Congenital carditis. Clinical patterns. Treatment.

Early congenital carditis occurs before the 7 th month of fetal development. Obligatory morphological substrate it is fibroelastoz or elastofibroz endo-and myocardium.

Late congenital carditis develops in a fetus after the 7 th month of gestation and without fibroelastoza elastofibroza.

Early rehabilitation provides a warning of heart failure. Appointed non-steroidal anti-inflammatory drugs, drugs that improve the trophic myocardium, as well as UFO with individually selected biodozoy.

Late rehabilitation during sanatorium treatment is carried out with an individual approach to the selection of rehabilitation factors. Reorganize foci of infection.

Restorative treatment in outpatient involves hardening of children. To this end, used spa treatment factors.

Further dynamic monitoring is carried out at an early carditis permanently in late cardio - within 5 years after the disappearance of signs of illness. Inspections pediatrician at the first year, 2 times a month, a cardiologist - a once in 2-3 months; ENT doctor, dentist - 2 times a year.

Chronic renal failure, Treatment. Prophylaxis.

Treatment of chronic renal failure in children includes conservative treatment prior to dialysis and treatment already on dialysis stage. Conservative therapy is aimed at some recommendations on diet, it is believed that an excess of protein causes the progression of renal failure. Typically, the diet in children with renal failure should include a restriction of products containing large amounts of potassium, are first of all, fresh fruit and phosphorus, fish and dairy products. This diet, which should include adequate amounts of calcium. Mandatory restriction of salt. Excess salt causes fluid retention, leading to the formation of arterial hypertension.

If, despite the best efforts of doctors, parents and young patients who develop end-stage chronic renal failure without renal replacement therapy, there is not enough.

Biliary dyskinesia. Causes. Clinics. Diagnosis.

Biliary dyskinesia in children - causes

Formation of biliary tract disease in children contribute to the qualitative and quantitative disorders diet: increased intervals between meals, early introduction into the diet of fatty and spicy food, overeating, excess of sweets, a sedentary lifestyle. To the development of pathology of biliary system in children predispose a violation of psycho-emotional sphere, transferred perinatal encephalopathy SVD, stressful situations. Play a significant role zabolivaniya associated gastric and duodenal ulcers, helminthic

infestations, giardiasis, developmental abnormalities of the gallbladder and biliary tract, food allergies, bacterial infections. Among the bacteria which causes inflammation of the gallbladder and bile ducts, is dominated by E. coli and various cocci, rarely are the cause of anaerobic organisms. Is of great importance, and genetic predisposition.

Various lesions of bile ducts are closely linked and have much in common at all stages of pathogenesis. The disease usually begins with the development of biliary dyskinesia, ie, functional motility disorders of the gallbladder, bile duct, sphincter Lyutkensa, Oddi and Miritstsi. Against this background, changes the physicochemical properties of bile, leading to the formation of crystals of bilirubin, cholesterol, etc. The result in the development of organic inflammatory lesions of the gallbladder and bile ducts, as well as the formation of gallstones.

In the occurrence of biliary dyskinesia important role played by the functional state of the stomach and duodenum. Violation of the sphincter duodenostasis, swelling and spasm of the major duodenal papilla lead to hypertension in the biliary system and violation of bile secretion. There are different mechanisms leading to violation of passage of bile.

Biliary dyskinesia in children - formsSecrete hypotonic (hypokinetic) and hypertensive (hyperkinetic) types of dyskinesias. It is also possible mixed form.

Hypotonic dyskinesia type

The main signs of hypotonic dyskinesias such as: reduction of muscle tone of the gallbladder, the weak and decline, the increase in gallbladder volume. Clinically, this option is accompanied by aching pain in the right upper quadrant or around the navel, general weakness, fatigue. Sometimes it is possible to palpate a large atonic gallbladder. When ultrasound reveals an enlarged, sometimes elongated gallbladder with normal or delayed emptying. When you receive a stimulus (egg yolk), the transverse dimension of the gallbladder is usually reduced by at least 40% (normally 50%). In fractional duodenal sounding reveal an increase in the portion of normal or high velocity outflow gallbladder bile, if the tone of the bladder has been saved. Reduction of tone accompanied by a decrease in volume of the portions.

Dyskinesia hypertensive type

The main signs of dyskinesias hypertensive type - reducing the size of the gallbladder, the acceleration of its discharge. Clinically, this variant is characterized by brief, but more intense episodes of pain localized in the region of the right hypochondrium or around the navel, sometimes indigestion. Ultrasonography for the decrease in the transverse dimension of the gallbladder after choleretic breakfast for more than 50%. In fractional duodenal sounding reveals a decrease of servings in an increase in the rate of outflow of bile.

Juvenile rheumatoid arthritis. Etiology. Pathogenesis. Clinical pattern. Treatment. Differential diagnosis.

Juvenile rheumatoid arthritis (JRA) - a chronic inflammatory joint disease of unknown cause, lasting more than 6 weeks in children under the age of 16 years and under.

EpidemiologyJuvenile rheumatoid arthritis is one of the most frequent and most disabling rheumatic disease that occurs in children. The incidence of JRA - 2 to 16 people per 100 000 child population under the age of 16 years. The prevalence of JRA in different countries - from 0,05 to 0,6%. Often suffer from rheumatoid arthritis girls.

CauseIn the development of JRA take part hereditary and environmental factors, among which the most important infection.There are many factors that triggers the disease. The most common are viral or mixed bacterial-viral infection, injury, joints, insolation, or hypothermia, immunizations, especially against the backdrop of spent or soon after undergoing SARS or bacterial infection. The possible role of infection in the development of JRA is expected, but it is still not fully proven. The relationship between onset of illness with a history of SARS, with carrying out preventive vaccination against measles, rubella and mumps. Interestingly, the debut of JRA after vaccination against mumps is more common in girls. There are cases when the JRA manifested after vaccination against hepatitis B. The role of intestinal infections, mycoplasma, beta-hemolytic streptococcus in the development of JRA most rheumatologists do not recognize. However, we know that these infections are a cause of reactive arthritis, which can be transformed into JRA. The role of viral infection in the development of chronic arthritis is less clear. It is known that more than 17 viruses can cause infection, accompanied by the development of acute arthritis (including viruses, rubella, hepatitis, Epstein-Barr virus, Coxsackie, etc.).In the development of chronic arthritis etiologic role of viruses has not been proved. Hereditary predisposition to JRA confirmed familial cases of this disease, studies of twin pairs, immunogenetic data.

Morbidity and mortalityAt JRA, 40-50% of children forecast favorable, may occur remission lasting from several months to several years. However, the aggravation of the disease may develop years after a stable remission. In 1 / 3 patients have continuously relapsing course of the disease. In children with early onset disease and adolescents with a positive revmatodnym high risk factors for severe arthritis, disability as musculoskeletal. In patients with late-onset possible transformation of the disease in ankylosing spondylitis. In 15% of patients with uveitis may develop blindness. Mortality in JRA is very low and noted the absence of timely treatment, accession of infectious complications or development of amyloidosis.

ClinicsThe main clinical manifestation of the disease is arthritis. Joint damage is manifested by pain, swelling, deformities and limitation of movement, increased skin temperature over joints (Fig. 1). Children most often affects large and medium-sized joints, especially knee, ankle, wrist, elbow, hip, at least - the small joints of the hand. Typical of the JRA is to engage the cervical spine and jaw-temporal joints. Pathological changes in the joint development of the reactions are characterized by inflammation that can lead to destruction of cartilage and bone joints, narrowing of the joint gaps (the space between the ends of the bones forming the joints) until the development of ankylosis (seam articular surfaces of bones forming the joints).In addition to joint damage may occur following extraarticular manifestations:

* Increased body temperature, sometimes to the high figures, develops, usually in the morning, may be accompanied by chills, increased joint pain, rash. The drop in temperature is often accompanied by heavy sweats. Febrile period can last weeks and months and sometimes years, and are often preceded by the defeat of the joints. * The rash may be diverse, not accompanied by itching, is located in the joints, on the face, chest, abdomen, back, buttocks and legs, is fast disappearing, growing at a height of fever (Figure 5a, 5b). * Cardiac, serous membranes, lungs and other organs. The clinical picture of heart disease in JRA: the pain behind the breastbone, in the heart, and in some cases - pain in the upper abdomen, a feeling of lack of air, forced position in bed (child is easier in a sitting position). Subjectively, the child complains of feeling short of breath. The child has been pale and blue nasolabial triangle, lips, fingers, swollen nostrils, swelling of legs and feet. If it affects the lungs of patients may show difficulty in breathing, wet or dry cough. If it affects the abdominal organs concerned abdominal pain. * Swollen lymph nodes can be marked up to 4-6 cm in diameter. Usually, the lymph nodes mobile, painless. * Enlarged liver and spleen. * Eye involvement is typical of girls with JRA younger age. Marked redness of the eyes, lacrimation, photophobia, irregular contour of the pupil, decreased visual acuity. In the end, may develop blindness and glaucoma. * Growth retardation and osteoporosis are among the manifestations of JRA. Stunting is particularly pronounced at the long and active course of the disease (Fig. 6). In osteoporosis a decline in bone density and increasing its fragility. It is manifested by pains in the bones. One of the severe manifestations osteoporpoza a compression fracture of the spine.

DiagnosisThe diagnosis of juvenile rheumatoid arthritis is based on the results of examination of the patient's physician, rheumatologist and a range of laboratory and instrumental methods.

Laboratory and instrumental methods of examination.

Analysis of peripheral blood (erythrocyte, hemoglobin, platelets, leukocytes, leukocyte formula, erythrocyte sedimentation rate - ESR), and analysis of biochemical parameters (total protein, protein fractions, the concentration of urea, creatinine, bilirubin, potassium, sodium, ionized calcium, transaminases, alkaline phosphatase), and analysis of immunological parameters (the concentration of immunoglobulin A, M, G, C-reactive protein, rheumatoid factor, presence of antinuclear factor - ANF). All the patients underwent electrocardiography, ultrasound of the abdomen, heart, kidneys, X-ray examination of the chest, damaged joints, if necessary, spine, krestsovo-iliac joints. Also, all children with involvement of joints is carried out a survey for infections: beta-hemolytic streptococci, coliforms (Yersinia, Shigella, Salmonella) and parasites (toxoplasmosis, toksokarr, etc.), herpes virus and cytomegalovirus, chlamydia. When you see the difficulties in diagnosis performed immunogenetic examination. Chronic administration of analgesic and hormonal preparations necessary to conduct esophagogastroscopy. Consultation eye and slit lamp examination showed that all children with a lesion of the joints.

TreatmentTreatment of juvenile rheumatoid arthritis is a serious problem and should be comprehensive, including adherence, diet, drug therapy, physical therapy and orthopedic correction.The goals of therapy JRA:- Suppression of the inflammatory process activity,- Disappearance of systemic manifestations, and articular syndrome- Preservation of the functional ability of joints,- Preventing or slowing joint damage, disability patients- To achieve remission,- Improving the quality of life of patients,- Minimizing the adverse effects of therapy.Drug therapy JRA is divided into two categories: symptomatic (non-steroidal anti-inflammatory drugs and corticosteroids) and immunosuppressive (suppresses immunity). The use of nonsteroidal anti-inflammatory drugs (NSAIDs) and glucocorticoids to quickly reduce pain and inflammation in joints, improve function, but does not prevent the destruction of joints. Immunosuppressive therapy stops the development of degradation, reduce disability.Nonsteroidal anti-inflammatory drugs (NSAIDs)Children are most often used with diclofenac, naproxen, nimesulide, meloxicam. Only NSAID treatment is carried out not more than 12.6 weeks, setting up a reliable diagnosis of JRA. After that NSAIDs should always be combined with immunosuppressive drugs. With prolonged use of NSAIDs or exceeded the maximum permissible dose of the possibility of side effects.GlucocorticoidsGlyukokotikoidy are hormonal drugs. They provide a quick anti-inflammatory effect. Glucocorticoids are used for intra-articular (methylprednisolone, betamethasone, triamsinolon), intravenous (prednisone, methylprednisolone) administration and oral (prednisolone, methylprednisolone).

It is not advisable to begin treatment of patients with JRA with the appointment of glucocorticoids inside. They should be appointed with the ineffectiveness of other treatments. Glucocorticoids is not recommended inside the children under 5 years (especially under 3 years), as well as in adolescence, it can lead to severe stunting (Fig. 7).Intravenous administration of glucocorticoids (pulse therapy) is rapidly inhibits the activity of the inflammatory process in patients, used mainly in the presence of systemic manifestations of JRA.Immunosuppressive therapyImmunosuppressive therapy is a leader in the treatment of rheumatoid arthritis. That is the choice of drug, the term of appointment, duration and regularity of treatment often depends on the prognosis for the patient's life and for the disease. Immunosuppressive therapy should be prolonged and continuous, to begin immediately after diagnosis. Cancel the drug might be effective if the patient is in a state of clinical and laboratory remission for at least 2 years. Cancel immunosuppressive drugs in most patients causes exacerbationThe main drugs for treatment of JRA are methotrexate, cyclosporin A, sulphasalazine, leflunomide, and combinations thereof. They are highly efficient, fairly good tolerability and low incidence of side effects even during long periods (years) admission.Cyclophosphamide, chlorambucil, azathioprine are used for the treatment of JRA are rare due to the high frequency of severe side effects. Hydroxychloroquine, D-penicillamine, gold salts is practically not used in connection with the lack of efficiency.In the treatment of immunosuppressive agents conducted a general analysis of control blood (erythrocyte, hemoglobin, platelets, leukocytes, leukocyte formula, erythrocyte sedimentation rate), and analysis of biochemical parameters (total protein, protein fractions, the concentration of urea, creatinine, bilirubin, potassium, sodium, ionized calcium, transaminases, alkaline phosphatase) - 1 every 2 weeks. By reducing the number of leukocytes, red blood cells, platelets below the norm, with increasing levels of urea, creatinine, transaminases, bilirubin above normal - immunosuppressants cancel at 5-7 days, after controlling for blood analysis, with normalization of the - to resume taking the drug.Biological agentsRecent advances in science helped to create a new group of drugs - the so-called biological agents. These include: infliximab, rituximab. These drugs are highly effective for the treatment of certain variants of the JRA. Treatment with these drugs should be conducted only in specialized rheumatology department, whose employees have experience in the use of such drugs.Surgical treatmentSurgical treatment is indicated in the development of pronounced deformation of the joints, impede the implementation of the simplest everyday actions, the development of severe ankylosis. Major surgery is a prosthetic joints.How to Prevent juvenile rheumatoid arthritis?Prevent the development of JRA is impossible due to lack of data on the causes of its occurrence.To prevent relapse of the disease is necessary to observe the following rules:

* Avoid insolation (location of the sun, regardless of latitude). * Avoid exposure.

* Try not to change the climate zone. * Reduce exposure. * Avoid contact with animals. * Patients with JRA is contraindicated conduct any vaccinations (except for the Mantoux test) and the use of drugs that enhance the immune response (Likopid, taktivin, polyoxidonium, immunofan, viferon, interferon, and others).

Treatment principles of chronic nonspecific pulmonary diseases caused by type II hypersensitivity reaction.

Chronic nonspecific lung diseases

Chronic nonspecific lung disease - a term adopted in 1958 at a symposium organizedpharmaceutical company «Ciba». The composition of COPD include lung diseases - chronic bronchitis, bronchial asthma,emphysema, chronic pneumonia, bronhektaticheskaya disease pneumosclerosis. Chronic bronchitis Chronic bronchitis - a diffuse progressive bronchial damage associated with prolonged stimulationairway harmful agents, characterized by inflammatory and sclerotic changes in the bronchialwall and peribronchial tissue, accompanied by a rearrangement of the secretory apparatus and mucus hypersecretion,show constant or peripheral cough with phlegm for at least 3 months a year for 2 andmore years, and the defeat of bronchial tubes - shortness of breath, leading to obstructive disorders of ventilation and the formation ofchronic pulmonary heart disease. Classification of chronic bronchitis I. Clinical forms: • chronic simple (non-obstructive) bronchitis, flowing with a constant or periodic release of mucoussputum, and without ventilation disorders; • chronic purulent (nonobstructive) bronchitis, flowing with a constant or periodic release of contaminatedsputum, and without ventilation disorders; • chronic obstructive bronchitis, flowing with blennoptysis and persistent obstructivedisorders of ventilation; • chronic suppurative obstructive bronchitis, accompanied by the release of purulent sputum with persistent obstructivedisorders of ventilation; • Special forms: hemorrhagic, fibrinous.

Obliterative bronchitis, bronchiolitis. Vascular pattern is deformed, irregular light pnevmotizatsiya

II. The level of destruction:

• bronchitis, mainly affecting large bronchi (proximal); • bronchitis with a primary lesion of small bronchi (distal). III. Current: • Patent; • with few exacerbations; • from frequent exacerbations; • continually recurring. IV. Availability bronhopasticheskogo (asthmatic) syndrome. V. Phase process: • aggravation; • remission. VI. Complications: • pulmonary emphysema; • coughing up blood; • respiratory failure (including power); • Chronic pulmonary heart (compensated or decompensated).

Obliterative bronchitis, bronchiolitis. On broncho-gram left distal bronchus and bronchi of the basal segmentsexpanded peripheral filling is absent. Upper lobe bronchus and the reed is not altered and performed to smallgenerations

The etiology of chronic bronchitis • Inhalation of pollutants - in the air of impurities of different nature and chemical structure, providingharmful irritant effect on the bronchial mucosa (tobacco smoke, dust, toxic fumes, gases, etc.). • Infection (bacteria, viruses, mycoplasma, fungi). • Endogenous factors - the stagnation in the lungs of circulatory failure, the allocation of the mucosabronchi products of nitrogen metabolism in chronic renal failure. • untreated acute bronchitis. Predisposing factors: • disturbance of nasal respiration; • nose and throat diseases - chronic tonsillitis, sinusitis, rhinitis; • cooling; • alcohol abuse; • Accommodation in the area where the atmosphere is polluted with contaminants (gases, dust, fumes of acids, alkalis, etc.). Pathogenesis of chronic bronchitis Impaired function of the system of local bronchopulmonary defense. Development of classical pathogenic triad - a hyper-Krini (giperfunktsionirovanie bronchial mucous glands,

hyperproduction of mucus), dyscrinia (increased viscosity of mucus due to changes in its physico-chemical properties andreducing its rheology) mukostaz (stagnation in the bronchi thick viscous mucus). Favorable conditions for the implementation of the bronchi of infectious agents. The development of sensitization to microbial flora and autosensibilizatsii. The basic mechanisms of bronchial obstruction: • bronchospasm; • inflammatory edema and infiltration of the bronchial wall; • hyper-and dyscrinia; • hypotonic dyskinesia of the large bronchi and trachea; • collapse of small bronchi on expiration; • hyperplastic changes in mucosal and submucosal layers of the bronchi. Clinical symptoms of chronic bronchitis Clinical manifestations of chronic non-obstructive bronchitis • a cough with mucopurulent sputum to 100-150 ml per day, mainly in the morning. • In the acute phase - weakness, sweating, and purulent bronchitis - increased body temperature. • With many years of purulent chronic bronchitis may develop clubbing ("drumsticks") andthickening of the nails ("hour glass"). • In light percussion in the case of emphysema percussion "box" and the restriction of the respiratorymobility of the lungs. • Auscultation is determined by hard breathing with prolonged exhalation, dry whistling and humming wheezing,variegated moist rales, depending on the caliber of the bronchi. Clinical manifestations of chronic obstructive bronchitis • Shortness of breath, mainly expiratory type. • The changing nature of dyspnea according to the weather, time of day, acute pulmonary infection. • Difficult and long exhalation as compared with the phase of inspiration. • Swelling of the neck veins during expiration, and wears off during inspiration. • prolonged unproductive cough. • When the percussion of the lungs: "boxed" sound, the omission of the lower boundary of the lungs (emphysema). • Auscultation: breath hard with extended expiration, whirring, wheezing, which can be heard ondistance. Sometimes tapped only in the supine position. • Palpation expiration of Votchanu: lengthening the exhalation and decrease its strength. • Positive test with a match on Votchanu: the patient can not pay a lighted match at a distance of 8 cm from the mouth. • In marked obstructive syndrome, symptoms of hypercapnia: sleep disturbance, headache, increasedsweating, anorexia, muscle twitching, a major tremor in more severe cases - confusion, seizures, and

coma. • Syndrome of dyskinesia of the trachea and major bronchi seen bouts of painful bitonal cough with difficultDetachable phlegm, accompanied by choking, sometimes loss of consciousness, vomiting. Laboratory data for chronic bronchitis • UAC: When purulent exacerbation of bronchitis, moderate increase in sedimentation rate, leukocytosis with a shift to the left. • LHC: an increase in blood sialic acid, fibrin, seromukoida, alpha-2-and gamma-globulin, the appearance of PSA. • Overall analysis of sputum: sputum light-colored mucous, purulent sputum - a yellowish-greenish color, candetected puromucous tube, with obstructive bronchitis - bronchial casts, with microscopic examinationpurulent sputum - a lot of neutrophils. In chronic obstructive bronchitis marked alkaline reaction of the morningsputum and neutral or acidic - daily. Rheological properties - viscosity, increased elasticity. Whenobstructive bronchitis may be determined by the spiral Kurshmana. Instrumental study of chronic bronchitis • Bronchoscopy plays a role in the verification of chronic bronchitis. In this case, are signs of chronicinflammation: cicatricial changes of the trachea and bronchi, mucous metaplasia. • X-ray of lungs: radiographic pattern in the lungs is changed only when the inflammatoryprocess covers the peribronchial or respiratory portion of the lungs. In this case, can be detected followingsymptoms of chronic bronchitis: Net pneumosclerosis, deformation lung pattern, diffuse increasetransparency of lung fields, low aperture distance and flattening its dome, the decrease in the amplitude of movement of the diaphragm.The central location of the heart, the pulmonary artery protrusion cone. • From spirograficheskih most important indicators are presented Tiffno index, the ratio of FEV, to VC andmeasure air velocity ratio (MVL and VC). Study of ventilation parameters to determinethe degree of the reversible component of airflow obstruction. • ECG is used to detect pulmonary hypertension. • Analysis of blood gases and acid-base status provides valuable information about the degree of hypoxemia andhypercapnia in chronic bronchitis. Indications for hospitalization in chronic bronchitis • Aggravation of the disease, reflected an increase in shortness of breath, cough, phlegm in the presence of one orseveral conditions: failure of outpatient treatment, a high risk of comorbidity, prolongedprogression of symptoms, increase in hypoxia, emergence or growth of hypercapnia. • Emergence of decompensation or pulmonary heart disease, not amenable to outpatient treatment. Treatment of chronic bronchitis Treatment of chronic bronchitis is made up of non-medical interventions and medical nature.

Drug-free methods of influence on a patient with chronic bronchitis include the following mandatoryelements: leveling the occupational hazards, improve environmental conditions at work and at home, avoidingsmoking, therapy and auditory training, dosed physical stress, vitamin and food-limitedsalt and total kalorazha (up to 800 kcal / day) with low-carb. Drug therapy of chronic bronchitis depend on the nosological diagnosis. In chronic (simplenonobstructive) bronchitis, occurring with a constant or periodic blennoptysis and withoutvent violations of basic therapy includes expectorant drugs. Choosing expectorants drugs depends on the type of cough. If a strong dry cough exhausting prescribe drugsdepressing the cough reflex (codeine, tekodin, dionin, glautsin). If a productive cough with sputum discharge shows good substance, reinforcing its selection:expectorants (Thermopsis, terpingidrat, etc.) and bronchodilators (aminophylline, theophylline). With unmodifiedrheological properties of sputum, but reduced mucociliary transport using derivatives of theophylline andsympathomimetics (teolong, teopek, sinekod). At high viscoelastic properties of sputum are used derivatives of thiols (acetyl-cysteine or mukosolvin)proteolytic enzymes (trypsin, chymotrypsin), and with significant adhesive performance prescribed substancesstimulating the formation of surfactant (Bromhexine-bisolvan, Mucosolvan-Ambroxol) and regidratata secretion (mineralsalt, essential oil). In chronic purulent (nonobstructive) bronchitis, occurring with a constant or periodic release of contaminatedsputum, and without ventilation disorders, except drugs that regulate mucociliary clearance, are shownantibacterials. Preference is given substance, active against pneumococcus and Hib. Since antibacterial drugs worsen the rheological properties of sputum, they must be combined with mucolytics.Antibiotics may be administered by mouth, parenteral and in the form of aerosols. Chronic obstructive bronchitis, with a flowingblennoptysis and persistent obstructive disorders of ventilation, requires the designation of bronchodilators(Anticholinergics, beta-2-agonists and methylxanthines), and expectorants drugs, and in case of hypoxemia,hypercapnia and pulmonary heart disease - treatment of these complications. When you join a pronounced obstructive bronchitispurulent component added antibacterial agents. Relief of bronchospasm is achieved with the appointment of agentsbronchodilatory effect of: • sympathomimetics selective or predominantly selective actions (izadrin, salbutamol, berotek,

Ventolin); • phosphodiesterase inhibitors (theophylline derivatives); • holinolitikov (platifillin, atropine); • corticosteroids, mostly of the inhalation (bekotid, beklomet, Pulmicort) did not inhibit the functionadrenal cortex. In the case of circulatory failure required cardiac glycosides, diuretics, oxygen therapy (malopotochnaya24-28% probability, the oxygen-air mixture through a mask). If, in spite of active treatment is progressing respiratoryacidosis are shown intubation and mechanical ventilation. When treating patients with chronic bronchitis are widely used physical therapyProcedure (MSS chest, ultrasound, inductothermy, UHF), chest compressions, breathing exercises,sanatorium treatment. If you frequently relapsing course of chronic bronchitis, 2 times a year, seasonal prophylaxis andpreventive treatment. Assign an immunomodulatory drugs, volatile, methods and tools aimed atimprove bronchial drainage. When pus forms of bronchitis every morning conducted "toilet" bronchial tree -patient performs positional drainage after prior acceptance expectorants, hot tea, bronhospazmolitikov.In secondary pulmonary hypertension and severe respiratory failure patients employ or restrictphysical activity. Along with bronhospazmolitikami they appoint peripheral vasodilators (nitrates or antagonistscalcium nifedipine group), if indicated, phlebotomy, oxygen therapy. The main tasks of medical examination • Early diagnosis of the disease. • as early as possible exception of external causal factors - smoking cessation, elimination of harmfulfactors of production, rehabilitation of chronic foci of infection, restoration of nasal breathing. • Selection of individual supportive therapy against non-drug therapies. • Organization of special treatment on an outpatient basis (aerosol therapy, endobronchial sanitation).Diagnosis of functional disorders of breathing, including the early diagnosis of bronchial obstruction. Measures toPrevention of relapse of chronic bronchitis suggest tempering the organism (regulated sports)prevention of viral infection (receiving ascorbic acid, rimantadine, interferon). Bronchial asthma Bronchial asthma - a chronic relapsing disease, mainly affecting the bronchi, whichcharacterized by their hyperreactivity due to specific (immunological) and (or) non-specific(Neimmunologicheskimi), congenital or acquired mechanisms, and the primary (mandatory) feature whichan attack of breathlessness and (or) asthma status due to spasm of bronchial smooth muscle, hypersecretion, and dyscriniaedema of the bronchial mucosa. Classification of asthma

Traditionally, the release: • atopic (exogenous, allergic, immunological); • nonatopic (endogenous, neimmunnologicheskuyu) bronchial asthma. Severity: • mild course; • During moderate; • severe course. Mild characterized by the absence of classic episodes of breathlessness. Symptoms of shortness of breath occurless than 1-2 times a week, are of short duration; drug therapy is usually not required. Night's sleeppatient in this stage of the disease is characterized by the awakening of respiratory discomfort at least 1-2 times a year. Outsideattacks the patient's condition is stable. In bronchial asthma, moderate attacks cropped sympathomimetics.Attacks at night, recorded more than twice a month. Asthma attacks are characterized by frequent severeprolonged exacerbations with the presence of complications, life threatening, frequent nocturnal symptoms, reduced physicalactivity, the presence of persistent symptoms in the interictal period. Phase of bronchial asthma: exacerbation, remission. Complications: • Pulmonary - pulmonary emphysema, pulmonary insufficiency, atelectasis, pneumothorax; • extrapulmonary - degeneration of the myocardium, lung, heart failure.

Bronchial asthma. Direct projection: total abdominal pulmonary vascular pattern is thinned, can be tracedmainly in the rhizospheres, the right root is deformed and shifted downwards

Stages of development of asthma development stages of bronchial asthma I. Availability of healthy people and congenital (or) the acquisition of biological defects and violations: a)local and general immunity, and b) a system of "rapid response" (mast cells, macrophages, eosinophils, platelets), c)mucociliary clearance, and d) the endocrine system, etc. The clinical implementation of biological defects leads to the developmentbronchial asthma. II. Condition predastmy. This is a sign of the threat of symptomatic asthma. III. Clinically decorated asthma - after the first attack of asthma or status asthmaticus.

Bronchial asthma. Lateral projection: middle lobe atelectasis with a decrease of up to 1 / 4 volume

Etiology and pathogenesis of asthma

Common pathogenetic mechanism inherent in various forms of asthma, is to changesensitivity and bronchial reactivity, determined by the reaction of bronchial patency in response to physical andpharmacological factors. Believe that 1 / 3 of patients with asthma have an autoimmune origin. In the eventAllergic asthma play the role of nonbacterial and bacterial allergens. The most studied allergicmechanisms of asthma, which are based on IgE and IgG caused the reaction. Central to the pathogenesis"Aspirin" of asthma withdrawn leukotrienes. With exercise-induced asthma is disruptive to the heat transfer from the surfacerespiratory tract. Clinical symptoms of asthma Predastma. The first group of symptoms predastmy - acute, recurrent or chronic bronchitis and pneumoniaphenomena of bronchial obstruction. The second group - the presence of extrapulmonary manifestations of allergy: vasomotor rhinitis, urticaria,angioedema. The third group - a hereditary predisposition to various allergic diseases, which revealedthe collection of family history. The fourth group - the blood and sputum eosinophilia. Bronchial asthma. In the development of bronchial asthma attack are three periods: the precursors, the height (suffocation) andreverse development. Period precursors occurs within minutes, hours, sometimes days before the attack and is manifested by the followingsymptoms: vasomotor reactions of the nasal mucosa, sneezing, itchy eyes, skin, paroxysmal cough,headache, often changes of mood. During the crisis period (suffocation) has the following symptoms. A feeling of lack of air, chest tightness,severe expiratory dyspnea. Breath becomes short, exhale - slow, accompanied by loudprolonged, wheezing, heard in the distance. The patient takes a forced position, sitting,leaning forward, elbows on knees, gasping for air. The face is pale with a bluish tint. Nostrilsinflated during inspiration. Thorax in the position of the maximum inspiratory muscles involved in breathing shoulder girdle,back, abdominal wall. Intercostal spaces and supraclavicular fossa retracted during inspiration. Swollen neck veins. Ina seizure cough with phlegm is very difficult to peel-off over the percussion sound can be easily determined fromtympanic shade lower limits of light are omitted, the mobility of lung edge is bounded on the background of a weakenedrespiration, particularly on the exhale, I hear a lot of dry wheeze. Pulse of teaching, weak filling, heart soundsmuted. Attack of asthma may become asthmatic status. Period of reverse development has a different duration. After the attack, people want to relax, some of them

experience hunger, thirst.

After an attack of asthma in the upper lobe of right lung is visible uniform rounded shape with a shadowclear margins - eosinophilic infiltration

Laboratory data in bronchial asthma • UAC: eosinophilia, increased ESR. • Overall analysis of sputum: a lot of eosinophils, Charcot-Leyden crystals, spirals Kurshmana, neutrophil leukocytes ininfektsionnozavisimoy patients with bronchial asthma. • LHC: an increase in the level of alpha-2-and gamma-globulin, sialic acids, seromukoida, fibrin.

Resorbed infiltration after a bout of bronchial asthma

Instrumental studies in bronchial asthma X-ray study: patients with atopic asthma attack is no change atinfektsionnozavisimoy bronchial asthma - symptoms of chronic bronchitis with emphysema and peribronchial sclerosislungs. During an attack of bronchial asthma revealed signs of acute pulmonary emphysema. Study of the nasopharynx. Patients predastmoy and asthma can be detected vasomotor disordersnasal mucosa, polyps, crooked nasal septum, inflammation of the sinuses and tonsils. ECG: signs of increased pressure on the right atrium, and sometimes partial or complete blockade of right bundle branch block,formation of pulmonary heart disease. ECG changes are formed earlier in patients with atopic asthma thaninfektsionnozavisimoy. Spirograficheskoe and pnevmotahometricheskoe Study: bronchial obstruction(Reduced forced expiratory volume in first second, maximum ventilation, reduced expiratory flow rate)with frequent exacerbations and the development of emphysema - reduced lung capacity. Diagnosis of clinical and pathogenetic variants of bronchial asthma Diagnostic criteria of atopic asthma: • Allergological history. Hereditary predisposition. Allergic constitution. Pollen allergy.Food allergy. Drug allergy. Occupational allergy. • Mostly young age (80% of patients aged 30 years). • Positive skin tests to specific allergens. • Positive provocative tests for certain allergens (conducted under strict indications). • Identify specific food allergies. • Laboratory criteria: elevated blood levels of IgE; elevated in the blood and sputum eosinophilbasophilic test Shelly; positive reaction alteration of neutrophils patient to the allergen, increasing the viscosity of sputumunder the influence of allergen. For the atopic form of bronchial asthma is characterized by periods of prolonged remission in case of

termination of contact withspecific allergens, relatively easy for the late development of complications, lack of signsinfection in the upper respiratory tract and bronchi. Diagnostic criteria for infection-dependent bronchial asthma: • Clinical examination: complaints, medical history, objective data indicating the relationship of asthma withtransferred respiratory infection, acute bronchitis, influenza, pneumonia. • UAC: leukocytosis, increased ESR. • LHC: the emergence of a PSA increase of sialic acid, alpha-2-and gamma-globulin seromukoida. • Overall analysis of sputum: muco-purulent, in a smear dominated by neutrophils, the detection of pathogenicBacteria in the diagnostic titre. • X-ray examination: identification of infiltrative fields with pneumonia symptoms pneumosclerosis,darkening of the paranasal sinuses. • Bronchoscopy: inflammation of the mucous membrane, dense puromucous secret predominance in bronchial secretionsneutrophil leukocytes, the detection of pathogenic bacteria. • Determination of bacterial sensitization: positive samples with the corresponding bacterial allergens. • Mycological sputum: sowing the yeast genus Candida. Virological research: identification of viral antigens in the epithelium of the nasal mucosa byimmunofluorescence, serodiagnosis. Identification of foci of chronic infection in the upper airways, nose and throat and oral cavity. Attack of asthma atThis version of bronchial asthma is characterized by gradual development, long,relative resistance to beta-agonists. The patients rapidly developed complications: pulmonary emphysema,pneumosclerosis diffuse, chronic pulmonary heart. Diagnostic criteria dyshormonal variant asthma. For dyshormonal option typicallydeterioration of patients before or during menstruation, pregnancy or menopause, amidhypothalamic syndrome after injury of skull, with lower doses of corticosteroids or their cancellation. Laboratory databased on the determination of blood levels of 11-ACS, ovarian hormone, radioimmunoassay studyestrogen and progesterone in blood plasma, cytology smear confirmed the diagnosis. Diagnostic criteria for autoimmune form of bronchial asthma. Heavy, continually relapsing course.Positive intradermal test with autolimfotsitami. The high level of acid phosphatase in the blood. Positive reactionblast transformation of lymphocytes with phytohemagglutinin. Decrease in blood levels of complement and identification of circulatingimmune complexes. Diagnostic criteria for neuro-psychological variant asthma. Mental factors can causeoccurrence of attacks of breathlessness, but far more often they provoke the development of

bronchospasm in patients already sufferingbronchial asthma. Psychogenic stimuli can cause bronchospasm through the blockade of beta-adrenoretsepotorov,stimulation of alpha-adrenoretsepotorov and vagus nerve. The patient revealed a history of violationsneuro-psychic sphere, psychic and traumatic brain injuries, conflicts within the family, at work, frustration atthe sexual sphere. Aspirin astmaAspirinovaya asthma (asthmatic triad). Bronchial asthma in the presence of recurrentpolyposis of the nose, chronic inflammation of the paranasal sinuses and the intolerance of one or more non-steroidalanti-inflammatory drugs (mostly aspirin) is known as "aspirin". The disease affects more peopleolder age groups. Prior to the development of attacks of breathlessness in patients over many years have polypous rhinosinusitis,about which repeatedly subjected to surgical treatment. Suddenly after taking aspirin, after 15-20 min,develops a severe attack of suffocation, sometimes ending in death. For laboratory parameters mostcharacterized by high blood and sputum eosinophilia. Exercise-induced asthma, or postnagruzochny bronchospasm, characterized by the occurrence of attacks of breathlessness inthe next 2-10 minutes after exercise. Among the different types of sports is the most powerful running, and swimming -the weakest stimulator of bronchospasm. Diagnosis of asthma Diagnosis of asthma (any form) is based on the following grounds (Pyktsy VI et al., 1991). • attacks of breathlessness with difficulty exhaling, accompanied by a characteristic pattern of auscultation in the form of elongationexpiratory wheezes and dry high above the entire surface of the chest, usually remote, that is audible atdistance. Determination of parameters of lung function during an attack reveals the obstructive type of violationrespiration. Characterized by dynamism of these disorders in zaAstma physical usiliyavisimosti from treatment or not. • Frequent combination with allergies or allergic-polypous rhinosinusopathy. • More or less pronounced eosinophilia in blood and sputum. • Positive response to sympathomimetics in the form of the elimination or substantial relief of shortness of breath andgrowth parameters of ERF at 20% or more. • Hypersensitivity of bronchial biologically active substances such as acetylcholine, histamine, etc. Indications for hospitalization With increasing frequency and severity of attacks of breathlessness, increasing demand for sympathomimetics and reducing theireffectiveness of patients require treatment in hospital. Admission subject to asthmatic patients withif they have complications and life-threatening, and severe concomitant diseases. Asthmatic condition - one of the most dangerous complication of asthma. Under the status

asthmaticus understandlong bouts of breathlessness, resistant to therapy, and sympathomimetic drugs flowing in the backgroundunproductive and ineffective cough. Mechanisms for the formation of status asthmaticus are associated with progressive blockadebeta-adrenergic receptors and obstruction of bronchi by mucus. On the severity of asthma are three stagesstate (Ado, AD, 1976; Chuchalin AG, 1985): 1 - relating to compensation, 2 - decompensation or "dumblung; 3 - hypoxic hypercapnic coma. Pathogenic variants of status asthmaticus: • anaphylactic; • Metabolic. Anaphylactic variant is characterized by sudden onset with rapid (within hours), developmentcoma. Its occurrence is usually associated with increased sensitivity to drugs.Metabolic variant asthmatic condition is formed by long-term (within a few days or weeks) under the influencerapid withdrawal of corticosteroids, respiratory infections, adverse weather factors on the backgroundfunctional beta-adrenoceptor blockade and intensive use of sympathomimetics. With increasing andincreasing severity of attacks of breathlessness the patient often resorts to non-selective beta-stimulants of action (apupent,astmoment, etc.). The use of such high doses of sympathomimetics leads to the fact that each subsequent attacksuffocation is heavier than the previous. This is the "rebound syndrome". There is another undesirable effectsympathomimetics. With chronic administration, they may contribute to edema, bronchial mucosa andmucus hypersecretion, resulting in a fit of choking can grow. The first stage of status asthmaticus (for compensation). The patient is able to basically giperventilirovatalveoli, accompanied by normo-or hypercapnia (35-40 rCO2 mmHg. cent.). Some patients may develophypoxemia (rO2 60-70 mmHg. cent.). Clinically, this stage is characterized by a prolonged bout of breathlessness, mildshortness of breath and tachycardia (100-120 beats per minute), nonproductive cough, and sometimes a slight cyanosis. Percussion over thesurface of the lung is determined by "a box" sound, auscultation revealed dry wheezing. The second stage is accompanied by a decrease in the ability of giperventilirovat alveoli ("silent lung"). This leads toincreased hypoxemia (PaO2 50-60 mmHg. cent.) and the appearance of hypercapnia (PaCO2 50-60 mmHg. cent.). The general condition of patientsheavy, there is a change of mentality (psychomotor agitation replaced by depression, hallucinations are possible). Importanthallmark of this stage is a discrepancy between the noisy, wheezing, and almost complete absence of wheezing in

lungs. Auscultation lung pattern is characterized by a mosaic: the place with impaired respiration are replaced by "dumb"sites. Tachycardia to 140 beats per minute, often recorded arrhythmia and hypotension. The third stage corresponds to the clinical picture gipoksimicheskoy and hypercapnic coma. The development of acidosis andsevere hypoxia (rO2 40-50 mmHg. cent.) and hypercapnia (rCO2 80-90 mmHg. cent.). The condition of patients is extremely difficult,express violation of nervous and mental activity precedes impairment of consciousness. An objectivestudy notes diffuse cyanosis, collapse, irregular breathing, thready pulse. Treatment of bronchial asthma Treatment of patients with asthma should be individualized and based on the concept ofallergic nature of the disease. Integrated Management of asthma include: • patient education program; • Dynamic control of disease severity and the adequacy of therapy with clinical andfunctional studies; • measures that exclude the impact on the patient's body, "the culprit allergen, or control of causative factors; • develop a plan of drug therapy; • prevention of relapses and develop a plan of treatment; • Dynamic monitoring of patients. The patient should have information about the causes and nature of the disease, the basic mechanisms that lead to the development ofsymptoms. Causal treatment is reduced to the elimination of the allergen that has entered the body through the respiratory tract.Removal of contact with the allergen - the most simple and effective method of treatment etiotrop (with pollen allergy) -suppression of contact at the time that the allergen is found in nature in the maximum number of (time to flowering), whenfood allergies - the use of elimination diets, and professional - a change of employment or working conditions, andhypersensitive to drugs - the rejection of their application. In the same vein, consider and surgicalsanitation of foci of infection. Specific hyposensitization is considered one of the most common methods