Hospital Pediatrics. Cheat sheet: briefly, the most important

Free technical library

Lecture notes, cheat sheets
Free library / Directory / Lecture notes, cheat sheets

Hospital Pediatrics. Cheat sheet: briefly, the most important

Lecture notes, cheat sheets

Directory / Lecture notes, cheat sheets

Comments on the article

Table of contents

1. Classification of primary immunodeficiency states in children

Immunity - a way to ensure and maintain antigenic homeostasis.

Immunodeficiencies Decrease in the functional activity of the main components of the immune system, leading to a violation of the antigenic homeostasis of the body and, above all, to a decrease in the body's ability to defend itself against microbes, manifested in increased infectious morbidity.

Classification of immunodeficiency states:

1) primary immunodeficiencies;

2) secondary immunodeficiencies.

Primary immunodeficiencies are genetically determined monogenic diseases transmitted by an autosomal recessive or X-linked trait. There is also an autosomal dominant mode of inheritance.

Primary immunodeficiencies are congenital disorders of the immune system with defects in one or more of its components (cellular or humoral immunity, phagocytosis, complement system).

Classification of primary immunodeficiency states:

1) pathology of the humoral link of immunity, i.e., insufficiency in the production of antibodies;

2) pathology of the cellular link of immunity mediated by T-lymphocytes;

3) combined forms (SCID) of humoral and lymphocytic insufficiency.

clinical picture immunodeficiency states has common features.

1. Recurrent and chronic infections of the respiratory tract, paranasal sinuses, skin, mucous membranes, gastrointestinal tract, caused by opportunistic infections, protozoa, fungi, tending to generalize, septicemia and torpid to the usual reaction.

2. Hematological deficiencies: leukocytopenia, thrombocytopenia, anemia.

3. Autoimmune disorders: arthritis, scleroderma, chronic active hepatitis, thyroiditis.

4. Sometimes IDS are combined with allergic reactions in the form of eczema, Quincke's edema.

5. Tumors and lymphoproliferative diseases are more common in IDS.

6. Often IDS are combined with malformations.

7. Patients with IDS have digestive disorders, diarrheal syndrome, malabsorption syndrome.

8. Patients with IDS have unusual reactions to vaccination.

9. Reticular dysgenesis (defect of maturation of lymphoid and myeloid cells).

Severe combined immune deficiency manifests itself in the first months of life: symptoms of a severe multiorgan infectious process with malnutrition. From the respiratory system - bronchopulmonary damage. From the gastrointestinal tract - diarrhea.

2. Diagnosis of primary immunodeficiencies. Principles of therapy

Diagnosis of primary immunodeficiency states is as follows:

1) selection of children at risk of primary CHD (attention must be paid):

a) the pedigree of the child, indicating in it cases of death of children in the family at an early age from inflammatory diseases;

b) the development of vaccination, repeated, chronic, multifocal and unusual current infections, parasitic and fungal diseases;

c) the presence in the pedigree of autoimmune, allergic and tumor processes, hemopathy and pathology associated with sex;

d) the presence of associated syndromes (lagging behind in physical development, endocrinopathy, skin and neurological manifestations, etc.);

2) when assessing the immune system of children, it is necessary to take into account:

a) negative Mantoux tests after vaccination and BCG revaccination;

b) thymus dysplasia in young and middle-aged children;

c) the absence of an increase in regional lymph nodes in response to the inflammatory process;

d) hypoplasia of the tonsils or, on the contrary, a pronounced hypertrophy of the tonsil tissue and lymph nodes in combination with recurrent inflammatory processes;

3) assessment of routine laboratory tests:

a) detection in a clinical blood test: hemolytic or hypoplastic anemia, neutropenia, thrombocytopenia, absolute lymphopenia (less than 1000 in 1 mm3), absence of plasma cells in response to an acute infection - all this may indicate a deficiency syndrome in T- and B- systems. b) analysis of the proteinogram - detection of low-level hypoproteinemia and hypoalbuminemia allows us to roughly but reliably judge the state of certain immune functions;

4) identification of bright clinical non-immunological markers:

a) ataxia and bulbar telangiectasias - with Louis-Barr syndrome;

b) malformations of the main vessels and convulsions against the background of hypocalcemia - with Di George's syndrome.

Treatment. Principles of therapy for primary immunodeficiency conditions:

1) hospitalization for in-depth immunological and molecular studies and the choice of the method of therapy;

2) adequate replacement immunotherapy, which allows many patients to lead a normal life;

3) bone marrow transplantation - a radical and almost routine treatment for many forms of IDS;

4) refusal to consider a patient with congenital IDS as therapeutically unpromising.

3. Secondary immunodeficiency states. Classification

Secondary immunodeficiency states are characterized by a violation of humoral and cellular immunity, the synthesis of complement components, the absence or decrease in the activity of cytotoxic lymphocytes and macrophages. In childhood, they lead to the breakdown of post-vaccination immunity and the ineffectiveness of vaccination programs.

Secondary immunodeficiency states - These are disorders of the immune system that develop in the post-neonatal period in children or adults and are not the result of genetic defects. Causes leading to the development of secondary immunodeficiency states: nutritional deficiencies, chronic viral and bacterial infections, chemo- and corticosteroid therapy, irrational use of drugs, age-related atrophy of the thymus, exposure to radiation, unbalanced diet, poor-quality drinking water, extensive surgical operations, excessive physical activity , multiple injuries, stress, exposure to pesticides, other environmental factors.

Classification- Classification of secondary immunodeficiency states 1. Systemic, developing as a result of damage to immunogenesis (with radiation, toxic, infectious and stress lesions).

2. Local, characterized by regional damage to immunocompetent cells (local disorders of the immune apparatus of mucous membranes, skin and other tissues, developed as a result of local inflammatory, atrophic and hypoxic disorders).

Diseases accompanied by secondary immunodeficiency states

1. Infectious diseases: protozoal and helminthic diseases; bacterial, viral and fungal infections.

2. Eating disorders: malnutrition, cachexia, malabsorption syndrome, etc.

3. Exogenous and endogenous intoxications - with renal and hepatic insufficiency, with poisoning, etc.

4. Tumors of lymphoreticular tissue (lympholeukemia, thymoma, granulomatosis and other neoplasms).

5. Metabolic diseases (diabetes mellitus).

6. Protein loss in intestinal diseases, nephrotic syndrome, burn disease, etc.

7. The action of various types of radiation.

8. Strong prolonged stress.

9. The action of drugs.

10. Blockade by immune complexes and antibodies of lymphocytes in allergic and autoimmune diseases.

With the syndrome of violation of anti-infective protection - adequate antibacterial, antiviral, antifungal and antiparasitic therapy; immunomodulatory drugs; rational mode of antigenic loads, including vaccination. Allergy syndrome treatment - dissociation from causally significant allergens, elimination of metabolic products, enzyme replacement therapy, hyposensitizing effects, immunomodulatory measures according to an individual program. In the treatment of diseases associated with the development of an autoimmune syndrome, antibacterial therapy is unpromising; cytostatics, extracorporeal methods of treatment, intravenous administration of immunoglobulin-containing drugs are indicated. In the stage of subsiding the inflammatory process - immunomodulatory therapy and drugs containing cytokines - leukinferon, interferon, reaferon, etc. In all cases, sanitation of foci of chronic infections.

4. Treatment of secondary immunodeficiency conditions

Treatment. Replacement therapy with various immune drugs (immunoglobulins; antitoxic, anti-influenza and anti-staphylococcal serums).

Correction of transient forms of secondary immunodeficiency states.

1. Achievement of the period of remission:

1) antigenic loads are excluded (dissociation of the patient from the team);

2) sanitation of foci of infections in the family;

3) reducing the influence of other social factors;

4) it is necessary to exclude contact with allergens by vaccines;

5) therapeutic measures are organized on an outpatient basis;

6) detoxification and enteral sorption are carried out;

7) complexes of vitamins, microelements and various antioxidants are used;

8) individual anti-inflammatory measures (if necessary - antibacterial drugs);

9) restoration of the functions of the gastrointestinal tract.

2. When the activity of pathological processes subsides:

1) immunotropic drugs containing thymus and bone marrow factors (taktavin, thymalin, thymogen, myelopid) are prescribed;

2) the choice of a specific drug is based on tests for determining the sensitivity of lymphocytes to drugs;

3) other drugs of this plan are prescribed only after the previous stage of rehabilitation of patients;

4) with an individual choice of a drug, the achievement of a positive result of therapy becomes natural;

5) it becomes possible to prevent acute and exacerbations of chronic diseases.

3. Treatment of the underlying pathology:

1) in case of neurological pathology - drugs that improve microcirculation and metabolic processes in the central nervous system, antihypertensive and diuretic drugs;

2) with primary vegetovascular dystonia - psychotherapy of family members; decrease in the predominant activity of the departments of the ANS;

3) in case of metabolic and constitutional disorders - membrane stabilizing agents, diet;

4) in chronic infectious processes - antibacterial, antiviral, antifungal and antiparasitic drugs; inducers of nonspecific defense of the body;

5) for all patients - drugs that improve metabolic processes.

5. Vegetative-vascular dystonia

The sympathetic department of the autonomic nervous system regulates mainly adaptation-trophic processes in situations requiring intense mental and physical activity. The parasympathetic department of the autonomic nervous system exhibits its main function outside the period of intense activity of the body, mainly during the period of “rest”, and regulates anabolic processes, the insular apparatus, digestive functions, emptying of hollow organs, and helps maintain the constancy of homeostasis. Autonomic reactivity is changes in autonomic reactions to internal and external stimuli. Irritants can be pharmacological drugs (mezaton, adrenaline, etc.), as well as physical influences (cold, heat, pressure on reflexogenic zones, etc.).

There are 3 types of vegetative reactivity:

1) normal (sympathicotonic);

2) hypersympathicotonic;

3) sympathicotonic.

Vegetative provision is the maintenance of the optimal level of functioning of the autonomic nervous system, ensures the adequate functioning of various organs and systems under load. Clinical manifestations in some patients in the form of fatigue, irritability, sleep disturbances, decreased pain sensitivity with various senestopathies. Signs of autonomic dysfunction may include palpitations with a tendency to sinus bradycardia or tachycardia; supraventricular extrasystole, paroxysmal tachycardia. Pathological vasomotor reactions can be manifested by a sensation of hot flashes, cold, a decrease or increase in blood pressure, pallor of the skin or hyperemia of the skin, general or local sweating, impaired secretory function, motor dysfunction of the gastrointestinal tract, sexual dysfunction.

Treatment.

1. Pathogenetic therapy, symptomatic therapy.

2. Long-term treatment to restore balance between the sections of the autonomic nervous system, this requires more time than to form an imbalance between them.

3. An integrated approach, including various types of effects on the body.

4. Selectivity of therapy, depending on the variant of vegetative dystonia, both with a constant (permanent) and crisis (paroxysmal) course.

The main sedatives in the treatment of vegetative dystonia in children.

1. Means of plant origin (valerian, motherwort, St. John's wort, viburnum, mint, oregano, sweet clover, lemon balm).

2. Tranquilizers (seduxen, tazepam, elenium, meproman).

3. Neuroleptics (sanopax, teralen, frenolone). Non-drug therapy includes: proper organization of work and rest; maintaining a daily routine; physical education classes; balanced diet; psychotherapy; hydrotherapy and balneotherapy; physiotherapy; massage; acupuncture (according to indications). Types of sports for vegetative dystonia in children (recreational swimming, cycling, race walking, skiing, skating). Hydrotherapy depending on the type of vegetative dystonia, physiotherapy.

6. Arterial hypertension

arterial hypertension - this is an increase in blood pressure from the mouth of the aorta to the arterioles inclusive.

Classifications of arterial hypertension: primary arterial hypertension and secondary arterial hypertension.

Etiology, pathogenesis. Etiopathogenesis of arterial hypertension.

1. Etiological factors: psycho-emotional effects, brain hypoxia, age-related neuroendocrine restructuring, perinatal disorders, salt overload.

2. Predisposing factors of the first line: hyperreactivity of the nerve centers that regulate blood pressure; dysfunction of norepinephrine deposympathetic structures. Borderline arterial hypertension develops.

3. Predisposing factors of the second line: weakening of the hypertensive function of the kidneys, disorders of the pressor system reninangiotensin 2-aldosterone, changes in cell membranes.

The development of hypertension in various forms.

Before prepubertal age, an increase in blood pressure is observed more often with kidney diseases, endocrine pathology, aortic coarctation, pheochromocytoma, etc.

Classification. Classification of blood pressure levels and severity of arterial hypertension.

1st degree. Systolic - 140-159 mm Hg. Art., diastolic - 90-99 mm Hg. Art.

Borderline degree: systolic - 140-149 mm Hg. Art., diastolic - 90-94 mm Hg. Art.

Second degree. Systolic - 160-179 mm Hg. Art., diastolic - 100-109 mm Hg. Art.

Third degree. Systolic - more than 180 mm Hg. Art., diastolic - more than 110 mm Hg. Art.

Clinical manifestations. Often detected by chance, with diseases of the urinary system, the numbers of both maximum and minimum pressure usually increase. Hypertension with coarctation of the aorta is diagnosed by low pressure in the lower extremities and the presence of systolic murmur.

In prepubertal and pubertal age, hypertensive conditions occur with vegetative-vascular dystonia. Hypertension is unstable, pressure fluctuates during the day, a close relationship with emotional factors can be noted. Complaints are noted of feeling unwell, irritability, easy fatigue, pain in the region of the heart, a feeling of heat, etc. On objective examination, tachycardia, inadequate response to physical activity, autonomic lability.

Treatment. Treatment of arterial hypertension in vegetative-vascular dystonia: sedative therapy is indicated - bromine with valerian, seduxen, normalization of the daily routine, mandatory stay in the fresh air, children are shown moderate physical activity and sports with gradually increasing loads. For arterial hypertension, according to indications, diuretics, ACE inhibitors, β2-blockers, L-blockers, L- and β-blockers, and calcium channel blockers can be used.

Prevention: the correct mode of the day, nutrition, physical education and sports, a sufficiently long sleep.

7. Cardiomyopia in children

Classification of cardiomyopathies:

1) dilated (DCMP);

2) hypertrophic (HCMP);

3) restrictive (RCMP);

4) arrhythmogenic right ventricle (AKMP).

Dilated cardiomyopathy represents a sharp expansion of the cavity of the ventricles, especially the left one.

Clinical manifestations. At any age, in any gender (more often in men), signs of heart failure (up to total), decreased blood pressure, expansion of the boundaries of the heart, cardiomegaly.

Auscultatory: deafness of the XNUMXst tone at the apex, bifurcation, gallop rhythm. Respiratory organs: tympanitis or dullness on the right, on the left - small bubbling wet rales.

Diagnostics.

ECG tachycardia, arrhythmia, the appearance of R wave and ("-") T wave; FCG - I tone weakened, systolic, proto-diastolic murmur; EchoCG - dilatation of all parts of the heart, EchoCG - dilatation of the cavity of the left ventricle (KDDlzh = 56 mm), decrease in myocardial contractility (fr. ejection 0,34), EchoCG - symmetric myocardial hypertrophy Tzspzh = Tmzhp = 28, mitral regurgitation.

Treatment. Principles of treatment.

I. Conservative.

1. ACE inhibitors (capoten, enalapril, renitek).

2. Angiotensin-2 receptor blockers (Cozaan, Diovan).

3. Diuretics.

4. β-blockers (carvediol).

5. Antiaggregants, anticoagulants. II. Surgical.

Hypertrophic cardiomyopathy

Hypertrophic cardiomyopathy is expressed by hypertrophy of the left ventricle and interventricular septum.

Clinical manifestations. More often in boys, there are familial forms, shortness of breath, pain in the heart, expansion of the borders of the heart, weakening of the first tone at the apex, emphasis of the second tone over the pulmonary artery, variable systolic-diastolic murmur along the left edge of the sternum, development of cardiovascular failure of the left ventricular type.

Diagnostics. ECG - signs of hypertrophy of the left atrium and left ventricle; the Q wave is changed in holes II-III, V4, V6.

EchoCG - thickening of the interventricular septum, a decrease in the volume of the left ventricle. X-ray examination of the chest - depends on the size of the heart, the displacement of the mitral valve forward.

Carnitine CMP

Ventricular hypertrophy: KDDlzh = 65 mm, atriomegaly, EF = 0,2, mitral regurgitation II-III degree.

Treatment. Surgical - septal myectomy.

1. Valve prosthetics - two-chamber constant stimulation.

2. Conservative:

1) limitation of physical activity;

2) diet with restriction of salt and water;

3) ?-blockers;

4) Ca-channel blockers;

5) antiarrhythmics of other groups;

6) ACE inhibitors.

Cardiac glycosides are contraindicated in HCM.

8. Diseases of the pericardium in children

Clinical and morphological classification of pericardial lesions

1. Malformations of the pericardium (anomalies):

1) the defects are complete;

2) partial defects;

3) pericardial lacing defects (diverticula and cysts).

2. Pericarditis:

1) acute (dry fibrinous, exudative);

2) chronic (duration - 3 months);

3) adhesive (asymptomatic, squeezing, with dysfunction of the cardiovascular system, but without signs of cardiac compression);

4) exudative (with moderate dysfunction of the cardiovascular system, but without cicatricial compression of the heart);

5) exudative squeezing.

3. Tumors of the pericardium (malformations of the pericardium):

1) pericardial defects (complete and partial);

2) pericardial lacing defects. Embryogenesis of these anomalies is associated with disturbances in the formation of the pericardium in the early stages of development (the first 6 weeks).

Congenital defects of the pericardium include the following.

1. Partial left-sided absence of the pericardium 70%. It is complicated by the formation of a hernia, infringement of the heart at the site of the defect. There are chest pains, shortness of breath, fainting, or sudden death. Surgical treatment - pericardioplasty.

2. The complete absence of the pericardium is manifested by the symptom of "free heart": pain in the region of the heart, shortness of breath, palpitations, sometimes fainting; with percussion, unusual mobility of the heart, on the left side it shifts to the axillary line, and when the head is lowered it moves up.

3. Partial right-sided absence of the pericardium - 17%.

4. Congenital lacing of the pericardium.

5. Pericardial cysts (tender, thin-walled formations that are not soldered to surrounding tissues and filled with a clear liquid - "spring water", but it can be bloody (in case of injury) and purulent (in case of inflammation).

6. Diverticula of the pericardium - cysts and diverticula of the pericardium in childhood are asymptomatic. Sometimes there may be pain and shortness of breath.

For partial defects of the pericardium, there are no direct clinical and radiological signs, they are found in concomitant diseases.

Pericardial cysts. Pericardial cysts are divided into pseudocysts and encysted and multilocular pericardial effusions, hydatid cysts (occur after the rupture of such cysts in the liver and lungs).

Clinic: in most cases, cysts are not clinically manifested and are detected incidentally on radiography as homogeneous radiopaque oval-shaped formations, usually in the right cardiodiaphragmatic angle. Complaints of discomfort in the chest, shortness of breath, coughing or palpitations due to compression of the heart.

Percutaneous aspiration and ethanol sclerosing are used to treat congenital and inflammatory cysts. Surgical excision of echinococcal cysts is not recommended.

9. Pericarditis. Clinic. Kinds. Diagnostics

Pericarditis is an inflammation of the visceral and parietal sheet, it can be fibrinous, purulent, hemorrhagic, serous.

Etiology- Viral diseases, severe septic, often staphylococcal, processes, rheumatism, diffuse connective tissue diseases.

Pathogenesis- Pathogenesis of an allergic or autoimmune nature; in infectious pericarditis, infection is the trigger; direct damage to the membranes of the heart by bacterial or other agents cannot be ruled out.

Clinical manifestations- Acute serous fibrinous pericarditis is manifested by the main symptoms - acute pain in the heart area, radiating to the shoulder and epigastric region and passing in an upright position and when bending forward. Sometimes abdominal pain simulating acute abdomen.

Acute exudative pericarditis develops when the inflammatory process of the heart membrane is accompanied by a total lesion.

Clinic: the apex beat of the heart is displaced upward and inward from the lower left border of dullness. The boundaries of the heart change depending on the position of the patient's body. Heart sounds in the lower parts are weakened.

Chronic exudative pericarditis. The clinical picture depends on the rate of exudate accumulation. Usually, the general condition worsens sharply, shortness of breath appears, dull pains in the region of the heart, the patient takes a forced position.

The apical impulse is weakened, the heart sounds are sharply muffled.

Chronic adhesive (adhesive, constrictive) pericarditis.

The pericardium and both of its leaves thicken, visceral and parietal, fuse both with each other and with the underlying myocardium.

The onset is gradual, edematous syndrome develops, protein-losing enteropathy appears, leading to hypoalbuminemia, followed by an increase in edematous syndrome, the development of hepatomegaly, ascites, and pronounced edema of the extremities. The pulse is small, blood pressure with a small amplitude. Heart sounds are weakened, gallop rhythm.

Diagnostics.

Diagnosis of acute pericarditis: during auscultation, pericardial friction noise (one-, two- and three-phase).

ECG.

Stage I: ST-segment concave in anterior and posterior leads, PR segment deviations opposite P-wave polarity.

Early stage II: ST connection returns to baseline, PR interval deviation persists. Late stage II: T waves gradually flatten and begin to invert.

Stage III: Generalized T-wave inversion.

Stage IV: restoration of the original ECG characteristics observed before the development of pericarditis.

Echocardiography: effusion types BD.

Signs of cardiac tamponade

Blood tests:

1) determination of ESR, the level of C-reactive protein and lactate dehydrogenase, the number of leukocytes (markers of inflammation);

2) determination of the level of troponin I and MB-fraction of creatine phosphokinase (markers of myocardial damage).

10. Chronic heart failure in children. Clinic. Diagnostics

Heart failure is a condition in which the heart, despite sufficient blood flow, does not provide the body's need for blood supply. Causes of chronic circulatory failure: direct effect on the myocardium (toxic, infectious, traumatic), cardiovascular diseases.

Classification. Classification of chronic heart failure (according to Strazhesko-Vasilenko).

I stage. Compensated.

IIA stage. Decompensated reversible.

IIB stage. Decompensated irreversible.

III stage. Terminal.

Pathogenesis. The pathogenesis of chronic heart failure is manifested by a decrease or increase in blood supply, blood flow and/or pressure in the central or peripheral parts of the circulation.

Clinical forms

1. Congestive left ventricular failure occurs more often with mitral valve disease.

Clinical manifestations: shortness of breath, orthopnea, signs of congestion in the lungs appear on auscultation.

2. Left ventricular failure is characteristic of aortic disease, coronary artery disease, arterial hypertension.

Clinical manifestations: cerebrovascular insufficiency, manifested by dizziness, darkening of the eyes, fainting, coronary insufficiency.

3. Congestive right ventricular failure manifests itself in mitral, tricuspid disease or constrictive pericarditis.

Clinical manifestations: swelling of the jugular veins, increased venous pressure, acrocyanosis, enlarged liver, peripheral and abdominal edema.

4. Right ventricular failure is observed with pulmonary artery stenosis and pulmonary hypertension.

Clinical manifestations of chronic heart failure

I stage chronic heart failure. Complaints of weakness. On physical examination, the skin is pale. Signs of heart failure only with great physical exertion: shortness of breath, tachycardia. Hemodynamics is not disturbed.

IIA stage chronic heart failure.

Complaints: sleep disturbance, increased fatigue. Signs of heart failure at rest:

1) left ventricular heart failure, shortness of breath (no cough), tachycardia;

2) right ventricular heart failure - an increase in the liver and its soreness, pastosity in the evening on the lower extremities (no edema).

IIB stage chronic heart failure.

Complaints: irritability, tearfulness. All signs of heart failure at rest: icterus, cyanosis of the skin, decreased diuresis, expansion of the boundaries of the heart, muffled tones, arrhythmia.

III stage chronic heart failure.

Cachexic circulation, emaciation, "light tan" skin. Edema-dystrophic circulation (thirst, edema, abdominal edema (pulmonary edema)).

11. Treatment of chronic heart failure in children

Principles of treatment

1. Cardiac glycosides.

2. Diuretics.

3. ACE inhibitors

4.?-blockers.

Tactics for the treatment of chronic heart failure

Stage I - basic therapy of the underlying disease.

Stage IIA - diuretics.

Stage IIB - diuretics, cardiac glycosides.

Stage III - diuretics, cardiac glycosides, peripheral vasodilators.

In stage I, it is necessary to observe the regime of work and rest, moderate physical exercises. In severe stages, physical activity should be limited, bed rest, semi-bed rest is prescribed. A complete, easily digestible food rich in proteins, vitamins, potassium. With a tendency to fluid retention and arterial hypertension, a moderate restriction of sodium chloride is indicated. Cardiac glycosides are prescribed in doses close to the maximum tolerated.

First, a saturating dose is used, then the daily dose is reduced by 1,5-2 times. With glycoside intoxication, unithiol is prescribed (5% solution of 5-20 ml IV, then IM 5 ml 3-4 times a day). According to the indications, antiarrhythmic therapy is carried out. Digoxin is prescribed 2 times a day in tablets of 0,00025 g or parenterally 0,5-1,5 ml of a 0,025% solution (saturation period), then 0,25-0,75 mg (maintenance dose) per day .

The selection of the dosage of cardiac glycosides should be done in a hospital. Diuretics are used for edema, liver enlargement, congestive changes in the lungs. Use the minimum effective dose during treatment with cardiac glycosides.

Hypotaazid is used in tablets of 0,025 g, loop diuretic furosemide or lasix in tablets of 0,04 g or parenterally. Peripheral vasodilators are prescribed in severe cases with the ineffectiveness of cardiac glycosides and diuretics. With stenosis (mitral, aortic), as well as with systolic (blood pressure is reduced from 100 mm Hg and below), they should not be used. Predominantly venous dilators, nitropreparations lower the ventricular filling pressure in case of congestive insufficiency, the arteriolar dilator hydralazine 0,025 g is prescribed 2-3 tablets 3-4 times a day, as well as the calcium antagonist nifedipine, corinfar. Venuloarteriolar vasodilators: captopril at a daily dose of 0,075-0,15 g.

Potassium preparations can be administered together with cardiac glycosides, diuretics and steroid hormones.

It is necessary to ensure the need for potassium through a diet (prunes, dried apricots, apricots, peach, apricot, plum juice with pulp). Potassium chloride is prescribed orally only in a 10% solution of 1 tbsp. l.

Potassium (aldosterone antagonist spironolactone (veroshpiron)) in tablets has a moderate diuretic effect, which manifests itself on the 2nd-5th day of treatment.

12. Violation of the heart rhythm in children. Violation of the function of automatism

Nomotopic rhythm disturbances. Sinus arrhythmia manifests itself in periodically occurring increases and decreases in heart rate. The patients do not make any complaints. Sinus arrhythmia is often associated with respiratory phases and can occur in healthy children. Respiratory arrhythmia occurs when the heart rate increases during inhalation and the heart rate decreases during exhalation.

Sinus bradycardia - a decrease in the number of heartbeats. It occurs in healthy children of athletes, with vegetative-vascular dystonia of the vagotonic type, with rheumatism, hypothyroidism, traumatic brain injury, brain tumors, and some infectious diseases. Patients do not present complaints. Sinus tachycardia - an increase in the number of heartbeats. Appears with physical and emotional stress, fever, organic heart disease, various infections and intoxications, thyrotoxicosis.

Heterotopic rhythm disturbances. Nodal rhythm - an increase in the automatic function of the atrioventricular node and a decrease in the automatic ability of the sinus node due to functional or organic changes. There are no complaints, sometimes complaints about pulsation in the neck, which is noted with simultaneous contraction of the atria and ventricles. Auscultation of the heart reveals an increase in the first sound. On the ECG, a negative P wave precedes the QRS complex, the R-R interval is shortened. There is a periodic change in rhythm from the sinus to the atrioventricular node.

In this case, the heart is excited under the influence of impulses emanating alternately from the sinus node, then from the atrial conduction system, then from the atrioventricular junction, and again the pacemaker migrates in the same sequence. No complaints, no objective changes.

The clinical picture is reduced to the underlying disease (rheumatism, intoxication). On the ECG, the shape, amplitude, position of the P wave changes, as well as the duration of the P-Q interval, which becomes shorter when moving to the atrioventricular node.

Extrasystole - premature contraction of the whole heart or a separate part of it, arising under the influence of an additional focus of excitation emanating from the sinus node.

Causes: inflammatory, dystrophic, degenerative, toxic, mechanical damage and neurogenic disorders.

Depending on the place of origin, there are ventricular, atrial, atrioventricular.

Extrasystoles can be single, multiple, can occur after each contraction in a certain sequence (bigemia) or after two contractions (trigemia). Extrasystoles that occur in various ectopic centers are called polytopic. Complaints are often not presented, sometimes there are unpleasant sensations in the region of the heart (fading, stopping, a strong push).

13. Extrasystole

Extrasystole - premature contraction of the whole heart or a separate part of it, arising under the influence of an additional focus of excitation emanating from the sinus node.

The reasons: inflammatory, dystrophic, degenerative, toxic, mechanical damage and neurogenic disorders. Depending on the place of origin, there are ventricular, atrial, atrioventricular. Extrasystoles can be single, multiple, can occur after each contraction in a certain sequence (bigemia) or after two contractions (trigemia). Extrasystoles that occur in various ectopic centers are called polytopic. Complaints are often not presented, sometimes there are unpleasant sensations in the region of the heart (fading, stopping, a strong push). Auscultation of the heart reveals additional pulse beats and additional heart sounds.

With atrial extrasystole, excitation from the ectopic focus occurs earlier than monotopic excitation, and after premature contraction of the heart, a long incomplete compensatory pause occurs. On the ECG - a deformed P wave is premature or superimposed on the previous P wave, shortening of the R-P interval, the QRS complex is not changed, the T-P interval is moderately increased.

On the ECG, ventricular extrasystoles appear:

1) premature occurrence of the QRS complex without the preceding P wave;

2) QRS complex with high voltage, broadened, split, serrated, transitional T wave without S-T interval;

3) discoordinate direction of the T wave in relation to the maximum wave of the QRS complex with high voltage, broadened, split, serrated, transitional T wave without ST interval;

3) discoordinate direction of the T wave in relation to the maximum tooth of the extrasystole ORS complex;

4) elongation of the compensatory pause after extrasystole, the distance between two RR intervals, including extrasystole, is equal to two normal cycles.

Right and left ventricular extrasystoles are distinguished: with right ventricular extrasystole in lead 1, the largest R wave of the QRS complex, extrasystoles are directed upwards, and in lead III, the S wave, directed downwards, is the largest.

With the left ventricular type, in lead 1, the largest S wave of the QRS complex of extrasystoles is directed downward, in lead III, the R wave, directed upward, is the largest. The origin of a functional extrasystole due to a violation of extracardiac, more often vegetative, regulation.

The main signs of a functional extrasystole (most common in prepubertal and pubertal age):

1) labile during the day, changes with a change in body position, with physical activity;

2) children show signs of vegetative-vascular dystonia, foci of chronic infection, endocrine disorders;

3) when using special research methods, violations of myocardial contractility are not detected.

14. Violation of the heart rhythm in children. Paroxysmal tachycardia. Atrial fibrillation

Arrhythmias - these are disorders of the heart rhythm and conduction, occur with congenital heart defects, acquired heart diseases, dysfunction of the central and autonomic nervous system.

Classification of cardiac arrhythmias.

1. Violation of the function of automatism - violation of the formation of an excitation impulse:

1) nomotopic arrhythmias (disturbances in the formation of an impulse in the sinus node) (sinus arrhythmia, sinus tachycardia, sinus bradycardia);

2) heterotopic rhythm disturbances (the impulse originates outside the sinus node).

2. Passive ectopic rhythms:

1) nodal rhythm;

2) migration of the pacemaker (from the sinus node to the atrioventricular junction).

3. Active ectopic rhythms:

1) extrasystole;

2) paroxysmal tachycardia;

3) atrial and ventricular fibrillation;

4) flutter of the atria and ventricles.

4. Disorders of the conduction function (blockade), slowdown, complete delay in the conduction of excitation through the conduction system:

a) sinoauricular blockade;

b) atrioventricular blockade;

c) intra-atrial blockade;

d) intraventricular blockade;

e) blockade of the legs of the bundle of His.

Paroxysmal tachycardia - this is an attack of a sharp increase in heart rate, 2-3 times the normal rhythm.

Complaints in older children about discomfort in the heart, a feeling of tension in the neck, dizziness, fainting, pain in the epigastric region, abdomen. In young children, paroxysmal tachycardia is accompanied by convulsive and dyspeptic symptoms. On physical examination, shortness of breath, cyanosis, pulsation of the veins, congestion in the lungs, enlargement of the liver, the pulse cannot be counted, low filling, and a decrease in blood pressure.

Allocate atrial, atrioventricular, ventricular forms of paroxysmal tachycardia.

On the ECG with atrial paroxysmal tachycardia, a long series of atrial extrasystoles with a sharp shortening of the T-P interval is detected, the layering of the P wave on the T wave with its deformation, the QRS complex is not changed or moderately deformed, atrioventricular paroxysmal tachycardia is characterized by repeated repetition of atrioventricular extrasystoles with negative P waves , or by shifting them to the QRS complex, or by merging them with the T wave.

Atrial fibrillation - this is a violation of the correct activity of the atria due to the appearance in the atria of one or more foci of excitation. Complaints about the deterioration of well-being, a sense of fear, anxiety.

On the ECG, the P wave is absent and is slowed down by waves of various sizes and shapes. The QRS complex is not changed, the S-T interval is below the isoelectric line, the T wave and the isoelectric line are deformed by flicker waves.

15. Disorders of the conduction function

blockades are manifested by a slowdown (incomplete blockade) or complete cessation (complete blockade) of the conduction of impulses from the sinus node to the terminal branches of the conduction system of the heart.

Classification.

1. Sinoauricular blockade.

2. Intra-atrial blockade.

3. Atrioventricular blockade (I-III degree).

4. Intraventricular blockade (blockade of the legs of the bundle of His).

Sinoauricular blockade is a violation of the conduction of excitation from the sinus node to the atrial myocardium.

Causes: autonomic dysfunction with vagotonia, immaturity of the sinus node in newborns, hyperkalemia, drug intoxication, degenerative and inflammatory changes in the sinus node and myocardium. There are no complaints.

Periodic dropouts of individual contractions of the heart (complete RR cycles) appear on the ECG, and a pause equal to a double RR interval is recorded in their place.

Intra-atrial blockade is a violation of the conduction of an impulse along the interatrial pathways, as a result of which the synchronism of the activity of both atria is disturbed. Occurs in diseases with atrial enlargement in rheumatism, cardiomyopathy, heart defects.

On the ECG - a change in the amplitude and duration of the P wave, which can be split, bifurcated in lead I, double-humped in leads I, II and V.

Atrioventricular blockade degree) appears as a result of a slowdown or complete cessation of the conduction of excitation from the atria to the ventricles.

Blockade classification:

1) incomplete (I, II degree);

2) complete (III degree);

3) functional, congenital, acquired.

Causes of vegetative-vascular dystonia according to the vagotonic type:

1) congenital malformations of the conducting system of the heart, combined with congenital heart defects;

2) rheumatism;

3) tachyarrhythmias;

4) progressive muscular dystrophy;

5) injuries;

6) embolism;

7) collagenosis;

8) drug intoxication (digoxin).

Treatment.

In the absence of vital indications, antiarrhythmic drugs should not be used. Of particular importance from antiarrhythmic drugs are: 10% solution of calcium chloride, 1 hour, des., Art. l. depending on age 3-4 times a day, procainamide 0,1-0,5 g 2-3 times a day, /3-blockers.

During an attack of paroxysmal tachycardia, means of mechanical excitation of the vagus nerve are used (pressure on the sinuses of the carotid artery, eyeballs, inducing a gag reflex by pressing on the root of the tongue), Isoptin is used intravenously at a dose of 0,3-0,4 ml for newborns up to 1 year - 0,4-0,8 ml, 1-5 years - 0,8-1,2 ml, 5-10 years - 1,2-1,6 ml, 10 years and older - 1,6-2,0 ml and digitalis preparations.

16. Systemic vasculitis in children

Microscopic polyangiitis (microscopic polyarteritis) - necrotizing vasculitis with little or no immune deposits, with a predominant lesion of small vessels.

Clinic. The clinical picture is dominated by symptoms of glomerulonephritis and pulmonary capillaritis.

Churg-Strauss syndrome is a granulomatous inflammation involving the respiratory tract associated with asthma and eosinophilia, and necrotizing vasculitis affecting small to medium vessels.

Wegener's granulomatosis is a granulomatous inflammation of the respiratory tract, necrotizing vasculitis of small and medium-sized vessels, usually associated with necrotizing glomerulonephritis.

There are three forms: localized, transitional, generalized. Laboratory criteria: ESR acceleration, leukocytosis, hypergammaglobulinemia.

Diagnosis criteria.

1. Ulcerative-necrotic lesion of the upper respiratory tract.

2. Progressive areas of necrosis of ENT organs with cartilage destruction.

3. Involvement of the eye orbit.

4. A large number of eosinophils, granulomas in the biopsy of the nasal mucosa, septum, palate.

Behçet's disease

Behçet's disease is a vasculitis that affects small to medium-sized arteries and presents with a clinical triad of recurrent aphthous stomatitis, necrotizing ulcers of the genital organs, and eye involvement.

Diagnostic criteria. Recurrent oral ulcer (at least 3 times during the year): minor aphthae, major aphthae, herpetiform rash. Also two of the following signs: recurrent genital ulcers, eye damage (anterior, posterior uveitis). Skin lesions (erythema nodosum, pseudopholliculitis, papulopustular inflammation, acneiform nodules). Formation of pustules at injection sites.

17. Polyarteritis nodosa

Systemic vasculitis is a heterogeneous group of diseases with primary inflammatory and necrotic changes in the vascular wall.

Etiology of systemic vasculitis: viruses (cytomegaloviruses, hepatitis virus), bacteria (streptococci, staphylococci, salmonella), parasitic diseases (ascaris, filariotosis).

Vasculitis classification 1. Primary vasculitis with granuloma formation (giant cell arteritis, Takayasu's arteritis, Wegener's granulomatosis, Churg-Strauss syndrome) and without granuloma formation (polyarteritis nodosa, Kawasaki disease, microscopic polyangitis).

2. Secondary vasculitis in rheumatic diseases (aortitis in rheumatoid arthritis, rheumatoid vasculitis, vasculitis in rheumatic diseases), infections (aortitis in syphilis, hepatitis B, HIV infection).

Polyarteritis nodosa

Polyarteritis nodosa is a necrotizing inflammation of the arteries of medium and small caliber without the formation of granulomas.

Clinic

clinical options.

1. Thromboangiitis (juvenile) - damage to the vessels of the skin.

2. Visceral (classic):

1) damage to the vessels of the lungs;

2) damage to the vessels of the gastrointestinal tract;

3) damage to the vessels of the kidneys;

4) damage to the vessels of the heart.

Diagnostic criteria. Loss of body weight by more than 4 kg, livedo reticularis on the skin, myalgia, weakness, decreased blood pressure (especially diastolic), arteriographic changes in blood vessels (aneurysm, occlusion). Biopsy - necrotizing vasculitis.

Treatment- Glucocorticoids, cytostatics, symptomatic therapy (angioprotectors, antihypertensives, anticoagulants). Hemorrhagic vasculitis is a systemic inflammatory disease of deposits, causing damage mainly to capillaries, arterioles and venules of the skin, joints, abdominal cavity and kidneys, which is based on multiple thrombovasculitis. It is more common in children 4-11 years old and is a classic immune complex disease.

Clinical syndromes- Skin syndrome: maculopapular rashes on the lower extremities, spreading to the buttocks and abdomen.

Articular syndrome - polyarthralgia, arthritis of large joints without deformation.

Abdominal syndrome - sharp spastic pains in the abdomen, aggravated after eating; nausea, vomiting.

Renal syndrome - micro, macrohematuria, severe capillary toxic glomerulonephritis.

CNS damage - headaches, strokes, subdural hematomas, subdural hematomas.

Diagnostic criteria- Palpable purpura, age of onset of the disease - younger than 20 years, attacks of abdominal pain, hematuria, in the biopsy - granulocytic infiltration in the walls of arterioles and venules.

Treatment. Exclusion of provoking factors, sanitation of foci of infection, treatment of the underlying disease, anticoagulants and antiplatelet agents, anti-inflammatory therapy, local treatment.

18. Kidney failure, its types

Renal insufficiency - this syndrome develops with severe disorders of the renal processes, leads to a disorder of hemostasis, is characterized by azotemia, a violation of the water-electrolyte composition and the acid-base state of the body.

Acute renal failure occurs suddenly due to acute, most often reversible, kidney disease.

Causes of acute renal failure:

1) violation of renal hemodynamics (shock, collapse, etc.);

2) exogenous intoxication: bites of poisonous snakes, insects, medicines, poisons that are used in the national economy, everyday life, medicines;

3) infectious diseases (hemorrhagic fever with renal syndrome and leptospirosis);

4) acute kidney disease (acute glomerulonephritis and acute pyelonephritis);

5) urinary tract obstruction;

6) arenal condition (trauma or removal of a single kidney).

Renal failure is characterized by a change in homeostatic constants (pH, osmolarity, etc.) as a result of a significant impairment of kidney function and is the outcome or complication of diseases conventionally divided into renal (glomerulonephritis, pyelonephritis), prerenal (hypovolemia, dehydration, DIC) and postrenal (obstructive uropathy). ).

Acute renal failure is characterized by a sudden disruption of homeostasis (hyperasotemia, electrolyte disturbances, acidosis) due to an acute violation of the basic functions of the kidneys (nitrogen excretion, regulation of CBS, water and electrolyte balance). Acute renal failure can develop in diseases manifested by hypotension and hypovolemia (shock, burns, etc.) with a subsequent decrease in renal blood flow; DIC in septic shock, HUS; with glomerulonephritis, pyelonephritis, with cortical necrosis of the kidneys in newborns, with difficulty in the outflow of urine from the kidneys. There are 4 periods of OPN:

1) initial period;

2) oligoanuric period;

3) polyuric period;

4) recovery period.

Chronic renal failure gradually develops as a result of progressive irreversible loss of functioning parenchyma.

It is diagnosed in children with diseases of the organs of the urinary system, if they persist for 3-6 months and reduce glomerular filtration rate less than 20 ml / min, increase the level of serum creatinine, urea. Over 50 diseases are manifested by kidney damage and lead to chronic renal failure, which is characterized by progression and irreversibility.

19. Clinical picture of acute renal failure

Clinic- The initial period is characterized by symptoms of the underlying disease (poisoning, painful shock, anaphylactic or bacterial), hemolysis, acute poisoning, infectious disease. On the first day, a decrease in diuresis (less than 500 ml/day) can be detected, i.e., a period of oliguria, anuria begins, and homeostasis changes. In plasma, the level of creatinine, urea, residual nitrogen, sulfates, phosphates, magnesium, potassium is increased, the level of sodium, chlorine, and calcium is decreased.

Adynamia, loss of appetite, nausea, vomiting appear; in the first days, oliguria and anuria can be observed. With increasing azotemia, the level of urea increases daily by 0,5 g/l; with increasing acidosis, overhydration and ectrolyte disorders, muscle twitching, lethargy, drowsiness are observed, shortness of breath appears due to acidosis, pulmonary edema, the early stage of which is determined by x-ray. Characteristic changes in the cardiovascular system: tachycardia, expansion of the borders of the heart, dull heart sounds appear on auscultation, systolic murmur at the apex, pericardial friction noise. Heart rhythm disturbances develop as a result of hyperkalemia, which can cause death. With hyperkalemia, the ECG shows a tall, pointed T wave, the QRS complex is widened, and the R wave is reduced. Heart block and ventricular fibrillation can lead to cardiac arrest. Anemia develops during all periods of acute renal failure. The period of oliguria and anuria is characterized by the appearance of leukocytosis.

There may be complaints of abdominal pain, liver enlargement, symptoms of acute uremia occur. Death in acute renal failure develops against the background of uremic coma, changes in hemodynamics, sepsis. In acute renal failure, hypoisostenuria appears.

The oligoanuric period is manifested by a rapid (within a few hours) decrease in diuresis to 100-300 ml / day with a low specific gravity of urine no more than 1012, lasts 8-10 days, a gradual increase in weakness, anorexia, nausea, vomiting, itching of the skin. With unlimited administration of fluid and salt, hypervolemia and hypertension occur; peripheral edema and pulmonary edema may occur.

Hyperazotemia rapidly increases (up to 5-1 mmol/day urea, creatinine more than 5 mmol/l), severe acidosis, hyperkalemia (up to 2 mmol/l), hyponatremia (below 9 mmol/l) cause uremic coma. Hemorrhages, gastrointestinal bleeding, decrease in hemoglobin, leukocytes to 115 X 2,0/l. The color of the urine is red due to gross hematuria, and proteinuria is usually small - up to 109%.

The recovery period lasts about 1 year and is manifested by the gradual restoration of renal functions.

In the treatment of peritoneal dialysis and hemodialysis in the complex therapy of acute renal failure, mortality decreased to 20-30%, the outcome in chronic renal failure is rarely noted, as well as the development of acute renal failure against the background of chronic renal failure.

20. Prerenal and renal renal failure

Prerenal acute renal failure. Etiology. Dehydration, hypovolemia, and hemodynamic disturbances lead to impaired renal blood flow.

Diagnosis prerenal acute renal failure is established on the basis of the level of sodium in the urine is less than 15 meq / l, the excreted fraction of sodium (30Na) is less than 1%. EF-Na = (Na + urine / Na + plasma) / (urine creatinine / / plasma creatinine). 100 %. Renal failure index (RII) < 1%, RPI = Na + urine / (urine creatinine / plasma creatinine). 100 %. Urinary urea/plasma urea ratio > 10, urinary creatinine/plasma creatinine > 40, urine osmolarity > 500 mos-mol/kg. The level of potassium in the urine is not less than 40 meq / l. Rehydration therapy increases diuresis and BCC. GFR increases as cardiac activity improves.

Treatment prerenal acute renal failure is aimed at restoring perfusion and renal function.

1. Vein catheterization is prescribed for the administration of drugs. Sometimes CVP monitoring is necessary.

2. Restore BCC.

3. If, after the restoration of BCC, oliguria, anuria persist, mannitol is prescribed - a 20% solution at a dose of 0,5 g / kg, intravenously for 10-20 minutes, and subsequently diuresis should increase by 6 ml / kg, if this does not occur, the introduction of mannitol is stopped.

4. After the restoration of the BCC, a test dose of furosemide is administered, 1 mg/kg intravenously.

5. If significant oliguria or anuria persists, parenchymal or postrenal AKI should be ruled out.

Renal (parenchymal) acute renal failure

Etiology. A long-term pronounced decrease in renal perfusion in the anamnesis indicates acute tubular necrosis. Other causes of parenchymal acute renal failure include glomerulonephritis, malignant arterial hypertension, hemolytic uremic syndrome, urate nephropathy, and vasculitis.

Assess kidney function.

Parenchymal acute renal failure is characterized by the following symptoms:

1) urine creatinine/blood creatinine ratio < 20;

2) urine osmolarity below 350 mosmol/kg;

3) urinary sodium level above 40 mEq/l, EFNa > 3%, PPI > 1%;

4) renal scintigraphy evaluates renal blood flow, kidney function, and with the help of this method it is possible to exclude cortical necrosis of the kidneys, ultrasound allows to exclude urinary tract obstruction.

It is necessary to monitor the level of glucose in the blood using the express method, prepare everything for hemodialysis. Emergency hemodialysis is indicated if the plasma potassium level is greater than 7,5 mEq/L and previous measures have not been effective. Acidosis is usually reduced by administration of glucose. Bicarbonate, citrate, lactate can be prescribed for administration at a dose of 1-3 meq / l. But we must remember that 1 meq / l contains 1 meq / l of sodium and potassium. Treatment of severe acidosis is difficult due to overhydration, and hemodialysis is indicated.

Diuretics are not used for anuria.

21. Postrenal acute renal failure. Diagnostics. Treatment

Etiology. Urinary tract obstruction develops with congenital valve anomalies, structural abnormalities of the urethra, hematuria, tumor or retroperitoneal fibrosis.

Examination and diagnostics. Obstruction of the urinary tract is established on the basis of anamnesis (congenital anomalies in the development of the urinary tract, genital organs, injuries of the lower abdomen); palpated volumetric formation in the lateral parts of the abdomen, overflowing bladder. Anuria may indicate bilateral ureteral obstruction. Conduct ultrasound and scintigraphy of the kidneys. If these methods cannot be carried out, determine the level of creatinine in serum, less than 5 mg /% - excretory urography is indicated.

Treatment. Pathogenetic therapy is prescribed based on the cause of acute renal failure. Plasmapheresis should be performed, the volume of which can be determined by the severity of the patient’s condition and the degree of intoxication. In case of hemodynamic disorders, anti-shock therapy is prescribed, replacement of blood loss with transfusion of blood components, blood substitutes (100-400 mg of prednisolone is administered intravenously). In case of hypotension (after replenishing blood loss), an intravenous drip of 1 ml of a 0,2% solution of norepinephrine in 200 ml of an isotonic sodium chloride solution is prescribed.

In case of poisoning, measures are used to remove the poison from the body. With large intravascular hemodialysis, if the hematocrit is below 20%, an exchange transfusion of blood or plasma is performed.

If the cause is bacterial shock, then anti-shock therapy and antibiotics are prescribed. In the initial period of oligurianuria, furosemide is prescribed intravenously at a dose of 160 mg 4 times a day to stimulate diuresis.

Further therapy should be aimed at regulating homeostasis. Assign a diet with limited intake of protein and potassium, but with sufficient calories from carbohydrates and fats. The amount of fluid injected should be more than diuresis, the amount of water lost with vomiting and diarrhea, no more than 500 ml, this volume should include 400 ml of a 20% glucose solution with 20 units of insulin, with hyperkalemia, 10- 20 ml of a 10% solution of calcium gluconate, also in / in drip 200 ml of a 5% solution of sodium bicarbonate (after establishing the degree of acidosis and under the control of blood pH). Indications for hemodialysis and peritoneal dialysis: if the level of urea in plasma is more than 2 g / l, potassium - more than 6,5 mmol / l; if there is decompensated metabolic acidosis; if there are clinical manifestations of acute uremia.

Contraindications are cerebral hemorrhage, gastric bleeding, intestinal bleeding, severe hemodynamic disorders, lowering blood pressure. A contraindication to peritoneal dialysis is a recent operation on the abdominal organs, adhesive process in the abdominal cavity. Treatment includes surgery or urinary diversion. Obstruction of the lower urinary tract is detected and eliminated by catheterization of the bladder, obstruction of the ureters is detected by ultrasound.

After restoration of the patency of the urinary tract, polyuria develops, which leads to dehydration; in these cases, 0,45% NaCl is injected.

22. Clinical manifestations of chronic renal failure

Clinic. Complaints of fatigue, decreased performance, headache, decreased appetite. CRF is characterized by the gradual development of weakness, pale skin, and anorexia. Sometimes an unpleasant taste in the mouth is noted, nausea and vomiting appear.

Muscle tone is reduced, small muscle twitching, tremor of fingers and hands are observed. There are pains in the bones and joints. Anemia develops, leukocytosis and bleeding appear. Arterial hypertension develops with underlying kidney disease. The boundaries of the heart are expanded, with auscultation, heart sounds are muffled, characteristic changes on the ECG (sometimes they are associated with dyskalemia). Conservative therapy regulates homeostasis, the general condition of the patient is satisfactory, but physical activity, mental stress, errors in diet, infection, surgery can lead to deterioration of kidney function and the appearance of uremic symptoms. Arterial pressure is normal in the initial and polyuric stages, arterial hypertension appears in the oligoanuric and uremic stages. In the polyuric stage of chronic renal failure (diuresis reaches 2-3 l / day), which can last for years, hyperazotemia is moderately expressed, glomerular filtration is 20-30 ml / min, the relative density of urine is lower than the relative density of blood plasma (1010-1012). With congenital nephropathy (proteinuria up to 1 g / day), proteinuria, hematuria, leukocyturia appear. In the oligoanuric stage, the patient's condition deteriorates sharply, which is due to the addition of hemorrhagic syndrome, cardiovascular insufficiency. When glomerular filtration is below 10 ml / min, conservative therapy is performed, homeostasis is impossible. The end stage of CRF is characterized by emotional lability (apathy is replaced by agitation), disruption of nocturnal sleep, lethargy, and inappropriate behavior. Puffy face, gray-yellow color, skin itching, scratching on the skin, dull, brittle hair, dystrophy, hypothermia is characteristic. Decreased appetite. The voice is hoarse. An ammonia smell appears from the mouth, aphthous stomatitis develops. Coated tongue, vomiting, regurgitation.

Sometimes diarrhea, stools are fetid, dark in color. Anemia, hemorrhagic syndrome, muscle twitches appear.

With prolonged uremia, pain in the arms and legs, brittle bones appear, which can be explained by uremic nephropathy and renal osteodystrophy. Uremic intoxication can be complicated by pericarditis, pleurisy, ascites, encephalopathy, and uremic coma. Children with chronic renal failure have symptoms of rickets (pain in the bones and muscles, bone deformities, growth retardation), which is associated with insufficient production of the biologically active metabolite of vitamin D.

During this period, anemia, hyperkalemia, and impaired renal function by osmotic dilution increase, which leads to the development of hypovolemia with inadequate fluid administration.

23. Treatment of chronic renal failure

Treatment. Treatment of chronic renal failure in conjunction with treatment of the underlying kidney disease, which leads to renal failure.

In the initial stage, when there is no impairment of renal processes, etiotropic and pathogenetic therapy is prescribed, which will cure the patient and prevent the development of renal failure or lead to remission and a slow course of the disease. In the stage of impaired renal processes, pathogenetic therapy is carried out with symptomatic treatment methods (hypotensive drugs, antibacterial treatment, protein restriction in the daily diet, spa treatment, etc.).

Conservative treatment of CRF is aimed at restoring homeostasis, reducing azotemia, and reducing symptoms of uremia.

The glomerular filtration rate is below 50 ml / min, the level of creatinine in the blood is above 0,02 g / l - it is necessary to reduce the amount of protein consumed to 30-40 g / day. The diet should be high in calories 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. To reduce the level of phosphates in the blood, use almagel 1-2 tsp. 4 times a day. During treatment, it is necessary to control the level of calcium and phosphorus in the blood. With acidosis, depending on the degree, 100-200 ml of a 5% sodium bicarbonate solution is injected intravenously.

With a decrease in diuresis, lasix is prescribed in doses (up to 1 g / day) that provide polyuria. Antihypertensive drugs are prescribed to lower blood pressure.

Anemia is treated with iron supplements. With a hematocrit of 25% and below, transfusions of erythrocyte mass by fractional administration are indicated. Antibiotics and their chemotherapeutic drugs in chronic renal failure are used carefully: doses are reduced by 2-3 times. Derivatives of nitrofurans in chronic renal failure are contraindicated. In heart failure and chronic renal failure, cardiac glycosides are used carefully in reduced doses, especially with hypokalemia. Hemodialysis may be indicated for exacerbation of renal failure, after the exacerbation subsides.

When the patient's condition improves, conservative therapy is carried out. Plasmapheresis courses give a good effect in chronic renal failure.

In the terminal stage, the patient is transferred to hemodialysis.

Regular hemodialysis is used when creatinine clearance is below 10 ml/min and plasma levels are above 0,1 g/l. CRF must be differentiated from acute renal failure, which is distinguished by a sudden onset with an oligoanuric stage and reverse development, from neurohypophyseal diabetes insipidus, the difference is that there is no hyperazotemia and other signs of chronic renal failure, from anemic syndrome and other diseases (hypoplastic anemia, etc.), in which there are no symptoms of CRF.

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

24. Classification of diffuse connective tissue diseases in children

Classification of rheumatic diseases.

1. Rheumatism.

2. Juvenile rheumatoid arthritis.

3. Ankylosing spondylitis.

4. Other spondyloarthropathies.

5. Systemic lupus erythematosus.

6. Vasculitis:

1) hemorrhagic vasculitis (Chilen-Genoch);

2) periarteritis nodosa (polyarteritis in young children, Kawasaki disease, Wegener's disease);

3) Takayasu's arteritis.

7. Dermatomyositis.

8. Scleroderma.

9. Difficult to classify rheumatic syndromes.

10. Various diseases associated with rheumatic symptoms and signs in children:

1) benign rheumatoid nodules;

2) erythema nodosum;

3) Lyme disease;

4) sarcoidosis;

5) Steven-Johnson syndrome;

6) Goodpasture's syndrome;

7) symptoms of fibrositis and fibromyalgia;

8) Behçet's syndrome;

9) Sjögren's syndrome.

11. Non-rheumatic diseases, clinically similar to rheumatic ones.

Diffuse connective tissue diseases (DBST, collagenoses) is an immunopathological lesion of connective tissue with systemic damage to blood vessels and various organs, with a progressive course.

In the etiology of DBST, 3 groups of leading factors can be distinguished.

1st factor - genetic predisposition, which is confirmed by epidemiological studies, the disease of close relatives, twins and the detection of markers of individual diseases according to the HLA system

The 2nd factor is a trigger mechanism, which is slow-reacting RNA-containing viruses (retroviruses), and a chronic persistent infection transmitted transplacentally.

3rd factor - resolving: stressful situation, hyperinsolation, hypothermia.

With all DBST, the degree of disease activity is determined; the nature of the flow; the presence of visceral lesions: the functional ability of the patient according to the state of the organs and systems involved in the process; the nature of the complications. In the DBST prodrome there are a number of common features that combine various nosological forms: unmotivated weakness, physical inactivity, loss of appetite and body weight; fever resistant to antibiotics, non-steroidal anti-inflammatory drugs and responsive to GC treatment; damage to the skin and mucous membranes; articular syndrome; lymphadenopathy; enlargement of the liver and spleen; persistent mono or polyviscerites.

In the DBST group, 4 "large collagenoses" are distinguished.

1. Systemic lupus erythematosus (SLE).

2. Systemic scleroderma (SSD).

3. Progressive sclerosis.

4. Dermatomyositis (DM).

25. Systemic lupus erythematosus

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

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

Family genetic predisposition, girls and women get sick more often. Provocative factors: 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 is observed. Polyarthritis, polyarthralgia are an early symptom of the disease. Damage to small joints of the hands, wrists, ankles, and less commonly, knee joints. Erythematous rashes on the skin of the face in the form of a “butterfly”, in the upper half of the chest in the form of a décolleté, and on the extremities are also a characteristic sign of systemic lupus erythematosus. Polyserositis, dermatitis, polyarthritis - diagnostic triad. Characterized by damage to the cardiovascular system with the development of pericarditis, which is accompanied by myocarditis. Lung damage may be associated with the underlying disease in the form of lupus pneumonitis, manifested by cough, shortness of breath, and moist rales on auscultation in the lower parts of the lungs. When examining the gastrointestinal tract, aphthous stomatitis is revealed, dyspeptic syndrome and anorexia develop. Damage to the reticuloendothelial system manifests itself in the form of enlargement of all groups of lymph nodes, enlargement of the liver, and spleen.

Every fifth patient with nephrotic syndrome may have systemic lupus erythematosus and damage to the neuropsychic sphere in patients may develop in all phases of the disease.

In the initial stage, asthenovegetative syndrome is diagnosed, then characteristic signs of damage to the central and peripheral nervous system appear in the form of encephalitis, polyneuritis, myelitis. Very rarely, epileptiform seizures can develop. Diagnosis based on clinical and laboratory data, which are of particular diagnostic value, determines 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. Nonsteroidal anti-inflammatory drugs are prescribed for articular syndrome. Immunosuppressants, B vitamins, ascorbic acid during the spring-autumn course. Patients are prescribed treatment in local sanatoriums (cardiological, rheumatological). Climatic-balneological, physiotherapeutic treatment is contraindicated, since ultraviolet irradiation, insolation and hydrotherapy can cause an exacerbation of the disease.

26. Scleroderma localized

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

Major criteria: scleroderma-like skin changes proximal to the major finger joints.

Small Criteria:

1) sclerodactyly;

2) dimpled scars or loss of soft tissue substance of the fingertips, hands and/or feet;

3) bilateral basal pulmonary fibrosis. Systemic scleroderma is a collagen disease that is associated with increased collagen formation and fibrosis, functionally defective fibroblasts and other collagen-forming cells. The predisposition is family genetic, women are ill 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.

Systemic scleroderma begins with a single symptom and quickly acquires the features of a multisyndromic disease. Skin lesions are a characteristic symptom of the disease.

The most common is dense edema, followed by thickening and atrophy of the skin. More often, changes are localized on the skin of the face, limbs, very rarely the skin of the entire body becomes dense.

Muscular syndrome manifests itself in the form of myalgia, characterized by progressive compaction, then muscle atrophy, and a decrease in muscle strength.

The damage to the joints is mainly associated with the pathological process of the periarticular tissue (skin, tendons, articular bags, muscles).

A special diagnostic sign is osteolysis of the terminal, as well as in severe cases, middle phalanges of the fingers, very rarely of the legs. Lung damage in the form of diffuse or focal pneumofibrosis, accompanied by emphysema and bronchiectasis. Complaints of shortness of breath, difficulty in deep breathing, hard breathing. Systemic scleroderma often has a chronic course, and the disease lasts for several decades with minimal activity of the process and the gradual spread of the lesion to various internal organs, the functions of which are not disturbed for a long time. These patients suffer mainly from diseases of the skin and joints with trophic disorders. The death of such patients occurs within 1-2 years from the onset of the disease. Forms of focal scleroderma.

1. Plaque form.

2. Keloid form.

3. Linear form.

4. Deep subcutaneous nodular form.

5. Atypical forms.

Treatment. The principles of treatment are as follows.

1. Antifibrotic agents.

2. The use of NSAIDs.

3. Treatment with immunosuppressive agents.

4. The use of antihypertensive drugs.

27. Dermatomyositis

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

Etiology- The etiology is unknown. A viral (Coxsackie B2) etiology of dermatomyositis is suggested. Provoking factors are insolation, cooling, trauma, pregnancy, drug intolerance, vaccination, and stressful situations.

Pathogenesis. Various immunopathological disorders.

Clinic. The disease begins with an acute or subacute course, with a muscle syndrome in the form of myasthenia gravis, myalgia, arthralgia also develops, fever appears, and when the skin is affected, the clinical picture is in the form of dense, widespread edema.

Skin lesions are diverse, more often purple para-orbital 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 at rest, manifested in the form of pain on pressure and increasing weakness. Significantly impaired active movements, the patient cannot sit down on his own, raise his head from the pillow and keep it sitting or standing, raise his limbs. With a large common process, patients are completely immobilized, and in severe cases they are in a state of complete prostration. When the skeletal muscles are affected, weakness, pain, swelling, muscle thickening, muscle wasting, calcification appear. The oculomotor muscles may be affected with the development of diplopia, strabismus, bilateral ptosis of the eyelids, etc. Polyarthralgia during movement is manifested by limited joint mobility up to the development of ankylosis, mostly due to muscle damage. Myocardial damage of an inflammatory or dystrophic nature is observed.

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

Diagnostics. The diagnostic criteria for dermatomyositis are as follows.

1. Proximal muscle weakness for at least one month.

2. Myalgia within one month in the absence of sensitivity disorders.

3. The ratio of the concentration of creatine in the urine to the sum of the concentrations of creatine and creatinine in the urine, exceeding 40%.

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 (half a tablet every 7-10 days), to a maintenance dose, against the background of delagil (0,25 g), plaquenil (0,2 g), 1 tablet after dinner.

In complex treatment, vitamins of group B, ascorbic acid are prescribed. With severe muscle fatigue, prozerin and its analogues are prescribed in normal doses, ATP.

28. Chronic constipation

Etiology. Reasons for development: improper diet, suppression of the urge to defecate, medications, local organic causes.

Clinic. The frequency of stool becomes less than three times a week, the consistency of the stool becomes denser (“sheep feces”), and difficulties associated with bowel movements appear. Chronic constipation is divided into:

1) functional, which are divided into alimentary, dyskinetic, psychoneurogenic, endocrine, inflammatory;

2) organic.

Functional chronic constipation includes cases of rare bowel movements, when it is not possible to identify any organic cause of this condition.

Diagnostics. Diagnosis of chronic constipation is as follows.

1. High proctolonoscopy.

2. Proctosigmoidoscopy in combination with irrigoscopy.

3. Fractional X-ray injection of barium through the small intestine.

Treatment. Diet therapy for chronic constipation.

1. Black and white bread with bran, legumes; cereals: oatmeal, buckwheat and barley.

2. Meat with a lot of connective tissue.

3. Raw vegetables and fruits, dried fruits.

4. Pickles, sweet kissels and compotes.

5. Dairy products. Water, fruit juices, mineral waters (Essentuki No. 4 and 17).

Diet therapy for constipation in infancy.

1. Fruit juices, vegetable purees.

2. Cabbage and beetroot juices, prune puree.

3. A mixture of "Fris" (for regurgitation, constipation, intestinal colic).

4. A mixture of "Semperbifidus" (lactolactulose), etc.

Diet therapy for constipation in other age groups.

1. Wheat bran.

2. Seaweed (kelp).

3. Thermal contrast liquids for drinking.

4. Biologically active additives (with dietary fiber).

Principles of treatment

1. Laxative antraglycosides (leaves of senna, rhubarb; tisasem, senadexin); synthetic (phenolphthalein, bisacodyl); lactulose (normaze, portalak), hilakforte.

2. Motility regulators (raglan, cerucal, motilium, coordinates).

3. For pain, a group of reserpine, antispasmodics. Anti-inflammatory in microclysters.

4. Phytotherapy.

5. Physiotherapy.

6. Therapeutic exercise.

7. Psychotherapy.

29. Organic disorders of the colon. Chronic colitis. Colon amyloidosis

Chronic colitis. Classification of chronic colitis.

1. By process localization:

1) right-handed;

2) left-sided;

3) transverse;

4) total.

2. Process phase:

1) exacerbation;

2) remission.

3. Type of intestinal dyskinesia:

1) hypomotor;

2) hypermotor;

3) mixed.

Diagnosis of chronic colitis.

1. Sigmoidoscopy (catarrhal or catarrhal-follicular proctosigmoiditis).

2. Irrigography, irrigoscopy (thickening and expansion of the folds and their discontinuity; smoothness of the haustra; narrowing of the intestine).

3. Colonofibroscopy (hyperemia, edema and hypertrophy of the mucosal folds, extended vascular pattern; the mucosa, as a rule, is devoid of luster, may be whitish).

4. Morphology (dystrophic changes, plethora of blood vessels and hemorrhages, edema, etc.).

Treatment of chronic colitis.

1. Diet number 4 (for 3-5 days), then diet number 4b.

2. Anti-inflammatory: sulfonamides; azo compounds (sulfasalazine), salofalk and salozinal; intetrix; 5-NOC (nitroxoline), nicodin.

3. Correction of intestinal dysbiosis.

4. Antispasmodic and myotropic (atropine, no-shpa, papaverine, etc.).

5. Vitamin therapy.

6. Phytotherapy.

7. Physiotherapy.

8. Local treatment.

9. Therapeutic exercise.

10. Mineral waters.

Amyloidosis of the colon. Amyloidosis of the colon is a partial or complete paralytic intestinal obstruction.

Gastrointestinal bleeding. Ulcers of the intestinal mucosa. Malabsorption Syndrome.

Treatment for amyloidosis of the colon.

1. Derivatives of 4-aminoquinoline (chloroquine, delagil, plaquenil); corticosteroids (prednisolone); immunocorrectors (T - and B activin, levamisole).

2. Means of stimulation of amyloid resorption: ascorbic acid, anabolic hormones.

3. Colchicine, dimethyl sulfoxide, prednisolone. In secondary amyloidosis, the underlying disease should be treated first.

30. Nonspecific ulcerative colitis

Nonspecific ulcerative colitis (NUC) is an autoimmune inflammatory-dystrophic lesion of the colon mucosa with the development of hemorrhages and erosions, the formation of extraintestinal manifestations of the disease and complications of a local and systemic nature.

The main reasons for the development of NUC:

1) viral or bacterial;

2) milk intolerance;

3) emotional stress reactions;

4) violation of the biocenosis of the intestine and the environment;

5) hereditary predisposition;

6) immunological changes and allergic reactions to food products (most often to cow's milk).

Diagnosis of nonspecific ulcerative colitis. When examining blood (anemia, accelerated ESR, leukocytosis, hypoproteinemia, dysproteinemia):

1) coprogram;

2) bacteriological examination of feces;

3) sigmoidoscopy;

4) irrigoscopy, irrigography.

Endoscopy for NUC: active stage - redness, loss of vascular pattern; granularity of the mucous membrane; vulnerability on contact, petechiae, bleeding; mucus, pus; ulceration of the mucous membrane, flat, confluent, superficial; pseudopolyps (inflammatory, not tumorous); continuous spread from the rectum in the proximal direction; "relapsing ileitis". The inactive stage is a pale, atrophic mucosa.

Treatment. Crohn's disease is a granulomatous inflammation of any part of the digestive tract with the development of ulcerations of the mucous membrane, narrowing of the lumen, fistulas and extraintestinal manifestations of the disease.

Treatment of UC and Crohn's disease.

1. Rational diet: frequent, fractional meals.

2. Basic drug therapy: azo compounds (sulfasalazine, salazopyrin, salazopyridazine; salofalk, salozinal); angioprotectors (trental, parmidine); multivitamins. Crohn's disease (azathioprine, cyclosporine, methotrexate).

3. Corticosteroids.

4. Eubiotics (intetrix, trichopolum, ercefuril, enterol).

5. Treatment of intestinal dysbacteriosis.

6. Infusion therapy. Hemosorption and plasmapheresis.

7. Anabolic hormones.

8. Treatment of anemia: iron preparations (ferrumlek, ectofer) parenterally.

9. Antihistamines (diazolin, suprastin, tavegil).

10. Normalization of bowel function antispasmodics and analgesics (papaverine, no-shpa, halidor); enzymes (pancreatin, panzinorm, digestal, mezimforte); imodium; fight against constipation (bran, vaseline oil).

11. Sedatives.

12. Dimephosphon.

13. Sandostatin is an analogue of somatostatin.

14. Phytotherapy.

15. Physiotherapy.

16. Local treatment.

17. Surgical treatment.

31. Intestinal microflora in children. Functions

Three phases of microbial colonization of the gastrointestinal tract in a child: the first - aseptic, lasting from 10 to 20 hours; the second - the initial colonization by microorganisms, the duration is from 2 to 4 days, depending on external environmental factors, the nature of nutrition and the time of breastfeeding; the third - stabilization of microflora (up to 1 month).

The intestinal microflora is a complex, dynamically balanced ecosystem. Contains over 500 different types of bacteria. 1 g of feces contains more than 1011 bacteria. The intestinal microflora is subject to frequent disturbances under the influence of adverse factors. Most of the intestinal microorganisms are the so-called obligate (indigenous) microflora (bifidobacteria, lactobacilli, non-pathogenic Escherichia coli, etc.). 92-95% of the intestinal microflora consists of obligate anaerobes.

Facultative (UP and saprophytic) microflora is unstable, has no significant biological functions, is represented by bacteria - citrobacters, micrococci, proteus, yeast-like fungi, clostridia. The composition of the intestinal microflora is quite individual and is formed in the first days of a child's life. An important factor in the formation of normal intestinal microflora is natural feeding.

Women's milk contains a large number of substances that contribute to the colonization of the intestines by certain types of microorganisms in certain quantities (staphylococcus, etc.). The composition of the intestinal flora of a child after two years is practically the same as that of an adult: the majority are anaerobes, which are difficult to cultivate.

The density of bacteria in the stomach, jejunum, ileum and colon is 1, 10, 100 and 1 thousand, respectively, in 000 ml of intestinal contents. Functions of the intestinal microflora.

1. Protective:

1) a barrier against microbial contamination (acidic environment, colony competition);

2) a decrease in the permeability of the mucous membrane for macromolecules.

2. Immune:

1) synthesis of immune defense factors (lysozyme, complement, properdin);

2) stimulation of the maturation of the lymphoid apparatus of the intestine and the synthesis of Ig;

3) stimulation of maturation of phagocytes.

3. Metabolic:

1) synthesis of B vitamins;

2) iron metabolism;

3) the exchange of bile acids.

4. Digestive:

1) the breakdown of carbohydrates;

2) synthesis of enzymes;

3) parietal digestion;

4) regulation of absorption;

5) stimulation of gastrointestinal motility.

32. Classification of dysbiosis. clinical forms. Stages

Classification of dysbacteriosis.

Stage I - a decrease in the number and level of activity of bifidus and lactobacilli. Aerobic flora changes.

Stage II - an increase or a sharp decrease in E. coli. The emergence of defective strains of E. coli and atypical species of enterobacteria.

Stage III - high titers of associations of opportunistic microflora. A sharp decrease in bifidus and lactobacilli or suppression of their activity.

Stage IV - a sharp decrease in bifido- and lactobacilli or suppression of their activity. Pronounced imbalance of microflora.

High titers of bacteria of the genus Proteus, Pseudomonas aeruginosa, Clostridia.

Clinical picture of intestinal dysbiosis: loose or unstable stools mixed with mucus, greens, or particles of undigested food. Less often - constipation; regurgitation, vomiting; flatulence, rumbling along the intestinal loops. Abdominal pain (intermittent).

Thrush, coated tongue; hyperemia around the anus. Anorexia, poor weight gain.

Clinical forms of dysbiosis.

1. Compensated (latent compensated): violation of the normal composition of the microflora. There are no clinical symptoms.

2. Subcompensated (local subcompensated): violation of the normal composition of the microflora, symptoms of intestinal inflammation with intoxication and bacteremia.

3. Decompensated (generalized decompensated): the appearance of metastatic inflammatory foci, intoxication and bacteremia, the development of sepsis and septicemia.

Examination plan and diagnosis of dysbacteriosis: hemogram, extended coprogram, cytocoprogram, bacteriological examination of feces, pH of feces; sugar curve, trypsin activity, biochemical blood test; elimination tests (exclusion of gluten, dairy products, sweet vegetables and fruits); determination of sweat chlorides, ultrasound of the abdominal organs.

Indications for the study of intestinal microflora (for dysbacteriosis):

1) intestinal dysfunction after the use of antibacterial drugs;

2) prolonged period of convalescence after OKI;

3) chronic intestinal disorders without isolation of pathogenic bacteria;

4) food allergy;

5) chronic diseases of the gastrointestinal tract in combination with flatulence, diarrhea and constipation;

6) irritable bowel syndrome.

Stages of correction of dysbacteriosis:

1) diet therapy;

2) normalization of intestinal microflora;

3) adsorption and excretion of toxic products from the intestine;

4) restoration of normal digestion;

5) relief of intestinal motility disorders;

6) correction of the immune status;

7) normalization of metabolism.

33. Diet therapy for persistent constipation and the absence of severe pain

Diet number 3 - stimulating intestinal motility.

1. Low-fat boiled meat, fish; buckwheat, rice or oatmeal; unleavened cottage cheese, white stale bread, pasta and vermicelli.

2. Adding bran to food, wholemeal bread.

3. Fruit juices, honey, sweet dishes, carbonated drinks, vegetables, salty foods, cold foods, white wines and highly mineralized mineral waters (Arzni, Yessentuki No. 17).

Diet therapy for diarrhea. Recommended.

1. White stale bread and crackers from it, dry biscuits.

2. Slimy rice and oatmeal soups; rice, oatmeal and semolina porridge; fresh cottage cheese, dishes from boiled vegetables; omelettes, soft-boiled egg; jelly, mousses and juices from quince, pear, dogwood, carrot, black currant and blueberry.

3. Warm and hot dishes, strong tea, cocoa, natural red wines.

Forbidden: fatty foods, raw fruits, milk, wheat and barley porridge.

Limited: vegetable fiber and sugar (no more than 40 g per day).

Diet therapy for fermentative dyspepsia (pronounced flatulence; profuse, frothy, sour stools).

Recommended.

1. Increase in the amount of boiled protein products (meat, fish).

2. Non-concentrated broths, fish soup, scrambled eggs, boiled or baked potatoes.

3. Use of cloves, bay leaf, pepper.

Forbidden: honey, jam, sweets, watermelons, bananas, grapes, milk and vegetable fiber - for 1-2 weeks.

Diet therapy for putrefactive dyspepsia (frequent headaches, signs of intoxication, moderate flatulence, spasms and pain in the distal intestines).

The following guidelines must be observed.

1. The first 2 days - hunger (broth of wild rose, slightly sweet tea).

2. From the 3rd day, dry biscuits, white bread crackers. From the 5-6th day, rice porridge on the water and sour-milk products.

3. In the future - a vegetable diet. Forbidden: protein foods and coarse fiber. Restricted: fats.

Antibacterial drugs: do not disturb the balance of the microbial flora in the intestine - intetrix - a combination of 3 antiseptics from the group of 8-hydroxyquinolones, effective against pathogenic bacteria and fungi.

34. Dietary supplements

biological active substances used to improve the function and regulation of microbiocenosis of the gastrointestinal tract, prevention and treatment: dietary supplements, functional nutrition, probiotics, prebiotics, synbiotics, bacteriophages, biotherapeutic agents.

Dietary Supplements - natural nutrients: vitamins, minerals, proteins, enzymes, plant products.

Requirements for dietary supplements that must contain one or more nutritional components: vitamins, minerals, herbs or other plants, amino acids.

Not intended to be used as the main ordinary food or the sole source of nutrition. They are used only as an addition to the main diet in order to increase the daily intake of certain nutritional components. Functional nutrition should be understood as ready-to-sell food products in which biological products have been added.

Functional food is defined as a modified food that provides better health benefits than the original food. Functional foods include antioxidants, carotenoids, digestive enzymes, yogurts and dairy products with added pro and prebiotics. Acidobeef is a food supplement for children over 1 year of age with lactase deficiency, milk protein intolerance and intestinal dysbiosis, containing lacto and bifidobacteria. Eugalan forte is a food supplement for adults and children over 3 years old, containing bifidobacteria and lactulose.

Probiotics are preparations based on microorganisms (lyophilized powders containing bifidobacteria and lactobacilli). Probiotics are drugs and food products that contain substances of microbial and non-microbial origin.

With a natural route of administration, they have a beneficial effect on the physiological functions and biochemical reactions of the body through the optimization of its microecological status. Probiotics (eubiotics) are live, weakened strains of microorganisms: more often bifidolactobacteria, less often yeast, which, based on the term "probiotic", refer to normal inhabitants of the intestines of a healthy person. Modern requirements for probiotics: natural origin, resistance to the action of gastric acid and bile, the ability to colonize the intestines, antagonism to pathogenic bacteria. Indications for the use of probiotics: diarrhea associated with taking antibiotics, infectious diarrhea, prevention of diarrhea, irritable bowel syndrome, gastrointestinal syndrome with allergies, inflammatory diseases.

Probiotics - preparations, mono and polycomponent preparations: bifidumbacterin, lactobacterin, bifikol, colibacterin, primadofilus, floradofilus, bifinorm, subamin.

Prebiotics are non-digestible food ingredients that selectively stimulate the growth and metabolic activity of one or more groups of bacteria (lactobacilli, bifidobacteria) in the colon. Substance prebiotics: fructozooligosaccharides, galactooligosaccharides (in dairy products, corn flakes, cereals, bread, onions, field chicory, garlic, bananas, and many others).

35. Classification of eximopathy

Classification.

pathogenic classification.

1. Exocrine pancreatic insufficiency:

1) cystic fibrosis of the pancreas;

2) chronic malnutrition with protein and calorie deficiency;

3) Shwachman-Diamond syndrome;

4) chronic pancreatitis with exocrine insufficiency;

5) specific enzyme defects (lipase, trypsinogen).

2. Insufficiency of bile acids:

1) obstruction of the biliary tract (biliary atresia, cholelithiasis, cancer of the pancreatic head);

2) resection of the ileum;

3) cirrhosis of the liver, chronic hepatitis (decreased secretion);

4) dysbacteriosis.

3. Violations of the functions of the stomach:

1) postgastrectomy syndrome;

2) vagotomy;

3) pernicious anemia caused by vitamin B12 deficiency.

4. Dysmotility:

1) hyperthyroidism;

2) diabetes mellitus;

3) scleroderma;

4) amyloidosis.

5. Pathology of the intestinal mucosa:

1) celiac disease;

2) lactase deficiency;

3) sucrase and isomaltase deficiency (combined);

4) exudative enteropathy;

5) cow’s milk (and/or soy) protein intolerance;

6) insufficiency of enterokinase;

7) α-, β-lipoproteinemia (Bassen-Kornzweig syndrome);

8) impaired transport of amino acids (tryptophan, methionine, lysine, etc.);

9) vitamin B12 malabsorption (transcobalamin-II deficiency);

10) congenital disorders of folic acid absorption processes;

11) chlorine-losing diarrhea;

12) vitamin D-dependent rickets;

13) enteropathic acrodermatitis;

14) Menkes syndrome (curly hair syndrome);

15) Crohn's disease;

16) malabsorption after suffering enteritis;

17) tropical sprue;

18) Whipple's disease;

19) chronic infections (immunodeficiency);

20) primary immune deficiency (Wiskott-Aldrich syndrome);

21) congenital short intestine;

22) short bowel syndrome after resection;

23) eosinophilic gastroenteritis.

36. Classification of chronic hepatitis. Fundamentals of chronic diffuse liver diseases

Classification of chronic hepatitis.

1. Viral (B, C, D, E, F, G).

2. Autoimmune (Epstein-Barr viruses, cytomegaly, Coxsackie, herpes simplex).

3. Medicinal (tuberculostatics, phenothiazines, poisonous mushrooms, DDT and its analogues).

4. Cryptogenic (etiology not established, possibly viral). Cirrhosis of the liver in childhood is rare, but occupies a significant place among liver diseases in children.

Etiology: acute viral hepatitis (B, C, D), vascular disorders (Buddy-Chiari syndrome and disease), narrowing v. portae - congenital or due to inflammation.

Clinical manifestations: enlarged, bumpy, dense liver with necessarily enlarged spleen. Pronounced systemic disorders, complications (dilation of the veins of the esophagus, stomach, hemorrhoidal veins (collaterals between v. portae and vena cava), morphological - massive inflammation in the portal tracts and hexagonal lobules, regenerated nodes, fibrosis, degeneration of hepatocytes in combination with their necrosis .

Basics of therapy for chronic diffuse liver diseases.

One of the main mechanisms of liver cell destruction is excessive activation of lipid peroxidation (LPO) and depletion of the antioxidant defense system.

Pharmacological regulation of lipid peroxidation by hepatoprotectors and antioxidants is the most important direction in the treatment of chronic liver diseases.

For viral CKD, antiviral drugs: viferon (recombinant interferon-referon with the addition of antioxidants, interferonintron A); it is possible with a preliminary short course of prednisolone.

Basic (non-drug) therapy is traditional and is prescribed to all patients, regardless of the etiology of liver damage. It includes a protective regimen (limitation of physical activity, bed rest during periods of exacerbations), adequate medical nutrition (table No. 5, during exacerbations - 5a), a complex of multivitamins.

Important - prevention of gastrointestinal dysfunction and intestinal autointoxication (appointment of enzymes, eubiotics, laxatives). Hepatoprotectors and antioxidants are used only in sick children with inflammatory activity and hyperenzymemia. Herbal preparations with membrane-stabilizing, antitoxic and choleretic effects (karsil, legalon, hepatofalk, LIV-52, galstena, hepabene, tykveol, hofitol, heptral, silimar, tanacechol, etc.). Relief of cholestasis - adsorbents (cholestyramine, bilignin, polyfepam), heptral, ursodeoxycholic acid preparations (ursofalk, ursosan), hemo and plasmasorption. With pronounced cytolysis and violation of the protein-synthetic and detoxification functions of the liver - intravenous administration of detoxification agents (polyionic buffer solutions, 5% glucose solution), protein preparations (albumin, plasma, freshly heparinized blood, coagulation factors), amino acid solutions (alvezin , aminofuzin, hepasteril, aminosteril); methods of extracorporeal detoxification.

37. Complications after the use of drugs

Complications divided into:

1) medication, which are divided into true side effects of drugs;

2) toxic effects of drugs;

3) complications associated with the sudden withdrawal of the drug;

4) individual intolerance to the drug.

Side effects of drugs: an undesirable effect of a drug, due to its structure and properties, which it has on the body along with its main actions. The toxic effects of drugs can be due to: overdose, rapid saturation of the body, rapid administration of medium and even minimal doses, insufficient excretion function of the body, impaired drug detoxification processes in the body (with primary liver failure).

Complications due to rapid withdrawal of drugs: withdrawal syndrome, withdrawal symptoms, exacerbation of those symptoms for which treatment was carried out. Individual intolerance to drugs is divided into unusual and perverted reaction. An unusual reaction of the body to normal doses of drugs that are harmless to most people. Individual intolerance is a disease of altered reactivity, a disease of the body.

Individual intolerance includes idiosyncrasy, an allergic reaction.

Idiosyncrasy - this is a genetically determined, peculiar response to a certain medicine at the first dose.

The cause of idiosyncrasy is an insufficient amount or low activity of enzymes (for example, a lack of the enzyme glucose-6-phosphate DG in response to taking certain drugs, quinidine, CA drugs, aspirin, pyrazalones, antibiotics leads to the development of hemolytic anemia). Factors in the development of drug disease are as follows.

1. Uncontrolled use of drugs by both doctors and patients themselves; the presence of the underlying disease changes the reactivity of the organism, and the altered reactivity manifests itself in unexpected effects when using drugs.

2. Polypharmacy, creating conditions for polyvalent sensitization; malnutrition during the use of drugs can change the reactivity of the body and the tolerance of drugs.

3. Age-related decrease in the participation of enzyme systems in the breakdown and neutralization of certain substances (higher sensitivity of children to barbiturates and salicylates, in the elderly - to SG).

4. Genetic conditionality of a number of drug-induced lesions.

5. The degree and rate of sensitization of the body partly depends on the routes of drug administration (local applications and inhalations lead to increased sensitivity of the body; with intravenous administration of drugs, sensitization of the body is less than with intramuscular and intramuscular injections).

38. Allergic reactions. Classification

Allergic reactions is the most common cause of intolerance to certain drugs.

Allergy is understood as an altered reactivity of the organism to the action of a given substance due to the hereditary high sensitivity of the organism.

A drug disease is one of the most significant clinical forms of an allergic reaction of the body to drugs.

Necessary steps for the development of drug allergies:

1) the transformation of the drug into a form that is able to interact with proteins;

2) the transformation of the drug into a form that can react with body proteins to form a complete antigen;

3) the body's immune response to this formed complex, which has become foreign, in the form of antibody synthesis through the formation of immunoglobulins.

Stages of allergic manifestations: preimmunological - this is the formation of complete (complete) allergens (antigens).

Immunological, when an antigen-antibody reaction occurs in the tissues of the shock organs. An antigen-antibody reaction is a specific reaction that is caused only by the introduction of a specific allergen.

pathochemical reaction - as a result of the formation of the antigen-antibody complex, biologically active substances (histamine, heparin, serotonin, etc.) are released, the reaction is nonspecific. The pathophysiological reaction is manifested by the action of biologically active substances on various organs and tissues.

Classification of allergic reactions

1. An immediate type reaction is associated with the presence of circulating antibodies in the blood. This reaction occurs 30-60 minutes after the administration of the drug and is then characterized by acute manifestations: local leukocytosis, eosinophilia in the blood test.

2. Delayed-type reaction due to the presence of antibodies in tissues and organs, accompanied by local lymphocytosis, occurs 1-2 days after taking the drug.

Classification of allergic reactions according to pathogenetic type.

1. True (allergic) reactions are divided into chimergic (B-dependent) and kitergic (T-dependent):

1) chimergic allergic reactions are caused by the reaction of an antigen with antibodies, the formation of which is associated with B-lymphocytes;

2) kytergic allergic reactions with allergen binding by sensitized lymphocytes.

2. False (pseudo-allergic, non-immunological) reactions - do not have an immunological stage in their development.

39. Classification of drug disease

1. Acute forms: anaphylactic shock, bronchial asthma, angioedema, vasomotor rhinitis, acute hemolytic anemia.

2. Prolonged forms: serum sickness, Lyell's syndrome, drug-induced vasculitis, etc.

3. Light (itching, angioedema, urticaria), in which the symptoms disappear 3 days after the use of antihistamines; moderate severity (urticaria, eczematous dermatitis, erythema multiforme, fever up to 39 ° C, poly- or monoarthritis, toxic-allergic myocarditis). Symptoms disappear after 4-5 days, but require the appointment of GC in average doses of 20-40 mg.

4. Severe form (anaphylactic shock, exfoliative dermatitis, Lyell's syndrome), damage to internal organs (myocarditis with rhythm disorders, nephrotic syndrome). All symptoms disappear after 7-10 days of combined administration of GCs, immunomodulators and antihistamines.

Diagnosis of drug disease: carefully collected allergic anamnesis. It should be borne in mind that many patients do not take drugs that they use daily (sedatives, laxatives, analgesics, eye drops, nasal drops) as medicines.

Allergic skin tests (in / to, scarification, application) give a sharply positive reaction with certain drug allergens.

Treatment of drug disease: bed rest; diet is not irritating, with sufficient fluid intake; cancellation of all medications; desensitizing therapy (calcium chloride, antihistamines, calcium, glucocorticoids); specific hyposensitization is ineffective; not performed for pancytopenia; symptomatic therapy.

Anaphylactic shock treatment

1. Subcutaneous injection of 0,5-1 ml of 0,1% adrenaline solution.

2. Prevention of aspiration of vomit.

3. Introduce 10,0 ml of a 10% solution of Ca chloride or 10,0 ml of a 10% solution of Ca gluconate intravenously.

4. In / in a jet, then drip 300-500 ml of a 5% glucose solution or saline + 0,5-1 ml of a 0,1% solution of adrenaline or 1,0 ml of a 1% solution of mezaton with HA.

5. With bronchospasm - 10 ml of a 2,4% solution of eufillin, novocaine blockade.

6. With laryngeal edema - tracheostomy, humidified oxygen.

7. Antihistamines (suprastin 2% - 2,0, tavegil 0,1% - 1,0, diphenhydramine 1% - 1,0).

8. Cardiac glycosides.

9. In anaphylactic shock of penicillin etiology - up to 1 million units of penicillinase, again - after 6-8 hours.

10. Resuscitation (artificial ventilation of the lungs, closed heart massage in case of cessation of respiratory and cardiac activity).

40. Helminthiases in children. Ascariasis

Helminthiasis - diseases that develop when parasitic helminth worms and their larvae are localized in the body.

Classification of helminthiases:

1) according to the biological principle: nematodes (roundworms), cestodoses (tape), trematodes (flukes);

2) epidemiologically: geohelminthiasis, biohelminthiasis, bon-contact.

Ascaridosis

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

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

Urticaria, vesicular rash on the hands and feet are possible, volatile infiltrates in the lungs may occur.

In the intestinal phase, the gastrointestinal form is distinguished, manifested by salivation, nausea, loss of appetite, cramping pains around the navel, sometimes disorder of the stool and gastric secretion; hypotonic form, manifested by a decrease in blood pressure, weakness; neurological form, manifested by dizziness, headache, fatigue, sleep disturbance, vegetative-vascular disorders.

Complications.

Ascariasis ileus, ascariasis appendicitis; perforative peritonitis; ascariasis of the liver with the occurrence of jaundice, subdiaphragmatic abscess; ascariasis of the pancreas with clinical manifestations of acute pancreatitis, creeping of ascaris into the respiratory tract with the development of asphyxia.

Diagnosis- Based on laboratory data, it is based on the detection of nematode larvae in sputum, antibodies in the blood, late intestinal phase of roundworm 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, the interval between taking the drug is 2-3 hours, for 2 days, the recommended dose is 1,5-2 g per dose (3-4 g/day). Effectiveness increases when piperazine is taken after dinner before bed. Decaris (levamisole) is prescribed after meals at a dose of 150 mg once, Pyrantel is prescribed once after meals at a dose of 10 mg/kg body weight.

Oxygen treatment is carried out on an empty stomach or 3-4 hours after a meal, preferably in the morning, 2-3 days in a row.

Prognosis and prevention.

The prognosis in the absence of complications that require surgical treatment is favorable.

Prevention: mass examination of the population and treatment of all persons infested with ascariasis. Protection of the soil of kitchen gardens, orchards, berry fields from contamination with feces. Thorough washing and scalding vegetables and fruits with boiling water.

41. Echinococcosis

Echinococcosis is a serious parasitic disease.

Etiology. The causative agent of hydatous echinococcosis is the larval stage of a small cestode, which has 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 of cells, outer and inner, which 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 final hosts are carnivores, domestic animals (dog, fox, wolf), which have a mature worm parasitizing in their intestines; its segments containing eggs are excreted with feces into the external environment. Intermediate hosts are herbivores and omnivores (sheep, goats, pigs, horses, rodents).

The mechanism of transmission of invasion: fecal-oral (as a result of ingestion of invasive echinococcus eggs upon contact with dogs, sheep, on the wool of which there may be helminth eggs), the route of transmission is 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 echinococcosis is formed. The growing bubble compresses the surrounding tissues, the lung, bronchi, 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 attachment 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 echinococcosis of the liver, patients lose their appetite, develop weakness, weight loss, headaches, decreased performance, and a feeling of heaviness in the epigastrium. Pain in the right hypochondrium, liver enlargement, thickening and pain on palpation, nausea, vomiting, upset stool. In rare cases, subecterism of the skin and the appearance of jaundice.

Diagnostics. Based on clinical 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.

42. Rheumatism. Classification. Clinic of rheumatic polyarthritis

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

Etiology, pathogenesis. The main etiological factor in acute forms of the disease is b-hemolytic streptococcus of group A. In patients with protracted and continuously recurrent forms of rheumatic carditis, it is often not possible to establish a connection between the disease and streptococcus. In the development of rheumatism, particular importance is attached to immune disorders.

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

Classification. It is necessary to identify the previously inactive or active phase of the disease.

Activity can be minimal (I degree), medium (II degree) and maximum (III degree).

To determine the degree of activity, the severity of clinical manifestations, as well as changes in laboratory parameters, are used.

Classification according to the localization of the activity of the rheumatic process (carditis, arthritis, chorea, etc.), the state of the blood circulation and the course of the disease.

Allocate an acute course of rheumatism, a subacute course, a protracted course, a continuously relapsing course and a latent course of the disease. The allocation of a 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, sometimes another infection.

In case of relapses, 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, rarely subacute. Polyarthritis develops quickly, accompanied by remitting fever up to 38-40 °C with daily fluctuations of 1-2 °C, severe sweating, but often without chills.

The first symptom of rheumatic polyarthritis is acute pain in the joints, increasing and intensifying with 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 joint is hot, there is sharp pain on palpation of the joint, the range of motion is limited due to pain.

A characteristic feature is a symmetrical lesion of large joints - more often knee, wrist, ankle, elbow. The "volatility" of inflammatory changes is typical, manifested in the rapid and reverse development of arthritic manifestations in some joints and the same rapid increase in other joints. All articular changes disappear without a trace even without treatment, they last no more than 2-4 weeks.

43. Pericarditis

Pericarditis in the clinic of rheumatism is rare.

Dry pericarditis clinically manifested by constant pain in the region of the heart and a pericardial friction rub, which is more often heard along the left edge of the sternum.

The intensity of the noise during auscultation is different, often it is determined in both phases of the cardiac cycle. The ECG shows an upward shift of the ST interval in all leads at the very beginning of the disease. With further development, these intervals return to the isoelectric line, and biphasic or negative T waves are also formed simultaneously. Dry pericarditis itself is not capable of causing an increase in the heart.

Exudative pericarditis is a further stage in the development of dry pericarditis. The main first clinical sign of the appearance of effusion is the disappearance of pain due to the separation of the inflammatory layers of the pericardium, accumulating exudate.

Clinical manifestations in the form of shortness of breath, which increases when the patient lies down. The region of the heart with a large amount of exudate swells, the intercostal spaces are smoothed, the apex beat is not palpable. The heart is greatly enlarged and takes the form of a trapezium or round graphite. The pulsation of the contours during fluoroscopy is small. On auscultation, the tones and noises are deaf (as there is an effusion). Pulse is frequent, small filling; arterial pressure is lowered. Venous pressure is always increased, swelling of the cervical and peripheral veins appears.

The electrocardiogram is the same as in dry pericarditis, an additional symptom may be a marked decrease in the voltage of the QRS complex. Of particular diagnostic importance is echocardiography, which determines the presence of fluid in the heart sac. When the skin is damaged, annular erythema is practically characteristic, which is pink ring-shaped elements that never itch and are located mainly on the skin of the inner surface of the arms and legs, as well as the abdomen, neck, torso. It is found only in 1-2% of patients. The "rheumatic nodules" described in the old manuals are now practically non-existent. Nodular erythema, hemorrhages, urticaria are also not characteristic. With kidney damage, mild proteinuria and hematuria are detected (due to generalized vasculitis and damage to the renal glomeruli and tubules).

Damage to the nervous system and sensory organs. Chorea minor, the most typical "nervous form" of rheumatism, occurs predominantly in children, especially girls. Chorea minor is characterized by a combination of emotional lability with muscular hypotension and violent movements of the trunk, mimic muscles and limbs.

Chorea minor occurs with relapses, but by the age of 17-18 it almost always ends. A feature of this form may be a relatively small lesion of the heart, as well as slightly pronounced laboratory indicators of the activity of rheumatism.

44. Diagnosis and treatment of rheumatism

Diagnostics: based on anamnesis, clinical and laboratory data. In the blood test, neutrophilic leukocytosis with a shift to the left, thrombocytosis, an increase in ESR to 40-60 mm/h. An increase in antistreptococcal antibody titers is characteristic: antistreptohiapuronidase and antistreptokinase more than 1: 300, antistreptolysin more than 1: 250. The height of antistreptococcal antibody titers and their dynamics do not indicate 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%, seromucoid above 0,16 g/l, and the appearance of C-reactive protein in the blood test. In many cases, biochemical activity indicators parallel the ESR value. There are broad diagnostic criteria for rheumatism: polyarthritis, carditis, ring erythema, chorea, rheumatic nodules. There are minor diagnostic criteria for rheumatism: fever, arthralgia, previous rheumatism, the presence of rheumatic heart disease, increased ESR, a positive reaction to C-reactive protein, prolongation of the P-Q interval on the ECG.

The diagnosis can be considered certain if the patient has two major diagnostic criteria and one minor diagnostic criterion, or one major and two minor diagnostic criteria, but only if both of the following evidence exist simultaneously, it is possible to judge a previous streptococcal infection: scarlet fever (which is an indisputable 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 3 weeks or more.

The diet shows the restriction of salt, carbohydrates, sufficient intake of proteins and vitamins. Exclusion of products that cause allergization. Antibacterial therapy of benzylpenicillin, sodium salt is used for 2 weeks, then prolonged action 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. Treatment in a hospital - 1,5-2 months, then treatment in a local sanatorium for 2-3 months, where chronic foci of infection are treated and dispensary observation is carried out by a local pediatrician and a cardiorheumatologist.

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. The prognosis is favorable.

45. Broncho-obstructive syndrome in children

Major Causes of Airway Obstruction in Children

1. Upper airway obstructions:

1) acquired:

a) allergic rhinitis;

b) nasal polyps;

c) hypertrophy of the tonsils;

d) inflammation of the epiglottis;

e) viral laryngotracheitis;

f) laryngospasm (with spasmophilia);

g) foreign body;

h) congenital stridor;

i) retraction of the tongue in an unconscious state;

j) mechanical compression of the trachea and bronchi;

2) congenital:

a) thymomegaly;

b) enlarged lymph nodes;

c) tumor.

2. Obstruction of large intrathoracic airways:

1) narrowing of the lumen (developmental anomaly, tumor, scar, foreign body);

2) compression from the outside (tumor, abnormal vessel);

3) excessive collapse due to weakness of the cartilaginous rings and (or) the membranous part (tracheomalacia).

3. Lower airway obstructions:

1) viral bronchiolitis;

2) bronchial asthma;

3) aspiration of vomit;

4) foreign bodies;

5) cystic fibrosis;

6) alpha1-antitrypsin deficiency.

Mechanisms of disorders in obstructive syndrome.

1. Reversible:

1) inflammatory edema and mucosal infiltration and submucosal edema;

2) violation of mucociliary transport, obturation of the bronchial lumen with a viscous secret;

3) bronchospasm.

2. Irreversible:

1) fibroplastic changes in the walls of the bronchi.

2) stenosis, deformation and obliteration of the bronchial lumen.

3) expiratory collapse of the bronchi, the presence of emphysema.

Protective mechanisms of the respiratory apparatus.

1. Mechanical.

2. Biochemical.

3. Immunological.

46. Acute bronchitis. Clinic

Broncho-obstructive syndrome - a clinical symptom complex observed in patients with a generalized violation of the patency of the bronchial tract, its leading manifestation is expiratory dyspnea, asthma attacks. Diseases associated with airway obstruction.

Acute bronchitis is a common disease: there are 1000-200 cases per 250 children of the first years of life.

Etiology. The vast majority of bronchitis are viral diseases. Respiratory syncytial virus - 50%, parainfluenza viruses - 21%, mycoplasma pneumonia - 8,3%, cytomegalo virus - 6,3%, rhinoviruses - 4,2%, coronaviruses - 4,1%, echoviruses I serotypes - 2%, virus influenza A - 2%, adenoviruses - 2%.

Bacterial agents are rare or play no role in the etiology of bronchitis. The bacterial flora is more often found in "non-whistlers" than in "wheezers".

Clinic. Clinical symptoms of bronchial obstruction against the background of ARVI in young children:

1) acute onset of the disease;

2) wheezing;

3) variability of dry and wet rales;

4) swelling of the chest;

5) shortness of breath (reaches 60-80 in 1 min);

6) retraction of the jugular fossa and intercostal spaces (hypoxemia);

7) low body temperature.

In addition to the main symptoms, there may be:

1) rhinitis;

2) frequent painful cough;

3) swelling of the wings of the nose (hypoxemia);

4) refusal of the breast;

5) loss of appetite;

6) the presence of small crepitant rales, often diffuse;

7) stool disorder;

8) poor sleep;

9) cyanosis (hypoxemia);

10) apnea (hypoxemia).

Laboratory data. Blood test: red blood - without features, accelerated ESR, leukocytosis. X-ray data are characterized by an increase in the transparency of the pulmonary fields, an increase in the anteroposterior diameter of the chest due to the overflow of the lungs with air, emphysema, a high standing dome of the diaphragm, and hilar infiltration. In almost 1/3 of patients, scattered areas of compaction are visible, which can be explained by the development of atelectasis in response to obstruction.

In about 44% of cases, the radiological picture remains normal. Sowing discharge from the nose and trachea is the usual flora.

Virological examination - by the method of immunofluorescence, an increase in the titer of antibodies in the blood.

47. Respiratory failure. Clinical picture

Respiratory failure

Respiratory (ventilatory pulmonary) insufficiency is characterized by such disorders in which pulmonary gas exchange is impaired or occurs at the cost of excessive energy costs.

Types of respiratory failure:

1) ventilation;

2) distribution-diffusion (shunt-diffusion, hypoxemic);

3) mechanical.

Clinic.

I degree. Shortness of breath varies without the participation of auxiliary muscles in the act of breathing; at rest, as a rule, is absent. Perioral cyanosis, intermittent, aggravated by anxiety, disappearing when breathing 40-50% oxygen; pallor of the face. Arterial pressure is normal, rarely moderately elevated. The ratio of the pulse to the number of breaths is 3,5-2,5: 1; tachycardia. Behavior is restless or not disturbed.

II degree. Shortness of breath at rest is constant, with the participation of auxiliary muscles in the act of breathing, retraction of compliant places of the chest; it can also be with a predominance of inhalation or exhalation, i.e., wheezing, grunting exhalation. Perioral cyanosis of the face, hands is permanent, does not disappear when breathing 40-50% oxygen, but disappears in an oxygen tent; generalized pallor of the skin, sweating, pallor of the nail beds. Arterial pressure is increased. The ratio of the pulse to the number of breaths is 2-1,5: 1, tachycardia. Behavior: lethargy, somnolence, adynamia, followed by short periods of excitement; decrease in muscle tone.

III degree. Severe shortness of breath (respiratory rate - more than 150% of the norm); shallow breathing, intermittent bradypnea, respiratory desynchronization, paradoxical breathing.

Decrease or absence of respiratory sounds on inspiration. Cyanosis is generalized; there is cyanosis of the mucous membranes, lips, does not go away when breathing 100% oxygen; generalized marbling or pallor of the skin with blue; sticky sweat. Arterial pressure is reduced. The ratio of pulse to number of breaths varies. Behavior: lethargy, somnolence, consciousness and reaction to pain are suppressed; muscular hypotension, coma; convulsions.

Causes of acute respiratory failure in children.

1. Respiratory - acute bronchiolitis, pneumonia, acute laryngotracheitis, false croup, bronchial asthma, congenital malformations of the lungs.

2. Cardiovascular - congenital heart disease, heart failure, pulmonary edema, peripheral dyscirculatory disorders.

3. Neuromuscular - encephalitis, intracranial hypertension, depression, poliomyelitis, tetanus, status epilepticus.

4. Injuries, burns, poisoning, surgical interventions on the brain, chest organs, poisoning with sleeping pills, narcotic, sedative drugs.

5. Renal failure.

48. Classification of malformations of the broncho-pulmonary system. Chronic and acquired diseases in children

A malformation is an anomaly in most cases of intrauterine development, resulting in gross changes in the structure and function of an organ or tissue.

Classification of malformations of the bronchopulmonary system.

1. Malformations associated with the underdevelopment of the organ as a whole or its anatomical, structural, tissue elements:

1) lung agenesis;

2) lung aplasia;

3) lung hypoplasia;

4) cystic hypoplasia (polycystic);

5) tracheobronchomegaly (Mounier-Kun's syndrome);

6) Williams-Campbell syndrome;

7) congenital lobar emphysema.

2. Defects associated with the presence of excess dysembryogenetic formations:

1) accessory lung (lobe) with normal blood supply or with abnormal blood supply;

2) lung cyst with normal blood supply or with abnormal blood supply;

3) hamartoma and other tumor-like formations.

3. Unusual anatomical arrangement of lung structures, sometimes of clinical significance:

1) reverse arrangement of the lungs (Kartegener's syndrome);

2) mirror lung;

3) tracheal bronchus;

4) share of the unpaired vein.

4. Localized violations of the structure of the trachea and bronchi:

1) stenosis;

2) diverticula;

3) tracheoesophageal fistulas. 5. Anomalies of blood and lymphatic vessels:

1) stenosis of the pulmonary artery and its branches;

2) varicose pulmonary veins;

3) multiple arteriovenous fistulas without clear localization.

Hereditary diseases of the respiratory system, according to various authors, range from 5 to 35% of the total number of patients with nonspecific lung diseases.

Chronic lung diseases in children (S. Yu. Kaganov, 2003).

1. Infectious and inflammatory diseases.

2. Congenital malformations of the bronchopulmonary system.

3. Hereditary lung diseases.

4. Lung lesions in other hereditary diseases.

5. Allergic diseases of the lungs. Acquired diseases:

1) a common type of pathological changes that cause obstruction;

a) allergic inflammation, bronchial asthma;

b) infectious inflammation;

2) recurrent and chronic obstructive bronchitis;

3) local type of pathological changes causing obstruction (mechanical factors);

4) foreign body, tumor, infectious granuloma, post-traumatic cicatricial stenosis.

49. Congenital malformations of the bronchopulmonary system

Congenital malformations are persistent morphological changes in an organ or organism that go beyond variations in their structure and occur in utero as a result of developmental disorders of the embryo, fetus, or sometimes after the birth of a child as a result of a violation of the further formation of organs. The vast majority of malformations are associated with hereditary pathology.

Only 3-5% of all malformations are associated with the actions of teratogenic factors.

Stages of impaired embryonic development of the lung (Monaldi, 1959).

The first stage includes lung agenesis as a result of the absence of a primary bronchial kidney.

At the second stage, there is a violation of the development of the primary bronchial kidney, leading to underdevelopment of the main bronchus and aplasia of the lung. These defects occur on the 3-4th week of the embryonic period.

The third stage of the violation occurs on the 30-40th day of intrauterine development and is characterized by the presence of lung hypoplasia.

The fourth stage (II-V months of the intrauterine period) is determined by a violation of the development of small bronchi and leads to the occurrence of polycystic lung disease.

Diagnosis of congenital and hereditary lung diseases: it is believed that of the numerous pulmonary symptoms, cough, sputum, and hemoptysis have the greatest objective significance in the diagnosis of respiratory diseases.

Other important symptoms: shortness of breath, cyanosis, change in the shape of the chest (retraction, flattening, keeled bulging of the sternum), "drumsticks", "watch glasses", percussion: shortening of percussion sound, displacement of the heart towards the pathologically altered lung, auscultation: constancy of auscultatory pictures (weakened breathing, its absence, various wheezing). Congenital malformations of the lungs.

1. Agenesia, aplasia and hypoplasia of the lungs.

2. Polycystic lungs.

3. Congenital lobar emphysema.

4. Williams-Campbell syndrome.

5. Tracheobronchomegaly (Mounier-Kuhn's syndrome).

6. Anomalies of branching of the bronchi.

Lung agenesis - Absence of the lung along with the main bronchus.

Aplasia of the lung - absence of a lung in the presence of a rudimentary main bronchus.

Hypoplasia of the lung - there are main and lobar bronchi, which end in a functionally imperfect rudiment, lung tissue is underdeveloped, agenesis, aplasia and hypoplasia of the lungs.

Clinical picture: cough, shortness of breath. Repeated pneumonia, bronchitis. Children are lagging behind in physical development. Deformation of the chest - retraction or flattening on the side of the defect. Children with lung hypoplasia have keeled bulging of the sternum (compensatory emphysema of the unaffected lung). The organs of the mediastinum are displaced towards the defect.

50. Pathology of connective tissue. Alveolar microlithiasis, alveolar proteinosis

Pathology of connective tissue can accompany hereditary pathology of connective tissue (Marfan syndrome, Ehlers-Danlos syndrome, achantitrypsin deficiency).

clinical picture. Sudden sharp stabbing pain in the chest, aggravated by a deep breath, shortness of breath, percussion on the side of the lesion "box" sound, a sharp weakening of the breath sounds (auscultation), a shift in cardiac dullness in the opposite direction.

X-ray is determined by the presence of air in the pleural cavity, the collapse of the lung.

Treatment. Treatment for spontaneous pneumothorax is drainage of the pleural cavity with constant active aspiration (according to Belau).

Alveolar microlithiasis characterized by the formation in the pulmonary alveoli of the smallest calculi, which consist of calcium carbonate and thiophosphates with a small admixture of iron salts and traces of magnesium.

As a result of the deposition of calculi, an alveolar-capillary block occurs, ventilation-perfusion relations are disturbed. It is inherited in an autosomal recessive manner.

Pathogenesis. The formation of stones in the alveoli is associated with disturbances in the production of alveolar fluid, as well as a disorder of carbonic acid metabolism - alveolar microlithiasis. The disease occurs in all age groups.

Clinical manifestations. The clinical picture is varied.

A discrepancy between the poor clinical picture and radiological changes is characteristic.

Symptoms may be absent altogether; shortness of breath, cyanosis, decreased exercise tolerance may be disturbing.

As the process progresses, signs of chronic inflammation of the lungs join: cough, sputum, fever, "drum sticks", cor pulmonale appear.

Diagnostics. X-ray examination reveals small diffuse shadows of stony density, located mainly in the lower and middle parts of the lungs; compaction of the pleura is noted (differentiated with tuberculosis).

Treatment. Symptomatic.

Forecast. Adverse; death from pulmonary heart failure.

Alveolar proteinosis is caused by the accumulation of a protein-lipoid substance in the alveoli. The histological picture is characterized by the presence in the alveolar lumen of a granular exudate with a PAS-positive reaction. It is transmitted in an autosomal recessive manner.

Pathogenesis. A genetic defect leading to the synthesis of a defective surfactant that does not have surface-active properties; this lipoprotein is characterized by a strong CHIC-positive reaction; filling the alveoli with lipoprotein causes changes in lung function and corresponding clinical symptoms: progressive shortness of breath, cough, chest pain, hemoptysis; subsequently, a pulmonary heart is formed with corresponding symptoms.

Diagnostics. X-ray examination reveals bilateral small-focal (small-pointed) darkening, which tends to merge, and subsequently fibrous changes are revealed.

Treatment. Therapeutic bronchoalveolar lavage; administration of trypsin, chymotrypsin.

51. Cystic fibrosis

Cystic fibrosis (cystic fibrosis of the pancreas) is characterized by a systemic lesion of the exocrine glands due to an increase in the viscosity of their secretion, which, in relation to the bronchopulmonary system, causes a sharp violation of the cleansing function of the bronchi and bronchial patency.

A frequent monogenic disease caused by a mutation in the cystic fibrosis gene, characterized by damage to the exocrine glands, vital organs and systems, and usually having a severe course and prognosis.

In most countries in Europe and North America, CF affects between 1:2000 and 1:4000 newborns. In Russia 1:12 newborns.

It is inherited in an autosomal recessive manner, i.e. both parents must be carriers of the mutant gene. The probability of the birth of a patient with CF in such a family is 25%, 2-5% of the population are carriers of the CF gene.

Clinic. In the bronchopulmonary system, a viscous secretion, accumulating in the lumen of the bronchi, leads to complete obstruction of the small bronchioles. As a result of infection with pathogenic microflora, purulent inflammation develops. The most common pathogens are staphylococcus and Pseudomonas aeruginosa. The bronchial wall is destroyed. Bronchiectasis and cor pulmonale are formed.

In patients with cystic fibrosis, the chlorine channel on the apical part of the cell membrane "does not work", leading to a disruption in the release of chlorine from the cell, which contributes to an increased escape of sodium ions from the lumen into the cell, followed by the aqueous component of the intercellular space. The consequence is a thickening of the secretions of the glands of external secretion (broncho-pulmonary system, pancreas, salivary glands, gonads).

The presence in the family of diseases of the lungs and intestines, stillbirths, spontaneous abortions.

From birth - dry, hacking cough.

Early onset of continuously recurrent bronchopulmonary inflammation. Exhaustion and lag in physical development. Respiratory failure. "Drumsticks".

Carinated protrusion of the sternum.

FVD - persistent obstructive and restrictive disorders. Often sowing Pseudomonas. Pulmonary heart. Almost all patients have excretory pancreatic insufficiency.

Gastrointestinal injury in cystic fibrosis:

1) reflux esophagitis;

2) ulcerative esophagitis;

3) gastritis;

4) duodenitis;

5) biliary reflux;

6) gastric and duodenal ulcer;

7) coprostasis;

8) meconium ileus;

9) delayed evacuation of meconium;

10) fecal ileus;

11) intestinal invagination;

12) biliary cirrhosis;

13) portal hypertension;

14) acute pancreatitis;

15) fatty degeneration of the pancreas;

16) diabetes mellitus.

52. Cystic Fibrosis Exclusion Search Groups

The following groups are distinguished. In infancy:

1) recurrent or chronic respiratory symptoms (cough, shortness of breath);

2) recurrent or chronic pneumonia;

3) lag in physical development;

4) unformed, profuse, oily and fetid stools;

5) chronic diarrhea;

6) prolonged neonatal jaundice;

8) heat stroke or dehydration in hot weather;

9) chronic hypoelectrolytemia;

10) family history data on the death of children in the first year of life or the presence of sibs with similar clinical manifestations;

11) hypoproteinemia/edema.

Search group for the exclusion of cystic fibrosis in preschool children:

1) persistent cough with or without purulent sputum;

2) diagnostically unclear recurrent or chronic shortness of breath;

3) lag in body weight and height;

4) prolapse of the rectum;

6) chronic diarrhea;

7) a symptom of "drum sticks";

8) salt crystals on the skin;

9) hypotonic dehydration;

10) hypoelectrolytemia and metabolic alkalosis;

11) hepatomegaly or diagnostically unclear liver dysfunction.

Search group to rule out cystic fibrosis in school-aged children:

1) chronic respiratory symptoms of unclear etiology;

2) pseudomonas aeruginosa in sputum;

3) chronic sinusitis;

4) nasal polyposis;

5) bronchiectasis;

6) a symptom of "drum sticks";

7) chronic diarrhea;

8) syndrome of distal intestinal obstruction;

9) pancreatitis;

10) prolapse of the rectum;

11) diabetes mellitus in combination with respiratory symptoms;

12) hepatomegaly;

13) liver disease of unknown etiology.

Search group for ruling out cystic fibrosis in adolescents and adults:

1) purulent lung disease of unclear etiology;

2) a symptom of "drum sticks";

3) pancreatitis;

4) syndrome of distal intestinal obstruction;

5) diabetes mellitus in combination with respiratory symptoms;

6) signs of liver cirrhosis and portal hypertension;

7) stunting;

8) delayed sexual development;

9) sterility with azoospermia in males;

10) reduced fertility in females.

53. Treatment of cystic fibrosis

Treatment. Goals of therapy for a patient with cystic fibrosis.

1. Supporting the patient's lifestyle as close as possible to the life of healthy children.

2. Control of respiratory infections.

3. Ensuring adequate nutrition. Mandatory directions in treatment:

1) physiotherapy exercises (physiotherapy, kinesitherapy);

2) mucolytic therapy;

3) antimicrobial therapy;

4) enzyme therapy (pancreatic preparations);

5) vitamin therapy;

6) diet therapy;

7) treatment of complications;

8) kinesitherapy. Methods:

1) postural drainage;

2) percussion and vibration of the chest (clopmassage);

3) active breathing cycle;

4) autogenous drainage;

5) breathing exercises with flutter and PEP mask.

Inhalation therapy (bronchodilators, mucolytics, antibiotics).

Recommendations from the Cystic Fibrosis Center.

1. Take a bronchodilator (salbutamol, etc.) 5 minutes before inhalation.

2. Thoroughly blow your nose.

3. Take the correct position: sit straight, straighten your chest, shoulders and shoulder blades are lowered down.

4. Inhalation of a mucolytic (cetylcysteine, saline solution, etc.) 8-10 minutes.

5. Kinesitherapy: breathing exercises, drainage, exercise therapy.

6. Antibiotic inhalation and topical corticosteroid spacer.

In the case of using pulmozyme, it is inhaled 30-40 minutes after inhalation of other drugs.

A stepwise approach to the treatment of cystic fibrosis. St. Aureus.

1. Antibiotics up to 2-4 months. per year, of which 1-2 courses in / in or / m (1-2 drugs).

2. PEP therapy. Pseudomonas aeruginosa.

1. Antibiotics - 2-4 IV courses for 14 days (2 drugs).

Total antibiotics up to 4-6 months a year.

2. Hepatotropic drugs.

3. Bacterial preparations.

1. Antibiotics - 4-6 IV courses for 14-20 days (2-3 drugs).

2. Hepatotropic drugs.

3. Bacterial preparations.

4. Antimycotics in inhalations.

5. NSAIDs.

6. Hormonal preparations.

54. Chronic bronchitis. Etiology. Pathogenesis

Chronical bronchitis - this is a progressive diffuse inflammation of the bronchi, not associated with local or generalized lung damage, manifested by cough. You can talk about chronic bronchitis if the cough continues for 3 months in the 1st year - 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 compounds of a chemical nature) and recurrent respiratory infection (a major role is played by respiratory viruses, Pfeiffer's bacillus, pneumococci), less commonly occurs in cystic fibrosis. Predisposing factors are chronic inflammatory, suppurative processes in the lungs, chronic foci of infection and chronic diseases localized in the upper respiratory tract, decreased reactivity of the body, hereditary factors.

Pathogenesis. The main pathogenetic mechanism is hypertrophy and hyperfunction of the bronchial glands with increased mucus secretion, a decrease in serous secretion and a change in the composition of the secretion, as well as an increase in acidic mucopolysaccharides in it, which increases the viscosity of sputum. Under these conditions, the ciliated epithelium does not improve the emptying of the bronchial tree; normally, the entire layer of secretion is renewed (partial cleansing of the bronchi is possible only with a cough). Long-term hyperfunction is characterized by depletion of the mucociliary apparatus of the bronchi, the development of dystrophy and atrophy of the epithelium. When the drainage function of the bronchi is disrupted, a bronchogenic infection occurs, the activity and recurrence of which depend on the local immunity of the bronchi and the occurrence of secondary immunological deficiency. With the development of bronchial obstruction due to hyperplasia of the epithelium of the mucous glands, swelling and inflammatory thickening of the bronchial wall, obstruction of the bronchi, excess viscous bronchial secretion, and bronchospasm are observed. With obstruction of the small bronchi, overstretching of the alveoli during exhalation and disruption of the elastic structures of the alveolar walls and the appearance of hypoventilated or unventilated zones develop, and therefore the blood passing through them is not oxygenated and arterial hypoxemia develops. In response to alveolar hypoxia, spasm of the pulmonary arterioles and an increase in total pulmonary and pulmonary arteriolar resistance develop; pericapillary pulmonary hypertension develops. Chronic hypoxemia leads to an increase in blood viscosity, which is accompanied by metabolic acidosis, which further increases vasoconstriction in the pulmonary circulation. Inflammatory infiltration in large bronchi is superficial, and in medium and small bronchi and bronchioles it is deep with the development of erosions and the formation of meso- and panbronchitis. The remission phase is manifested by a decrease in inflammation and a large decrease in exudation, proliferation of connective tissue and epithelium, especially with ulceration of the mucous membrane.

55. Clinical manifestations and diagnosis of chronic bronchitis

Chronic bronchitis is the most common form of chronic nonspecific lung disease.

The onset of the disease is gradual. The first and main symptom is a cough in the morning with sputum discharge, gradually the cough begins to occur at any time of the day, intensifies in cold weather and becomes constant over the years. The amount of sputum increases, the sputum becomes mucopurulent or purulent. Shortness of breath appears. With purulent bronchitis, purulent sputum may occasionally be released, but bronchial obstruction is not very pronounced.

Obstructive chronic bronchitis is manifested by persistent obstructive disorders. Purulent-obstructive bronchitis is characterized by the release of purulent sputum and obstructive ventilation disorders. Frequent exacerbations during periods of cold damp weather: coughing increases, shortness of breath, the amount of sputum increases, malaise appears, fatigue. The body temperature is normal or subfebrile, hard breathing and dry rales over the entire lung surface can be determined.

Diagnostics. A slight leukocytosis with a band shift in the leukocyte formula is possible. With exacerbation of purulent bronchitis, a slight change in the biochemical parameters of inflammation occurs (reactive protein, sialic acids, fibronogen, seromucoid, etc. increase). Sputum examination: macroscopic, cytological, biochemical. With a severe exacerbation, the sputum becomes purulent in nature: a large number of neutrophilic leukocytes, an increased content of acidic mucopolysaccharides and DNA fibers, the nature of the sputum, predominantly neutrophilic leukocytes, an increase in the level of acidic mucopolysaccharides and DNA fibers, which increase the viscosity of the sputum, a decrease in the amount of lysozyme, etc.

Bronchoscopy, which evaluates the endobronchial manifestations of the inflammatory process, the stages of development of the inflammatory process: catarrhal, purulent, atrophic, hypertrophic, hemorrhagic and its severity, but mainly to the level of subsegmental bronchi.

Differential diagnosis is carried out with chronic pneumonia, bronchial asthma, tuberculosis. Unlike chronic pneumonia, chronic bronchitis always develops with a gradual onset, with widespread bronchial obstruction and often emphysema, respiratory failure and pulmonary hypertension with the development of chronic cor pulmonale. In x-ray examination, the 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 differs from bronchial asthma in the absence of asthma attacks, with pulmonary tuberculosis it is associated with the presence or absence of symptoms of tuberculosis intoxication, Mycobacterium tuberculosis in sputum, the results of X-ray and bronchoscopic examination, tuberculin tests.

56. Treatment of chronic bronchitis

Treatment. In the phase of exacerbation of chronic bronchitis, therapy is aimed at eliminating the inflammatory process, improving bronchial patency, as well as restoring impaired general and local immunological reactivity. Anti-biotibacterial therapy is prescribed, which is selected taking into account the sensitivity of the sputum microflora, administered orally or parenterally, and sometimes combined with intratracheal administration. Inhalations are indicated. Use expectorants, mucolytic and bronchospasmolytic drugs, and drink plenty of fluids to restore and improve bronchial patency.

Herbal medicine using marshmallow root, mother and stepmother leaves, plantain. Proteolytic enzymes (trypsin, chymotrypsin) are prescribed, which reduce the viscosity of sputum, but are currently rarely used. Acetylcysteine has the ability to break disulfide bonds of mucus proteins and promotes strong and rapid liquefaction of sputum. Bronchial drainage is improved with the use of mucoregulators that affect secretions and the production of glycoproteins in the bronchial epithelium (bromhexine). In case of insufficient bronchial drainage and existing symptoms of bronchial obstruction, bronchospasmolytics are added to treatment: aminophylline, anticholinergic blockers (atropine in aerosols), adrenergic stimulants (ephedrine, salbutamol, Berotec). In a hospital setting, intratracheal lavage for purulent bronchitis must be combined with sanitation bronchoscopy (3-4 sanitation bronchoscopy with a break of 3-7 days). When restoring the drainage function of the bronchi, physical therapy, chest massage, and physiotherapy are also used. When allergic syndromes develop, calcium chloride and antihistamines are used; if there is no effect, a short course of glucocorticoids can be prescribed to relieve allergic syndrome, but the daily dose should not be more than 30 mg. The danger of activation of infectious agents does not allow long-term use of glucocorticoids. In patients with chronic bronchitis, complicated respiratory failure and chronic cor pulmonale, the use of veroshpiron (up to 150-200 mg/day) is indicated.

The food of patients should be high-calorie and fortified. Ascorbic acid 1 g per day, nicotinic acid, B vitamins are used; if necessary, aloe, methyluracil. With the development of complications of a disease such as pulmonary and pulmonary-heart failure, oxygen therapy and auxiliary artificial ventilation are used.

Anti-relapse and supportive therapy is prescribed in the phase of exacerbation subsidence, is carried out in local and climatic sanatoriums, this therapy is prescribed during clinical examination.

It is recommended to allocate 3 groups of dispensary patients.

1st group. It includes patients with cor pulmonale, with severe respiratory failure and other complications, with disability.

2nd group. It includes patients with frequent exacerbations of chronic bronchitis, as well as moderate respiratory dysfunction.

3rd group. It includes patients in whom anti-relapse therapy led to a cessation of the process and the absence of relapses for 2 years.

Author: Pavlova N.V.

We recommend interesting articles Section Lecture notes, cheat sheets:

▪ Logistics. Crib

▪ Customs law. Lecture notes

▪ Internal illnesses. Lecture notes

See other articles Section Lecture notes, cheat sheets.

Read and write useful comments on this article.

<< Back

Latest news of science and technology, new electronics:

Artificial leather for touch emulation 15.04.2024

In a modern technology world where distance is becoming increasingly commonplace, maintaining connection and a sense of closeness is important. Recent developments in artificial skin by German scientists from Saarland University represent a new era in virtual interactions. German researchers from Saarland University have developed ultra-thin films that can transmit the sensation of touch over a distance. This cutting-edge technology provides new opportunities for virtual communication, especially for those who find themselves far from their loved ones. The ultra-thin films developed by the researchers, just 50 micrometers thick, can be integrated into textiles and worn like a second skin. These films act as sensors that recognize tactile signals from mom or dad, and as actuators that transmit these movements to the baby. Parents' touch to the fabric activates sensors that react to pressure and deform the ultra-thin film. This ... >>

Petgugu Global cat litter 15.04.2024

Taking care of pets can often be a challenge, especially when it comes to keeping your home clean. A new interesting solution from the Petgugu Global startup has been presented, which will make life easier for cat owners and help them keep their home perfectly clean and tidy. Startup Petgugu Global has unveiled a unique cat toilet that can automatically flush feces, keeping your home clean and fresh. This innovative device is equipped with various smart sensors that monitor your pet's toilet activity and activate to automatically clean after use. The device connects to the sewer system and ensures efficient waste removal without the need for intervention from the owner. Additionally, the toilet has a large flushable storage capacity, making it ideal for multi-cat households. The Petgugu cat litter bowl is designed for use with water-soluble litters and offers a range of additional ... >>

The attractiveness of caring men 14.04.2024

The stereotype that women prefer "bad boys" has long been widespread. However, recent research conducted by British scientists from Monash University offers a new perspective on this issue. They looked at how women responded to men's emotional responsibility and willingness to help others. The study's findings could change our understanding of what makes men attractive to women. A study conducted by scientists from Monash University leads to new findings about men's attractiveness to women. In the experiment, women were shown photographs of men with brief stories about their behavior in various situations, including their reaction to an encounter with a homeless person. Some of the men ignored the homeless man, while others helped him, such as buying him food. A study found that men who showed empathy and kindness were more attractive to women compared to men who showed empathy and kindness. ... >>

Random news from the Archive

Sending a message using electronic telepathy 05.09.2014

The technology of "reading" brain waves has reached a new stage of development. A scientist from India conveyed a message to his colleague in France through the "power of thought". This case was the first time that people managed to exchange information virtually directly from brain to brain.

Using electroencephalogram (EEG) technology, scientists compared thoughts with electrical impulses in the brain. If earlier the information reproduced by a person sent signals to the gadget, then in the course of the latest study it was decided to connect another person to the data transfer process.

The experiment went like this: a volunteer from Thiruvananthapuram (India) sent a "mental message" in the form of a greeting to another subject in Strasbourg (France). There, the computer "translated" the greeting, after which, with the help of electrical stimulation, it communicated the received thoughts to the second subject, in whose brain the sensor was implanted. The message was recorded as a light flash in the viewing angle of the recipient's vision. A sequence of flashes of light allowed the addressee to decipher the received information. Later, a second experiment was carried out, where a similar message was transmitted from Spain to France.

It is also noted that errors were made during the second experiment, but their share was only 15%. Of these, 5% of errors were recorded at the coding stage, 10% at decryption.

According to scientists, this was the first time that people were able to transmit information virtually directly, from brain to brain. Also, the authors of the project argue that in the near future the human brain will be able to easily interact with computers.

The technology for "reading" brain waves was developed as part of a collaboration between Axilum Robotics, Starlab Barcelona, the University of Barcelona and Harvard Medical School.

This technology of brain waves is actively used in various fields, ranging from conventional computer simulators to the control of military equipment by the "power of thought".

Other interesting news:

▪ paper battery

▪ Ultra-Flash CSFB Technology

▪ The most powerful gantry crane

▪ GPS signal will measure wind speed over water

▪ How a laser cuts flesh

News feed of science and technology, new electronics

Interesting materials of the Free Technical Library:

▪ section of the site Microcontrollers. Article selection

▪ article Human factor. Popular expression

▪ article Which goalkeeper has scored more goals in his career than many outfield players? Detailed answer

▪ article A wood finisher who applies finishing materials in pneumatic spray booths. Standard instruction on labor protection

▪ article Black mordant for aluminum. Simple recipes and tips

▪ article Automatic charger for lead-acid batteries. Encyclopedia of radio electronics and electrical engineering

Leave your comment on this article:

All languages of this page

Home page | Library | Articles | Website map | Site Reviews