 2 years after the primary revaccination. This is usually done at the age of 7 years.

Contraindications to BCG revaccination: past tuberculosis, positive or doubtful Mantoux tests with 2TE PPD-L, complicated reactions to the previous administration of BCG (keloid scars, chronic diseases in the acute stage, allergic diseases in the acute stage, malignant neoplasms and blood diseases, immunodeficiency states).

Complications after BCG vaccinations are usually rare. They are expressed in the form of lymphadenitis, keloid scars and cold abscesses.

DTP vaccination

It is carried out with a DPT-vaccine - a mixture of purified concentrated diphtheria and tetanus toxoids adsorbed on aluminum oxide hydrate, as well as pertussis vaccine. The first vaccination is carried out at 3 months. Vaccination 3 times. The second - at 4,5 months, the third - at 6 months. The first revaccination is carried out at the age of 18 months. The second - in 7 years.

The vaccination dose is 0,5 ml, administered intramuscularly. The vaccine is highly effective, but can cause a general reaction in the form of fever, sleep disturbance, appetite, and allergic reactions. Children prone to allergic manifestations (exudative diathesis, asthmatic bronchitis, bronchial asthma, neurodermatitis) are vaccinated with ADS vaccine without a pertussis component.

Polio vaccination

An oral live polio vaccine is used, which is a mixture of attenuated Sabin strains of the 1st, 2nd, 3rd types, cultivated on a primary culture of green monkey kidney cells. Produced in liquid form in 5 ml bottles and in the form of dragees. Dragees with a mixture of 3 immunological types are white, type 1 - pink, type 2 - lilac, type 3 - blue. Each tablet contains one vaccination dose. Liquid polio vaccine is available as a monovaccine and a trivaccine. The grafting dose of liquid monovaccine is contained in 2 drops (0,1 ml), trivaccine - in 4 drops (0,2 ml). To prevent paralytic poliomyelitis, 5 injections of the vaccine are needed.

Specific prophylaxis against polio for all children is carried out from the age of 3 months three times with an interval of 1,5 months. Revaccination is carried out at 1-2 and 2-3 years twice with an interval of 1,5 months and once at 6-7 years and at 14 years. The vaccine has virtually no adverse reactions and can be combined with the DTP vaccine.

Rubella vaccination

The rubella vaccine is a live lyophilized attenuated vaccine that also contains neomycin. It is produced in the form of a monovaccine and a divaccine (mumps-rubella). It is recommended to vaccinate girls of pubertal age and women of childbearing age who do not plan pregnancy in the next few months.

Mumps vaccination

Mumps vaccine is a live, attenuated, contains antibiotics of the aminoglycoside group. Children from 12 months to 7 years of age who have not previously been ill are vaccinated. Vaccination is mandatory for boys, since one of the complications after mumps may be orchitis and subsequently infertility. The vaccine is administered subcutaneously, under the shoulder blade or in the shoulder area. Immunity is maintained for 8 years.

Measles prevention provides for the introduction of measles vaccine to all children at 12 months and 7 years, and from 1990 to those who do not have measles antibodies.

Vaccination against viral hepatitis B.

Specific prophylaxis has been carried out since 2001 for all newborns in the first 12 hours after birth, then one month and 6 months after the first administration of the drug. The recombinant vaccine "KOMBITEKS" is used

For children whose mothers are carriers of viral hepatitis B or have had it in the last trimester of pregnancy, the vaccine is administered according to the following scheme: 0-1-2-12. In view of the fact that in recent years the incidence of viral hepatitis B among adolescents has increased, it is advisable to vaccinate children aged 8-11 years according to the scheme: 2 vaccinations at a monthly interval and subsequent administration after 6 months.

Показания for vaccinations:

1) scheduled vaccinations for children according to the calendar and military personnel;

2) unscheduled vaccinations in case of a threat of an occupational disease, residence and upcoming trip to the epidemiological territory, emergency vaccination of persons in contact with the source of infection.

Противопоказания for vaccinations:

1) severe reaction (fever, swelling at the site of the vaccine, hyperemia during the first or repeated administration);

2) complications during the first or repeated administration;

3) immunosuppression;

4) immunodeficiency state;

5) malignant blood diseases, neoplasms;

6) progressive diseases of the nervous system;

7) pregnancy;

8) allergic reactions, anaphylactic shock.

LECTURE No. 6. Rickets, rickets-like diseases

Rickets is a disease of infants and young children with a disorder of bone formation and lack of bone mineralization, the leading link is the deficiency of vitamin D and its active metabolites during the period of the most intensive growth of the body.

Etiology. The main factor is hypovitaminosis D, vitamin D deficiency of exogenous or endogenous origin. Lack of sun exposure and exposure to fresh air, especially in winter and autumn in cities, since vitamin D is endogenously formed in the skin under the influence of solar radiation. Nutritional factors: improper feeding and nutritional deficiency of vitamin D, long-term artificial feeding with unadapted milk formulas.

Perinatal factors: prematurity (immaturity of enzyme systems). The rapid growth of the child, diseases accompanied by acidosis, insufficient intake of calcium and phosphorus salts.

Pathogenesis. Vitamin D is a steroid compound and is known as vitamin D₂ (ergocalciferol) and vitamin D₃ (cholecalciferol), which are similar in structure, physical, chemical properties and effect on the human body. Vitamin D supplied with food is converted in the liver and kidneys, resulting in the formation of 1,25-dihydroxy-vitamin D, which has a hormone-like effect, this compound affects the genetic apparatus of intestinal cells, increases the synthesis of a protein that binds calcium and ensures its transport in the body.

With a lack of vitamin D, the absorption and metabolism of calcium is disturbed, its concentration in the blood decreases, which causes a reaction of the parathyroid glands and an increase in the secretion of parathyroid hormone, which regulates the metabolism of calcium and phosphorus.

Increased secretion of parathyroid hormone leads to the mobilization of calcium from bone tissue, suppression of phosphate reabsorption in the renal tubules, and therefore the content of inorganic phosphates in the blood falls and the activity of alkaline phosphatase sharply increases. Violations of phosphate-calcium metabolism lead to the development of acidosis, which is accompanied by impaired excitability of the nervous system.

Clinic. The following degrees of rickets are distinguished by severity:

1) mild - small changes in the nervous and muscular systems; does not give residual effects (I degree);

2) moderate severity - pronounced changes in the bone, muscle, nervous and hematopoietic systems, moderate dysfunction of internal organs, a slight increase in the size of the liver and spleen, anemia (grade II);

3) severe - pronounced changes in the central nervous, bone and muscle systems, internal organs (III degree).

The initial period is more often noted in the second or third month, or manifests itself throughout the first year of life. From the side of the autonomic nervous system: sweating, nape baldness. From the nervous system: anxiety, irritability, tearfulness, disturbed sleep, muscular dystonia. Unsharp softening of the edges of the large fontanel and bones along the swept and lambdoid sutures.

Laboratory data. Biochemical studies: mild decrease in the amount of phosphorus, normal calcium content, increase in phosphatase activity. Increased phosphorus in daily urine. There are no radiological changes.

In the period of the height of the disease, along with the phenomena of inhibition of the nervous system, changes in the bones appear (softening of the bones of the skull, chest, limbs, pelvic bones, lower jaw) and is manifested by craniotabes, arched curvature of the forearms, deformities of the chest. Frontal and parietal tubercles, rosaries on the ribs, thickening of the epiphyses of tubular bones in the form of pearl strands, pronounced muscular hypotension of the muscles of the anterior abdominal wall with the formation of a frog belly, hypotension of the heart muscle (deafness of tones, tachycardia, gentle systolic murmur), weakness of the ligamentous apparatus, leading to spinal deformities. Bone changes, hardly noticeable with rickets of the I degree and distinct with the II degree, turn into deformation with rickets of the III degree. With rickets II and III degree, the spleen and liver are enlarged.

Biochemical studies: hypophosphatemia, hypocalcemia, increased activity of alkaline phosphatase. On radiographs, the contours of the bones are blurred, stripes are visible that correspond to zones of calcification in the metaphyses during the repair period. The epiphyses of the tubular bones are goblet, the edges of the metaphyses are fringed.

Late rickets include rare cases of the disease, when its active manifestations are observed at the age of over 4 years. Late rickets, observed in the war and the first post-war years, was characterized by the presence of common symptoms of the disease: anorexia, sweating, pain in the legs, fatigue. Bone deformities were noted only in some cases.

Convalescence period: neurological and vegetative symptoms disappear, condition improves, muscle tone increases, motor and static functions are restored, constipation disappears. The level of phosphorus, calcium is restored, decreases, and the level of alkaline phosphatase approaches the norm.

The period of residual effects: rachitic changes in the internal organs disappear, the tone of the muscles and ligamentous apparatus is restored. All biochemical parameters are normalized.

Diagnostics is carried out on the basis of clinical, laboratory data and X-ray data.

Differential diagnosis is carried out with a number of rickets-like diseases of a hereditary nature - phosphate diabetes, renal tubular acidosis, Debre - de Toni - Fanconi syndrome, as well as with congenital dislocation of the hip, chondrodystrophy, osteopathy in chronic renal failure, congenital bone fragility.

Treatment. Vegetables and fruits should be introduced into the child’s diet in a timely manner. Complementary foods should contain sufficient amounts of vitamins, salts, and foods containing natural vitamin D₃ (egg yolk, fish oil). Normalization of the regime with sufficient exposure to fresh air, massage, gymnastics. At the initial manifestations, full-term children are prescribed vitamin D supplements.₂ 300 - 800 IU per day, per course 400-000 IU; during the peak period for moderate and severe rickets, 600-000 IU per day is prescribed in 10-000 doses, for a course of 16 - 000 IU. During treatment, monitor the sensitivity of the child’s body to vitamin D using the Sulkovich test to prevent hypervitaminosis.

Ultraviolet therapy has a beneficial effect in the initial period and in the subacute course of rickets in young children. Massage and gymnastics are used at any time, but not in acute cases.

Forecast with timely treatment and elimination of the cause, it is favorable. In severe cases, psychomotor developmental delay, skeletal deformity, and posture disorders are possible.

Prevention. Rational nutrition, better natural feeding, vegetable and fruit juices, additional vitamins, sufficient insolation, sanitary and hygienic regime, hardening, therapeutic nutrition, massage, proper education. Antenatal prophylaxis in pregnant women in the last 2-3 months of pregnancy with vitamin D is advisable₂ 500-1000 IU per day. A long stay in the open air and a balanced diet are necessary. In the autumn-winter period, ultraviolet irradiation of children for preventive purposes should begin from 1-1,5 months of life. Two courses should be carried out with an interval of 2 months. The physiological requirement for vitamin D of a healthy full-term baby in the first year of life ranges from 400-500 IU per day. In cases where a child for some reason does not receive ultraviolet irradiation for prophylactic purposes, an artificial vitamin D preparation should be prescribed.₂ or D₃. For the purpose of antenatal prophylaxis in the last 3-4 months of pregnancy, Gendevit is recommended 1-2 tablets per day (250-500 IU vitamin D₂), under unfavorable conditions - 4 tablets per day. Contraindications: maternal age over 30 years, maternal illness. Postnatal prophylaxis is carried out from 2-3 weeks of age at 500 IU per day (1 drop of videohol), for a course of 150-000 IU.

LECTURE No. 7. Diseases of the respiratory system. Classification, clinic, diagnosis, treatment

1. Acute bronchitis

Acute bronchitis is an acute, diffuse inflammation of the tracheobronchial tree. Classification: acute bronchitis (simple), acute obstructive bronchitis, acute bronchiolitis, acute bronchiolitis obliterans, recurrent bronchitis, recurrent obstructive bronchitis, chronic bronchitis, chronic bronchitis with obliteration.

Etiology. The disease is caused by viral infections (influenza viruses, adenoviruses, parainfluenza, respiratory syncytial, measles, pertussis, etc.) and bacterial infections (staphylococci, streptococci, pneumococci, etc.); physical and chemical factors (dry, cold, hot air, nitrogen oxides, sulfur dioxide, etc.). Cooling, chronic focal infection in the nasopharyngeal area, impaired nasal breathing, and chest deformation predispose to the disease.

Pathogenesis. The damaging agent penetrates the trachea and bronchi with inhaled air through hematogenous and lymphogenous routes. Acute inflammation of the bronchial tree is accompanied by a violation of bronchial patency by an edematous-inflammatory or bronchospastic mechanism. Characterized by hyperemia, swelling of the mucous membrane, mucous, mucopurulent or purulent secretion on the walls of the bronchi in their lumen, and degenerative changes in the ciliated epithelium. In severe forms, the inflammatory process affects not only the mucous membrane, but also the deep tissues of the bronchial wall.

Clinic. Bronchitis of infectious etiology begins with rhinitis, nasopharyngitis, moderate intoxication, increased body temperature, weakness, a feeling of weakness, rawness behind the sternum, dry cough turning into wet. Auscultatory signs are absent, or harsh breathing and dry wheezing are detected over the lungs. There are no changes in peripheral blood. This course is observed more often with damage to the trachea and large bronchi.

With a moderate course, general malaise, weakness are significantly expressed, a strong dry cough appears with difficulty breathing and shortness of breath, pain in the lower parts of the chest and abdominal wall associated with muscle strain when coughing. Cough gradually becomes wet, sputum acquires a mucopurulent or purulent character. In the lungs during auscultation, hard breathing, dry and moist small bubbling rales are heard. Body temperature subfebrile. There are no pronounced changes in peripheral blood.

A severe course of the disease is observed with a predominant lesion of the bronchioles. Acute symptoms of the disease subside by the 4th day and, with a favorable outcome, completely disappear by the 7th day. Acute bronchitis with impaired bronchial patency tends to protracted course and transition to chronic bronchitis.

Acute bronchitis of toxic-chemical etiology is severe. The disease begins with a painful cough with the release of mucous or bloody sputum, bronchospasm quickly joins (dry whistling rales are heard against the background of an extended exhalation), shortness of breath progresses (up to suffocation), symptoms of respiratory failure and hypoxemia increase. Radiological symptoms of acute pulmonary emphysema can be determined.

Diagnostics based on clinical and laboratory data.

Treatment. Bed rest, plenty of warm drinks with honey, raspberries, linden blossom. Prescribe antiviral and antibacterial therapy, vitamin therapy (ascorbic acid up to 1 g per day, vitamin A 3 mg 3 times a day), mustard plasters, chest cups. For severe dry cough, antitussive drugs codeine, libexin, etc. are prescribed.

For wet cough - mucolytic drugs bromhexine, ambrobene, etc. Inhalation of expectorants, mucolytics, heated mineral alkaline water, eucalyptus, anise oil using a steam inhaler is indicated. Inhalations are carried out for 5 minutes 3-4 times a day (for 3-5 days). Bronchospasm is relieved by prescribing aminophylline (0,15 g 3 times a day). Antihistamines are indicated.

Prevention. Elimination of the etiological factor of acute bronchitis (hypothermia, chronic and focal infection in the respiratory tract, etc.).

2. Chronic bronchitis

Chronic bronchitis is a progressive, diffuse inflammation of the bronchi, not associated with local or generalized lung damage and manifested by cough. It is customary to talk about the chronic nature of the process if the cough lasts at least 3 months in the first year for 2 years in a row.

Etiology. The disease is associated with prolonged irritation of the bronchi by various harmful factors (inhalation of air contaminated with dust, smoke, carbon monoxide, sulfur dioxide, nitrogen oxides and other chemical compounds), smoking, recurrent respiratory infection (the main role is played by respiratory viruses, Pfeiffer's bacillus, pneumococci), occurs less frequently in cystic fibrosis. Predisposing factors: chronic inflammatory, suppurative processes in the lungs, chronic foci of infection in the upper respiratory tract, decreased body reactivity, hereditary factors.

Pathogenesis. The main pathogenetic mechanism is hypertrophy and hyperfunction of the bronchial glands with increased mucus secretion, a decrease in serous secretion, a change in the composition of the secretion - an increase in acidic mucopolysaccharides in it, which increases the viscosity of sputum. Under these conditions, the ciliated epithelium does not ensure emptying of the bronchial tree and the normal renewal of the entire layer of secretion (emptying of the bronchi occurs only when coughing). Long-term hyperfunction leads to depletion of the mucociliary apparatus of the bronchi, dystrophy and atrophy of the epithelium.

In case of violation of the drainage function of the bronchi, a bronchogenic infection occurs, the activity and relapses of which depend on local immunity of the bronchi and the development of secondary immunological deficiency, bronchial obstruction develops due to hyperplasia of the epithelium of the mucous glands, edema and inflammatory infiltration of the bronchial wall, obstruction of the bronchi with an excess of viscous bronchial secretion, bronchospasm . Obstruction of the small bronchi leads to overstretching of the alveoli on expiration and disruption of the elastic structures of the alveolar walls and the appearance of hypoventilated or non-ventilated zones, and therefore the blood passing through them is not oxygenated, arterial hypoxemia develops.

In response to alveolar hypoxia, spasm of the pulmonary arterioles and an increase in total pulmonary and pulmonary arteriolar resistance occur, precapillary pulmonary hypertension occurs. Chronic hypoxemia leads to an increase in blood viscosity, accompanied by metabolic acidosis, which further enhances vasoconstriction in the pulmonary circulation. Inflammatory infiltration in large bronchi is superficial, and in medium and small bronchi, bronchioles - deep with the development of erosion and the formation of meso- and panbronchitis.

The remission phase is manifested by a decrease in inflammation, a significant decrease in exudation, proliferation of connective tissue and epithelium, especially with ulceration of the mucous membrane.

Clinic. The beginning is gradual. The first symptom is a cough in the morning with mucous sputum, gradually the cough begins to occur both at night and during the day, intensifies in cold weather and becomes constant over the years. The amount of sputum increases, it becomes mucopurulent or purulent. Shortness of breath appears.

With purulent bronchitis, purulent sputum is periodically released, but bronchial obstruction is not pronounced. Obstructive chronic bronchitis is characterized by persistent obstructive disorders. Purulent-obstructive bronchitis occurs with the release of purulent sputum and obstructive ventilation disorders.

Frequent exacerbations during periods of cold, damp weather: cough and shortness of breath increase, the amount of sputum increases, malaise and fatigue appear. The body temperature is normal or subfebrile, hard breathing and dry wheezing over the entire surface of the lungs can be determined.

Diagnostics. A slight leukocytosis with a rod-nuclear shift in the leukocyte formula is possible. With exacerbation of purulent bronchitis, the biochemical indicators of inflammation (C-reactive protein, sialic acids, seromucoid, fibrinogen, etc.) change slightly. Sputum examination: macroscopic, cytological, biochemical. With severe exacerbation, the purulent nature of the sputum is detected, predominantly neutrophilic leukocytes, an increase in the content of acidic mucopolysaccharides and DNA fibers that increase the viscosity of the sputum, a decrease in the content of lysozyme, etc. Bronchoscopy is indicated, with the help of which endobronchial manifestations of the inflammatory process are assessed (catarrhal, purulent, atrophic, hypertrophic, hemorrhagic) and its severity (but only to the level of the subsegmental bronchi).

Differential diagnosis carried out with chronic pneumonia, bronchial asthma, tuberculosis. Unlike chronic pneumonia, chronic bronchitis always proceeds with the gradual development of widespread bronchial obstruction and often emphysema, respiratory failure and pulmonary hypertension (chronic cor pulmonale). X-ray changes are also diffuse in nature: peribronchial sclerosis, increased transparency of the lung fields due to emphysema, expansion of the branches of the pulmonary artery.

Chronic bronchitis is distinguished from bronchial asthma by the absence of asthma attacks.

Differences with pulmonary tuberculosis are associated with the presence or absence of signs of tuberculosis intoxication, Mycobacterium tuberculosis in sputum, X-ray and bronchoscopic examination data, and tuberculin tests.

Treatment. In the phase of exacerbation of chronic bronchitis, therapy should be aimed at eliminating the inflammatory process in the bronchi, improving bronchial patency, and restoring impaired general and local immunological reactivity.

Bacterial therapy is prescribed, which is selected taking into account the sensitivity of the sputum microflora, administered orally or parenterally, sometimes combined with intratracheal administration. Showing inhalation.

Apply expectorant, mucolytic and bronchospasmolytic drugs, drink plenty of water to restore and improve bronchial patency. Phytotherapy using marshmallow root, coltsfoot leaves, plantain. Assign proteolytic enzymes (trypsin, chymotrypsin), which reduce the viscosity of sputum, but are now rarely used. Acetylcysteine ​​has the ability to break the disulfide bonds of mucus proteins and causes a strong and rapid liquefaction of sputum.

Bronchial drainage improves with the use of muco-regulators that affect the secretion and synthesis of glycoproteins in the bronchial epithelium (bromhexine). In case of insufficiency of bronchial drainage and the presence of symptoms of bronchial obstruction, bronchospasmolytic agents are added to therapy: eufillin, anticholinergics (atropine in aerosols), adrenergic stimulants (ephedrine, salbutamol, berotek).

In a hospital setting, intratracheal lavages for purulent bronchitis are combined with sanitation bronchoscopy (3-4 sanitation bronchoscopy with a break of 3-7 days). The restoration of the drainage function of the bronchi is also facilitated by physical therapy, chest massage, and physiotherapy.

In the event of allergic syndromes, calcium chloride is prescribed orally and intravenously with antihistamines. If there is no effect, it is possible to conduct a short (until the allergic syndrome is removed) course of glucocorticoids (daily dose should not exceed 30 mg). The risk of infection activation does not allow recommending long-term use of glucocorticoids.

In patients with chronic bronchitis complicated by respiratory failure and chronic cor pulmonale, the use of veroshpiron (up to 150-200 mg per day) is indicated. The diet should be high-calorie and fortified. Prescribe ascorbic acid in a daily dose of 1 g, B vitamins, nicotinic acid, aloe, if necessary, methyluracil.

When the disease is complicated by pulmonary and pulmonary heart failure, oxygen therapy, auxiliary artificial ventilation of the lungs are used. Anti-relapse and supportive therapy begins in the phase of subsiding exacerbation, is carried out in local and climatic sanatoriums, it is also prescribed during clinical examination.

It is recommended to distinguish three groups of dispensary patients. The first group includes patients with severe respiratory failure, cor pulmonale and other complications of the disease, with loss of ability to work; patients need systematic maintenance therapy, which is carried out in a hospital or by a local doctor. These patients are examined at least once a month. The second group consists of patients with frequent exacerbations of chronic bronchitis and moderate respiratory dysfunction. Patients are examined by a pulmonologist 3-4 times a year, anti-relapse courses are prescribed in spring and autumn, as well as after acute respiratory diseases. An effective method of taking medications is inhalation. According to indications, the bronchial tree is sanitized by intratracheal lavage and sanitary bronchoscopy. For active infection, antibacterial drugs are used. The third group consists of patients in whom anti-relapse therapy led to the subsidence of the process and the absence of relapses for 20 years. They are indicated for seasonal preventive therapy, including agents aimed at improving bronchial drainage and increasing reactivity.

3. Pneumonia

Pneumonia is an inflammation of the lungs, characterized by inflammation of the parenchymal, respiratory part of the lungs. Classification by form: acute pneumonia is divided into community-acquired, nosocomial, with perinatal infection and in patients with immunodeficiency. According to the morphological form: focal, focal - confluent, segmented, lobar, interstitial. Downstream: acute, protracted (in the absence of resolution of the pneumonic process within 6 to 8 weeks). According to the development of complications: pulmonary (synpneumonic pleurisy, metapneumonic pleurisy, pulmonary destruction, lung abscess, pneumothorax, pyopneumothorax), extrapulmonary (toxic shock, DIC, cardiovascular insufficiency, respiratory distress syndrome).

Etiology. Various bacteria act as the etiological factor: pneumococci, staphylococci, streptococci, Klebsiella pneumoniae, gram-negative flora and mycoplasmas (community-acquired form); staphylococcus, Pseudomonas aeruginosa (nosocomial form); chlamydia, cytomegalovirus (for perinatal infection); various bacteria in patients with immunodeficiency.

In the occurrence of the disease, an important role can be played by viral-bacterial associations, chemical and physical agents - exposure to light chemicals (gasoline, etc.), thermal factors (cooling or burns), radioactive radiation (etiological factors are usually combined with infectious ones). Pneumonia can be the result of allergic reactions in the lungs or a manifestation of a systemic disease (interstitial pneumonia in connective tissue diseases).

Pathogenesis. The pathogen penetrates into the lung tissue by bronchogenic, hematogenous and lymphogenous routes from the upper respiratory tract, usually in the presence of acute or chronic foci of infection or from infectious foci in the bronchi (chronic bronchitis, bronchiectasis). A special role in pathogenesis is played by violations of the protective mechanisms of the bronchopulmonary system, as well as the state of humoral and tissue immunity. The survival of bacteria in the lungs, their reproduction and spread through the alveoli depend on their aspiration with mucus from the upper respiratory tract and bronchi (which is favored by cooling), on the excessive formation of edematous fluid, covering an entire lobe or several lobes of the lungs in lobar (pneumococcal) pneumonia. At the same time, immunological damage and inflammation of the lung tissue is possible due to a reaction to the antigenic material of microorganisms and other allergens.

A viral infection, causing inflammation of the upper respiratory tract and bronchi, and in some cases pneumonia, even more often favors the activation of a bacterial infection and the occurrence of bacterial focal or lobar pneumonia. The appearance of bacterial pneumonia usually at the end of the first or at the beginning of the second week after a respiratory viral disease corresponds to a significant decrease in the bactericidal activity of the alveolar-macrophage system of the lungs. Chronic pneumonia can occur due to unresolved acute pneumonia with slowing down and stopping the resorption of exudate in the alveoli and the formation of pneumosclerosis, inflammatory cell changes in the interstitial tissue, often of an immunological nature (lymphocytic and plasma cell infiltration).

The protracted course of acute pneumonia, their transition to a chronic form is facilitated by immunological disorders that are caused by repeated respiratory viral infection, chronic infection of the upper respiratory tract (chronic tonsillitis, sinusitis, etc.) and bronchi.

Clinic. Depends on the etiology, nature and phase of the course, morphological substrate of the disease and its prevalence in the lungs, as well as complications (pulmonary suppuration, pleurisy, etc.). Acute pneumonia usually begins abruptly, often after cooling: the patient experiences tremendous chills; body temperature rises to febrile levels of 39-40 ° C, less often to 38 or 41 ° C; pain when breathing on the side of the affected lung increases with coughing, first dry, then wet, with purulent viscous sputum. The patient's condition is serious. The skin of the face is hyperemic and cyanotic. Breathing is rapid, shallow, with flaring of the wings of the nose.

After the application of antibiotic therapy, the high temperature gradually decreases. The chest lags behind in the act of breathing on the side of the affected lung, the percussion of which, depending on the morphological stage of the disease, reveals dull tympanitis (tide stage), shortening (dulling) of the pulmonary sound (stage of red and gray hepatization) and pulmonary sound (resolution stage).

Depending on the staging nature of morphological changes, auscultation reveals, respectively, increased vesicular respiration, bronchial respiration, and vesicular or weakened vesicular respiration. In the hepatization phase, increased voice trembling and bronchophony are determined. Due to the uneven development of morphological changes in the lungs, percussion and auscultatory patterns can be variegated.

Due to the defeat of the pleura (parapneumonic serous-fibrinous pleurisy), a pleural friction rub is heard. At the height of the disease, the pulse is quickened, soft, corresponds to reduced blood pressure, from the side of the cardiovascular system, the first tone is muffled and the second tone is accentuated on the pulmonary artery. In the blood test - neutrophilic leukocytosis, increased ESR, anemia.

On x-ray, homogeneous shading of the entire affected lobe or part of it is determined, especially on lateral radiographs. Fluoroscopy may be insufficient in the early hours of illness. Similar to pneumococcal, staphylococcal pneumonia can occur. More often it proceeds more severely, accompanied by destruction of the lungs with the formation of thin-walled air cavities, lung abscesses.

With the phenomena of severe intoxication, staphylococcal (usually multifocal) pneumonia occurs, complicating a viral infection of the bronchopulmonary system (viral-bacterial pneumonia). This kind of pneumonia is characterized by a pronounced intoxication syndrome, manifested by hyperthermia, chills, hyperemia of the skin and mucous membranes, dizziness, headache, severe shortness of breath, hemoptysis, tachycardia, nausea, and vomiting.

With severe infectious-toxic shock, vascular insufficiency develops (BP 90 - 80 / 60-50 mm Hg, pallor of the skin, cold extremities, the appearance of sticky sweat). With the progression of intoxication syndrome, cerebral disorders, an increase in heart failure, cardiac arrhythmias, the development of shock lung, hepatorenal syndrome, disseminated intravascular coagulation syndrome, and toxic enterocolitis are revealed. Such pneumonia can lead to rapid death.

Focal pneumonia, bronchopneumonia arise as a result of complications of acute or chronic inflammation of the upper respiratory tract and bronchi, in patients with congestive lungs, severe diseases that debilitate the body, in the postoperative period, as a result of fat embolism in injuries, and thromboembolism. The disease may begin with chills, but not as severe as with lobar pneumonia. Body temperature rises to 38-38,5 °C, rarely higher. A cough appears and intensifies, dry, then with mucopurulent sputum. Chest pain may occur when coughing and when inhaling.

With confluent focal (usually staphylococcal) pneumonia, the condition worsens: severe shortness of breath, cyanosis, shortening of the lung sound, breathing can be enhanced vesicular with bronchial foci, foci of fine and medium bubbling rales are heard.

On the radiograph (sometimes only on the tomogram), lobular, subsegmental and segmental shadows, increased lung pattern are revealed, bullae and foci of abscess formation can be detected radiologically.

Diagnostics. Based on clinical and laboratory data, shortening of the percussion sound is taken into account, an increase in vesicular breathing is noted, sometimes with foci of bronchial breathing, crepitus, small- and medium-bubble rales, and focal shadowing on radiographs (sometimes on tomograms). Examine sputum or throat swabs for bacteria, including Mycobacterium tuberculosis, viruses, and Mycoplasma pneumoniae.

Differential diagnosis carried out with acute bronchitis and exacerbation of chronic bronchitis (in contrast to pneumonia, intoxication is less pronounced, foci of shading are not detected radiologically).

Treatment pneumonia with mild course and favorable living conditions can be carried out at home, but most patients need inpatient treatment. According to emergency indications, patients with lobar and other pneumonias and severe infectious-toxic syndrome are hospitalized. At the height of the disease, bed rest is shown, a mechanically and chemically sparing diet with limited salt and a sufficient amount of vitamins, especially A and C. With the disappearance or a significant decrease in the phenomena of intoxication, the regimen is expanded, physiotherapy exercises are prescribed, in the absence of contraindications (diseases of the heart, digestive organs) the patient is transferred to diet No. 15.

Immediately after taking sputum, swabs or swabs for bacteriological examination, etiotropic antibiotic therapy is started, which is carried out under the control of clinical efficacy, and subsequently, taking into account the inoculated microflora and its sensitivity to antibiotics.

With community-acquired pneumonia, semi-synthetic penicillins, penicilli, macrolides of a new generation are prescribed; with nosocomial pneumonia, "protected" penicillins, aminoglycosides, second-third generation cephalosporins, fluoroquinolones and other antibiotics of the reserve group are prescribed; for pneumonia with intrauterine infection - new generation macrolides (spiromycin, roxithromycin, azithromycin); in pneumonia in patients with immunodeficiencies, third-fourth generation cephalosporins, fluoroquinolones are prescribed.

For severe viral-bacterial pneumonia, which often occurs as a result of the interaction of the influenza virus and staphylococcus, along with intravenously administered broad-spectrum antibiotics, the administration of specific donor anti-influenza γ-globulin 3-6 ml is indicated. Combinations of antibiotics for the treatment of complicated pneumonia: cephalosporins + semisynthetic penicillins; semisynthetic penicillins + aminoglycosides; cephalosporins + aminoglycosides. Detoxification agents (hemodesis, etc.) are also used. Mucolytic therapy, bronchodilator therapy, physiotherapy, immunocorrective therapy, exercise therapy are prescribed.

With severe tachycardia, a decrease in systolic pressure to 100 mm Hg. Art. and below, patients with pneumonia are prescribed strophanthin, sulfokamphokain. Discharged from the hospital during the period of clinical recovery or remission, persons who have had pneumonia should be taken under dispensary observation. For rehabilitation, they are sent to local sanatoriums. The prognosis for pneumonia has improved significantly since the start of the use of antibacterial agents. But it remains serious with staphylococcal and Friedlander pneumonias, with often recurrent chronic pneumonias complicated by an obstructive process, respiratory and pulmonary heart failure, as well as with the occurrence of pneumonia in people with severe diseases of the cardiovascular and other systems. Mortality from pneumonia in these cases remains high.

4. Bronchial asthma

Bronchial asthma is a chronic relapsing disease with a primary lesion of the respiratory tract, which is based on chronic allergic inflammation of the bronchi, accompanied by their hyperreactivity and intermittent attacks of shortness of breath or suffocation as a result of widespread bronchial obstruction, which is caused by bronchospasm, mucus hypersecretion, swelling of the bronchial wall.

There are two forms of bronchial asthma - immunological and non-immunological - and a number of clinical and pathogenetic variants: atopic, infectious-allergic, autoimmune, dyshormonal, neuropsychic, adrenergic imbalance, primary altered bronchial reactivity (including "aspirin" asthma and asthma of physical effort ), cholinergic.

Etiology and risk factors for the occurrence of bronchial asthma in children: atopy, bronchial hyperreactivity, heredity. Causes (sensitizing): household allergens (house dust, house dust mites), epidermal allergens of animals, birds, and insects, fungal allergens, pollen allergens, food allergens, drugs, viruses and vaccines, chemicals.

Pathogenesis. The general pathogenetic mechanism is a change in the sensitivity and reactivity of the bronchi, determined by the reaction of bronchial patency in response to the influence of physical and pharmacological factors.

It is believed that in 1/3 of patients (mainly in persons suffering from an atonic variant of the disease), asthma is of a hereditary origin. The most studied allergic mechanisms of asthma, which are based on IgE- or IgG-mediated reactions. The central place in the pathogenesis of "aspirin" asthma is given to leukotrienes. With asthma of physical effort, the process of heat transfer from the surface of the respiratory tract is disturbed.

Clinic. The disease often begins with a paroxysmal cough, accompanied by shortness of breath with the discharge of a small amount of glassy sputum (asthmatic bronchitis). The full picture of bronchial asthma is characterized by the appearance of mild, moderate or severe attacks of suffocation. An attack may begin with a precursor (profuse discharge of watery secretion from the nose, sneezing, paroxysmal cough, etc.).

An attack of bronchial asthma is characterized by a short inhalation and an extended exhalation, accompanied by wheezing audible at a distance. The chest is in the position of maximum inspiration, the patient takes a forced position, sitting on the bed, hanging his legs down, tilting his body slightly forward. The muscles of the shoulder girdle, back, and abdominal wall take part in breathing. On percussion over the lungs, a box sound is determined, and a lot of dry rales are heard during auscultation. The attack often ends with the separation of viscous sputum.

Severe prolonged attacks can turn into an asthmatic state - one of the most formidable options for the course of the disease.

5. Asthmatic condition

The asthmatic condition is manifested by increasing resistance to bronchodilatory therapy and unproductive cough. There are two forms of asthmatic condition - anaphylactic and metabolic. In the anaphylactic form, caused by immunological or pseudo-allergic reactions with the release of a large number of mediators of an allergic reaction (most often in people with hypersensitivity to drugs), an acute severe asthma attack occurs.

The metabolic form, due to the functional blockade of β-adrenergic receptors, occurs as a result of an overdose of sympathomimetics during a respiratory tract infection, and is formed within a few days.

In the initial, stage I, sputum ceases to come out, pain appears in the muscles of the shoulder girdle, chest and in the abdominal area. Hyperventilation, loss of moisture with exhaled air leads to an increase in the viscosity of sputum and obstruction of the bronchial lumen with a viscous secret.

The formation of mute lung areas in the posterior lower sections of the lungs indicates the transition of the status to stage II with a clear discrepancy between the severity of remote wheezing and their absence during auscultation. The condition of the patients is extremely serious. The chest is emphysematous, swollen. Pulse exceeds 120 beats per minute. Arterial pressure tends to increase. On the ECG - signs of overload of the right heart. Respiratory or mixed acidosis is formed.

In stage III (with hypoxic-hypercapnic coma), shortness of breath and cyanosis increase, sudden excitement is replaced by loss of consciousness, convulsions are possible. The pulse is paradoxical, blood pressure decreases. The course of the disease is cyclical: an exacerbation phase with characteristic symptoms and data from laboratory and instrumental studies is replaced by a remission phase. Complications of bronchial asthma: emphysema, often the addition of infectious bronchitis, with a long and severe course of the disease, the appearance of cor pulmonale.

Diagnostics is carried out on the basis of a carefully collected anamnesis, typical attacks of expiratory dyspnea, eosinophilia in the blood, especially in sputum, an allergological examination with skin and in some cases provocative inhalation tests, an examination of immunoglobulins E and G. A good analysis of anamnestic, clinical, radiological and laboratory data allows exclude bronchial obstruction syndrome in nonspecific and specific inflammatory diseases of the respiratory system, connective tissue diseases, helminthic invasions, bronchial obstruction (foreign body, tumor), endocrine-humoral pathology (hypoparathyroidism, etc.), hemodynamic disorders in the pulmonary circulation, affective pathology and etc.

Treatment in bronchial asthma, it should be strictly individualized, taking into account the variant of the course, the phase of the disease, the presence of complications, concomitant diseases, the tolerance of drugs to patients and the most rational use of them during the day. A polyclinic - an allergological office - a specialized department of a hospital and, subsequently, constant monitoring in an allergological office - are approximate stages of continuity in the treatment of such patients.

In atonic bronchial asthma, first of all, alimination therapy is prescribed - the most complete and permanent cessation of contact with the allergen. If the allergen is identified, but the patient cannot be isolated from it, specific hyposensitization is indicated in specialized allergological institutions in the remission phase. Patients with atonic asthma (especially in uncomplicated forms of the disease) are prescribed sodium cromolyn (Intal), spraying it with a special inhaler.

If asthma is combined with other allergic manifestations, oral ketotifen 1 mg 2 times a day is preferable. The effect of both drugs comes gradually.

If there is no effect, glucocorticoids are prescribed; in moderate cases, it is advisable to administer them in the form of inhalations (becotide 50 mcg every 6 hours). For severe exacerbations, oral glucocorticoids are indicated, starting with prednisolone 15-20 mg per day; after achieving a clinical effect, the dose is gradually reduced. For food allergies, the use of fasting-dietary therapy carried out in a hospital is indicated. Patients with an infectious-allergic form of asthma are recommended treatment with autovaccine, sputum autolysate, heterovaccines, which are currently being prepared using new technology. Vaccine treatment is carried out in a specialized hospital.

In case of violations in the immune system, appropriate immunocorrective therapy is prescribed. During the period of remission, sanation of foci of chronic infection is carried out. With an infectious-dependent form of asthma, recreational activities are indicated: physical activity, regular therapeutic exercises, tempering procedures.

In connection with the violation of mucociliary clearance, sputum thinning therapy is necessary: ​​plentiful warm drink, alkaline warm inhalations, decoction of herbs - rosemary, coltsfoot and others, mucolytic agents. Physical training is advisable: swimming or a quiet run in a warm room. With good tolerance, every week increase the load by 1 minute (up to 60 minutes).

With "aspirin" asthma, foods containing acetylsalicylic acid (berries, tomatoes, potatoes, citrus fruits) are excluded from the diet. Non-steroidal anti-inflammatory drugs are strictly prohibited.

If necessary, appoint intal, zaditen or corticosteroids.

With severe emotional disorders, a qualified examination and treatment by a psychotherapist with an individual selection of psychotropic drugs is necessary. Assign psychotherapy, reflexology.

For the relief of asthma attacks, an individually selected bronchodilator therapy is prescribed. The optimal dose of bronchodilators is selected empirically (from a small dose to the most effective). Selective stimulants β have a positive effect in most patients.₂-adrenergic receptors (salbutamol, berotek, etc.), which are produced in the form of metered-dose manual (pocket) inhalers.

During an attack, two breaths of an aerosol help. In mild cases, such drugs can be used in the form of tablets.

For more severe attacks, intravenous aminophylline injections are used (5-10 ml of a 2,4% solution, the drug is also used in the form of tablets (0,15 g) and suppositories (0,3 g)). An overdose of these drugs (especially during hypoxia) can have a cardiotoxic effect; in addition, frequent use of sympathomimetics causes blockade of β-receptors.

Anticholinergics (atropine, belladonna, platyphylline) are preferable for the infectious-allergic form of the disease, especially with obstruction of large bronchi. Often these drugs are combined with other bronchodilators. An effective drug in this group is Atrovent, produced in metered dose inhalers; it can be used to prevent attacks by taking two breaths 3-4 times a day.

The drug has little effect on mucociliary clearance. Different mechanisms of bronchial obstruction in each patient determine the appropriateness of a combination of drugs. An effective drug is berodual - a combination of berotek and atrovent in the form of a metered dose inhaler.

Treatment of status asthmaticus carried out differentially depending on its stage, form, cause of occurrence. In case of anaphylactic form, a subcutaneous solution of adrenaline is administered and glucocorticoids are immediately used, prescribing 100 mg of hydrocortisone intravenously. If no obvious improvement occurs in the next 15-30 minutes, the hydrocortisone infusion is repeated and intravenous drip administration of aminophylline (10-15 ml of a 2,4% solution) is started. At the same time, oxygen therapy is administered through a nasal catheter or mask (2-6 l/min). Treatment should be carried out in an intensive care unit. Treatment of the metabolic form of status asthmaticus is carried out depending on its stage. First, it is necessary to eliminate an unproductive cough, improve sputum discharge through warm alkaline inhalations and plenty of warm drinks. If the asthmatic condition is caused by withdrawal or overdose of sympathomimetics, drip administration of prednisolone 30 mg every 3 hours IV is indicated until the status is relieved. If acidosis develops, it is necessary to administer an intravenous infusion of a 2% sodium bicarbonate solution. Rehydration must be carried out by administering large amounts of fluid. At stage II of the asthmatic condition, the dose of glucocorticoids is increased (prednisolone to 60 - 90-120 mg every 60 - 90 minutes). If the picture of a silent lung does not disappear within the next 1,5 hours, controlled ventilation with active liquefaction and suction of sputum is indicated. In stage III, intensive therapy is carried out together with a resuscitator. After recovery from the asthmatic state, the dose of glucocorticoids is immediately reduced by half, and then gradually reduced to maintenance. It is necessary to monitor such patients, to reduce the maintenance dose of glucocorticoids as much as possible, to switch to inhaled use if possible, to combine them with other drugs (Zaditene, Intal, bronchospasmolytics, etc.), and to intermittently use glucocorticoids. The use of psychotropic medications and physical rehabilitation can minimize complications of glucocorticoid therapy.

During the period of remission, hyposensitizing therapy, sanitation of foci of infection, physiotherapy exercises, physical training (walking, swimming), physiotherapy, and spa treatment are carried out. Treatment at local resorts is of the greatest importance, since it has become obvious that the processes of adaptation to new climatic conditions and after a short time readaptation do not have a training effect. Qualified psychotherapy significantly improves the effect of complex therapy.

Forecast. With clinical observation (at least 2 times a year) and rationally selected treatment, the prognosis is favorable. Death may be associated with severe infectious complications, untimely and irrational therapy, and progressive pulmonary heart failure in patients with cor pulmonale.

LECTURE No. 8. Diseases of the digestive system in children. Chronic gastroduodenitis. Stomach ulcer

1. Chronic gastroduodenitis

Chronic gastroduodenitis is a chronic inflammation of the mucous membrane of the antrum of the stomach and duodenum, accompanied by a violation of the physiological regeneration of the epithelium, the secretory and motor functions of the stomach.

Etiological factors: endogenous factors (hereditary predisposition, high type of acid formation, impaired mucus formation, chronic diseases accompanied by hypoxia, local vascular disorders, intoxication, chronic diseases of the liver and biliary tract); exdogenic factors (malnutrition, poor-quality roughage, eating dry, in a hurry, long breaks in eating; past food poisoning, prolonged and frequent medication, psycho-emotional stress, neurogenic stress, colonization of the mucous membrane of the antrum of the stomach and duodenum with bacteria). Classification according to the period of the disease: exacerbations, subremissions, remissions. According to the mechanism of development, there are: chronic gastritis type A, based on an autoimmune mechanism of development with the production of antibodies to the parietal cells of the mucous membrane and the internal factor; chronic type B gastritis develops as a result of the action of various factors (long-term medication, nutritional disorders, persistence in the mucosa of Helicobacter pylori); chronic gastritis type C has a reflux mechanism of development or medication as a result of taking NSAIDs.

Clinic. Abdominal pain is localized in the epigastric and pyloroduodenal zones, most often occurs on an empty stomach and decreases after eating. Sometimes early pain is observed, appearing 20-30 minutes after eating; hunger pain is less common - 1,5-2 hours after eating. The rhythm of pain in older children: hunger - pain - eating - relief - hunger. Eating a small amount of food helps reduce pain, but overeating, eating spicy, sour foods, and physical activity increases the pain. Dyspeptic syndrome is caused by a violation of the motor and secretory functions of the stomach and duodenum, manifested by nausea, vomiting, belching, heartburn, bowel dysfunction in the form of constipation, or unstable stool with polyfecal matter. Asthenovegetative syndrome is manifested by weakness, fatigue, and neurosis-like conditions. Palpation of the abdomen reveals moderate diffuse pain in the epigastric and pyloroduodenal areas.

Diagnostics performed on the basis of anamnesis of clinical and laboratory data. In the blood test - a decrease in erythrocytes, hemoglobin, moderate leukocytosis. During endoscopic examination, superficial gastroduodenitis is isolated, where hyperemia and mucosal edema are revealed. With hypertrophic gastroduodenitis, the mucosa is edematous, hyperemic, has a granular appearance, small punctate hemorrhages. With erosive gastritis against the background of hyperemia, there are multiple, less often single, erosions with a flat bottom. With atrophic (subatrophic) gastroduodenitis, the mucosa is pale, the folds are thinned, smoothed, the vascular pattern is enhanced. In all forms, there may be signs of duodenogastric reflux (pylorus gaping, an admixture of bile in the contents of the stomach).

Carry out tests for the determination of Helicobacter pylori. This is enzyme immunoassay, determination of antibodies in blood, urine, saliva, microscopy of smears - prints of the gastric mucosa. X-ray examination - according to indications, if there are changes in the folds, a large amount of contents on an empty stomach, spasms of the pylorus, duodenum, a change in the shape of the stomach.

Differential diagnostics. It is carried out with chronic pancreatitis, in which pain is localized on the left above the navel with irradiation to the left (sometimes girdle pain), in blood and urine tests there is an increase in amylase, an increase in trypsin activity in the stool, steatorrhea, creatorrhea, and on ultrasound examination - an increase in the size of the pancreas and changes in its echo density. With chronic cholecystitis, in which pain is localized in the right hypochondrium, upon palpation there is pain in the projection of the gallbladder; ultrasound examination shows thickening of the wall of the gallbladder and flakes of mucus in it. With chronic enterocolitis, in which pain is localized throughout the abdomen and decreases after defecation, there is bloating, poor tolerance of milk, vegetables, fruits, unstable stools, in the coprogram - amilorrhea, steatorrhea, mucus, creatorrhoea, possibly leukocytes, erythrocytes, dysbacteriosis. With peptic ulcer disease, in which pain occurs acutely, 1-2 hours after eating, including severe pain on palpation of the abdomen, tension in the abdominal muscles; endoscopic examination reveals a deep mucosal defect surrounded by a hyperemic shaft; there may be multiple ulcers.

Treatment. You should adhere to a therapeutic and protective regime, sleep at least 8 hours at night, the head of the bed should be higher than the foot. Sharp physical exertion and heavy physical labor are contraindicated; timely treatment of carious teeth, nasopharyngeal diseases, and giardiasis is necessary. Diet therapy: nutrition should be complete and varied, contain a sufficient amount of vegetables, fruits, and dairy products. Food is taken 5-6 times a day, the last meal no later than 19.00. Dry food is not allowed. You should not take a horizontal position for 2-3 hours after eating. Highly carbonated drinks and chewing gum are contraindicated for consumption, especially on an empty stomach. Antacid therapy is carried out (Almagel, Maalox, Phosphalugel are prescribed) and antisecretory therapy (N₂-histamine blockers, ranitidine 150 mg morning and evening, M-anticholinergics, gastrocepin 35 mg 2 times a day before meals). Prescribed drugs that improve the protective properties of the mucosa. These are protective basic drugs (Venter, de-nol, before meals and at night, the tablet is chewed and washed down with water); synthetic prostaglandins (Cytotec); nonspecific mucosal protectors (actovegin, folic acid, vitamins A, E, B). Anti-Helicobacter therapy is carried out, using bismuth preparations (denol, bismofalk), antibacterial drugs (amoxacillin), antimicrobial drugs (metronidazole). If the motor-evacuation function is impaired, motilium is used; to correct the pathological reflux of duodenal contents into the stomach, adsorbents (smecta, enterosgel, wheat bran) are prescribed. Physiotherapy is prescribed: UHF, laser therapy, inductothermy.

2. Peptic ulcer of the stomach or duodenum

Peptic ulcer of the stomach or duodenum is a chronic disease, a characteristic feature of which is the formation of ulcers in the digestive tract during the period of exacerbation. The main etiological factor is Helicobacter pylori infection. An important role in the formation of pathology is played by psychosocial factors (stress, psychotrauma, conflicts in the family and school), toxic-allergic factors (frequent medication, substance abuse, smoking, food and drug allergies), hereditary-constitutional factors (genetic predisposition, asthenic physique) .

Pathogenesis. An imbalance between aggressive factors (hydrochloric acid, bile, pepsin, nicotine, NSAIDs) and protective factors of the gastric and duodenal mucosa (a mucosal barrier consisting of three layers of protection - a layer of mucus and bicarbonates, a layer of epithelial cells producing bicarbonates and mucus). Classification by localization: stomach, duodenal bulb, mixed localization; by phase: exacerbation, incomplete clinical remission, clinical remission by form: complicated, uncomplicated (bleeding, perforation, penetration, pyloric stenosis); according to the course: newly identified, often recurrent for less than 3 years, rarely recurrent for more than 3 years; according to the nature of the acid-forming function: with preserved function, with increased function, with decreased function. Clinical and endoscopic stage: fresh ulcer, beginning of epithelization of the ulcerative defect, healing of the ulcerative defect of the mucous membrane with preserved duodenitis, clinical and endoscopic remission.

Clinic. Pain of a persistent and persistent nature, localized in the epigastric or pyloroduodenal zone. The rhythm of pain in older children: hunger - pain - eating - relief - hunger. The appearance of pain at night and pain in the early morning hours is typical. The course of a peptic ulcer can be latent, and for a long time children do not complain of abdominal pain; nausea, vomiting, belching, a feeling of rapid satiety, and heaviness in the abdomen are occasionally observed. Asthenovegetative syndrome is manifested by sleep disturbance, emotional lability, irritability, arterial hypotension, and loss of appetite.

Diagnostics. Based on anamnesis, clinical and laboratory data, fibrogastroduodenoscopy with biopsy can identify an ulcer. Tests are carried out to determine Helicobacter pilori. This is enzyme immunoassay diagnostics, determination of antibodies in blood, urine, saliva, microscopy of smears - imprints of the gastric mucosa. X-ray examination is used in cases where there is a suspicion of an abnormal structure of the organs of the upper digestive tract.

1. Direct signs - niche, convergence of folds.

2. Indirect - fasting hypersecretion, bulb deformity, pyloroduodenospasm, spastic peristalsis.

Differential diagnosis performed with chronic gastritis, gastroduodenitis, hernia of the esophageal opening of the diaphragm, pathology of the biliary tract.

Treatment. Bed rest, diet No. 1a, No. 1b, then No. 1.

Treatment is directed to:

1) to suppress the aggressive properties of gastric juice. Selective blockers are used₁-cholinergic receptors: gastrocepin, pirenzepine; H blockers₂- histamine receptors: ranitidine, famotidine; antacids: almagel, phosphalugel, gastrogel;

2) to increase the protective layer of the mucous membrane. Cytoprotectors are prescribed: bismuth preparations, cytotec, sucralfate;

3) on neurohumoral regulation. Psychotropic drugs, dopamine receptor blockers are shown.

In addition, antibacterial and antiprotozoal drugs are prescribed; physiotherapy (EHF, magneto and laser therapy, hyperbaric oxygenation).

Treatment regimens for anti-Helicobacter therapy for children under 5 years of age are not prescribed. First-line therapy for newly diagnosed infection: children under 7 years old: de-nol (120 mg 2 times a day) + metronidazole (250 mg 2 times a day) + amoxacillin (500 mg 2 times a day). For children over 7 years old: de-nol (240 mg 2 times a day) + metronidazole (500 mg 2 times a day) + amoxacillin (1000 mg 2 times a day). Quality control of eradication after 6 months using endoscopic techniques.

Second-line therapy (in the absence of eradication or recurrence of peptic ulcer): children under 7 years old: de-nol (120 mg 2 times a day) + metronidazole (250 mg 2 times a day) + amoxacillin (500 mg 2 times a day) + ranitidine (150 mg 2 times a day). For children over 7 years old: de-nol (240 mg 2 times a day) + metronidazole (500 mg 2 times a day) + amoxacillin (1000 mg 2 times a day) + omeprazole (10 mg 2 times a day).

LECTURE No. 9. Diseases of the biliary system in children

1. Classification of pathological conditions of the biliary tract in childhood

I. Dyskinesia of the gallbladder and biliary tract:

1) hypermotor - hypertension, hyperkinesia;

2) hypomotor - hypotension, hypokinesia;

3) mixed.

II. Dyskinesia of the gallbladder.

III. Inflammatory diseases (cholecystitis, cholangitis, cholecystocholangitis) differ in course: acute, chronic; according to the phase of the disease: exacerbation, remission.

IV. Congenital malformations of the gallbladder and biliary tract.

V. Gallstone disease.

VI. Parasitic diseases (opisthorchiasis, echinococcus, helminthiases).

VII. Tumor diseases.

2. Biliary dyskinesia

Biliary dyskinesia is a functional disorder of the motility of the gallbladder and biliary tract, manifested by pain in the right hypochondrium, leading to a violation of the outflow of bile into the duodenum. Dyskinesias are divided into primary, which include changes in neurohumoral mechanisms, they develop with intoxication against the background of allergic diseases, endocrine-hormonal disorders, neurosis, and secondary, which occur reflexively in diseases of the abdominal cavity according to the type of viscero-visceral reflexes, joining chronic cholecystocholangitis , cholelithiasis. The occurrence of impaired motility of the biliary tract and biliary hypertension leads to a change in the normal blood flow in the gallbladder and bile ducts, which causes hypoxia with a subsequent change in the permeability of cell membranes and biochemical processes in the cells of the gallbladder mucosa and liver.

Clinic. It manifests itself as abdominal pain, mainly in the right hypochondrium. Pains of aching or cramping nature are accompanied by dyspeptic disorders (nausea, vomiting, bitterness in the mouth, intolerance to fatty foods, unstable stools), a characteristic feature is the connection of pain with neuropsychic and physical overload. Pain syndrome with hypotonic dyskinesia is characterized by constant, periodically intensifying pain and a feeling of fullness in the right hypochondrium. The pain syndrome in hypertensive dyskinesia is characterized by pain of a paroxysmal nature (cramping, stabbing, cutting) associated with emotional and physical stress with irradiation to the right shoulder, epigastric and periumbilical region. On examination, attention is drawn to asthenovegetative disorders, pain on palpation in the right hypochondrium, positive symptoms of Kerr, Ortner, Murphy, Mussi.

Diagnostics carried out on the basis of anamnesis, clinical and laboratory data. With fractional duodenal intubation, hypertonicity of the sphincters of Oddi and Lütkes can be detected; there is an increase in the duration of the second and third phases of FDD from 10 to 30 minutes; with hypotension, a decrease to 1-3 minutes; hyperkinesia of the gallbladder is characterized by rapid emptying, occurring immediately or in the first 3-5 minutes; with hypokinesia, gallbladder reflux is normal or slow, the amount of bile in portion B is greater than normal. Microscopic and biochemical examination of bile reveals an increase in the number of cholesterol crystals and calcium bilirubinates. Ultrasound cholecystography reveals disturbances in the contractile function of the gallbladder. Ultrasound of the liver and gallbladder shows signs of bile stagnation and gallbladder abnormalities.

Treatment. Diet therapy: table No. 5, mechanical, chemical, thermally gentle nutrition. You should consume fermented milk products in the morning and evening. Exclude from the diet dishes containing extractive substances, essential oils, peppers, onions, garlic, smoked meats, pastries, chocolate, coffee. For hypomotor dyskinesia, foods with a choleretic effect are indicated (butter and vegetable oil, eggs, cream, sour cream, black bread, vegetables and fruits). If you have hypermotor dyskinesia, you should not eat rye bread, peas, cold drinks, or ice cream. Choleretic therapy for hypomotor dyskinesia: drugs that stimulate bile formation are used (cholagol, cholenzyme); preparations containing bile acids (allochol, lyobil); drugs that cause an increase in the tone of the biliary tract (sorbitol, xylitol, magnesium sulfate); herbal preparations: dandelion, rose hips, mint, corn). Choleretic therapy for hypermotor dyskinesia: drugs are used that cause relaxation of the tone of the biliary tract (aminophylline); herbal preparations (St. John's wort, chamomile, stinging nettle). Tubages provide a good cholekinetic effect. Mineral waters for hypermotor dyskinesia are low-mineralized "Slavyanovskaya", "Smirnovskaya"; for hypomotor dyskinesia - mineral waters with high and medium mineralization (Essentuki).

3. Chronic cholecystitis

Chronic cholecystitis is an inflammatory process in the wall of the gallbladder of bacterial, viral origin, as well as as a result of anomalies of the gallbladder, violations of the colloidal composition of bile, helminth invasion.

Clinic. The onset of the disease is often delayed with periodic exacerbations, the causes of which are errors in nutrition, physical activity, psycho-emotional disorders, and intercurrent diseases. During the period of exacerbation, symptoms of intoxication increase, and dyspeptic disorders intensify. Complaints of pain in the right hypochondrium of a paroxysmal or dull nature, intensifying after eating fatty foods, when running, walking. Duration from several minutes to 1-2 hours. When palpating the abdomen, pain is noted in the right hypochondrium.

Diagnostics carried out on the basis of anamnesis, clinical and laboratory data. In the blood test, in the acute course there is leukocytosis, neutrophyllosis, increased ESR; in the chronic course, the inflammatory reaction is moderate and constant; in a biochemical blood test during an exacerbation - an increase in the content of sialic acids, fibrin, transaminases, alkaline phosphatase. An echographic examination reveals a decrease or enlargement of the gallbladder, wall thickening of more than 1 mm, impaired contraction of the gallbladder. When studying bile - a decrease in specific gravity (normal specific gravity in portion A is 1006-1007, portion B is 1024-1032, portion C is 1007-1010), a shift in pH to the acidic side (normally 6,2 - 7,5), microscopy of sediment reveals mucus, leukocytes, cylindrical epithelium, an increase in cholesterol crystals, calcium bilirubinate, the presence of Giardia cysts or opisthorchiasis eggs.

Differential diagnosis carried out with duodenitis, gastritis, pancreatitis, peptic ulcer, helminthic invasion, appendicitis.

Treatment. Diet therapy No. 5. Antibacterial therapy (semi-synthetic penicillins, macrolides, cephalosporins), antiparasitic drugs when helminths and protozoa are detected. Choleretics and cholekinetics depending on the type of dyskinetic disorders. Vitamin therapy. Drugs to improve liver function (Carsil, Essentiale, Legalon). Reflexology, physiotherapy, physical therapy depending on dyskinetic disorders. Spa treatment.

LECTURE No. 10. Acute and chronic viral hepatitis in children

1. Acute hepatitis

Acute hepatitis is an inflammatory disease of the liver.

Etiology. The most common cause of acute liver damage in humans is viral hepatitis. Acute hepatitis can also be caused by enteroviruses, pathogens of intestinal infections, infectious mononucleosis viruses, and septic bacterial infections.

There are also acute toxic hepatitis caused by drugs (MAO inhibitors - hydrazine derivatives, PAS, isonicotinic acid derivatives, male fern extract, etc.), industrial poisons (phosphorus, organophosphorus insecticides, trinitrotoluene, etc.), mushroom poisons of pale grebe, morels (muscarine, afalotoxin, etc.).

Acute hepatitis can occur as a result of radiation (radiation) damage, with extensive burns of the body, severe infectious diseases, and toxicosis of pregnant women.

Pathogenesis consists in the direct effect of a damaging factor on the hepatic parenchyma or in immunological disorders that occur in response to a primary liver lesion, followed by cytolysis of affected and intact hepatocytes. In some cases, disturbance of microcirculation in the liver and intrahepatic cholestasis are of additional importance.

Clinic. In mild cases, acute hepatitis is practically asymptomatic, being detected only during a random examination.

In more severe cases (with toxic hepatitis), the clinical symptoms of the disease develop rapidly, combined with signs of general intoxication and toxic damage to other organs and systems.

At the height of the disease, icteric staining of the skin and mucous membranes, whitish-clay-colored stools, rich dark (beer-colored) urine, and hemorrhagic phenomena are characteristic. The skin is orange or saffron. In mild cases, jaundice is visible only in daylight, icteric staining of the sclera and mucous membrane of the soft palate appears most early. Sometimes there are nosebleeds, petechiae; patients are concerned about pruritus, bradycardia, depressed mental state, irritability, insomnia and other signs of damage to the central nervous system. Enlargement of the liver and spleen on palpation is slightly painful.

Diagnostics. Based on clinical and laboratory data, hyperbilirubinemia (100-300 µmol/l or more), increased activity of a number of serum enzymes: aldolase, aspartate aminotransferase and especially alanine aminotransferase (significantly above 40 units), lactate dehydrogenase, hypoalbuminemia, hyperglobulinemia are detected. The indicators of protein-sedimentary samples (thymol, sublimate, etc.) are far from normal. The liver's production of fibrinogen, prothrombin, VII, V coagulation factors is impaired, resulting in hemorrhagic phenomena.

Differential diagnosis. Of great importance is a carefully collected anamnesis, establishing the possibility of professional or household intoxication, taking into account the epidemiological situation in identifying the nature and cause of the disease. In unclear cases, the first consideration should be viral hepatitis.

The detection of the so-called Australian antigen is characteristic of serum hepatitis B (it is also detected in virus carriers, rarely in other diseases). Mechanical (subhepatic) jaundice occurs acutely, usually only when the common bile duct is blocked by a stone in cholelithiasis. But in this case, the appearance of jaundice is preceded by an attack of biliary colic; direct bilirubin in the blood is noted, the stool is discolored.

With hemolytic adrenal jaundice, free (indirect) bilirubin is determined in the blood, the stool is intensely colored, the osmotic resistance of erythrocytes is usually reduced.

With false jaundice (due to staining of the skin with carotene with prolonged and abundant consumption of oranges, pumpkins, carrots), the sclera are usually not stained, hyperbilirubinemia is absent.

Treatment. Hospitalization in special departments of infectious diseases hospitals is mandatory, and sanitary and epidemiological measures are carried out at the source of infection. Prescribe bed rest, a gentle diet with limited fat and increased carbohydrate content, and a large amount of fruit juices. In severe cases, detoxification therapy is carried out.

Forecast depends on the etiology of the disease, the severity of liver damage, the timeliness of therapeutic measures.

Prevention acute hepatitis consists in observing the rules of personal hygiene, carrying out sanitary and epidemic measures, ensuring appropriate sanitary and technical supervision at enterprises, which prevents the possibility of industrial poisoning with hepatotropic poisons. You should not eat obviously inedible or unknown mushrooms, as well as edible, but old ones (which can also cause severe poisoning).

2. Chronic hepatitis

Chronic hepatitis - polyetiological chronic liver lesions of an inflammatory-dystrophic nature with moderately severe fibrosis and predominantly preserved lobular structure of the liver, occurring without improvement for at least 6 months, clinically characterized by asthenic-vegetative, dyspeptic syndromes, hepatomegaly, impaired liver function, morphological persistence of necrosis, inflammation, fibrosis while maintaining the overall architectonics of the liver.

Etiology. The greatest importance is caused by viral, toxic and toxic-allergic liver damage due to viral hepatitis, chronic drug intoxication, and less commonly - viruses of infectious mononucleosis, herpes, and cytomegaly.

Pathogenesis. The direct effect of an etiological factor (virus, hepatotoxic substance) on the liver parenchyma, causing degeneration and necrobiosis of hepatocytes and reactive proliferation of mesenchyme.

One of the pathogenetic mechanisms of the transition of acute viral and toxic hepatitis to chronic and further progression of the latter are specific immunological disorders.

Clinic. Pain in the liver area is dull, constant. Characterized by enlarged liver, pain or a feeling of heaviness, fullness in the right hypochondrium, dyspeptic symptoms; Jaundice, skin itching, and low-grade fever are less common. There is no enlargement of the spleen, or it is slightly enlarged. Lethargy, fatigue, loss of appetite, belching, nausea, poor fat tolerance, flatulence, unstable stool, general weakness. The skin is pale, dry, and sometimes some patients exhibit mild (subicteric sclera and palate) or moderate jaundice.

Diagnostics. Based on clinical and laboratory data, moderate hyperbilirubinemia is detected. Positive results of protein-sedimentary tests - thymol, sublimate, etc. In the blood serum of patients, the content of aminotransferases is increased: ALT, AST and LDH, with difficulty in the outflow of bile - alkaline phosphatase. Ultrasound of the liver and liver scan allows you to determine its size; with hepatitis, sometimes there is a reduced or uneven accumulation of the radioisotope drug in the liver tissue, in some cases there is an increased accumulation in the spleen. Liver puncture biopsy and laparoscopy make it possible to more accurately distinguish between these two forms of hepatitis, as well as to carry out differential diagnosis with other liver diseases.

Treatment. A diet is prescribed with the exception of hot, spicy foods, refractory animal fats, and fried foods. Cottage cheese (up to 100-150 g daily), mild cheeses, low-fat boiled fish (cod, etc.) are recommended. In case of toxic and toxic-allergic hepatitis, it is extremely important to completely stop contact with the corresponding toxic substance. The use of hepatoprotectors (Karsila, Essentiale, etc.), cytostatics, antiviral drugs, and immunocorrectors is indicated.

LECTURE No. 11. Kidney diseases in children. Classification

1. Classification of kidney diseases in children

I. Hereditary and congenital nephropathies:

1) anatomical anomalies in the structure of the kidneys and urinary organs:

a) malformations of the kidneys: quantitative (agenesis, aplasia, accessory kidneys), positional (dystopia, nephroptosis, rotation), formal (horseshoe-shaped s- and l-shaped kidneys);

b) malformations of the ureters;

c) anomalies in the structure of the bladder and urethra;

d) anomalies in the structure and location of the renal vessels, including the lymphatic system;

e) anomalies of the innervation of the urinary system with the syndrome of neurogenic bladder;

2) impaired differentiation of the renal structure:

a) with cysts;

b) without cysts;

3) hereditary nephritis (without hearing loss, with hearing loss);

4) tubopathies;

5) dysmetabolic nephropathy with crystalluria (oxalaturia, uraturia);

6) nephro- and uropathy in chromosomal diseases;

7) amyloidosis;

8) embryonic tumors.

II. Acquired diseases of the kidneys and urinary organs:

1) glomerulonephritis;

2) interstitial nephritis;

3) pyelonephritis;

4) urinary tract infection;

5) kidney tumors;

6) injuries of the kidneys and urinary organs;

7) urolithiasis;

8) secondary kidney disease in acute infections, diabetes, burn disease.

2. Pyelonephritis

Pyelonephritis is a nonspecific infectious disease of the kidneys that affects the renal parenchyma, predominantly with damage to the interstitial tissue. Causes: infection, impaired urodynamics, impaired immunity.

Etiology. Most often, pyelonephritis is caused by Escherichia coli, Enterococcus, Proteus, staphylococci, streptococci. In some patients with acute pyelonephritis and in 2/3 of patients with chronic pyelonephritis, the microflora is mixed. During treatment, the microflora and its sensitivity to antibiotics change, which requires repeated urine cultures to determine adequate urinary antiseptics.

Pathogenesis. The development of pyelonephritis largely depends on the general condition of the macroorganism and a decrease in its immunobiological reactivity. The infection penetrates into the kidney, pelvis, then into its calyces by hematogenous or lymphogenous route, from the lower urinary tract along the wall of the ureter, along its lumen - in the presence of retrograde reflux. Of particular importance in the development of pyelonephritis are urinary stasis and disturbances of venous and lymphatic outflow from the kidney. According to the current, acute and chronic pyelonephritis are distinguished; by period: period of exacerbation, period of partial remission, period of complete clinical and laboratory remission.

Clinic. The disease begins acutely, with an increase in body temperature to 40 ° C, chills, sweating, pallor of the skin and mucous membranes, pain in the lumbar region, severe pain in the costovertebral angle, general malaise, thirst, dysuria or pollakiuria, painful urination. Additional headache, nausea, and vomiting indicate rapidly increasing intoxication. Pasternatsky's symptom is usually positive. With bilateral acute pyelonephritis, signs of renal failure often appear. Acute pyelonephritis can be complicated by paranephritis and necrosis of the renal papillae.

Diagnosis put on the basis of an anamnesis indicating a recent acute purulent process or the presence of chronic diseases, clinical and laboratory data. In the blood test, neutrophilic leukocytosis, anemia, aneosinophilia, and an increase in ESR are noted. In the analysis of urine - leukocyturia, pyuria with moderate proteinuria and hematuria. In the Zimnitsky test - a decrease in the density of urine during the day. In the sample according to Nechiporenko - leukocytosis. In a biochemical study of blood - an increase in the content of sialic acids, creatinine, urea, the appearance of C-reactive protein. On a survey radiograph, an increase in one of the kidneys in volume is detected, with excretory urography - a sharp restriction of the mobility of the affected kidney during breathing, the absence or later appearance of a shadow of the urinary tract on the side of the lesion. prescribe an ultrasound examination of the kidneys, excretory pyelography to detect changes in the pelvicalyceal system. Voiding urethrography reveals anatomical and functional features, the presence of reflux.

Treatment. Treatment objectives: elimination and reduction of the microbial inflammatory process in the renal tissue and urinary tract; normalization of metabolic disorders and functional state of the kidneys; stimulation of regenerative processes; reduction of sclerotic processes in interstitial tissue. In the acute period, table No. 7a is prescribed, consumption of up to 2 liters of liquid per day. A balanced diet is prescribed to reduce the load on the tubular transport systems and correct metabolic disorders. Then the diet is expanded, increasing its protein and fat content. Proper organization of the general and motor regime is carried out, ensuring a reduction in the functional load on the kidneys and improving the elimination of metabolic products from the body. Early sanitation of foci of infection that contribute to the occurrence and progression of the disease is carried out. Restoration of urine passage, blood and lymph circulation in the renal tissue.

To improve local blood circulation and reduce pain, thermal procedures (warming compresses, heating pads, diathermy of the lumbar region) are prescribed. If the pain does not subside, then antispasmodics are used. Antibacterial therapy is carried out with nalidixic acid (nevigramon, negram), the course of treatment of which should last at least 7 days (0,5-1 g 4 times a day), nitroxoline (5-NOK), prescribed at 0,1 - 0,2 g 4 times a day for 2-3 weeks, nitrofuran derivatives (furadonin 0,15 g 3-4 times a day, course of treatment 5 - 8 days). The use of these drugs should be alternate. Nalidixic acid and nitrofuran derivatives should not be prescribed simultaneously, as this weakens the antibacterial effect. Combined treatment with antibiotics and sulfonamides is effective. The selection of antibiotics is carried out depending on the sensitivity of the microflora to them. Penicillin group drugs (ampicillin, aminoglycoside drugs, long-acting sulfonamides), and herbal medicine are prescribed. Symptomatic and replacement therapy is carried out when signs of renal failure develop.

3. Chronic pyelonephritis

Chronic pyelonephritis may be the result of untreated acute pyelonephritis, i.e., it can proceed without acute events from the onset of the disease.

Clinic. Unilateral chronic pyelonephritis is manifested by dull, constant pain in the lumbar region on the side of the affected kidney. There are no dysuric phenomena in most patients.

Diagnosis put on the basis of anamnesis, clinical and laboratory data. In the blood test, neutrophilic leukocytosis is noted. In the analysis of urine in the urine sediment, the predominance of leukocytes over other formed elements of urine is determined. The relative density of urine remains normal, one of the symptoms of the disease is bacteriuria. If the number of bacteria in 1 ml of urine exceeds 100, then it is necessary to determine their sensitivity to antibiotics and chemotherapy drugs. Arterial hypertension is a common symptom of chronic pyelonephritis, especially a bilateral process. The functional state of the kidneys is examined using chromocystoscopy, excretory urography, and clearance methods.

In chronic pyelonephritis, the concentration ability of the kidneys is disturbed early, while the nitrogen excretion function persists for many years. With infusion urography, a decrease in the concentration ability of the kidneys, a delayed release of a radiopaque substance, local spasms and deformations of the cups and pelvis are first determined. Subsequently, the spastic phase is replaced by atony, the calyxes and pelvises expand.

RџSЂRё differential diagnosis with chronic glomerulonephritis, the nature of the urinary syndrome (the predominance of leukocyturia over hematuria, the presence of active leukocytes, significant bacteriuria in pyelonephritis), and excretory urography data are of great importance. Nephrotic syndrome indicates the presence of glomerulonephritis. In case of arterial hypertension, differential diagnosis is carried out between pyelonephritis, hypertension and renovascular hypertension.

Treatment should be carried out for a long time. Treatment should begin with the appointment of nitrofurans (furadonin, furadantin, etc.), 5-NOC, nalidixic acid (negram, nevigramone), sulfonamides (urosulfan, atazol, etc.), alternating them alternately. At the same time, it is advisable to treat with cranberry extract.

With the ineffectiveness of these drugs, exacerbations of the disease, broad-spectrum antibiotics are used. The appointment of an antibiotic each time should be preceded by a determination of the sensitivity of the microflora to it.

4. Glomerulonephritis

Glomerulonephritis, an immunoallergic disease with a predominant lesion of the glomerular vessels, proceeds as an acute or chronic process with repeated exacerbations and remissions. Variants of glomerulonephritis:

1) nephritic - manifested by hematuria, proteinuria, hypertension, oliguria, cylindruria, leukocyturia, hypovolemia, hypocomplementemia, encephalopathy;

2) nephrotic - high proteinuria, edema, hypoproteinemia, possibly arterial hypertension, erythrocyturia, azotemia;

3) mixed - severe nephrotic syndrome, significant hematuria, hypertension;

4) hematuric - hematuria predominates in the urinary syndrome;

5) isolated urinary syndrome, manifested by extrarenal symptoms that are slightly expressed.

5. Acute glomerulonephritis

Acute glomerulonephritis is a cyclical infectious-allergic kidney disease that often develops 1-3 weeks after an infectious disease (usually of streptococcal etiology). Acute glomerulonephritis can develop at any age, but most patients are under 40 years of age.

Etiology, pathogenesis. The disease most often occurs after tonsillitis, tonsillitis, upper respiratory tract infections, scarlet fever, etc. 12-β-hemolytic group A streptococcus, pneumococcus, respiratory viruses, parasitic infestation, hypothermia, and trauma play a major role in the occurrence of glomerulonephritis. It may occur under the influence of a viral infection, after the administration of vaccines and serums (serum, vaccine nephritis). Cooling causes reflex disorders of the blood supply to the kidneys and affects the course of immunological reactions. The generally accepted idea is that glomerulonephritis is an immune complex pathology. The appearance of symptoms after an infection is preceded by a long latent period, during which the body’s reactivity changes and antibodies to microbes or viruses are formed.

Antigen-antibody complexes, interacting with complement, are deposited on the surface of the basement membrane of capillaries, mainly glomeruli.

Clinic. Clinical manifestations of glomerulonephritis in children:

1) extrarenal:

a) neurovegetative syndrome (malaise, anorexia, lethargy, nausea, vomiting, poor appetite, headache);

b) cardiovascular syndrome (hypertension, muffled heart sounds, murmurs and accents of heart sounds, enlargement of the liver);

c) edematous syndrome, manifested by pastosity, limited or generalized edema;

2) renal manifestations:

a) urinary syndrome (oliguria, proteinuria, hematuria, cylindruria, transient lymphocytic-mononuclear leukocyturia);

b) pain syndrome. Manifested by pain in the lumbar region or undifferentiated abdominal pain;

c) renal failure syndrome (azotemia is manifested by three main symptoms - edematous, hypertonic and urinary).

Diagnostics. Protein and red blood cells are found in the urine. The amount of protein in the urine usually ranges from 1 to 10 g/l, but often reaches 20 g/l or more. Slight proteinuria may be present from the very beginning of the disease, and in some periods it may even be absent. Small amounts of protein in the urine of patients who have had acute nephritis are observed for a long time and disappear only after 3-6, and in some cases even 9-12 months from the onset of the disease. Hematuria is a mandatory sign of acute hepomerulonephritis. There are macrohematuria and microhematuria, sometimes the number of red blood cells may not exceed 10-15 in the field of view. Cylindruria is not a necessary symptom of gpomerulonephritis. Leukocyturia is insignificant, but sometimes 20-30 or more leukocytes are found in the field of view. At the same time, there is always a quantitative predominance of erythrocytes over leukocytes, which is better revealed when counting the formed elements of urine sediment using the Addis-Kakovsky and Nechiporenko methods. Oliguria (400 - 700 ml of urine per day) is the first symptom of acute nephritis. In a blood test, the hemoglobin content and the number of red blood cells decrease, an increase in ESR is determined, and there is slight leukocytosis. A Rehberg, McClure - Aldrich test is performed. The function of the proximal convoluted tubules is examined, excretory urography, ultrasound examination of the kidneys, and radioisotope renography are prescribed.

There are two forms of acute glomerulonephritis.

Cyclic form It starts off stormy. Swelling, shortness of breath, headache, pain in the lumbar region appear, and the amount of urine decreases. Urine tests show high levels of proteinuria and hematuria. Blood pressure rises. The swelling lasts for 2-3 weeks, during the course of the disease a turning point occurs: polyuria develops and blood pressure decreases. The recovery period may be accompanied by hyposthenuria. However, often when patients feel well and have almost completely restored their ability to work, slight proteinuria (0,03 - 0,1 g/l) and residual hematuria may be observed for a long time, for months.

latent form is rare, and its diagnosis is of great importance, since often with this form the disease becomes chronic. This form of glomerulonephritis is characterized by a gradual onset, without any significant subjective symptoms, and is manifested only by slight shortness of breath or swelling in the legs. In such cases, it is possible to diagnose glomerulonephritis only with a systematic examination of urine. The duration of the relatively active period in the latent form of the disease can be significant (2-6 months or more).

Differential diagnosis. Conducted between acute glomerulonephritis and exacerbation of chronic glomerulonephritis. What is important here is to clarify the period from the onset of the infectious disease to the acute manifestations of nephritis. In acute cases, this period is 1-3 weeks, and in case of exacerbation of the chronic process - only a few days (1-2 days). Urinary syndrome may be the same in severity, but a persistent decrease in the relative density of urine (below 1,015) and a decrease in the filtration function of the kidneys are more typical for exacerbation of the chronic process.

Treatment. Hospitalization in a hospital, bed rest and diet are prescribed. A sharp restriction of table salt in food (no more than 1,5-2 g per day) in itself can lead to increased release of water and the elimination of edematous and hypertensive syndromes. In the future, watermelons, pumpkins, oranges, and potatoes are given, which provide almost completely sodium-free nutrition. Liquids can be consumed up to 600-1000 ml per day. Long-term restriction of protein intake is not sufficiently justified, since retention of nitrogenous wastes, as a rule, is not observed, and the sometimes supposed increase in blood pressure under the influence of protein nutrition has not been proven. Of the protein products, it is better to eat cottage cheese, as well as egg whites. Fats are allowed in the amount of 50 - 80 g per day. Carbohydrates are added to provide daily caloric intake. Antibacterial therapy is indicated when there is a clear connection between glomerulonephritis and an existing infection, for example, chronic tonsillitis. For chronic tonsillitis, tonsillectomy is indicated 2-3 months after the acute symptoms of the disease have subsided. The use of steroid hormones - prednisone, dexamethasone is possible no earlier than 3-4 weeks from the onset of the disease, when general symptoms (in particular, arterial hypertension) are less pronounced. Corticosteroid hormones are also indicated for the nephrotic form or prolonged course of acute glomerulonephritis. Corticosteroid therapy affects both edema and urinary syndrome. Moderate arterial hypertension is not a contraindication to the use of corticosteroid drugs. Vitamin therapy.

Forecast. Full recovery.

Prevention. It comes down to the prevention and early intensive treatment of acute infectious diseases, elimination of focal infection, especially in the tonsils. Prevention of sudden hypothermia of the body is also of preventive importance.

6. Subacute diffuse glomerulonephritis

Subacute diffuse glomerulonephritis has a malignant course.

Clinic. Rapid onset of the disease, characterized by edema, severe albuminuria (up to 10-30 g/l), as well as severe hypoproteinemia (45-35 g/l) and hypercholesterolemia (up to 6-10 g/l), i.e. signs of lipoid nephrotic syndrome. At the same time, hematuria and oliguria are observed. In urine analysis, the relative density is high only at the beginning, and then it becomes low. The filtration function of the kidneys progressively decreases. Already from the first weeks of the disease, azotemia may increase, which leads to the development of uremia. Arterial hypertension in this form of nephritis can be very high and is accompanied by severe changes in the fundus (retinal hemorrhages, swelling of the optic discs, formation of exudative white retinal spots).

Diagnosis. Taking into account the rapid development of renal failure, severe arterial hypertension is established, often of a malignant type. Subacute glomerulonephritis is indicated by the greater severity of edematous-inflammatory and lipoid-nephrotic syndromes.

Treatment. Treatment with steroid hormones for this form of glomerulonephritis is less effective, and in some cases is not indicated due to high and progressive arterial hypertension (BP above 200/140 mm Hg). Recently, it has been recommended to use immunosuppressants with careful monitoring of the morphological composition of the blood. Treatment with immunosuppressants is more effective in combination with corticosteroid hormones, which are prescribed in lower doses (25-30 mg per day). This combination not only promotes the effectiveness of treatment, but also reduces the risk of complications from both corticosteroids and immunosuppressants (in particular, severe leukopenia).

To combat edema and arterial hypertension, antihypertensive drugs, hypothiazide (50-100 mg/day), etc. are used. If signs of heart failure appear, diuretics and digitalis preparations are prescribed.

7. Chronic diffuse glomerulonephritis

Chronic diffuse glomerulonephritis is a long-term (at least a year) immunological bilateral kidney disease, in which changes in the urine persist without significant changes for over a year or edema and hypertension are observed for over 3-5 months. This disease ends (sometimes after many years) with the shrinking of the kidneys and the death of patients from chronic renal failure. Chronic glomerulonephritis can be either the outcome of acute glomerulonephritis or primary chronic, without a previous acute attack.

Etiology, pathogenesis. See Acute glomerulonephritis.

Clinic. As with acute glomerulonephritis: edema, arterial hypertension, urinary syndrome and impaired renal function. During chronic glomerulonephritis, two stages are distinguished:

1) renal compensation, i.e. sufficient nitrogen excretion function of the kidneys (this stage may be accompanied by a pronounced urinary syndrome, but sometimes it is latent for a long time, manifesting only a slight albuminuria or hematuria);

2) renal decompensation, characterized by insufficiency of the nitrogen-excreting function of the kidneys (urinary symptoms may be less significant; high arterial hypertension is observed, edema is often moderate; at this stage, hypoisosthenuria and polyuria are expressed, which end in the development of azotemic uremia).

The following clinical forms of chronic glomerulonephritis are distinguished.

1. Nephrotic form - the most common form of primary nephrotic syndrome. This form, in contrast to pure lipoid nephrosis, is characterized by a combination of nephrotic syndrome with signs of inflammatory kidney damage. The clinical picture of the disease can be determined by the nephrotic syndrome for a long time, and only later does the progression of glomerulonephritis itself occur with a violation of the nitrogen excretion function of the kidneys and arterial hypertension.

2. Hypertensive form. Arterial hypertension predominates among the symptoms, while urinary syndrome is less pronounced. Occasionally, chronic glomerulonephritis develops according to the hypertensive type after the first violent attack of glomerulonephritis, but more often it is the result of the occurrence of a latent form of acute glomerulonephritis. Blood pressure reaches 180/100-200/120 mm Hg. Art. and may be subject to large fluctuations during the day under the influence of various factors. Hypertrophy of the left ventricle of the heart is broken, an accent of the second tone is heard over the aorta. Hypertension does not become malignant; blood pressure, especially diastolic blood pressure, does not reach high levels. Changes in the fundus of the eye in the form of neuroretinitis are observed.

3. Mixed form. In this form, there are simultaneously nephrotic and hypertensive syndromes.

4. latent form. This is a fairly common form; It usually manifests itself only as a mild urinary syndrome, without arterial hypertension and edema. It can have a very long course (10-20 years or more), later leading to the development of uremia. The hematuric form should also be distinguished, since in some cases chronic glomerulonephritis can manifest as hematuria without significant proteinuria and general symptoms (hypertension, edema). All forms of chronic glomerulonephritis can periodically produce relapses that resemble or completely repeat the picture of the first acute attack of diffuse glomerulonephritis. Exacerbations are often observed in autumn and spring and occur 1-2 days after exposure to an irritant, most often a streptococcal infection. In any course, chronic diffuse glomerulonephritis passes into the final stage - a secondary wrinkled kidney.

Diagnosis. It is established on the basis of a history of acute glomerulonephritis and the clinical picture. However, in the latent form, as well as in the hypertensive and hematuric forms of the disease, its recognition can be difficult. If the history does not have specific indications of acute glomerulonephritis, then with moderately severe urinary syndrome, differential diagnosis is carried out with one of many unilateral or bilateral kidney diseases.

Differential diagnosis. When differentiating hypertensive and mixed forms of chronic glomerulonephritis with hypertension, it is important to determine the time of onset of urinary syndrome in relation to the onset of arterial hypertension. In chronic glomerulonephritis, urinary syndrome long precedes arterial hypertension or occurs simultaneously with it. Chronic glomerulonephritis is characterized by less severe cardiac hypertrophy, less propensity to hypertensive crises (with the exception of exacerbations occurring with eclampsia) and rare or less intense development of atherosclerosis, including the coronary arteries.

In favor of the presence of chronic glomerulonephritis in differential diagnosis with chronic pyelonephritis, the predominance of erythrocytes over leukocytes in the urine sediment, the absence of active and pale leukocytes when stained according to Sternheimer - Mapbin, the same size and shape of the two kidneys and the normal structure of the pelvis and calyces, which is detected by X-ray examination . The nephrotic form of chronic glomerulonephritis should be differentiated from lipoid nephrosis, amyloidosis, and diabetic glomerulosclerosis. In the differential diagnosis of amyloidosis of the kidneys, the presence in the body of foci of chronic infection and amyloid degeneration of another localization is important.

Treatment. It is necessary to eliminate foci of infection (removal of tonsils, sanitation of the oral cavity, etc.). Long-term dietary restrictions (salt and protein). Patients with chronic nephritis should avoid cooling, especially exposure to damp cold, and a dry and warm climate is recommended. If the general condition is satisfactory and there are no complications, sanatorium treatment is indicated. Bed rest is necessary only during the period of significant edema or the development of heart failure, with uremia. For the treatment of patients with chronic glomerulonephritis, diet is of great importance, which is prescribed depending on the forms and stage of the disease. In nephrotic and mixed forms (there is edema), the intake of sodium chloride from food should not exceed 1,5-2,5 g per day, and stop adding salt to food. With sufficient excretory function of the kidneys (no edema), food should contain a sufficient amount of animal protein, rich in complete phosphorus-containing amino acids, which normalizes nitrogen balance and compensates for protein losses.

In the hypertensive form, it is recommended to moderately limit the consumption of sodium chloride to 3-4 g per day with a normal content of proteins and carbohydrates in the diet. The latent form of the disease does not require large restrictions in the diet of patients; it must be complete, varied and rich in vitamins. Vitamins (C, B complex, A) should be included in the diet for other forms of chronic glomerulonephritis. The basis of pathogenetic therapy for this disease is the prescription of corticosteroid drugs. For the course of treatment, 1500-2000 mg of prednisone is used, then the dose is gradually reduced. It is recommended to carry out repeated courses of treatment during exacerbations or small maintenance courses. While taking corticosteroid hormones, an exacerbation of hidden foci of infection is possible, and therefore antibiotics are prescribed simultaneously or after removal of foci of infection (for example, tonsillectomy). A contraindication to the use of corticosteroids in chronic glomerulonephritis is progressive azotemia.

For moderate arterial hypertension (BP 180/110 mm Hg), antihypertensive drugs are added to treatment. In case of high arterial hypertension, a preliminary reduction in blood pressure is required. If corticosteroid therapy is contraindicated or if it is ineffective, the use of non-hormonal immunosuppressants is recommended. These are drugs of the 4-aminoquinoline series - hingamine (delagil, resokhin, chloroquine), hydroxychloroquine (plaquenil). In mixed forms of chronic glomerulonephritis (edematous and severe hypertensive syndromes), the use of natriuretics is indicated, as they have a diuretic and hypotensive effect. Hypothiazide is prescribed 50-100 mg 2 times a day, Lasix 40-120 mg per day, ethacrynic acid (uregit) 150-200 mg per day. It is better to combine saluretics with the aldosterone antagonist aldactone (veroshpiron) - 50 mg 4 times a day, which increases sodium excretion and reduces potassium excretion. The diuretic effect is accompanied by the release of potassium in the urine, which leads to hypokalemia with the development of general weakness, adynamia and impaired cardiac contractility. Therefore, a solution of potassium chloride is prescribed at the same time.

In the treatment of the hypertensive form of chronic glomerulonephritis, antihypertensive drugs used in the treatment of hypertension (reserpine, adelfan) should be prescribed. However, sharp fluctuations in blood pressure and its orthostatic fall should be avoided, which can worsen renal blood flow and the filtration function of the kidneys.

LECTURE No. 12. Kidney diseases in children. Acute renal failure (ARF). Chronic renal failure (CRF).

1. Kidney failure

The main functions of the kidneys (excretion of metabolic products, maintaining a constant water-electrolyte composition and acid-base state) are carried out by the following processes: renal blood flow, glomerular filtration and tubules (reabsorption, secretion, concentration ability). Not every change in these renal processes leads to severe impairment of renal function and can be called renal failure.

Acute renal failure is a syndrome that develops in connection with a sudden shutdown of kidney function as a result of severe violations of renal processes leading to a disorder of homeostasis, and is characterized by azotemia, a violation of the water-electrolyte composition and the acid-base state of the body. Acute kidney failure can occur suddenly due to acute (often reversible) kidney disease. Acute renal failure is indicated with oligoanuria less than 300 ml / m16 per day, an increase in blood urea up to XNUMX mmol / l, with signs of impaired renal tubular functions.

2. Prerenal acute renal failure

1. Violation of renal hemodynamics - shock (traumatic, anaphylactic, bacterial, burn, with loss of fluid and electrolytes).

2. Obstruction of the urinary tract and blood vessels (thrombosis and embolism of various etiologies or their spasm of drug genesis).

3. Disorder of electrolyte metabolism without shock - acute hypercalcemia, hyperkalemia, hyponatremia.

4. Hemolysis and myolysis during transfusion of incompatible blood, acute hemolytic anemia, crush syndrome.

5. Endogenous intoxications associated with intestinal obstruction.

3. Renal acute renal failure

1. Kidney damage associated with exogenous nephrotoxins (poisoning with salts of heavy metals, poisonous mushrooms, bites of poisonous snakes and insects).

2. Toxic-allergic lesions associated with an overdose of drugs or the presence of hypersensitivity to them.

3. Infectious diseases (hemorrhagic fever with renal syndrome, anaerobic sepsis, leptospirosis, hemolytic-uremic syndrome).

4. Absence of a kidney (agenesis).

5. Complications of diffuse renal disease (acute glomerulonephritis and acute pyelonephritis, nephritis with hemorrhagic vasculitis, systemic lupus erythematosus).

Postrenal acute renal failure is classified according to the location of the urinary tract obstruction and the cause leading to the obstruction (such as tumor, urolithiasis). Stages of development of acute renal failure: initial or shock, oligoanuric, recovery of diuresis, recovery. Renal hemodynamic disorders and exogenous intoxications cause 90% of all cases of acute renal failure. The main mechanism of kidney damage in these forms of acute renal failure is anoxia of the renal tubules, the development of necrosis of the epithelium of the tubules, edema and cell infiltration of the interstitial tissue, damage to the capillaries of the kidneys (necrotic nephrosis develops). Most of these damages are reversible.

Clinic. In the initial period of acute renal failure, symptoms appear due to shock (painful, anaphylactic or bacterial), acute poisoning, hemolysis, infectious disease, and already on the first day a decrease in diuresis is detected (less than 500 ml per day), i.e. a period of oliguria-anuria develops , and homeostasis is disrupted. In plasma, along with an increase in the levels of urea, creatinine, residual nitrogen, phosphates, sulfates, magnesium, and potassium, the levels of chlorine, sodium and calcium decrease. The combination of these disorders leads to an increase in the symptoms of acute uremia. Adynamia, loss of appetite, nausea, vomiting, and oliguria-anuria are also observed. With increasing azotemia (urea level increases by 0,5 g/l daily), acidosis, overhydration and electrolyte disturbances, drowsiness, mental retardation, muscle twitching appear, shortness of breath increases due to acidosis and pulmonary edema, the early stage is determined by x-ray. Abdominal pain and liver enlargement may occur. Characteristic changes in the cardiovascular system (tachycardia, muffled tones, systolic murmur at the apex, expansion of the borders of the heart, arterial hypertension). Rhythm disorders are associated with hyperkalemia: it is especially dangerous and can cause sudden death.

With hyperkalemia of more than 6,5 mmol/l on the ECG, the T wave is high, pointed, the QRS complex widens, and sometimes the R wave decreases. Heart block and ventricular fibrillation can result in cardiac arrest. The blood test shows anemia, leukocytosis, which is characteristic of the period of oliguria-anuria. Death in acute renal failure often occurs from uremic coma, hemodynamic disorders and sepsis. In acute renal failure, hypoisosthenuria is detected. The period of diuresis restoration begins with an increase in diuresis of more than 500 ml per day. Improvement occurs gradually, even after the onset of polyuria and as the level of azotemia decreases and homeostasis is restored. During the period of polyuria, hypokalemia (less than 3,8 mmol/l) with ECG changes (low voltage of the T wave, U wave, decreased ST segment) and extrasystole is possible. The recovery period is observed when the content of residual nitrogen in the blood normalizes. Homeostasis is restored. During this period, renal processes are restored. It lasts up to a year or more. But in some patients, the decrease in glomerular filtration and the concentrating ability of the kidneys remains, and in some, renal failure takes a chronic course, with associated pyelonephritis playing a major role.

Diagnosis established on the basis of clinical and laboratory data, this is a sudden decrease in diuresis, an increase in azotemia and other typical homeostasis disorders.

Differential diagnosis carried out with an exacerbation of chronic renal failure or its terminal stage, where history data help, a decrease in the size of the kidneys in chronic glomerulonephritis and pyelonephritis, or the identification of a chronic urological disease. In acute glomerulonephritis, high proteinuria is observed.

Treatment should be aimed at stopping the action of the damaging factor that caused acute renal failure, correcting homeostasis disorders, preventing and treating complications. Etiotropic therapy. If acute renal failure is caused by shock, then antishock therapy is carried out; if acute renal failure is caused by acute hemolysis, then a replacement blood transfusion, plasmapheresis, elimination of the agent that caused hemolysis, and administration of large doses of steroids are performed to prevent antibody formation; if acute renal failure develops as a result of poisoning, then hemosorption is carried out using antidotes; in case of poisoning with sulfonamides, a 4% solution of sodium bicarbonate is administered with catheterization of the ureters; if acute renal failure develops as a result of kidney disease, antihypertensive drugs are prescribed in combination with diuretics, anticoagulants, plasmapheresis, and extracorporeal dialysis. If the cause of acute renal failure is bacterial shock, then, in addition to anti-shock measures, antibiotics are prescribed. At the beginning of acute renal failure, a 10% solution of mannitol is administered intravenously at the rate of 1 g per 1 kg of the patient’s body weight. If anuria continues for 2-3 days, treatment with mannitol is not advisable. In the initial period of oliguria-anuria, diuresis is stimulated with furosemide (160 mg IV 4 times a day).

If diuresis increases, then the use of furosemide is continued, then therapy is aimed at regulating homeostasis. The diet (restriction of protein and potassium intake) should be high in calories due to a sufficient amount of carbohydrates and fats. The amount of fluid administered should exceed diuresis, as well as the amount of water lost through vomiting and diarrhea, by no more than 500 ml. This volume includes 400 ml of a 20% glucose solution with 20 units of insulin. Syndromic therapy: for hyperhydration, hypertonic glucose solutions are administered in combination with diuretics, rheopolyglucin and other blood substitutes. For hyperkalemia, a glucose solution and a 3-4% sodium bicarbonate solution are administered intravenously.

For hyponatremia, perfusion treatment is carried out aimed at eliminating overhydration. For hypocalcemia, calcium supplements are administered. For hyperphosphatemia, solutions of sodium bicarbonate, cocarboxylase, and B vitamins are administered. Antibiotics are prescribed for prophylactic purposes, but their dose is reduced by 2-3 times. Streptomycin, monomycin, neomycin in conditions of anuria have a pronounced ototoxic property and should not be used (for example, penicillin is prescribed at a dose of 50 mg/kg per day, oxacillin 200 mg/kg per day, cephalothin 100 mg/kg per day, methicillin 200 mg/kg per day). With continued oliguria and increasing symptoms of uremia, the patient is transferred to the hemodialysis department, where extracorporeal cleansing is performed using an artificial kidney or peritoneal dialysis. Types of dialysis: intestinal, peritoneal, extracorporeal.

Indications for hemodialysis: oligoanuria for more than 1-2 days, pulmonary edema, hyperhydration with symptoms of cerebral edema, hypertension, hyperkalemia, increasing azotemia, drug and chemical poisoning, plasma urea level more than 2 g/l, potassium 6,5 mmol/ l, decompensated metabolic acidosis and the clinical picture of acute uremia.

Contraindications to hemodialysis: cerebral hemorrhages, gastric and intestinal bleeding, severe hemodynamic disorders with a decrease in blood pressure. Contraindications to peritoneal dialysis are a recent operation on the abdominal organs and adhesions in the abdominal cavity.

Forecast. With timely and correct application of adequate treatment methods, patients with acute renal failure recover and return to normal life.

Chronic renal failure develops gradually as a result of irreversible impairment of homeostatic renal functions with severe progressive renal disease that occurs in its final stage. CRF is a condition in which the filtration capacity of the kidneys is reduced to 25% of normal, and creatinine in the blood exceeds 0,176 mmol / l.

4. Partial CRF

Partial CKD is an isolated dysfunction of one or more mechanisms that maintain homeostasis. Total CRF is the presence of a complete symptom complex of homeostatic disorders associated with the inclusion of all elements of the nephron in the process.

Etiology. The causes of chronic renal failure are chronic glomerulonephritis, chronic pyelonephritis, nephritis in systemic diseases, hereditary nephritis, polycystic kidney disease, diabetic glomerulosclerosis, renal amyloidosis, tubopathies, chromosomal diseases, dysmetabolic nephropathies. The pathogenetic mechanism of chronic renal failure is a progressive decrease in the number of active nephrons, which leads to a decrease in the efficiency of renal processes and impaired renal function. The morphological picture of the kidney in chronic renal failure depends on the underlying disease, but more often there is replacement of the parenchyma with connective tissue and wrinkling of the kidney. Risk factors for chronic renal failure: presence in the family of cases and deaths from chronic renal failure at a young age; early, torpid onset of pathology with decreased renal function; detection of signs of disembryogenesis and sclerosing variants of glomerulonephritis during biopsy in renal tissue; the presence of a persistent hypoimmune state with signs of auto-aggression; increasing instability of cell membranes in the absence of a family predisposition to dysmetabolic nephropathies.

Stages of development of CRF:

1) latent;

2) Azotemic;

3) uremic.

Pathogenesis. Chronic kidney disease can last from 2 to 10 years or more before ESRD develops. They go through a number of stages, the identification of which is necessary for proper planning of treatment for both kidney diseases and chronic renal failure. When glomerular filtration and tubular reabsorption are maintained at normal levels, the underlying disease is in a stage not accompanied by disturbances in renal processes. Over time, glomerular filtration becomes lower than normal, the ability of the kidneys to concentrate urine decreases, and the disease progresses to the stage of impaired renal processes. At this stage, homeostasis is preserved (no renal failure). With a further decrease in the number of active nephrons and the glomerular filtration rate below 50 ml/min in the blood plasma, the levels of creatinine (more than 0,02 g/l) and urea (more than 0,5 g/l) increase. At this stage, conservative treatment of chronic renal failure is required. When filtration is below 10 ml/min, azotemia and other homeostasis disorders increase, despite conservative therapy, and the end stage of chronic renal failure occurs, in which the use of dialysis is necessary. With the gradual development of chronic renal failure, homeostasis slowly changes - the level of creatinine, urea, sulfates, phosphates and other metabolites in the blood increases.

When diuresis is preserved (polyuria is observed), water is excreted in sufficient quantities, and the level of sodium, chlorine, magnesium and potassium in the plasma does not change. Constantly observed hypocalcemia associated with impaired metabolism of vitamin D and absorption of calcium in the intestine. Polyuria leads to hypokalemia. Metabolic acidosis often develops. In the terminal stage (when oliguria occurs), azotemia rapidly increases, acidosis worsens, hyperhydration increases, hyponatremia, hypochloremia, hypermagnesemia and hyperkalemia develop. The combination of these humoral disorders causes the symptoms of chronic uremia.

Clinic. Complaints of fatigue, decreased performance, appetite, headache. Sometimes an unpleasant taste in the mouth, nausea and vomiting are noted. The skin is pale, dry, flabby, muscle tone is reduced, small muscle twitching, tremors of the fingers and hands are observed, pain in the bones and joints rarely appears. There is arterial hypertension, which is often caused by underlying kidney disease. Changes in the cardiovascular system: the boundaries of the heart are expanded, sounds are muffled, changes are detected on the ECG.

Blood tests revealed anemia, leukocytosis and bleeding. Conservative therapy makes it possible to regulate homeostasis, and the patient’s general condition allows him to work, but increased physical activity, errors in diet, mental stress, limited drinking, infection, and surgery can lead to deterioration of kidney function. When glomerular filtration is below 10 ml/min, conservative correction of homeostasis is impossible. The terminal stage of chronic renal failure is characterized by emotional lability (apathy is replaced by excitement), night sleep disturbances, daytime drowsiness, lethargy and inappropriate behavior, and decreased appetite. The face is puffy, gray-yellow in color, the skin is itchy, there are scratches on the skin, the hair is dull and brittle. There is an ammonia smell from the mouth. Aphthous stomatitis occurs, the tongue is coated, the abdomen is swollen, vomiting, regurgitation, and sometimes diarrhea are repeated, fetid, dark-colored stools. Dystrophy increases, hypothermia is characteristic. Anemia, hemorrhagic syndrome increases, muscle twitching becomes frequent and painful. With long-term uremia, pain in the arms and legs and bone fragility are observed, which is explained by uremic neuropathy and renal osteodystrophy. Noisy breathing is often due to acidosis, pulmonary edema, or pneumonia. Uremic intoxication is complicated by fibrinous pericarditis, pleurisy, ascites, encephalopathy and uremic coma.

Diagnosis established on the basis of history of chronic kidney disease, clinical and laboratory data.

Differential diagnosis carried out with acute renal failure, where anamnestic data help. Encephalopathy in chronic renal failure differs from an attack of encephalopathy in acute glomerulonephritis by a gradual development, not always accompanied by a deep coma, small convulsive twitches of individual muscle groups, noisy breathing, while in renal eclampsia, an acute onset, accompanied by complete loss of consciousness, dilated pupils, large convulsions and asphyxia.

Treatment CRF is inseparable from the treatment of kidney disease that has led to kidney failure. At the stage not accompanied by disturbances in renal processes, etiological and pathogenetic therapy is carried out, which can lead to remission and a slower course of the disease. At the stage of violation of renal processes, pathogenetic therapy and symptomatic methods of treatment are prescribed (antihypertensive drugs, antibacterial agents, protein restriction in the daily diet - no more than 1 g per 1 kg of body weight, spa treatment, etc.).

The combination of these measures allows you to delay the onset of CRF, and periodic monitoring of the level of glomerular filtration, renal blood flow and the concentration ability of the kidneys, the level of creatinine and urea in plasma makes it possible to predict the course of the disease. Conservative treatment of CRF is aimed at restoring homeostasis, reducing azotemia and reducing the symptoms of uremia. The protein content in the daily diet depends on the degree of impaired renal function.

When glomerular filtration is below 50 ml/min and the level of creatinine in the blood is above 0,02 g/l, it is recommended to reduce the amount of protein consumed to 30-40 g per day, and when glomerular filtration is below 20 ml/min, a diet with a protein content of no more than 20 is prescribed -24 g per day. The diet should be high-calorie (about 3000 kcal) and contain essential amino acids (potato-egg diet without meat and fish).

Food is prepared with a limited (up to 2-3 g) amount of table salt, and for patients with high hypertension - without salt. Disorders of calcium metabolism and the development of osteodystrophy require long-term use of calcium gluconate and vitamin D up to 100 IU per day, but the administration of vitamin D in large doses for hyperphosphatemia can lead to calcification of internal organs.

To reduce the level of phosphates in the blood, use almagel 1-2 tsp. 4 times a day. Treatment requires regular monitoring of calcium and phosphorus levels in the blood. For acidosis, depending on its degree, a 5% solution of sodium bicarbonate is administered intravenously. When diuresis decreases, furosemide (Lasix) is prescribed in doses (up to 1 g per day) that provide polyuria.

To reduce blood pressure, antihypertensive drugs are used in combination with furosemide. The treatment of anemia is complex and includes the appointment of testosterone propionate to enhance erythropoiesis (1 ml of a 5% oil solution IM daily) and iron preparations.

When the hematocrit is 25% and below, red blood cell transfusions are prescribed in fractional doses. Antibacterial therapy for chronic renal failure should be used with caution: the doses of penicillin, ampicillin, methicillin, ceporin and sulfonamides are reduced by 2-3 times. Streptomycin, monomycin, neomycin in chronic renal failure, even in reduced doses, can cause auditory neuritis and other complications. Nitrofuran derivatives are contraindicated in chronic renal failure.

In heart failure, glycosides are used with caution, in reduced doses, especially with hypokalemia.

In the treatment of pericarditis, small doses of prednisolone are prescribed, but hemodialysis is more effective. Hemodialysis can be indicated during exacerbation of renal failure, and after the patient's condition improves, conservative therapy is carried out for a long time.

A good effect is obtained after plasmapheresis. In the terminal stage, if conservative therapy does not work and there are no contraindications, the patient is transferred to hemodialysis treatment. Regular hemodialysis is used when creatinine clearance is below 10 ml / min and its plasma level becomes above 0,1 g / l.

Forecast. Hemodialysis and kidney transplantation change the fate of patients with chronic renal failure, allowing them to prolong their lives and achieve rehabilitation for years. The selection of patients for these types of treatment is carried out by specialists from hemodialysis and organ transplantation centers.

LECTURE № 13. Diffuse connective tissue diseases. Systemic lupus erythematosus. Dermatomyositis. Systemic scleroderma

1. Systemic lupus erythematosus

Systemic lupus erythematosus is a chronic polysyndromic disease of connective tissue and blood vessels that develops due to genetically determined imperfection of immunoregulatory processes.

Etiology. The significance of a viral infection against the background of genetically determined immune disorders is assumed.

Pathogenesis. The formation of circulating autoantibodies, of which antinuclear antibodies are of the most important diagnostic and pathogenetic importance; the formation of circulating immune complexes, which, deposited on the basement membranes of various organs, cause their damage and inflammation. This is the pathogenesis of nephritis, dermatitis, vasculitis, etc. This hyperreactivity of humoral immunity is associated with disorders of cellular immunoregulation.

Recently, importance has been attached to hyperestrogenemia, accompanied by a decrease in the clearance of circulating immune complexes, etc. A family genetic predisposition has been proven. Mostly young women and teenage girls are ill. Provoking factors are insolation, pregnancy, abortion, childbirth, the onset of menstrual function, infections (especially in adolescents), drug or post-vaccination reactions.

Clinic. The disease begins gradually with recurrent polyarthritis and asthenia. Less common is an acute onset (high fever, dermatitis, acute polyarthritis). Subsequently, a relapsing course and characteristic polysyndromic character are noted. Polyarthritis and polyarthralgia are the most common and early symptom of the disease. Mostly small joints of the hands (wrist, ankle) are affected, and less commonly the knee joints. A non-erosive type of polyarthritis is characteristic, even in the presence of deformation of the interphalangeal joints, which develops in 10-15% of patients with a chronic course. Erythematous rashes on the skin of the face in the form of a butterfly, on the upper half of the chest in the form of a décolleté, on the extremities are also a common sign of systemic lupus erythematosus. Polyserositis is considered a component of the diagnostic triad along with dermatitis and polyarthritis. It is observed in almost all patients in the form of bilateral pleurisy and pericarditis, less commonly perihepatitis and (or) perisplenitis. Characterized by damage to the cardiovascular system with the development of pericarditis, which is accompanied by myocarditis.

Relatively often observed warty endocarditis Libman-Sacks with damage to the mitral, aortic and tricuspid valves.

Signs of vascular damage are included in the picture of damage to individual organs. Nevertheless, it should be noted the possibility of developing Raynaud's syndrome (long before the typical picture of the disease), damage to both small and large vessels with corresponding clinical symptoms.

Lung lesions may be associated with the underlying disease in the form of lupus pneumonitis, characterized by cough, shortness of breath, unvoiced moist rales in the lower parts of the lungs. X-ray examination in such patients reveals an increase and deformation of the pulmonary pattern in the basal sections of the lungs, at times focal-like tones can be detected.

Since pneumonitis usually develops against the background of current polyserositis, the described radiographic symptoms are supplemented by a high standing of the diaphragm with signs of pleurodiaphragmatic and pleuropericardial adhesions and discoid atelectasis (linear shadows parallel to the diaphragm). In the study of the gastrointestinal tract, aphthous stomatitis, dyspeptic syndrome and anorexia are noted.

Painful abdominal syndrome can be associated both with the involvement of the peritoneum in the pathological process, and with vasculitis proper - mesenteric, splenic, etc. Segmental ileitis develops less frequently.

The defeat of the reticuloendothelial system is expressed in an increase in all groups of lymph nodes - a very frequent and early sign of the systemic nature of the disease, as well as in an increase in the liver and spleen. Actually lupus hepatitis develops extremely seldom. However, liver enlargement may be due to heart failure with pancarditis or severe effusion pericarditis, as well as the development of fatty liver.

Lupus diffuse glomerulonephritis (lupus nephritis) develops in half of the patients, usually during the period of generalization of the process.

There are various variants of kidney damage - urinary, nephritic and nephrotic syndromes.

For the recognition of lupus nephritis, intravital puncture biopsy with immunomorphological and electron microscopic examination of the kidney biopsy is of great importance. The development of renal pathology in patients with recurrent articular syndrome, fever and persistently elevated ESR requires the exclusion of lupus nephritis. It should be remembered that almost every fifth patient with nephrotic syndrome has systemic lupus erythematosus.

The defeat of the neuropsychic sphere occurs in many patients in all phases of the disease. At the onset of the disease - asthenovegetative syndrome, subsequently develop signs of damage to all parts of the central and peripheral nervous system in the form of encephalitis, myelitis, polyneuritis. Damage to the nervous system in the form of meningoencephalomyelopolyradiculoneuritis is characteristic. Epileptiform seizures are less common. Hallucinations (auditory or visual), delusional states, etc. are possible.

Diagnostics is carried out on the basis of clinical and laboratory data that are of diagnostic value: the determination of a large number of LE cells, high titers of antibodies to DNA, especially to native DNA, to deoxyribonucleoprotein, Sm antigen.

Treatment. Non-steroidal anti-inflammatory drugs and aminoquinoline derivatives are indicated. The first ones are recommended for articular syndrome.

Immunosuppressants: B vitamins, ascorbic acid in the form of a spring-autumn course. Patients are shown treatment in sanatoriums of the local type (cardiological, rheumatological).

Climatobalneological, physiotherapeutic treatment is contraindicated, since ultraviolet irradiation, insolation and hydrotherapy can exacerbate the disease.

2. Scleroderma localized

Localized scleroderma is a chronic systemic disease of connective tissue and small vessels with widespread fibro-sclerotic changes in the skin and stroma of internal organs and symptoms of obliterating endarteritis in the form of systemic Raynaud's syndrome.

Big Criterion. Scleroderma-like skin changes proximal to the major finger joints.

Small criteria.

1. Sclerodactyly.

2. Dimpled scars or loss of soft tissue substance at the fingertips and/or feet.

3. Bilateral basal pulmonary fibrosis.

The diagnosis of scleroderma is considered reliable if either a major criterion or at least two minor criteria are met.

Etiology. Unknown. Provoking factors are cooling, trauma, infection, vaccination, etc.

Pathogenesis. Of leading importance is a violation of collagen metabolism associated with the functional hyperactivity of fibroblasts and smooth muscle cells of the vascular wall. Also a factor in pathogenesis is a violation of microcirculation caused by damage to the vascular wall and changes in the intravascular aggregate properties of blood.

Systemic scleroderma is a typical collagen disease associated with excessive collagen formation (and fibrosis), functionally defective fibroblasts and other collagen-forming cells. Family genetic predisposition matters. Women get sick 3 times more often than men.

Clinic. The clinical picture usually begins with Raynaud's syndrome (vasomotor disturbances), trophic disorders and persistent arthralgia, weight loss, increased body temperature, and asthenia. Having begun with any one symptom, systemic scleroderma gradually or quite quickly acquires the features of a multi-syndromic disease.

Skin lesions are a pathognomonic sign of the disease. This is a common dense edema, followed by thickening and atrophy of the skin. More often, changes are localized on the skin of the face and extremities, often the skin of the entire body is dense.

At the same time, focal or widespread pigmentation develops with areas of depigmentation, telangiectasia. Ulcerations and pustules on the fingertips are characteristic, which do not heal for a long time and are extremely painful, deformation of the nails, hair loss up to baldness. Fibrosing interstitial myositis often develops.

Muscular syndrome is accompanied by myalgia, progressive thickening, then muscle atrophy, and a decrease in muscle strength. And rarely there is acute polymyositis with pain, muscle swelling, etc.

Fibrosing changes in the muscles are accompanied by tendon fibrosis, which leads to muscle-tendon contractures.

Joint damage is mainly associated with pathological processes in periarticular tissues (skin, tendons, articular bags, muscles). Arthralgias are accompanied by a pronounced deformity of the joints due to proliferative changes in the periarticular tissues. X-ray examination does not reveal significant destruction.

An important diagnostic sign is osteolysis of the terminal, and in severe cases, the middle phalanges of the fingers, less often the legs. The deposition of calcium salts in the subcutaneous tissue is localized mainly in the area of ​​​​the fingers and periarticular tissues, expressed in the form of painful uneven formations, sometimes spontaneously opening with rejection of crumbly calcareous masses.

Damage to the cardiovascular system observed in almost all patients: the myocardium and endocardium are affected. Scleroderma cardiosclerosis is clinically characterized by pain in the region of the heart, shortness of breath, extrasystole, muffled tones and systolic murmur at the apex, expansion of the heart to the left. In X-ray examination, a weakening of the pulsation and smoothness of the contours of the heart are noted, with X-ray kymography - silent zones in areas of macrofocal cardiosclerosis, and in the most severe cases, an aneurysm of the heart is formed due to the replacement of muscle tissue with fibrous tissue. On the ECG, a decrease in voltage, conduction disturbances up to atrioventricular blockade are usually observed; heart attack-like ECG occurs with the development of massive foci of fibrosis in the myocardium.

If the process is localized in the endocardium, the development of scleroderma heart disease and damage to the parietal endocardium is possible. The mitral valve is usually affected. Scleroderma heart disease is characterized by a benign course.

Damage to small arteries, arterioles causes such peripheral symptoms of scleroderma as Raynaud's syndrome, gangrene of the fingers. Damage to the vessels of internal organs leads to severe visceral pathology - hemorrhages, ischemic and even necrotic changes with a clinical picture of severe visceritis (decay of lung tissue, "true scleroderma kidney", etc.). Vascular pathology determines the speed of the process, its severity and often the outcome of the disease.

At the same time, it is possible to damage large vessels with a clinical picture of thromboangiitis obliterans; ischemic phenomena develop, and often gangrene of the fingers, toes, migrating thrombophlebitis with trophic ulcers in the feet and legs, etc.

Lung injury in the form of diffuse or focal pneumofibrosis, accompanied by emphysema and bronchiectasis. Complaints of shortness of breath, difficulty in taking a deep breath, hard breathing, when auscultating the lungs, wheezing is heard, a boxy tint of percussion sound, a decrease in vital capacity to 40-60% of the expected value, bilateral strengthening and deformation of the pulmonary pattern, sometimes with a fine-mesh structure (honeycomb); X-ray examination shows signs that usually characterize scleroderma pneumofibrosis.

Kidney damage manifests itself more often with focal nephritis, and diffuse glomerulonephritis with hypertension and renal failure may develop. With a rapidly progressive course of systemic scleroderma, a true scleroderma kidney often develops, leading to focal necrosis of the cortex and renal failure.

Esophageal injury, manifested by dysphagia, expansion, weakening of peristalsis and rigidity of the walls with a slowdown in the passage of barium during X-ray examination, is observed very often and is of great diagnostic value. In connection with the defeat of the vessels, the development of ulcers, hemorrhages, ischemic necrosis and bleeding in the digestive tract is possible.

Damage to the nervous system manifested by polyneuritis, vegetative instability (impaired sweating, thermoregulation, vasomotor skin reactions), emotional lability, irritability, tearfulness and suspiciousness, insomnia. Only in rare cases does a picture of encephalitis or psychosis occur. Possible symptoms of sclerosis of cerebral vessels due to their scleroderma lesions, even in young people.

There is damage to the reticuloendothelial (polyadenia, and in some patients hepatosplenomegaly) and endocrine (pluriglandular insufficiency or pathology of one or another endocrine gland) systems. More often there is a chronic course, the disease lasts for decades with minimal activity of the process and the gradual spread of lesions to various internal organs, the function of which is not disturbed for a long time.

Such patients suffer mainly from lesions of the skin, joints and trophic disorders. Within the framework of chronic systemic scleroderma, CRST syndrome (calcinosis, Raynaud's syndrome, sclerodactyly and telangiectasia) is distinguished, characterized by a long benign course with an extremely slow development of visceral pathology.

In the subacute course, the disease begins with arthralgia, weight loss, visceral pathology quickly increases, and the disease takes on a steadily progressive course with the spread of the pathological process to many organs and systems. Death usually occurs 1-2 years from the onset of the disease.

Forms of focal scleroderma: plaque - puffiness, erythema, violations of the skin pattern and pigmentation with a lilac-pink "corolla", induration, fibrosis, atrophy. Keloid form - dense strands resembling a keloid scar. Linear form - a lesion along the neurovascular bundle, affecting the fascia, muscles and bones; areas of lipodystrophy, amyotrophy, shortening of the tendons and dysplasia of the limb. Deep subcutaneous nodular form is localized on the thighs and buttocks with the involvement of the fascia. Isolated nodules along the tendons, resembling rheumatoid, and transforming calcifications. Atypical forms - idiopathic atrophoderma (bluish-violet spots on the body without previous seals); Buschke's scleroma is a pseudoscleroderma disease (dense swelling of the dermis and subcutaneous tissue).

Diagnostics. Based on clinical and laboratory data: moderate, normo- or hypochromic anemia, moderate leukocytosis and eosinophilia, and transient thrombocytopenia are usually observed. ESR is normally or moderately increased in chronic cases and significantly increased (up to 50-60 mm/h) in subacute cases.

Treatment. Antifibrotic agents (D-penicillamine, diuciphone, colchicine, enzymatic drugs, dimethyl sulfoxide). Use of NSAIDs. Treatment with immunosuppressants (suppress the autoimmune inflammatory process in connective tissue, inhibit excessive fibrosis formation), prescription of glucocorticoids. The use of antihypertensive and microcirculation-improving agents. Local therapy, massage, exercise therapy. Symptomatic treatment for damage to the digestive organs. Spa treatment.

3. Dermatomyositis

Dermatomyositis is a systemic disease of the skeletal and smooth muscles and skin.

Etiology. Unknown. Suspected viral (Coxsackie B₂) the etiology of dermatomyositis. Provocative factors - cooling, insolation, trauma, pregnancy, drug intolerance, vaccination, stressful situations.

Pathogenesis. Various immunopathological disorders.

Clinic. The disease begins acutely or subacutely with muscle syndrome (myasthenia gravis, myalgia), arthralgia, fever, skin lesions, dense widespread edema. Skin lesions are varied. More often it is purple paraorbital erythema with or without edema, erythema over the extensor surfaces of the joint, sometimes with atrophic scars. Damage to skeletal muscles is observed in the form of myalgia during movement and even at rest, with pressure and increasing muscle weakness. The muscles of the shoulder and pelvic girdle become denser, increase in volume, active movements are significantly impaired, the patient cannot sit down independently, lift his limbs, lift his head from the pillow, or hold it while sitting or standing.

With a significant spread of the process, patients are essentially completely immobilized, and in severe cases they are in a state of complete prostration. Damage to skeletal muscles (weakness, pain, swelling, induration, malnutrition, calcification).

Visceral-muscular syndrome, damage to symmetrical (mainly proximal) muscle groups, facial muscles leads to masking of the face, damage to the pharyngeal muscles leads to dysphagia, and damage to the intercostal and diaphragm muscles leads to respiratory failure, a decrease in lung capacity, and hypoventilation. The oculomotor muscles may be affected with the development of diplopia, strabismus, bilateral ptosis of the eyelids, etc. Polyarthralgia during movement and limitation of joint mobility up to the development of ankylosis are mostly due to muscle damage.

An inflammatory or dystrophic myocardial injury is observed, which is manifested by persistent tachycardia and pulse lability, enlargement of the heart to the left, muffled tones, systolic murmur at the apex, arterial hypotension.

Lung damage is associated with the underlying disease, more often it is due to infection, to which patients are predisposed due to hypoventilation of the lungs. The gastrointestinal tract is involved in the process: anorexia, abdominal pain, symptoms of gastroenterocolitis, hypotension of the upper third of the esophagus are noted. Damage to the peripheral and central nervous system.

Diagnostics. Weakness of the proximal muscles for at least 1 month, myalgia for 1 month in the absence of sensory impairment, the ratio of the concentration of creatine in the urine to the sum of the concentrations of creatine and creatinine in the urine exceeds 40%, A significant increase in the blood level of creatine phosphokinase or transaminases in the absence of other causes, degenerative changes muscle fibers on biopsy.

Four signs - a reliable diagnosis, three signs - a probable diagnosis, two signs - a possible diagnosis.

The diagnosis is made on the basis of clinical, laboratory data. In the blood, moderate leukocytosis with severe eosinophilia, a moderate increase in ESR, and hypergammaglobulinemia are usually observed. Biochemical studies of blood and urine and muscle biopsy are of diagnostic importance, especially in chronic and subacute course (thickening of muscle fibers is detected with loss of transverse striation, fragmentation and dystrophy up to necrosis, a significant cellular reaction is observed - accumulation of lymphocytes, plasma cells, etc. ).

Treatment. In acute and subacute cases, glucocorticoids are indicated in large daily doses (prednisolone). After achieving the effect, the dose of corticosteroids is reduced very slowly (0,5 tablets every 7-10 days) to a maintenance dose against the background of delagil (0,25 g), plaquenil (0,2 g) 1 tablet after dinner. With the development of stable remission, glucocorticoids can be completely discontinued. In complex treatment, B vitamins and ascorbic acid are recommended.

With severe muscle fatigue, prozerin and its analogues in normal doses, ATP are indicated. With early treatment with adequate doses of corticosteroids in patients with acute dermatomyositis, a stable recovery occurs. In the subacute course, it is usually possible to achieve only remission, supported by glucocorticoids. In chronic dermatomyositis, the disease becomes undulating.

LECTURE No. 14. Hemorrhagic diseases in children, hemorrhagic diathesis, thrombocytopenic purpura, hemorrhagic vasculitis. Hemophilia, emergency treatment for bleeding

1. Hemorrhagic diathesis and syndromes

Hemorrhagic diathesis and syndromes are forms of pathology characterized by a tendency to bleeding.

Etiology, pathogenesis. There are hereditary (familial) forms with bleeding starting in childhood and acquired forms, most of them secondary. Most of the hereditary forms are associated with abnormalities of megakaryocytes and platelets, dysfunction of the latter, or with a deficiency or defect of plasma coagulation factors, as well as von Willebrand factor, less often - with inferiority of small blood vessels (telangiectasia, Osler-Rendu disease). Most acquired forms of bleeding are associated with DIC syndrome, immune and immunocomplex lesions of the vascular wall and platelets (most thrombocytopenias), with disorders of normal hematopoiesis, and damage to blood vessels. In many of the listed diseases, hemostasis disturbances are of a mixed nature and sharply intensify due to the secondary development of DIC syndrome, most often in connection with infectious-septic, immune, destructive or tumor (including leukemia) processes.

Pathogenesis. According to pathogenesis, the following groups of hemorrhagic diathesis are distinguished:

1) caused by disorders of blood clotting, fibrin stabilization or increased fibrinolysis, including treatment with anticoagulants, streptokinase, urokinase, defibrinating drugs;

2) caused by a violation of platelet-vascular hemostasis;

3) caused by violations of both coagulation and platelet hemostasis:

a) von Willebraid's disease;

b) disseminated intravascular coagulation (thrombotic hemorrhagic syndrome);

c) with paraproteinemia, hemoblastoses, radiation sickness, etc.;

4) due to the primary lesion of the vascular wall with possible secondary involvement in the process of coagulation and platelet mechanisms of hemostasis.

Diagnostics. General diagnosis of hemorrhagic diseases and syndromes is based on the following criteria:

1) on determining the timing of the onset, duration and characteristics of the course of the disease (appearance in early childhood, adolescence or in adults and the elderly, acute or gradual development of hemorrhagic syndrome, chronic, relapsing course, etc .;

2) to identify, if possible, a family (hereditary) genesis of bleeding or an acquired nature of the disease, to clarify the possible connection between the development of hemorrhagic syndrome and previous pathological processes and background diseases;

3) on determining the predominant localization, severity and type of bleeding. So, with Osler-Rendu disease, persistent nosebleeds prevail and are often the only ones, with platelet pathology - bruising, uterine and nasal bleeding, with hemophilia - deep hematomas and hemorrhages in the joints.

2. Types of bleeding

The capillary, or microcirculatory type, is characteristic of thrombocytopenia and thrombocytopathy, von Willebrand disease, as well as deficiency of prothrombin complex factors (VII, X, V and II), some variants of hypo- and dysfibrinogenemia, and moderate overdose of anticoagulants. Often combined with bleeding of the mucous membranes and menorrhagia. Mixed capillary-hematoma type of bleeding - petechial-spotted hemorrhages in combination with extensive, dense hemorrhages and hematomas. With the hereditary genesis of bleeding, this type is characteristic of severe deficiency of factors VII and XIII, severe forms, von Willebrand disease, and among acquired ones, it is characteristic of acute and subacute forms of DIC syndrome, significant overdose of anticoagulants. Hemorrhagic diathesis caused by disorders in the blood coagulation system. Among hereditary forms, the vast majority of cases are due to deficiency of the components of factor VIII (hemophilia A, von Willebrand disease) and factor IX (hemophilia B), 0,3-1,5% each are due to deficiency of factors VII, X, V and XI. Rare forms associated with hereditary deficiency of other factors are XII Hageman defect, XIII (fibrin-stabilizing factor deficiency). Among the acquired forms, in addition to DIC syndrome, coagulopathies associated with deficiency or depression of prothrombin complex factors (II, VII, X, V) predominate - liver disease, obstructive jaundice.

3. Thrombocytopenic purpura

Thrombocytopenic purpura is a primary hemorrhagic diathesis caused by quantitative and qualitative insufficiency of the platelet link of homeostasis. In children under 10 years of age, it occurs with the same frequency, over 10 years of age and in adults - more often in females. This group of diseases is united according to the principle of a single pathogenesis of thrombocytopenia, shortening of the life of platelets caused by the presence of antibodies to platelets or another mechanism of their lysis. The etiology is unknown. The mechanism of development has not been studied. Provoking factors: hereditary predisposition, viral infections, preventive vaccinations, mental and physical trauma. Classification by reason of development: congenital, acquired; downstream: acute, chronic, chronic with frequent relapses, chronic continuously recurrent; in form: transimmune, isoimmune, heteroimmune, autoimmune. Complications: posthemorrhagic anemia, posthemorrhagic encephalopathy.

Clinic. Characteristic is the spontaneous appearance of bruises after minor contusions, and the appearance of hemorrhages of various sizes and shapes on the skin, asymmetrical, polymorphic in nature; bleeding from the nose, gums, uterus, sometimes from the kidneys, gastrointestinal tract is possible; bleeding occurs spontaneously. There is no splenomegaly. The disease is complicated by chronic iron deficiency anemia of varying severity. The course of the disease can be mild, moderate or severe.

Diagnosis established on the basis of clinical and laboratory data. In peripheral blood tests - prolongation of bleeding time according to Duke, Ivey or Borchgrevink - Waaler, positive tests for capillary fragility, increased or normal content of megakaryocytes in the bone marrow. Positive tests for capillary resistance. The diagnosis of autoimmune thrombocytopenia is suggested based on the absence of a family history and other signs of hereditary platelet deficiency, as well as a positive result of steroid therapy.

Differential diagnosis carried out with hemorrhagic vasculitis, leukemia, infectious diseases, DIC.

Treatment. Diet, strict bed rest, during a hemorrhagic crisis. Conservative treatment: prescribing prednisolone at an initial dose of 2 mg/kg per day orally for at least 2-3 weeks, after which the dose is reduced, then switched to a continuous course. Prescribe fibrinolysis inhibitors epsilon-aminocaproic acid when disseminated intravascular coagulation is excluded, drugs that improve the adhesive-aggregation functions of platelets (etamsylate, dicinone, adroxon, magnesium preparations), herbal medicine (nettle, shepherd's purse), platelet transfusion in severe hemorrhagic crisis. Surgical methods of treatment when drug therapy is ineffective: splenectomy. Therapy with immunosuppressants (azathioprine, leukeran, cyclophosphamide, vincristine, etc.) alone or in combination with prednisolone is prescribed only if steroid therapy and splenectomy are ineffective in a specialized hospital (and only for health reasons). Hemostasis is carried out by tamponade, the use of aminocaproic acid, the administration of adroxoc, etamsylate and other symptomatic agents. Dispensary observation for 5 years. Vaccinations with live viral vaccines are contraindicated. During treatment, the use of aspirin, analgin, nitrofurans, UHF, ultraviolet radiation, and NSAIDs should be avoided.

Forecast different. With immunological reduction of the megakaryocytic germ, as well as with ineffective splenectomy, the prognosis worsens. Patients are subject to mandatory medical examination. The frequency of visits to the doctor is determined by the severity of the disease and the treatment program at the moment.

4. Hemorrhagic vasculitis (Schonlein-Genoch disease)

Hemorrhagic vasculitis (Schonlein - Henoch disease) is a systemic infectious-allergic disease, which is based on a generalized inflammation of small vessels, characterized by a polymorphism of clinical manifestations with lesions of capillaries, arterioles, venules of the skin, joints, abdominal cavity and kidneys.

The disease occurs in 20-25% per 10 children, boys are more often affected.

Etiology. The cause of the disease has not been established, but there has been a connection with a previous viral or bacterial infection (streptococcal tonsillitis or exacerbation of tonsillitis, pharyngitis), as well as after the introduction of preventive vaccinations, vaccines and serums, due to drug intolerance, helminthiases, cooling and other adverse environmental influences.

Pathogenesis is associated with immune disorders - an increase in the level of circulating immune complexes, which are associated with damage to the walls of blood vessels, which leads to an increase in their permeability, edema, hypercoagulability mechanisms are triggered, the rheological properties of blood deteriorate, depletion of the anticoagulant link of blood coagulation is possible, which leads to ischemia and purpura of various localization.

Clinic. The disease manifests itself as a triad: pinpoint red, confluent hemorrhagic skin rashes (purpura), transient arthralgias of predominantly large joints and abdominal syndrome. Initial skin rashes are located on the extensor surfaces of the extremities, spreading to the buttocks, upper extremities, lower back, and neck. The elements are small erythematous spots, which at first turn pale when pressed, and after some time the rash becomes hemorrhagic, the elements acquire a red-purple color. Further, the rash turns pale, but does not bloom, and ends with residual pigmentation, which can persist for a long time. Typical for hepatitis B is that the rash is maculopapular with exudative-hemorrhagic elements located symmetrically, mainly on the extensor surfaces of the lower and upper extremities, buttocks, ears, inner thighs, less often on the chest, back, face.

But sometimes a different character of the rash is possible - with necrosis, erythema-like, vesicle-necrotic. Skin lesions are polymorphic due to rashes.

Itching is not typical. Large joints (knee, elbow, ankle) are affected. Swelling, pain, hyperemia of the joints are noted. More often the lesion is asymmetrical.

Arthritis resolves quickly without causing permanent deformities. Migrating symmetrical polyarthritis, usually of large joints, is accompanied by pain of a different nature - from short-term aches to the most acute, leading patients to immobility.

Arthritis often coincides in time with the appearance and localization of purpura. Paleness of the skin, haggard face, sunken eyes, pointed facial features, dry tongue.

Abdominal syndrome is characterized by sudden cramping, very sharp pains in the abdomen, often near the navel, simulating appendicitis, cholecystitis, pancreatitis, intestinal colic. The pain increases with palpation, there may be signs of irritation of the peritoneum. Patients usually lie on their side, pressing their legs to their stomach, rushing about.

Often, the kidneys are involved in the pathological process in the form of hematuric glomerulonephritis due to damage to the glomerular capillaries. However, with the outcome of glomerulonephritis in chronic renal pathology can be varied - from urinary syndrome to diffuse glomerulonephritis of hypertensive or mixed type.

With a generally favorable course of nephritis, outcomes in chronic progressive nephritis with renal failure are possible. Other clinical signs (CNS lesions, hemorrhagic pneumonia, myocarditis and serositis) are rare and are recognized during special studies.

Diagnostics performed on the basis of anamnesis, clinical and laboratory data. In the blood test - moderate leukocytosis, neutrophilia, eosinophilia, increased ESR.

In the biochemical analysis of blood, dysproteinemia is observed. An increase in C-reactive protein, AST, ALT, immunoglobulins in the urine test, moderate proteinuria with microhematuria.

Differential diagnosis carried out with rheumatism, skin diseases, diseases of the gastrointestinal tract.

Treatment. Bed rest. Hypoallergenic diet, limitation of table salt, extractives. Enterosorption, anti- or disaggregant therapy and antioxidant therapy are carried out to improve microcirculation (chirantil, trental, ticlopidine).

Anticoagulants are prescribed - heparin 150-300 units/kg per day (in 3-4 doses s.c.). Antihistamines - diazolin, tavegil, fenkarol. Glucocorticoids are indicated in all severe cases. Infusion therapy is used to improve the rheological properties of blood, normalize the volume of circulating blood, and reduce the coagulation potential of the blood (iv drip rheopolyglucin, contrical, gordox, trasylol).

Antibiotic therapy is prescribed if there is a connection with a previous bacterial infection or in the presence of decompensated foci of chronic infection.

With undulating course and relapses, alternative treatments are needed: non-steroidal anti-inflammatory drugs (ortofen, diclofenac sodium, piroxicam, movalis). Membrane stabilizers (vitamin E, retinol, rutin) are indicated for severe skin purpura, nephritis. Immunocorrective drugs (dibazol, interferon). Antimetabolites (azathioprine), cytostatics. Symptomatic therapy includes rehabilitation of chronic foci, deworming, painkillers, antispasmodics, antacids. The prognosis is favorable.

Dispensary observation for 5 years, medical exemption from preventive vaccinations for 2 years from the onset of stable remission.

5. Hemophilia A and B

Hemophilia A and B are recessively inherited, sex-linked (X-chromosome) diseases characterized by a sharply slow blood clotting and increased bleeding due to insufficient coagulation activity of VIII or IX plasma coagulation factors; males are ill, inherited through the female line, transmitted through the daughters of a hemophilic to his grandchildren. Genetic defects are characterized by insufficient synthesis or anomaly of factors VIII - hemophilia A, factor IX - hemophilia B, factor XI - hemophilia C, factor XII - hemophilia D. Temporary (from several weeks to several months) acquired deficiency of factors VIII, less often - IX, accompanied by severe bleeding, observed in both men and women (especially in the postpartum period, in people with immune diseases) due to the appearance in the blood in a high titer of antibodies to these factors.

Pathogenesis. Violation of the initial stage of the internal mechanism of blood coagulation, as a result of which the total clotting time of whole blood and the indicators of more sensitive tests - autocoagulation, activated, partial, thromboplastin time, etc. are sharply prolonged.

Prothrombin time (index) and the final stage of coagulation, as well as all parameters of platelet hemostasis (the number of platelets and all types of their aggregation) are not violated. Tests for fragility of microvessels (cuff, etc.) remain normal.

Clinic. From early childhood, males have experienced heavy and prolonged bleeding after any, even minor, injuries and operations, including extraction of teeth, biting the lips and tongue, etc. There is a tendency to focal massive hemorrhages in the subcutaneous tissue, muscles, joints, internal organs. Children with hemophilia are frail, have pale, thin skin and a poorly developed subcutaneous fat layer. Bleeding is always excessive compared to the cause that caused it. Large joints are most often affected. Repeated hemorrhages in the same joint lead to inflammatory changes, deformation and ankylosis. Persistent recurrent gastrointestinal and renal bleeding are possible.

The severity of the disease corresponds to the degree of deficiency of antihemophilic factors: in extremely severe forms their level is below 1%, in severe forms - 1-2%, moderate - 3-5%, mild - more than 5%. However, during injuries and operations, the threat of life-threatening bleeding remains in mild forms of hemophilia, and only maintaining the level of factors VIII or IX above 30-50% ensures reliable hemostasis.

Diagnosis established on the basis of clinical and laboratory data, analysis of pedigree data (maternally bleeding men), lengthening of the total blood clotting time (norm 8 min according to Lee White) with normal prothrombin and thrombin tests. Prenatal diagnosis: determination of the antigen of factors VIII, IX and their coagulation activity in the blood of the fetus (from the 10th week of gestation by chorion puncture). early amniocentesis. Sonography. Puncture of the umbilical cord.

Differential diagnosis carried out with acquired vasopathies, von Willebrand's disease, parahemophilia.

Treatment based on the replacement replacement of the missing factor, concentrates of VIII, IX factors are used, in the absence of - cryocypitate (contains factor VIII), native plasma concentrate (contains factor XI), fresh frozen plasma.

In hemophilia, human and animal serum can be used as a hemostatic agent. A bleeding wound should be well packed.

In hemophilia A, fresh blood should be transfused, since antihemophilic globulin A is rapidly inactivated during storage in canned blood.

In hemophilia B, ordinary donated blood can be transfused, because it contains a sufficient amount of the plasma thromboplastin component. Erythromass transfusions are indicated for acutely developed severe anemia according to vital indications.

Local homeostasis and a general increase in blood coagulability in patients with hemophilia is carried out using the application of thrombin, hemostatic sponges, fibrin films, gelatin, pressure bandages, and immobilization of the limbs.

With the introduction of antihemophilic drugs, E-amicaproic acid is prescribed intravenously or orally. Small-dose blood transfusions are usually sufficient to stop bleeding. Wounds should be cleaned of clots and washed with a solution of penicillin in isotonic sodium chloride solution. Then gauze is applied, impregnated with one of the hemostatic (adrenaline, hydrogen peroxide, etc.) and thromboplastin-rich agents (hemostatic sponges, breast milk). In the treatment of hemorrhages in the joints, glucocorticoid hormones are used (intra-articular), surgical correction with the removal of the altered synovial membrane.

With hemorrhages in the joint and muscle hematomas, it is necessary to ensure the rest of the affected limb, cold on the joint, hemostasis. Carrying out massage, exercise therapy, physiotherapy is indicated after the bleeding stops.

Features of patient management. IM injections are prohibited; all drugs are prescribed only orally or IV. For any location and severity of bleeding, if the integrity of the skin is compromised, indications for immediate (even at night) administration of antihemophilic drugs. Any surgical interventions are possible only after the administration of antihemophilic globulin preparations. The patient should visit a dentist once a quarter who has experience in treating patients with hemophilia.

If it is necessary to extract the tooth 30 minutes before the operation, a transfusion of cryoprecipitate is performed and aminocaproic acid is administered orally. After 6 hours, the cryoprecipitate is reintroduced. Aminocaproic acid is given within a week. Cryoprecipitate is infused daily for 3 days, and then every other day until the hole is epithelized.

Forecast with modern treatment favorable.

Prevention. Medical genetic counseling.

LECTURE No. 15. Anemia and leukemia in children

1. Anemia

Anemia (anemia) is a polyetiological disease characterized by a decrease in hemoglobin content, often in combination with a decrease in the number of red blood cells.

Clinic. The disease is manifested by changes in external signs (pallor of the skin, mucous membranes, sclera), weakness, dizziness, shortness of breath, tachycardia, memory impairment, the appearance of disorders of the muscular system (weakness, decreased tissue turgor), deviations in the central nervous system (lethargy, apathy, mild excitability), functional disorders of the cardiovascular system (expansion of boundaries, the appearance of systolic murmur), the development of hepatomegaly and splenomegaly, a decrease in the total amount of hemoglobin in the blood, red blood cells, and their osmotic resistance.

Anemia classification. Primary (hereditary) and secondary (acquired).

Because of:

1) deficiency anemia, iron deficiency, vitamin deficiency, protein deficiency;

2) hypo- and aplastic anemia: Fanconi congenital anemia, Diamond-Blackfan anemia, acquired anemia;

3) hemolytic anemia: spherocytic, sickle cell, autoimmune.

By severity:

1) mild anemia - hemoglobin in the range of 90-110 g/l, the number of red blood cells decreases to 3 million;

2) moderate anemia - hemoglobin 70 - 80 g/l, the number of red blood cells decreases to 2,5 million;

3) severe anemia - hemoglobin is below 70 g / l, the number of red blood cells is below 2,5 million.

By color index:

1) normochromic;

2) hyperchromic;

3) hypochromic.

iron deficiency anemia characterized by a decrease in hemoglobin content due to iron deficiency, associated with a violation of the synthesis of porphyrins, thalassemia, erythrocyte content as a result of its violation upon admission, assimilation or pathological losses.

Etiology. Antenatal reasons:

1) violation of the uteroplacental circulation, placental insufficiency (toxicosis, the threat of interruption and re-carrying of pregnancy, hypoxemic syndrome, exacerbation of somatic and acute infectious diseases);

2) feto-maternal and feto-placental bleeding;

3) intrauterine melena;

4) prematurity, multiple pregnancy;

5) deep and prolonged iron deficiency in the body of a pregnant woman.

Internal causes:

1) fetoplacental transfusion;

2) premature or late ligation of the umbilical cord;

3) internal bleeding due to traumatic obstetric aids and (or) anomalies in the development of the placenta and umbilical cord vessels.

Postnatal:

1) insufficient intake of iron with food (early artificial feeding, the use of unadapted milk formulas, feeding with cow or goat milk, an unbalanced diet devoid of a sufficient content of meat products);

2) an increase in the need for iron in children with accelerated growth rates (premature, children with high birth weight, children with a lymphatic type of constitution, children of the pre- and pubertal period);

3) increased loss of iron due to bleeding of various etiologies, intestinal absorption disorders (hereditary and acquired malabsorption syndromes, chronic bowel disease, hemorrhagic uterine bleeding in girls during the formation of the menstrual cycle in puberty), impaired iron metabolism in the body due to hormonal disorders (pre- and pubertal hormonal imbalance), violations of iron transport due to a decrease in the activity or content of transferrin in the body.

Clinic. History: insufficient, unhealthy diet, lethargy, increased fatigue, dryness, roughness of the skin, brittle nails, curvature and cross-striations of nails, hair loss, perversions of taste and smell, asthenovegetative disorders, disturbances in intestinal absorption processes, palpitations, shortness of breath during physical exertion . Based on the content of hemoglobin and red blood cells, anemia is divided into mild (hemoglobin within 90-109 g/l, red blood cells less than 4-3,5 x 10¹²), anemia of moderate severity (hemoglobin in the range of 89 - 70 g / l, red blood cells less than 3,5 x 10¹²), severe anemia (hemoglobin less than 70 g/l, erythrocytes less than 2,5 x 10¹²).

Diagnostics - based on clinical and laboratory data. in a blood test - a decrease in red blood cells, hemoglobin, serum iron concentration, a decrease in blood elements, anisocytosis, poikilocytosis. The color index is usually low (sometimes below 0,5); pronounced hypochromia of erythrocytes, their anisocytes, poikilocytosis; ESR is usually slightly increased. The most important indicator of the disease is a decrease in serum iron levels (normal is 13-28 mmol/l for men; 11-26 mmol/l for women). Low levels of serum iron and ferritin, as well as an increase in the level of total iron-binding capacity of serum.

Treatment aimed at eliminating iron deficiency and restoring the necessary supply of iron in the body. Therapy must begin with the elimination of the causes of its cause and the organization of a proper, balanced diet (foods rich in vitamins and iron, especially meat, should be included in the diet). Treatment with parenteral iron preparations is less effective than taking it in the form of oral tablets.

For intramuscular administration, Jectofer, Ferbitol, Ferrum Lek, etc. are used. The latter drug is also produced for intravenous administration. Indications for parenteral administration of iron for iron deficiency anemia are severe enteritis, conditions after extensive resections of the small intestine (but not gastric resections). Doses are prescribed at the rate of 1,5 mg of iron per 1 kg of body weight per day. Jectofer is administered intramuscularly at 2 ml per day to a patient weighing 60 kg. Blood transfusion when the hemoglobin level is below 60 g/l. Taking iron supplements increases bone marrow production of red blood cells and is accompanied by an increase in the level of reticulocytes in the blood 8-12 days after the start of therapy (a fact that has differential diagnostic significance).

Forecast favorable. Dispensary observation for 12 months.

Anemia associated with vitamin B deficiency₁₂ regardless of the reasons for this deficiency, they are characterized by the appearance of megaloblasts in the bone marrow, intramedullary destruction of erythrocytes, thrombocytopenia and neutropenia, atrophic changes in the mucous membrane of the gastrointestinal tract and changes in the nervous system.

Etiology. Vitamin deficiency is rarely of an exogenous (usually endogenous) nature, associated with increased consumption (with helminosis) and impaired absorption of various natures (with stomach diseases, malabsorption syndrome).

Pathogenesis. Vitamin B deficiency₁₂ more often associated with a violation of the production of a glycoprotein that combines with dietary vitamin B₁₂ and providing its absorption (intrinsic factor). Often the first signs of the disease appear after suffering enteritis, hepatitis. In the first case, this is due to malabsorption of vitamin B₁₂ in the small intestine, in the second - with the expenditure of its reserves in the liver, which is the main depot of vitamin B₁₂. Development B₁₂- deficiency anemia after total gastrectomy (when the secretion of the intrinsic factor is completely eliminated) occurs 5-8 years or more after the operation. During this period, patients live with vitamin reserves in the liver with minimal replenishment due to insignificant absorption in the small intestine, not connected with the internal factor of the vitamin. Rare form B₁₂-deficiency anemia is a violation of the assimilation of the vitamin during invasion with a wide tapeworm, when the parasite absorbs a large amount of vitamin B₁₂. Causes of impaired absorption of vitamin B₁₂ with intestinal damage, there may be severe chronic enteritis, diverticulosis of the small intestine, terminal ileitis, the occurrence of a blind loop of the small intestine after surgery on it.

Clinic vitamin B deficiency₁₂ characterized by damage to the hematopoietic tissue, digestive and nervous systems. There are weakness, fatigue, palpitations during physical exertion. Gastric secretion is depressed, persistent achlorhydria is possible. Often there are signs of glossitis - a polished tongue, a burning sensation in it. The skin is slightly icteric, the level of indirect bilirubin in the blood serum is increased (due to the increased death of hemoglobin-containing megaloblasts in the bone marrow). A slight increase in the spleen is determined, less often the liver.

Diagnostics - based on clinical and laboratory data. In the blood test - hyperchromic anemia, leukopenia, thrombocytopenia, pronounced anisocytosis of erythrocytes along with very large (more than 12 microns in diameter) cells - megapocytes, the sharpest poikilocytosis, increased saturation of erythrocytes with hemoglobin - hyperchromia, the appearance of polysegmented neutrophils, hyperchromic, less often normochromic nature of anemia , thrombocytopenia, leukopenia. A study of the bone marrow reveals a sharp increase in the number of elements of the erythroid series in it with a predominance of megaloblasts. Red cells, very reminiscent of megaloblasts, may occur in acute erythromyelosis, which, like B₁₂- deficiency anemia, accompanied by a slight icterus, often combined with leuko- and thrombocytopenia. However, with this leukemia, there is no such pronounced aniso- and poikilocytosis as with B₁₂-deficiency anemia, and most importantly - in the bone marrow, along with megaloblast-like cells, there are a large number of myeloblasts or undifferentiated blasts. In doubtful cases, vitamin B therapy should be started after bone marrow puncture.₁₂, which at B₁₂-deficiency anemia in 8-10 days will lead to a sharp increase in the percentage of reticulocytes in the blood (recyclic cell crisis), an increase in hemoglobin levels, the disappearance of pronounced anisocytosis in the blood, and in the bone marrow - megaloblasts.

Treatment. Cyanocobalamin (vitamin B₁₂) is administered daily subcutaneously at a dose of 200-500 mg once a day for 1-4 weeks. After normalization of hematopoiesis and blood composition, which occurs after 6-1,5 months, the vitamin is administered once a week for 2-1 months, then 2 times a month for six months (in the same doses as at the beginning of the course). In the future, patients should be registered at the dispensary; they are given prophylactic vitamin B₁₂ 1-2 times a year in short courses of 5-6 injections. This recommendation may be changed depending on the dynamics of blood counts, intestinal condition, and liver function.

folate deficiency anemia - megaloblastic anemia similar to B₁₂- deficiency anemia; develops with folic acid deficiency. Violation of the absorption of folic acid is observed in pregnant women suffering from hemolytic anemia, in premature babies, when feeding them with goat's milk, in persons who have undergone resection of the small intestine, with celiac disease, as well as with long-term use of anticonvulsants such as phenobarbital, diphenin.

Clinic similar to vitamin B deficiency₁₂.

Diagnostics - based on clinical and laboratory data. In the blood test - a decrease in the level of folic acid in erythrocytes and blood serum.

Prevention. Prescription of folic acid to persons who have suffered from its deficiency, pregnant women, and those suffering from hemolytic anemia.

Hypo- and aplastic anemias. The basis of this disease is a decrease in the production of bone marrow cells.

Hemolytic anemia develop as a result of the destruction of erythrocytes, are characterized by an increase in the blood content of erythrocyte decay products - bilirubin or free hemoglobin, or the appearance of hemosiderin in the urine. An important sign is a significant increase in reticulocytes in the blood due to an increase in the production of red blood cells. The bone marrow in hemolytic anemia is characterized by a significant increase in the number of red cells.

Anemia posthemorrhagic acute - anemia due to acute blood loss for a short period of time.

Etiology. The cause of blood loss can be trauma, surgery, bleeding from a stomach or duodenal ulcer, from dilated veins of the esophagus, from impaired hemostasis, ectopic pregnancy, lung diseases, etc.

Pathogenesis consists of the phenomena of acute vascular insufficiency caused by acute devastation of the vascular bed, loss of plasma; with massive blood loss, hypoxia also occurs due to the loss of erythrocytes, when this loss can no longer be compensated by the acceleration of circulation due to increased heart rate.

Clinic. Vascular disorders (palpitations, shortness of breath, drop in arterial and venous pressure, pallor of the skin and mucous membranes).

Treatment start by stopping the bleeding.

hereditary anemiaassociated with a violation of the synthesis of porphyrins (sideroahrestic anemia), are characterized by hypochromia of erythrocytes, an increase in the level of serum iron, iron deposition with a picture of hemosiderosis of organs.

Pathogenesis associated with a violation of the synthesis of protoporphyrin, which leads to a violation of the binding of iron and its accumulation in the body with a sharply disturbed formation of hemoglobin.

Clinic. There are no complaints or slight weakness and fatigue. Men are more often affected. The disease is inherited in a recessive manner, inheritance linked to the X chromosome. At the beginning of the disease, a slight enlargement of the spleen is noted, later, due to increased iron deposition in the organs, hemosiderosis of the liver (the liver enlarges and becomes dense) and the pancreas (a picture of diabetes mellitus appears) develops. The accumulation of iron in the heart muscle leads to severe circulatory failure, testicular hemosiderosis is accompanied by the development of eunuchoidism. Sometimes the skin takes on a gray tint.

Diagnostics - based on clinical and laboratory data. In the blood test - pronounced hypochromia of erythrocytes (color index 0,4 - 0,6), the level of hemoglobin is reduced, the number of erythrocytes is changed to a lesser extent, the level of serum iron is increased. Morphologically, anisocytosis, poikilocytosis, and sometimes a small number of target-shaped forms are noted. The content of reticulocytes is usually normal.

Treatment. Prescribe pyridoxine (vitamin B₆) 1 ml of a 5% solution i/m 2 times a day. With effective therapy, after 1,5 weeks, the content of reticulocytes sharply increases, and then the level of hemoglobin also increases.

Megaloblastic anemias - a group of anemias, a common feature of which is the detection in the bone marrow of peculiar erythrokaryocytes with structural nuclei that retain these features in the later stages of differentiation (the result of impaired DNA and RNA synthesis in cells called megaloblasts), in most cases megaloblastic anemia is characterized by a color index above one. Since the synthesis of nucleic acids concerns all bone marrow cells, frequent signs of the disease are a decrease in the number of platelets, leukocytes, and an increase in the number of segments in granulocytes.

2. Leukemia

Leukemia is the general name for malignant tumors arising from hematopoietic cells and affecting the bone marrow. The incidence ranges from 1 to 5 per 1 child population, with a peak between the ages of 000 and 000 years. Chronic myeloid leukemia is a tumor that arises from differentiating cells - the precursors of myelopoiesis.

Etiology. Not established, but the most common theory is viral-genetic. The role of factors that weaken the body’s reactivity: immunodeficiency states, chromosomal abnormalities, congenital and hypoplastic Fanconi anemia, ionizing radiation, acceleration with lymphatism.

Pathogenesis. Leukemia cells are the offspring of one mutated bone marrow hematopoietic cell that has lost the ability to mature, but retains the ability to reproduce.

Tumor progression in leukemia: inhibition of normal hematopoietic growths, changes in the morphology of the affected hematopoietic cell and the clone of tumor cells emanating from it, metastasizing and growing outside the hematopoietic organs; release by leukemia cells of substances that inhibit normal hematopoiesis; self-maintenance of the leukemic clone and the dynamism of its properties during treatment with the acquisition of high aggressiveness and resistance to the action of cytostatics.

Classification: acute leukemias (may be lymphoblastic and myeloblastic) and chronic leukemias.

Clinic. The main syndromes are anemic, intoxication, hemorrhagic, proliferative, osteoarticular, damage to internal organs, the nervous system, and infectious complications.

Diagnostics - based on clinical and laboratory data, analysis of peripheral blood, myelogram, cytochemical study of blood and bone marrow blasts.

Differential diagnosis carried out with infectious mononucleosis, infectious lymphocytosis, leukemoid reactions in infectious diseases, drug disease and poisoning.

Treatment drugs with immunosuppressive and cytostatic effects on periods of induction, consolidation, reinduction. Symptomatic therapy, treatment of infectious complications.

LECTURE No. 16. Pathology of the neonatal period. Perinatal pathology of the central nervous system. Hemolytic disease of the newborn. intrauterine infection. Sepsis

1. Perinatal CNS pathology

Etiology. Damage to the central nervous system occurs as a result of a lack of oxygen in the blood of the fetus or newborn, which can be caused by a number of reasons: fetal asphyxia caused by diseases and intoxications of the mother or caused by diseases of the fetus, disorders of the uteroplacental circulation.

Pathogenesis. The development of diseases can be caused by a discrepancy between the sizes of the birth canal of the mother and the fetus, prolonged labor, and obstetric assistance during childbirth. With the development of damage to the central nervous system as a result of hypoxia, metabolic acidosis, hyperkalemia, hyponatremia, hypoglycemia, and circulatory disorders develop, leading to cerebral edema, death of nerve cells and the development of encephalopathy. The following periods of action of the harmful factor are distinguished: embryonic, early fetal (28 weeks), perinatal. Periods of illness: acute until the first month; subacute up to 3-4 months; recovery from 2-4 to 12 months, sometimes up to 2 years.

Clinic. According to the degree of severity, they are distinguished: mild degree (Apgar score 6 - 7 points), manifested by hemocerebrospinal fluid dynamics disturbances, which is associated with a short-term hypoxic state, reversible morphofunctional changes, in children - sleep disturbances, motor restlessness, horizontal nystagmus, muscle tone is not changed, the function of sucking and swallowing is preserved. The moderate degree is a consequence of the unfavorable course of the ante- and intranatal periods of development. It is manifested by an Apgar score of 4-5 points, there is depression of reflexes, decreased muscle tone, cyanosis of the skin, and disturbances in thermoregulation. Hypertension syndrome is characterized by impaired cerebral circulation, bulging fontanelles, seizures, setting sun symptoms, severe hemorrhagic phenomena, congenital failure of functional systems, and degenerative changes.

A severe degree is a consequence of damaging factors during pregnancy and childbirth, characterized by cerebral edema, massive hemorrhages, profound metabolic disorders, degenerative changes, atrophies, gliosis.

Apgar score of at least 3 points, atony and inhibition of reflexes, impaired cardiac activity. Children are inactive, the cry is weak or absent, the skin is gray-cyanotic, cold to the touch. Breathing is uneven, shallow, heart sounds are deaf, a tendency to bradycardia. There is a disorder of sucking and swallowing. Children lie with their heads thrown back. Convulsive syndrome may occur.

Treatment. Brain dehydration is carried out by administering dry plasma, magnesium sulfate, antihemorrhagic agents, and sedative therapy.

Means that improve redox processes (cocarboxylase, ATP), in order to prevent hypoxic brain damage, intensive therapy may include methods of hyperbaric oxygenation.

Prevention. Timely treatment of maternal obstetric pathology, health education among mothers, the fight against alcoholism and smoking, rational management of childbirth.

2. Hemolytic disease of the newborn

Hemolytic jaundice of newborns is caused by an immunological conflict between mother and fetus due to incompatibility for erythrocyte antigens.

Etiology. Most often caused by incompatibility of the fetus and mother for Rh conflict or ABO antigens, less often there is incompatibility for other Rhesus (C, E, c, d, e) or M-, M-, Kell-, Duffy-, Kidd- antigens.

Pathogenesis. Any of these antigens (usually D-Rh antigen), penetrating into the blood of a Rh-negative mother, causes the formation of specific antibodies in her body, which enter the blood of the fetus through the placenta, where they destroy the corresponding antigen-containing red blood cells.

In the pathogenesis of the immunological conflict between the mother and the fetus, three stages can be distinguished: the first stage is the immunization of the mother in case of antigenic incompatibility. Occurs when incompatible blood is transfused at any time in life. Repeated abortions due to violation of the integrity of the placental barrier in late toxicosis of pregnancy and maternal diseases. The formation of isoantibodies occurs, and an isoimmunological conflict begins with the defeat of the fetus. Antibodies damage the membrane and disrupt the metabolism of red blood cells, which leads to premature intravascular hemolysis and increased production of indirect bilirubin. When antibodies occur during pregnancy, hemolytic disease of the newborn develops in utero. If antibodies penetrate during childbirth, then the disease develops after childbirth in the form of an icteric form.

The most severe complication of hemolytic disease of the newborn is kernicterus, caused by the toxic effect of indirect bilirubin on the nuclei of the base of the brain. Risk factors for kernicterus are prematurity, asphyxia, cooling, hypoglycemia. There are three main forms: edematous, icteric, anemic.

Clinic. The edematous form is the most severe: children are born prematurely, manifested by general edema at birth, accumulation of fluid in the cavities (pleural, cardiac sac, abdominal), severe pallor with jaundice, enlarged liver and spleen. Blood tests show severe anemia, a significant number of normo- and erythroblasts.

The combination of severe anemia and hypoproteinemia contributes to the development of heart failure, which leads to death (in utero or immediately after birth). The prognosis is unfavorable.

The icteric form is the most common clinical form and appears on the first or second day of a child’s life. There is icteric staining of the sclera and mucous membranes, the liver and spleen are enlarged, and tissue pastiness is observed. Children are lethargic, adynamic, and do not suck well. Reflexes are reduced. Anemia is pronounced (hemoglobin level below 160 g/l), pseudoleukocytosis, reticulocytosis, erythro- and normoblastosis are noted. A striking specter is the increased content of indirect bilirubin in the blood (100-265-342 µmol/l or more). Urine is dark, feces are of normal color. In the future, an increased level of direct bilirubin may be observed. Bilirubin intoxication increases and is manifested by lethargy, regurgitation, vomiting, pathological yawning, and decreased muscle tone. Then the classic signs of kernicterus appear: muscle hypertonicity, nuchal rigidity, opisthotonus, a sharp “brain” cry, hyperesthesia, bulging of the large fontanelle, convulsions, muscle twitching, positive sunset sign, nystagmus, apnea and complete cessation of breathing. After 2-3 weeks, the patient’s condition improves, but subsequently signs of cerebral palsy are revealed (athetosis, choreoathetosis, paralysis, paresis, delayed psychophysical development, deafness, dysarthria, etc.).

The anemic form is the most benign, occurs in 10-15% of cases and is manifested by pallor of the skin, poor appetite, lethargy, enlarged liver and spleen, anemia, reticulocytosis, normoblastosis, and a moderate increase in bilirubin.

Diagnosis is established on the basis of anamnesis and clinical symptoms, determination of the blood group and Rh affiliation of the mother and child, a blood test of the child, determination, bilirubin level, titer of Rh antibodies or α- and β-agglutinins in the mother's blood and milk. For the purpose of antenatal diagnosis, the level of bilirubin in amniotic fluid and Rh antibodies is determined.

Differential diagnosis carried out with hereditary hemolytic jaundice, hemorrhage, polycythemia.

Treatment can be both conservative and operational (according to indications). Conservative treatment: carrying out infusion therapy to correct metabolic changes and detoxification (in / in infusion of 5% glucose solution, albumin, plasma, ATP, phenobarbital 10 mg / (kg per day).

Mechanical removal of bilirubin by exchange transfusion. Phototherapy (blue or light blue lamps, 3-hour session at 2-hour intervals, total irradiation time per day is 12-16 hours). Symptomatic therapy (diuretics, B vitamins).

Surgical treatment: the absolute indication for replacement blood transfusion is hyperbilirubinemia above 342 µmol/l, with a rate of increase in bilirubin above 6 µmol/l and when its level in umbilical cord blood is above 60 µmol/l. In most cases, exchange transfusion is performed using the Diamond method through the umbilical vein using a polyethylene or metal catheter. For these purposes, freshly preserved single-group blood (preferably Rh-negative) is used. Calculation: 120-170 ml of blood per 1 kg of body weight.

The course and prognosis of the disease depend on the form. With a bilirubin level of 257-342 µmol/l or more, even if kernicterus has not developed, almost 1/3 of children have deviations in their neuropsychic status. If a replacement blood transfusion is performed, then normochromic hypo- or normoregenerative anemia is observed within 1-2 months.

In order to prevent all pregnant women are examined for Rh-affiliation.

In case of Rh-negative blood in a pregnant woman, the titer of anti-Rhesus antibodies is determined every 1-1,5 months. As the titer increases, administration of anti-D-globulin is indicated. It is recommended to maintain the first pregnancy and take a break of 4-5 years before the next one. Children who have had hemolytic disease of newborns are monitored at the dispensary with monthly examination by a neurologist, orthopedist, and ophthalmologist. A waiver from vaccinations is granted for up to 1 year.

3. Bacterial sepsis of the newborn

Bacterial sepsis of a newborn is a generalization of a bacterial infection, characterized by a breakthrough of local and regional protective barriers, the release of the pathogen into the general circulation, the development of toxicosis and multiple organ failure against the background of immunological restructuring and suppression of nonspecific resistance of the organism.

Etiology. The causative agent of neonatal sepsis is various pathogenic and conditionally pathogenic hospital strains of microorganisms, both gram-negative (Escherichia coli, Pseudomonas aeruginosa, Klebsiella, Enterobacteriaceae, Proteus) and gram-positive (staphylococcus, streptococcus, anaerobes, clostridia), etc.

Predisposing factors for sepsis are factors that reduce the protective properties of natural pathways - multiple catheterizations of the umbilical and central veins, tracheal intubation, mechanical ventilation, birth defects, acute respiratory viral infections, skin lesions; factors that inhibit the immunological reactivity of the newborn - complicated antenatal period, pathological course of childbirth, leading to asphyxia, intrauterine hypoxia, immaturity of the newborn, intracranial birth trauma; factors that increase the risk of massive bacterial contamination of the child are a long anhydrous period, especially if the mother has chronic foci of infection, and an unfavorable sanitary and epidemiological situation in the maternity hospital.

Pathogenesis. The entrance gates of infection are the umbilical wound, injured skin and mucous membranes, as well as intact skin and mucous membranes of the upper respiratory tract and gastrointestinal tract. Infection of a child can occur intrauterinely, during childbirth and after birth. At the site of infection, a primary inflammatory focus is formed, and adjacent vessels and tissues are affected. Degenerative-necrotic changes in the walls of blood vessels develop, from where pathogenic microbes spread hematogenously throughout the newborn’s body, exerting a damaging effect on tissues and organs through their enzymes and toxins, causing a severe pathological process with profound disturbances of homeostasis. Under the influence of microorganism enzymes, cell lysis occurs, resulting in increased intoxication.

Clinic. There are acute (within 3-6 weeks), subacute (1,5-3 months), prolonged (more than 3 months) and fulminant course of the disease. Depending on the entrance gate of the infection, umbilical, cutaneous, pulmonary, intestinal, and otogenic sepsis are distinguished.

If the septic process occurs in the antenatal period and the child is already born sick, his condition is severe: fever, pale gray skin with extensive dermatitis, hemorrhagic rash, swelling, exsicosis, regurgitation, vomiting, jaundice, enlarged liver and spleen, large initial loss of body weight, greenish color near the amniotic fluid.

Sepsis that has developed intra- and postnatally is more often manifested by a gradual onset of the disease - deterioration in the general condition in the first or second week of a child's life, subfebrile temperature, pale skin with a gradual acquisition of a gray or earthy hue, lethargy, refusal of the breast, regurgitation, vomiting, weight loss body, flattening of the body weight curve, an increase in the duration and severity of jaundice, hemorrhagic phenomena on the mucous membranes, pyoderma, swelling of the anterior abdominal wall and limbs.

There is a delay in mummification and separation of the umbilical residue, prolonged bleeding of the umbilical wound with late epithelization, a bloody crust in the center of the navel that does not fall off for a long time, a symptom of a secondarily opened navel, omphalitis, unstable mortar, interstitial pneumonia, etc.

Weakening of physiological reflexes, weakness, muscle hypotension, anxiety, stools with mucus and greenery, bloating, swelling or pastosity of the abdominal wall, hyperemia of the skin over the arteries, increased network of subcutaneous venous vessels, thickening of the umbilical vein or artery, increased bleeding of the umbilical wound.

The septicopyemic form is characterized by the occurrence of purulent foci most often in the brain with the development of purulent meningitis. The development of pneumonia, ulcerative necrotic enterocolitis, pyelonephritis, otitis media, conjunctivitis, etc.

Diagnostics is carried out on the basis of the clinical picture and laboratory data. In the peripheral blood, anemia, neutrophilic leukocytosis with shifts of the leukocyte formula to the left, monocytosis, thrombopenia, an increase in the level of bilirubin in the blood serum, alkaline phosphatase, thymol test, a violation of the ratio of aspartic and alanine transaminases; in the urine - transient albuminuria, bacterio- and leukocyturia. Isolation of the pathogen from the child's blood is a valuable but optional diagnostic criterion.

Treatment. Urgently hospitalize in specialized neonatal pathology departments if surgical intervention is necessary. Feeding with mother's milk (mother's breast or expressed breast milk through a tube, from a nipple).

Treatment is symptomatic with the use of broad-spectrum antibiotics in combination with drugs that stimulate defense mechanisms and restore biological balance.

When the patient's condition improves, active immunization agents are used - staphylococcal toxoid, autovaccine, staphylococcal bacteriophage, drugs that stimulate immunogenesis. All this is used in combination with such biologically active substances as lactobacterin, bifidumbacterin and vitamins.

Septicemia due to Staphylococcus aureus proceeds with a rapid malignant course, with the rapid development of multiple organ failure, rapid exhaustion, decompensation of all types of metabolism, toxic delirium, septic endocarditis, hepatolienal syndrome, infectious toxic nephrosis, endotoxic shock.

Etiology. The causative agents are various pathogenic and opportunistic microorganisms (staphylococcus, streptococcus, Escherichia coli, Proteus, Pseudomonas aeruginosa, anaerobic bacteria).

Clinic. Symptoms of intoxication predominate. General exhaustion, yellowness of the skin and mucous membranes, hemorrhages on the skin, mucous membranes, serous membranes, hemorrhages in the stomach cavity, internal organs and adrenal glands develop. On the part of the central nervous system - violations. Septicemia is characterized by intoxication of the body without local purulent-inflammatory foci, while with septicopyemia, pyemic foci are detected (abscesses, phlegmon, meningitis, otitis, pneumonia of a destructive type with pleural complications, etc.).

LECTURE No. 17. Parasitic diseases in children

1. Helminthiases

Helminthiases are diseases caused by parasitic worms that have settled in the body - helminths and their larvae.

Classification of helminthiases. According to the biological principle: nematodes (roundworms), cestodes (tapeworms), trematodes (flukes).

According to the epidemiological: geohelminthiases, biohelminthiases, contact.

Ascaridosis

Etiology. The causative agent is roundworm, which parasitizes in the adult stage in the small intestine. The lifespan of roundworms is about a year. In the migratory stage (the first 6 - 8 weeks after infection), roundworm larvae have a mechanical and sensitizing effect, causing hemorrhages and eosinophilic infiltrates in the tissues of various organs. In the intestinal phase (8 weeks after infection), adult roundworms cause general toxic-allergic and neuro-reflex reactions of the body and a variety of local mechanical effects.

Clinic. The migratory phase often occurs under the guise of acute respiratory infections, bronchitis (including malaise, dry cough or scanty sputum, low-grade fever, dry and moist rales in the lungs).

Possible urticaria, vesicular rash on the hands and feet, volatile eosinophilic infiltrates in the lungs. In the intestinal phase, the gastrointestinal form is distinguished (salivation, nausea, loss of appetite, cramping pains around the navel, sometimes disorders of the stool and gastric secretion); hypotonic (decrease in blood pressure, weakness) and neurological (dizziness, headache, fatigue, sleep disturbance, vegetative-vascular disorders) forms.

Complications. Ascariasis intestinal obstruction, ascariasis appendicitis, perforated peritonitis, ascariasis of the liver with the development of jaundice, subdiaphragmatic abscess, ascariasis of the pancreas with symptoms of acute pancreatitis, crawling of ascaris into the respiratory tract with the development of asphyxia.

Diagnosis is based on laboratory data, on the detection of nematode larvae in sputum and antibodies in the blood, in the late intestinal phase - ascaris eggs in feces.

Treatment. Piperazine, levamisole, and combantrin are used to expel young and adult roundworms. Piperazine is prescribed after meals 2 times a day with an interval between doses of 2-3 hours for 2 days in a row at a dose of 1,5-2 g per dose (3-4 g per day). Efficiency increases when taking piperazine after dinner, before bed. Levamisole (Dekaris) is prescribed after meals at a dose of 150 mg once, pyrantel is recommended once after meals at a dose of 10 mg/kg. Oxygen treatment is carried out on an empty stomach or 3-4 hours after breakfast for 2-3 days in a row.

Forecast. In the absence of complications requiring surgical intervention, favorable.

Prevention. Mass examination of the population and treatment of all those infected with ascariasis. Protection of the soil of vegetable gardens, orchards, and berry fields from contamination with feces. Thorough washing and scalding of vegetables and fruits with boiling water. Personal hygiene measures.

2. Alveococcosis

Etiology, pathogenesis. The causative agent is the larval stage of alveococcus. Infection occurs after oncospheres enter the mouth after contact with contaminated skins of foxes, arctic foxes, dogs, with the water of stagnant reservoirs and by eating wild berries collected in endemic areas. Clusters of larvae (usually in the liver) infiltrate and grow into tissues, disrupt the blood supply to organs, and cause tissue degeneration and atrophy.

Clinic. It remains asymptomatic for a long time, there is a progressive enlargement of the liver, heaviness and pressure appear in the right hypochondrium, and a dull aching pain.

After a few years, the liver becomes bumpy and very dense. Jaundice may develop, sometimes the spleen is enlarged. With the disintegration of the nodes, the body temperature rises, sweating is observed.

Diagnosis. Based on laboratory data - leukocytosis, eosinophilia, increased ESR, hyperproteinemia, hypergammaglobulinemia. Serological tests with alveococcal antigen are performed. To clarify the localization, X-ray and ultrasound examinations, liver scans, and computed tomography are used. Test puncture is prohibited due to the risk of contamination of other organs.

Differential diagnosis. Differentiate with tumors, echinococcosis and cirrhosis of the liver.

Treatment. Surgical and symptomatic.

3. Ankylostomiasis (ankylostomiasis and necatoriasis)

Etiology, pathogenesis. The causative agents are hookworm and necator, parasitizing in the human small intestine, most often in the duodenum. Infection occurs when larvae penetrate the skin or when they are ingested with contaminated vegetables, fruits, or water. The larvae migrate through the systemic and pulmonary circulation, lasting 7-10 days. In the small intestine, the larvae turn into sexually mature individuals and after 4-6 weeks begin to lay eggs. The lifespan of hookworms ranges from several months to 20 years. During the migration period, the larvae cause toxic-allergic phenomena.

Adult helminths are hematophages. When fixed to the intestinal mucosa, they injure tissues, lead to the formation of hemorrhage, cause bleeding, anemia, maintain an allergic state, dyskinesia of the gastrointestinal tract and dyspepsia.

Clinic. Skin itching and burning, asthmatic phenomena, fever, eosinophilia. In the late stage, nausea, drooling, vomiting, abdominal pain, intestinal dysfunction (constipation or diarrhea), and bloating appear.

Diagnosis. Confirmed by the detection of eggs in the stool and occasionally in the duodenal contents.

Treatment. Deworming is carried out with combantrin or levamisole. For severe anemia (hemoglobin below 67 g/l), iron supplements and red blood cell transfusions are used.

Forecast. In most cases favorable.

Prevention. In areas of hookworm infection, you should not walk barefoot or lie on the ground without bedding. It is necessary to thoroughly wash and scald fruits, vegetables, and berries with boiling water before eating them; you should not drink unboiled water.

4. Diphyllobothriasis

Etiology, pathogenesis. The causative agent is the broad tapeworm. Its lifespan is tens of years. Human infection occurs when eating fresh, insufficiently salted caviar and raw fish (pike, perch, omul, etc.). The tapeworm attaches to the intestinal mucosa with its bothria and injures it. Large accumulations of the parasite can clog the intestinal lumen. Helminth metabolic products sensitize the body.

Clinic. Characterized by nausea, weakness, dizziness, abdominal pain, unstable stools, and the release of strobile fragments during bowel movements.

Diagnosis. This is confirmed by the detection of tapeworm eggs and strobila fragments in feces.

Treatment. In case of severe anemia, before helminthization, vitamin B is prescribed at 300-500 mcg intramuscularly 2-3 times a week for a month, iron supplements, hemostimulin, hematogen. For deworming, fenasal, male fern extract, and a decoction of pumpkin seeds are used.

Forecast. In the absence of complications - favorable.

Prevention. You should not eat raw, uncooked or insufficiently salted and dried fish, as well as “live” pike caviar.

5. Opisthorchiasis

Etiology, pathogenesis. The causative agent is the cat fluke, which parasitizes the bile ducts of the liver, gallbladder and pancreatic ducts of humans, cats, dogs, etc. The parasite lives in the human body for 20-40 years. Infection occurs when eating raw (frozen), lightly salted and insufficiently fried fish of carp species (ide, chebak, dace, etc.). Opisthorchises injure the mucous membranes of the pancreatic and bile ducts, create obstacles to the outflow of bile, and contribute to the development of cystic enlargements and liver tumors. They have toxic and neuro-reflex effects.

Clinic. The incubation period is about 2 weeks. In the early period there may be fever, pain in muscles and joints, vomiting, diarrhea, pain and enlargement of the liver, less often the spleen, leukocytosis and high eosinophilia, allergic skin rashes. In the chronic stage, complaints of pain in the epigastric region, right hypochondrium, radiating to the back and left hypochondrium, attacks of pain such as gall bladder colic.

Frequent dizziness, various dyspeptic phenomena. Muscle resistance in the right hypochondrium, enlargement of the liver, occasionally icterus of the sclera, enlargement of the gallbladder, symptoms of pancreatitis are revealed. Most often, with opisthorchiasis, the phenomena of cholecystitis, biliary dyskinesia, chronic hepatitis and pancreatitis develop, less often - symptoms of gastroduodenitis, enterocolitis. Opisthorchiasis may be asymptomatic.

Diagnosis. Based on the detection of helminth eggs in feces and duodenal contents.

Treatment. Deworming is carried out with mebendazole (Vermox).

Prevention. Explaining to the population the dangers of eating raw, thawed and frozen (stroganina), lightly salted and insufficiently fried fish.

6. Teniasis

Etiology. The causative agent is the pork tapeworm, which can parasitize humans not only in the sexually mature stage, but also in the larval stage, causing the disease cysticercosis. The adult helminth parasitizes the small intestine for many years. Humans become infected with taeniasis by eating raw or half-raw meat containing taeniasis.

Diagnosis put on the basis of a repeated study of feces for the presence of segments of helminths and mucus from the perianal folds (by scraping) for the presence of tapeworm eggs.

Treatment. Vermox treatment. Sometimes ethereal extract of male fern and pumpkin seeds are used.

Prevention. You should not eat undercooked or undercooked pork.

7. Trichuriasis

Etiology, pathogenesis. The causative agent is the whipworm, which parasitizes the human colon. The lifespan of the parasite is about 5 years. Whipworms injure the intestinal mucosa, are hematophagous and promote inoculation of microflora, causing reflex reactions in other organs of the abdominal cavity. Their metabolic products sensitize the body.

Clinic. Worries include drooling, decreased (less often increased) appetite, pain in the right half of the abdomen and epigastrium, nausea, constipation or diarrhea, sometimes headache, dizziness, restless sleep, irritability; moderate hypochromic anemia and slight leukocytosis are possible. At low intensity, whipworm infestation is asymptomatic.

Diagnosis. Installed when whipworm eggs are detected in the feces.

Treatment. Mebendazole and other anthelmintic drugs are prescribed. The patient is first given a cleansing enema.

Forecast. Favorable.

8. Fascioliasis

Etiology, pathogenesis. The causative agents are liver fluke and giant fluke. The main source of human invasion is various farm animals. Human infection usually occurs in the warm season when fasciola larvae are ingested in water, sorrel, lettuce and other greens. The lifespan of helminths in the body is about 10 years. Trauma and toxic-allergic damage to the hepatobiliary system are important. Fasciolae can be carried into other tissues and organs.

Clinic. The disease is characterized by eosinophilia, allergic phenomena, disorders of the liver and gall bladder, reminiscent of the symptoms of opisthorchiasis (jaundice and attacks of gall bladder colic are more common).

Diagnosis. Diagnosis of the early stage of fascioliasis is difficult, since helminth eggs are released only 3-4 months after infection. Immunological methods are used. In the late stage, the diagnosis is based on the detection of fasciola eggs in the duodenal contents and feces.

Treatment. Anthelmintic drugs are prescribed, and after deworming, choleretic drugs are prescribed for 1-2 months. Long-term (at least a year) medical examination of patients is necessary.

Forecast favorable in treatment.

Prevention. Prohibition of drinking water from stagnant reservoirs, thorough washing and scalding of greens with boiling water.

9. Echinococcosis

Etiology. The causative agent of hydatid echinococcosis is the larval stage of a small cestode with a scolex with 4 suckers and hooks and 3-4 proglotids filled with eggs. The larva is a single-chamber bubble, the wall of which consists of two layers (outer and inner), of cells that form small parietal protrusions. The bladder cavity is filled with liquid. Echinococcus eggs are highly resistant in the external environment and can withstand drying and exposure to low temperatures.

Epidemiology. It is widespread throughout the world, infection of the population is very widespread, shepherds, hunters and people who have constant contact with the definitive hosts of echinococcus are most often affected.

Reservoir and source of invasion. The definitive hosts are carnivores, domestic animals, dogs, foxes, wolves, in which a mature worm parasitizes in the intestines; its segments containing eggs are excreted with feces into the external environment. Intermediate hosts are herbivores and omnivores (sheep, goats, pigs, horses, rodents).

Mechanism of transmission of invasion. Fecal-oral (as a result of ingestion of invasive Echinococcus eggs upon contact with dogs, sheep, on whose fur there may be helminth eggs), transmission routes are food, water, household.

Pathogenesis. When a person swallows Echinococcus eggs in the stomach and intestines, they are released from the oncosphere, penetrate through the intestinal wall into the blood, then into the liver, where the larval stage of Echinococcus is formed. The growing bubble compresses the surrounding tissues (lung, bronchi, blood vessels) and involves the pleura in the pathological process with the appearance of symptoms of a space-occupying formation. The death of the parasite leads to the addition of a bacterial infection and the formation of a lung abscess.

Clinic. Chest pain of various types, dry cough, then with purulent sputum, hemoptysis, shortness of breath. If a bubble breaks into the bronchus, a severe cough, cyanosis, suffocation appears, and the contents of the bubble may be detected in the sputum. When echinococcal blisters suppurate, a lung abscess develops.

With liver echinococcosis, patients lose their appetite, weakness, weight loss, headaches, decreased performance, a feeling of heaviness in the epigastrium appear. Pain in the right hypochondrium, liver enlargement, induration, and tenderness on palpation, nausea, vomiting, upset stool. In rare cases, subekterichnost skin and the appearance of jaundice.

Diagnostics. Based on clinical and laboratory data using serological reactions (RSC, RNGA, latex agglutination reaction with antigen from the fluid of echinococcal blisters), additional research methods, chest x-ray, computed tomography of the lungs, ultrasound of the lungs.

Treatment. Usually surgically.

Prevention. Prevention of infection of animals and humans, compliance with personal hygiene rules, periodic helminthological examination of dogs and timely deworming of infected animals and humans. Information from medical and veterinary institutions is of particular importance.

10. Enterobiasis

Etiology. The causative agent of the pinworm is a female 9-12 cm long, males 3-4 cm. Males die after fertilization, females emerge from the anus and lay eggs on the perianal area and in the perineum. Infection occurs as a result of ingestion of infective eggs. Autoinvasion is possible. In the upper part of the small intestine, the infective larvae leave the egg membranes and reach sexual maturity in the large intestine. Pinworms stick to the intestinal mucosa and penetrate to the muscle layer, producing toxins.

Clinic. With minor infestation, there may be no complaints. Itching around the anus, scratching, infection, and frequent bowel movements with pathological impurities appear. Symptoms of intoxication, vulvovaginitis in girls.

Diagnostics. Based on the detection of pinworm eggs in feces or by scraping for pinworm eggs. In the blood - eosinophilia.

Treatment. Mebendazole (Vermox) from 2 to 10 years 25-50 mg/kg once, pyrantel (Combantrin) 10 mg/kg (once after breakfast, chew), piperazine up to 1 year 0,2 2 times 5 days; 2-3 years - 0,3; 4-5 years - 0,5; 6 - 8 years - 0,5; 9-12 years - 1,0; 13-15 years old - 1,5.

Prevention. Maintain personal hygiene.

LECTURE No. 18. Rheumatism in children and adolescents

Rheumatism is a systemic inflammatory disease of the connective tissue with a primary lesion of the heart.

Etiology, pathogenesis. The main etiological factor in acute forms of the disease is group A β-hemolytic streptococcus.

In patients with prolonged and continuously recurrent forms of rheumatic heart disease, it is often not possible to establish a connection between the disease and streptococcus. In the development of rheumatism, immune disorders are of particular importance.

It is assumed that sensitizing agents (streptococcus, virus, nonspecific antigens, etc.) can lead at the first stages to immune inflammation in the heart, and then to a change in the antigenic properties of its components with their transformation into autoantigens and the development of an autoimmune process. An important role in the development of rheumatism plays a genetic predisposition.

Classification of rheumatism: it is necessary to highlight the previously inactive or active phase of the disease. Activity can be minimal (I degree), medium (II degree) and maximum (III degree). To judge it, both the severity of clinical manifestations and changes in laboratory parameters are used.

Classification is also carried out according to the localization of the active rheumatic process (carditis, arthritis, chorea, etc.), the state of blood circulation and the course of the disease. There is an acute course of rheumatism, subacute, protracted, continuously reviewing and latent (clinically asymptomatic).

Isolation of the latent course is justified only for the retrospective characteristics of rheumatism: the latent formation of heart disease, etc.

Clinic. Most often, the disease develops 1-3 weeks after a sore throat or, less commonly, another infection. For repeated attacks, this period may be shorter. Relapses of the disease often develop after any intercurrent diseases, surgical interventions, or physical overload. A manifestation of rheumatism is a combination of acute migratory and completely reversible polyarthritis of large joints with moderately severe carditis.

The onset of the disease is acute, violent, less often subacute. Polyarthritis quickly develops, accompanied by remitting fever up to 38-40 ° C with daily fluctuations of 1-2 ° C and profuse sweating, but usually without chills.

The first symptom of rheumatic polyarthritis is a growing acute pain in the joints, aggravated by the slightest passive and active movements. The pain is accompanied by swelling of the soft tissues in the area of ​​the joints, and at the same time an effusion appears in the joint cavity. The skin over the affected joints is hot, their palpation is sharply painful, the range of motion is limited due to pain.

A symmetrical lesion of large joints is characteristic - usually knee, wrist, ankle, elbow. The "volatility" of inflammatory changes is typical, which is manifested in the rapid and reverse development of arthritic phenomena in some joints and their equally rapid increase in others.

All articular manifestations disappear without a trace; even without treatment they last no more than 2-4 weeks. Rheumatic myocarditis, in the absence of a concomitant defect, is not severe with complaints of mild pain or vague discomfort in the heart area, mild shortness of breath during exercise, and, less often, palpitations or irregularities.

With percussion, the heart is of normal size or moderately enlarged to the left, with auscultation and FCG, satisfactory sonority of tones or a slight muffling of the I tone, sometimes the appearance of III, less often IV tone, soft muscle systolic murmur at the apex of the heart and the projection of the mitral valve are characteristic.

Blood pressure is normal or moderately low. On the ECG - flattening, broadening and serration of the P wave and the QRS complex, less often the lengthening of the PQ interval for more than 0,2 s. In a number of patients, a slight shift of the ST interval downwards from the isoelectric line and changes in the T wave (low, negative, less often biphasic, primarily in leads V1 - V3) are recorded. Extrasystoles, atrioventricular block II or III degree, intraventricular block, junctional rhythm are rarely observed.

Diffuse rheumatic myocarditis is manifested by violent inflammation of the myocardium with its pronounced edema and dysfunction. From the onset of the disease, severe shortness of breath, forcing to take the position of orthopnea, constant pain in the region of the heart, and palpitations have been disturbing. Characterized by "pale cyanosis", swelling of the jugular veins.

The heart is significantly and diffusely dilated, the apex beat is weak. The tones are sharply muffled, a clear third tone (protodiastolic gallop rhythm) and a distinct but soft systolic murmur are often heard. The pulse is frequent, weak filling. Arterial pressure is lowered.

Venous pressure rises rapidly, but with the onset of collapse it also falls. On the ECG, a decrease in the voltage of all teeth, flattening of the G wave, a change in the ST interval, and atrioventricular blockade are noted.

The outcome of rheumatic myocarditis in the absence of active treatment may be myocardial cardiosclerosis, the severity of which often reflects the extent of myocarditis. Focal cardiosclerosis does not impair myocardial function.

Diffuse myocarditis cardiosclerosis is characterized by signs of a decrease in the contractile function of the myocardium: weakening of the apex beat, muffled tones (especially I), systolic murmur.

Rheumatic endocarditis, which is the cause of rheumatic heart disease, is very poor in symptoms. Its essential manifestation is a clear systolic murmur with sufficient sonority of tones and the absence of signs of pronounced myocardial damage.

Unlike the murmur associated with myocarditis, endocardial murmur is coarser and sometimes has a musical tinge. Its sonority increases with a change in the position of the patient or after exercise.

A reliable sign of endocarditis is the variability of already existing noises and especially the emergence of new ones with unchanged (especially with normal) heart boundaries. Light and rather quickly disappearing diastolic murmurs, sometimes heard at the beginning of a rheumatic attack on the projection of the mitral valve or vessels, can also be partly associated with endocarditis.

Deep endocarditis (valvulitis) of the cusps of the mitral or aortic valves in a number of patients is reflected on the echocardiogram: thickening of the cusps, their "shaggy", multiple echoes from them. Pericarditis in the clinic of modern rheumatism is rare.

Dry pericarditis It is manifested by constant pain in the region of the heart and a pericardial friction noise, heard more often along the left edge of the sternum. The intensity of the noise is different, usually it is determined in both phases of the cardiac cycle. The ECG is characterized by an upward shift in the ST interval in all leads at the onset of the disease. In the future, these intervals gradually return to the isoelectric line, at the same time biphasic or negative T waves are formed. Sometimes ECG data are indicative. Dry pericarditis does not cause enlargement of the heart by itself.

Exudative pericarditis - essentially a further stage in the development of dry pericarditis. Often the first sign of an effusion is the disappearance of pain due to the separation of the inflamed pericardial layers by the accumulating exudate. There is shortness of breath, aggravated in the supine position. The region of the heart with a large amount of exudate swells somewhat, the intercostal spaces are smoothed, the apex beat is not palpated.

The heart is greatly enlarged and takes the characteristic shape of a trapezoid or round decanter. The pulsation of the contours during fluoroscopy is small. Tones and noises are very muffled (due to effusion). The pulse is frequent, small filling, blood pressure is reduced. Venous pressure is almost always increased, there is swelling of the cervical and even peripheral veins. The electrocardiogram is basically the same as in dry pericarditis; an additional symptom is only a marked decrease in the voltage of the QRS complex.

Echocardiography is of significant diagnostic importance, as it undoubtedly establishes the presence of fluid in the heart sac. When the skin is affected, ring erythema is almost pathognomonic, which is pink ring-shaped elements, never itchy, located mainly on the skin of the inner surface of the arms and legs, abdomen, neck and torso. It is found in only 1-2% of patients. Rheumatic nodules, described in the old manuals, are now practically never encountered. Erythema nodosum, hemorrhages, and urticaria are completely uncharacteristic.

With kidney damage, slightly pronounced proteinuria and hematuria (due to generalized vasculitis and damage to the renal glomeruli and tubules), changes in the nervous system and sensory organs are found.

Chorea minor, the typical "nervous form" of rheumatism, occurs predominantly in children, especially girls. It is manifested by a combination of emotional lability with muscular hypotension and violent frilly movements of the torso, limbs and mimic muscles.

Minor chorea can occur with relapses, but by the age of 17-18 it almost always ends. Features of this form are relatively small damage to the heart and slightly expressed laboratory indicators of the activity of rheumatism.

Diagnostics will be checked based on medical history, clinical and laboratory data. The blood test revealed neutrophilic leukocytosis with a shift to the left, thrombocytosis, an increase in ESR to 40-60 mm/h. An increase in titers of antistreptococcal antibodies is characteristic: antistreptohiapuronidase and antistreptokinase more than 1: 300, antistreptolysin more than 1: 250. The height of titers of antistreptococcal antibodies and their dynamics do not reflect the degree of activity of rheumatism.

In a biochemical study, an increase in the level of plasma fibrinogen above 4 g / l, globulins above 10%, γ-globulins above 20%, seromucoid above 0,16 g / l, the appearance of C-reactive protein in the blood.

In most cases, biochemical indicators of activity are parallel to the values ​​of ESR.

There are large diagnostic criteria for rheumatism (carditis, polyarthritis, chorea, erythema annulare, rheumatic nodules) and small ones (fever (not lower than 38 ° C), arthralgia, past rheumatism or the presence of rheumatic heart disease, increased ESR or a positive reaction to C- reactive protein, prolonged PQ interval on ECG).

The diagnosis is considered certain if the patient has two major criteria and one minor, or one major and two minor, but only if one of the following evidence of a previous streptococcal infection simultaneously exists: recent scarlet fever (which is an undisputed streptococcal disease) ; sowing group A streptococcus from the mucous membrane of the pharynx; increased titer of antistreptolysin O or other streptococcal antibodies.

Treatment. Maintain bed rest for 2-3 weeks or more. In the diet, it is recommended to limit table salt, carbohydrates, and sufficient intake of proteins and vitamins. Exclusion of allergenic products.

Antibacterial therapy of benzylpenicillin sodium salt for 2 weeks, then long-acting drugs (bicillin-5).

With intolerance to penicillins, replacement with cephalosporins, macrolides. Prescribe vitamin therapy, potassium preparations. Pathogenetic therapy: glucocorticoids (prednisolone). Non-steroidal anti-inflammatory drugs (indomethacin, voltaren).

Aminoquinoline preparations (rezokhin, delagil) - with a sluggish, protracted and chronic course. Immunosuppressants are rarely used. Symptomatic therapy of heart failure is carried out. When indicated, diuretic therapy is prescribed. Antirheumatic drugs do not directly affect the manifestations of chorea minor.

In these cases, it is recommended to add luminal or psychotropic drugs such as chlorpromazine or especially seduxen to ongoing therapy. For the management of patients with chorea, a calm environment, a friendly attitude of others, and inspiring the patient with confidence in a full recovery are of particular importance.

In necessary cases, it is required to take measures to prevent self-harm of the patient as a result of violent movements.

Treatment in a hospital is 1,5-2 months, then treatment in a local sanatorium is 2-3 months, where chronic foci of infection are treated and follow-up with a local pediatrician and cardio-rheumatologist is carried out.

Prevention: primary correct treatment of streptococcal infection, sanitation of foci of chronic infection, rational nutrition.

Secondary prevention includes bicillin drug prophylaxis for all patients, regardless of age and the presence or absence of heart disease, who have undergone a significant rheumatic process.

Forecast favorable.

Author: Gavrilova N.V.

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