Dust can affect the organ of vision, lead to inflammatory processes in the conjunctiva (conjunctivitis). Cases of conjunctivitis and keratitis are described in workers in contact with dust of arsenic-containing compounds, aniline dyes and acriquine.

Dust of trinitrotoluene with prolonged exposure, settling in the lens, causes the development of professional cataracts. Workers who have long-term contact with the dust of sulphide and bromide silver salts have professional argyrosis of the conjunctiva and cornea as a result of the deposition of reduced silver in the tissues.

The dust of coal tar pitch has a strong sensitizing effect on the mucous membrane and cornea of ​​the eye, causing severe keratoconjunctivitis - "pitch ophthalmia" when working outdoors in sunny weather.

Skin diseases from exposure to dust

Contaminating the skin, dust of various composition can have an irritating, sensitizing and photodynamic effect.

Dust of arsenic, lime, calcium carbide, superphosphate irritates the skin, causing dermatitis. Prolonged contact with aerosols of cutting fluids (products of petroleum and mineral oils) causes the development of oily follicles. The action on the skin of industrial allergens - dust of synthetic adhesives, epoxy resins, nylon, nylon and other polymeric materials, as well as dust of chromium, copper, nickel, cobalt leads to the development of allergic pro-dermatoses (dermatitis and eczema).

Allergic dermatitis and eczema have been reported in workers exposed to cement dust. Substances with photodynamic (photosensitizing) action include products of processing of coal and oil (tar, tar, asphalt, pitch).

Contamination of the skin with these compounds against the background of insolation causes photodermatitis of open skin areas.

Many dusts of plant and animal origin have a pronounced allergic effect - dust of grass, cotton, flax, grain, flour, straw, various types of wood, especially pine, silk, wool, leather, feathers, rosin, etc.

Dust disease prevention measures

Measures to combat dust formation in order to prevent occupational diseases in the USSR are carried out widely and systematically. As a result of persistent work on improving working conditions, the number of dust-borne diseases of the lungs in our country has sharply decreased and at present there are only isolated cases.

Hygienic regulation.

The basis for carrying out measures to combat dust is hygienic regulation.

The maximum permissible concentration of fibrogenic dusts in the air of working rooms has been established - a list of them is presented in the regulatory documents. The development of standards is carried out in accordance with guidelines- "Substantiation of maximum permissible concentrations (MPC) of aerosols in the working area", approved by the USSR Ministry of Health in 1983

Considering that dust containing free silicon dioxide is the most aggressive among aerosols of fibrogenic action, the maximum permissible concentration of such dusts, depending on the percentage of the latter, is 1 and 2 mg / m 3. For other types of dusts, MPCs are set from 2 to 10 mg / m 3.

The task of sanitary supervision in the field of dust control and prevention of dust lung diseases is to determine the level of this factor, identify the causes and sources of dust formation, hygienic assessment of the degree of air pollution in the working area with dust and the development of recreational measures.

The requirement to comply with the maximum permissible concentration established by GOST is the main one in the implementation of preventive and current sanitary supervision. Systematic monitoring of the state of the level of dust is carried out by the SES laboratory, factory sanitary and chemical laboratories. The administration of the enterprises is responsible for maintaining the conditions that prevent the exceeding of MPCs for dust in the air.

When developing a system of health-improving measures, the basic hygienic requirements should be imposed on technological processes and equipment, ventilation, construction and planning solutions, rational medical care for workers, and the use of PPE. In this case, it is necessary to be guided by the sanitary rules for organizing technological processes and hygienic requirements for production equipment, as well as industry standards for production with dust emissions at enterprises of various sectors of the national economy.

Measures to reduce dust at work and prevent pneumoconiosis should be comprehensive and include measures of a technological, sanitary-technical, medical-biological and organizational nature.

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Ministry of Education and Science of Ukraine

Ukrainian Engineering and Pedagogical Academy

on the topic of: « Occupational Diseases Caused by Exposure to Industrial Dust»

Kharkoin 2013

Introduction

The topic of this essay is very relevant in our time, when heavy industry is very developed. In the post-Soviet countries, they are accustomed to violating safety measures, which leads to numerous accidents, and even more people suffering from occupational diseases. Therefore, I will try to study diseases caused by long-term exposure to dust. At the moment, science is developing rapidly, but in the wrong direction. Therefore, I believe that the research conducted in this essay will be useful, firstly, for managers, and secondly, for the workers themselves who are in contact with dust.

I will try to investigate pneumoconiosis from the point of view of medicine, their manifestations and symptoms, their treatment and prevention.

Pnevmoconiosis

Under the name "pneumoconiosis" (from the Greek pneumon - "lungs", konis - "dust"), they combine a number of diseases caused by the ingress of large amounts of dust particles into the lungs for a long time. The term "pneumoconiosis" was proposed by F.A. Zenker (1866). These diseases belong to the group of professional processes. Pneumoconiosis is found in some workers who have been breathing various types of dust for 5-15 years or more. Small dust particles that enter the respiratory tract cause an interstitial reaction connective tissue, as a result of which pulmonary fibrosis develops and progresses.

The negative impact of industrial dust on humans is determined by its total toxicological effect on various organs. The respiratory organs, skin, eyes, blood and the digestive tract are most affected by dust.

When dust is inhaled, pneumoconiosis occurs, associated with the deposition of dust in the lungs and the reaction of tissue to its presence.

Along with the chemical composition of dust, other factors are also important: the shape and size of particles, their solubility, degree of hardness, distribution of electron density over their surface, etc. Particles of industrial dust are divided into visible (more than 10 microns in diameter), microscopic (from 0 , 25 to 10 μm) and ultramicroscopic (less than 0.25 μm), detectable with an electron microscope. The greatest danger is posed by particles less than 5 microns in size, penetrating into the deep parts of the pulmonary parenchyma. The shape, consistency of dust particles and their solubility in tissue fluids are of great importance. Dust particles with sharp, serrated edges injure the mucous membrane of the respiratory tract. Fibrous particles of animal and vegetable origin cause chronic rhinitis, laryngitis, tracheitis, bronchitis, pneumonia. When dust particles dissolve, chemical compounds are produced that have irritating, toxic and histopathogenic effects. They have the ability to induce the development of connective tissue in the lungs, i.e. pneumosclerosis.

The nature of the resulting pneumoconiosis, the features of its course, depend on the characteristics and concentration of dust entering the respiratory system during work. possible complications, forecast. The most dangerous is dust containing free silicon dioxide, in particular in the form of small crystals, i.e. quartz particles. This dust has the most pronounced fibrogenic properties. Dust containing most silicates has similar, but much less pronounced properties; even lower (but still noticeable) fibrogenic activity of the dust of some metals, in particular beryllium. The fibrogenic properties of most types of organic dust are poorly expressed. When dust of different composition gets into the lungs, the lung tissue can react in different ways.

The reaction of the lung tissue can be:

1.inert, for example, with the usual pneumoconiosis - anthracosis of coal miners;

2. fibrosing, for example, with massive progressive fibrosis, asbestosis and silicosis;

3. allergic, for example, with exogenous allergic pneumonitis;

4. neoplastic, for example in mesothelioma and lung cancer with asbestosis.

The localization of the process in the lungs depends on the physical properties of the dust. Particles less than 2-3 microns in diameter can reach the alveoli, larger particles are retained in the bronchi and nasal cavity, from where they can be removed from the lungs by mucociliary transport. An exception to this rule is asbestos, which particles of 100 microns in size can settle in the terminal sections of the respiratory tract. This is due to the fact that the asbestos particles are very fine (about 0.5 microns in diameter). Dust particles are phagocytosed by alveolar macrophages, which then migrate to the lymphatic vessels and are sent to the hilar lymph nodes. Pneumoconiosis is a very common form of chronic dust lung disease. For all types of pneumoconiosis, a pulmonary fibrotic process is required. However, the course, clinical and radiological and pathological pictures different types pneumoconiosis have some features that largely depend on the composition of industrial dust, which caused the development of pulmonary fibrosis. It is assumed that the destruction of alveolar macrophages by dust plays a significant role in the development of pulmonary fibrosis, which is most noticeable when inhaling dust containing quartz, as well as coal and asbestos dust. In addition, the action of dust stimulates the formation of a significant amount of collagen. A common feature of all types of pneumoconiosis is the development of interstitial fibrosis, however, each type of pneumoconiosis has its own characteristics, determined by histological examination. In addition to the nature and amount of inhaled dust, the onset and development of the disease is also influenced by the previous state of the respiratory system, immunological status, allergic reaction and etc.

This explains the differences in the health status of workers who spend the same time in similar occupational conditions.

Classification

By the nature of the course, the following types of pneumoconiosis are distinguished:

1. rapidly progressing;

2. slowly progressing;

3. late;

4. regressive.

With a rapidly progressive form of pneumoconiosis, stage I of the disease can be detected 3-5 years after the start of work in contact with dust or with the progression of the pneumoconiotic process, i.e. the transition of stage I of pneumoconiosis to stage II is observed after 2-3 years. This form of pneumoconiosis, in particular, should include the so-called acute silicosis, which is essentially a rapidly progressive form of silicosis.

Slowly progressive forms of pneumoconiosis usually develop 10-15 years after the start of work in contact with dust, and the transition from stage I to stage II of the disease lasts at least 5-10 years.

Pneumoconiosis that develops several years after the cessation of contact with dust is usually called late.

Regressive forms of pneumoconiosis are found only when radiopaque dust particles accumulate in the lungs, which give the impression of a more pronounced stage of pulmonary fibrosis according to X-ray studies. When the patient's contact with dust ceases, there is usually a partial removal of radio-opaque dust from the lungs.

This explains the “regression” of the pneumoconiotic process.

Depending on the nature of the dust inhaled, different types of pneumoconiosis are emitted.

1. Silicosis is a disease caused by inhalation of dust containing free silicon dioxide (SiO2).

2. Silicatosis (asbestosis, talc, cement, mica, nepheline, olivine and other silicatoses, kaolinosis). Silicatoses arise from the inhalation of silicate dust containing silicon dioxide in a bound state.

3. Metalloconiosis (beryllium, siderosis, aluminosis, baritosis, stanyosis, pneumoconiosis caused by the dust of rare earth hard and heavy alloys).

4. Carboconiosis (anthracosis, graphitosis, soot pneumoconiosis). These diseases are the result of the inhalation of carbonaceous dust.

5. Pneumoconiosis caused by inhalation of mixed dust containing free silicon dioxide (anthracosilicosis, siderosilicosis, silicosilicatosis), with an insignificant content of it (pneumoconiosis of grinders, electric welders) and not containing silicon dioxide.

6. Pneumoconiosis caused by inhalation of organic dust (cotton, grain, cork, reed pneumoconiosis).

According to international classification ICD-10 diseases distinguish the following types of lung diseases caused by external agents (J60 - J70).

J60. Pneumoconiosis of the coal miner.

Anthracosilicosis.

Anthracosis.

The coalman's lung.

J61. Pneumoconiosis caused by asbestos and other minerals.

Asbestosis.

Excluded: pleural plaque.

J92.0. With asbestosis.

J65. With tuberculosis.

J62. Pneumoconiosis caused by dust containing silicon.

Includes: silicate fibrosis (extensive) of the lung.

J65. Excludes: pneumoconiosis with tuberculosis.

J62.0. Pneumoconiosis due to talc dust.

J62.8. Pneumoconiosis due to other dusts containing silicon.

J63. Pneumoconiosis due to other inorganic dust.

J65. Excluded: with tuberculosis.

J63.0. Aluminosis (lung).

J63.1. Bauxitis fibrosis (lung).

J63.2. Beryllium disease.

J63.3. Graphite fibrosis (lung).

J63.4. Siderosis.

J63.5. Stannosis.

J63.8. Pneumoconiosis due to other specified inorganic dust.

J64. Pneumoconiosis, unspecified.

J65. Excluded: with tuberculosis.

J65. Pneumoconiosis associated with tuberculosis.

Any condition covered by J60 to J64 in combination with tuberculosis classified in A15 to A16.

J66. Respiratory tract disease caused by specific organic dust. J67.1. Excluded: bagassosis.

J67.0. Farmer's lung.

J67. Hypersensitive pneumonitis caused by organic dust.

J68.3. Reactive airway dysfunction syndrome.

J66.0. Byssinosis.

Respiratory tract disease caused by cotton dust.

J66.1. Flax flapper disease.

J66.2. Cannabinosis.

J66.8. Respiratory tract disease due to other specified organic dust.

J67. Hypersensitive pneumonitis caused by organic dust.

Includes: allergic alveolitis and pneumonitis caused by inhalation of organic dust and particles of fungi, actinomycetes or particles of other origin.

J68.0. Excludes: pneumonitis due to inhalation of chemicals, gases, fumes and vapors.

J67.0. Farmer's (agricultural worker's) lung.

Reaper's lung.

Easy mismatch.

Disease caused by moldy hay.

J67.1. Bagassos (from sugar cane dust).

Bogaznaya (th):

pneumonitis.

J67.2. Poultry breeder lung.

A disease, or lung, of a parrot lover.

A disease, or lung, of a pigeon lover.

J67.3. Suberose.

Disease, or lung, of the cork processor.

Disease, or lung, working in the cork industry.

J67.4. Malt's easy.

Alveolitis caused by Aspergillus clavatus.

J67.5. Easy to work with mushrooms.

J67.6. Maple bark gatherer's easy.

Cryptostroma corticale alveolitis.

Cryptostromosis.

J67.7. The lung is in contact with the air conditioner and air humidifiers.

Allergic alveolitis caused by fungal mold, thermophilic actinomycetes and other microorganisms that multiply in ventilation (air conditioning) systems.

J67.8. Hypersensitive pneumonitis caused by other organic dust.

Cheese washer's lung.

Light coffee grinder.

Easy worker of a fish-and-meal enterprise.

Furrier's (furrier's) light.

Easy to work with sequoia.

J67.9. Hypersensitive pneumonitis due to unspecified organic dust.

Alveolitis is allergic.

Hypersensitive pneumonitis.

J68. Respiratory conditions caused by inhalation of chemicals, gases, fumes and vapors.

An additional code is used to identify the reason. external causes(class XX).

J68.0. Bronchitis and pneumonitis caused by chemicals, gases, fumes and vapors. Chemical bronchitis (acute).

J68.1. Acute pulmonary edema caused by chemicals, gases, fumes and vapors.

Chemical pulmonary edema (acute).

J68.2. Inflammation of the upper respiratory tract due to chemicals, gases, fumes and vapors, not elsewhere classified.

J68.3. Other acute and subacute respiratory conditions caused by chemicals, gases, fumes and vapors.

Reactive airway dysfunction syndrome.

J68.4. Chemical respiratory conditions caused by chemicals, gases, fumes and vapors.

Emphysema (diffuse) (chronic).

Obliterating bronchitis (chronic) subacute.

Pulmonary fibrosis (chronic) of fumes and vapors.

J68.8. Other respiratory conditions caused by chemicals, gases, fumes and vapors.

J68.9. Unspecified respiratory conditions due to chemicals, gases, fumes and vapors.

J69. Pneumonitis due to solids and liquids.

P24. Excludes: neonatal aspiration syndrome.

J70. Respiratory conditions caused by other external agents.

An additional external reason code (class XX) is used to identify the cause.

J70.0. Radiation-induced acute pulmonary manifestations.

Radiation pneumonitis.

J70.1. Chronic and other pulmonary manifestations caused by radiation.

Fibrosis of the lung due to radiation.

Therapeutic and preventive measures include high-quality nutrition with a high content of proteins and vitamins, competent organization of recreation, active sports, breathing exercises, smoking cessation, water procedures.

Modern fitness clubs are ready to offer you various types of training, selected specifically for your level of physical fitness or the presence of certain diseases. We recommend the site gogym.ru, where it is very easy to find the fitness clubs closest to your home.

From medications, various adaptogens are used. They have general stimulating properties, increase nonspecific reactions of the body, promote quick recovery damaged organs. Most often, patients are prescribed tincture of Eleutherococcus, pantocrine, nicotinic acid, vitamins of groups B, C and P.

If the patient does not have a pronounced pulmonary insufficiency, he is recommended: potassium chloride, iontophoresis with novocaine and ultrasound to the chest. All these procedures stimulate blood and lymph circulation, significantly improve the ventilation function of the lungs. With the onset and development of bronchitis, the patient is additionally prescribed expectorants and drugs that thin phlegm (marshmallow root, thermopsis, iodine preparations).

Patients with a severe stage of the disease are transferred to inpatient or sanatorium treatment of pneumoconiosis. The most widely used techniques are hyperbaric oxygenation and oxygen inhalation. Bronchodilators and drugs are effective that reduce pressure in the pulmonary circulation (reserpine, papaverine, aminophylline). With decompensation of cor pulmonale, patients are prescribed diuretics and cardiac glycosides. Corticosteroids are also widely used.

The prognosis of treatment and recovery depends on the stage of pneumoconiosis and those complications that often arise during the development of the disease. The prognosis is unfavorable in such forms as silicosis, beryllium and asbestosis, when the progression of the disease continues even after the termination of contact with harmful compounds. The rest of the forms are characterized by a benign course and favorable prognosis.

Prophylaxis

dust pneumoconiosis treatment prophylactic

In recent years, studies have been conducted on the antifibrogenic action of polymeric drugs, the positive effect of which, according to modern concepts, is based on the protection of cell membranes of phagocytes from the toxic action of quartz and the interaction of polymers with silicon dioxide, which, when adsorbed on the polymer, loses its activity. The experiment studied a number of polymer drugs, and, in particular, poly-2-vinyl-pyridine-N-oxide (polyvinoxide), which has a pronounced antifibrogenic effect and prevents the progression of silicosis, and according to some data, and contributes to the reverse development of the process. However, in a clinical trial of the drug, no positive effect was found for the course of the progressive silicotic process. Experimental studies continue in the direction of searching for new polymeric drugs that undergo faster resorption in the body and have fewer side properties.

The currently used means and methods for the prevention and treatment of pneumoconiosis include general strengthening measures aimed at hardening the body and increasing its reactivity, improving functional state bronchopulmonary system, prevention and treatment of heart failure and control of complications.

Among the measures for the medical prevention of pneumoconiosis, the leading role belongs to preliminary and periodic medical examinations of workers. The correct organization of medical examinations using X-ray and functional diagnostic methods that provide early detection of respiratory pathology is of great importance in preventing dust pathology of the respiratory system. When conducting periodic examinations, the selection of workers who need to carry out preventive and therapeutic measures aimed at preventing dust diseases is also carried out, and if the latter are detected, to combat complications that aggravate their course.

Prolonged exposure to industrial dust often leads to the appearance of changes, which are expressed primarily in a decrease in the functional activity of the mucous membrane of the upper respiratory tract and bronchi, as well as in a change in the indicators of the general reactivity of the body. It is known that modern forms of pneumoconiosis and dusty bronchitis develop on average 10 years or more after starting work in the dusty profession, therefore, persons with more than 10 years of work experience, even without special respiratory abnormalities, should be classified as a risk group for the possibility of dust pathology. The same group should include those workers who show individual signs of dust exposure, regarded as suspicion of pneumoconiosis and dust bronchitis, as well as persons suffering from chronic inflammatory diseases of the upper respiratory tract and frequent acute respiratory diseases, predisposing to the development of dust pathology of organs. breathing.

Persons working in underground conditions need to carry out ultraviolet irradiation in the conditions of mine photoaria, which increases the general reactivity of the body and resistance to infectious bronchopulmonary diseases. Irradiation is recommended to be carried out 2 times a year in the autumn-winter and spring periods, in courses of 20 sessions. When determining the dose of ultraviolet radiation, it is necessary to take into account that with an increase in underground experience, miners become more sensitive to ultraviolet rays, therefore, irradiation should be started with minimum doses.

Various adaptogens that have general stimulating properties and increase the non-specific reactivity of the body (tincture of Eleutherococcus, pantocrine, Chinese magnolia vine in conventional doses in courses of 3-4 weeks) can be used quite widely in relation to this group of workers. The use of a complex of various vitamins is also shown.

In addition to physiotherapy exercises, other wellness activities are recommended: massage, health path, walking. Of the means of hardening, it is possible to recommend the use of hydro-procedures, especially therapeutic showers (circular shower, Charcot's shower) with a gradual decrease in the water temperature. Patients with pneumoconiosis without severe pulmonary insufficiency are shown the whole complex of the above preventive measures. In addition, it is additionally advisable to prescribe currents or ultrasound to the chest, stimulating lymph and blood circulation, as well as improving the ventilation function of the lungs. These procedures are carried out in a hospital setting, taking into account contraindications (tuberculosis, hemoptysis, hypertension, etc.). In the presence of viscous sputum, inhalation of proteolytic enzymes (lidase, hyaluronidase, ribonuclease, fibrinolysin, etc.) can also be recommended. The presence of mild signs of impaired bronchial patency (complaints of paroxysmal cough or difficulty breathing, decreased expiratory power according to pneumotachometry data or a one-second forced expiratory volume) is an indication for inhalation of aminophylline, as well as adrenostimulants (ephedrine) or vagoblockers (atropine, possible platyphylline), taking into account side effects of the latter in the form of an increase blood pressure and tachycardia. It is recommended to conduct courses of treatment and prophylactic measures for patients of this group twice a year in a sanatorium or in a hospital.

With rapidly progressing forms of silicosis, the use of glucocorticoid hormones is justified, since they have an anti-inflammatory, antiproliferative, and, according to some reports, an inhibitory effect on the development of silicosis. Hormone therapy for silicosis is carried out in courses of 1-2 months, mainly with prednisolone or urbazone at doses of 20-25 mg per day, followed by a gradual decrease. When prescribing glucocorticoids, prophylactic protection with anti-tuberculosis drugs (tubazide, PASK) is mandatory. The courses can be repeated 1-2 times a year. Instead of hormonal drugs or in addition to them, delagil, plaquinil and other drugs of the quinoline series can be used. In terms of further research, an attempt to use anti-fibrotic agents that have found application in pulmonary practice for the treatment of progressive forms of silicosis is promising. These include D-penicillamine and large immunosuppressants (imuran, cyclophosphamide, etc.). It is possible that in the future, drugs that have an immunostimulating effect will find their place in the treatment of silicosis.

Treatment of patients with pneumoconiosis with pulmonary insufficiency of the II-III degree should be carried out annually in a hospital setting, as well as in sanatoriums-dispensaries and sanatoriums of a specialized pulmonary profile. Pulmonary insufficiency in pneumoconiosis is of a restrictive nature, which is primarily due to a decrease in tidal volumes and impaired gas exchange due to anatomical damage to the alveolar system and vessels of the pulmonary circulation. A certain role is also played by the violation of the drainage function of the bronchi, due to their deformation and obstruction of bronchial secretions. In patients, blood oxygen saturation decreases with normal carbon dioxide tension. At the same time, the pressure in the pulmonary circulation rises and a chronic cor pulmonale is formed. Based on the concepts of the pathogenesis of respiratory and cardiovascular insufficiency: with pneumoconiosis, therapeutic measures it is necessary to focus primarily on improving blood oxygenation, bronchial drainage function and reducing pressure in the pulmonary circulation. In the absence of contraindications, the above treatment complex can be used. It should be borne in mind that the use of the inhalation method of drug administration is very limited in the presence of severe pulmonary insufficiency due to low tidal volumes. It is imperative to prescribe oxygen therapy in the form of oxygen inhalation or, better, hyperbaric oxygenation. Various prescriptions of bronchodilators and drugs that reduce pressure in the pulmonary circulation (aminophylline, papaverine, reserpine, etc.) are recommended. When prescribing reserpine to patients with bronchospastic syndrome, the possible side effect in the form of increased bronchospasm. The most effective intravenous infusion of aminophylline, which has a bronchodilatory effect, reduces the pressure in pulmonary artery, as well as having weak cardiotonic and diuretic properties. In the presence of chronic cor pulmonale in the stage of decompensation, hospital treatment is indicated. In addition to funds aimed at improving the respiratory function of the lungs and reducing pressure in the pulmonary circulation, it is necessary to prescribe cardiac glycosides (korglikon, strophanthin) in combination with panangin, potassium orotate and other potassium-containing drugs that prevent glycoside intoxication, potassium metabolism disorders. Antialdosterone drug veroshpiron, which removes mainly sodium, has a mild diuretic effect. With severe decompensation with peripheral edema, stronger diuretics (furosemide, diacarb, ethacrynic acid, hypothiazide, etc.) are used in short courses. Before prescribing these diuretics, it is necessary to carry out therapy with cardiac glycosides within 3-4 days, since the abundant excretion of fluid from the body increases the load on the heart muscle.

The normalization of metabolic processes in the myocardium is facilitated by the appointment of anabolic hormones (methandrostenolone, phenobolin, retabolil), as well as vitamins of group B. With persistent edematous syndrome, corticosteroid hormones are sometimes effective. In cases where it is necessary to appoint several drugs, including bronchodilators, vasodilators and cardiotonic agents, it is advisable to introduce them by the drip method in saline. In this case, it is recommended to inject small doses of heparin (5000-10,000 U), which has a general resorptive effect and improves coronary blood flow. The anticoagulant properties of the drug in these dosages are insignificant. After the symptoms of decompensation have been removed, the patient can be transferred to the administration of lantoside, digoxin or isolanide in combination with drugs that reduce the pressure in the pulmonary circulation.

Treatment of other complications of silicosis is carried out according to the usual methods and treatment regimens for chronic nonspecific lung diseases, taking into account the activity of bronchopulmonary infection and the severity of bronchospasm.

Conclusion

Pneumoconioses combine a number of diseases caused by the ingress of large amounts of dust particles into the lungs for a long time. These diseases belong to the group of professional processes. They are found in some workers who have been breathing various types of dust for 5-15 years or more. Penetrating small dust particles into the respiratory tract cause a reaction of the interstitial connective tissue, as a result of which pulmonary fibrosis develops and progresses.

Pneumoconiosis cannot be especially treated if the lungs are damaged, they cannot be restored. Therefore, the main way to fight is to prevent the disease, that is, prevention.

The basis for the prevention of pievmoconiosis is primarily technical and sanitary measures to combat dust, detailed in the special literature. They must be combined with medical measures, the first place among which is taken by preliminary (upon admission to work) and periodic medical examinations with the obligatory use of X-ray examination.

Literature

Occupational diseases caused by exposure to industrial dust (pneumoconiosis). URL: http://www.medkurs.ru/sickness_catalog/breath_in/ (date of access: 9.12.2013).

Pneumoconiosis [electronic library]. URL: http://www.eurolab.ua/diseases/1491/ (date of access: 9.12.2013).

Pneumoconiosis [Handbook]. URL: http://zabolevaniya.ru/zab.php?id=14045&act=full (date of access: 12/9/2013).

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TO professional include diseases that develop as a result of exposure to the body of pathogenic factors of the working environment in the conditions of human labor.

Etiology and classification. There is no unified classification of occupational diseases. The most accepted classification is based on etiological principle. Guided by it, there are 5 groups of occupational diseases caused by exposure: 1) chemical production factors; 2) industrial dust; 3) physical factors; 4) overvoltage; 5) biological factors.

Pathogenesis. Among the mechanisms of development of occupational diseases, along with specific, due to the peculiarities of the action of a pathogenic professional factor, there are also nonspecific. In modern conditions, the features of the pathogenesis of occupational diseases can be determined complex exposure to various factors: chemical, dust, vibration, altered microclimatic conditions, etc. It should also be noted that many occupational factors have different long-term effects. About oncogenic effect you can speak with asbestosis, when pleural mesothelioma and lung cancer often occur, with beryllium disease, when lung cancer develops. Long-term exposure to nickel, chromium and zinc can cause in the long term malignant tumor in the place of contact with them and in various organs. Some professional factors have gonadotropic effect, cause atrophy of the testicles and ovaries - nickel, antimony, manganese, electromagnetic waves (EMW) of radio frequencies, ionizing radiation. In the long-term period, many types of occupational factors can have not only gonadotropic, but also mutagenic and embryotropic effects(miscarriages, malformations, etc.).

Occupational diseases caused by exposure to chemical production factors

This group of diseases is wide and varied. It is represented by acute and chronic intoxications, as well as their consequences,

1 Prof. M.S. Tolgskaya and prof. N.N. Shatalov, to whom the authors are very grateful.

proceeding with the defeat of various organs and systems; skin diseases (contact dermatitis, onychia and paronychia, melasma, etc.); foundry or fluoroplastic (Teflon) fever.

Etiology. There are a large number poisonous substances, which are used in industry and can cause poisoning and diseases of an acute and chronic nature. Such substances include lead, tetraethyl lead, manganese, nitrogases, or nitrogen oxides, arsenic and its compounds, arsenous hydrogen, phosphorus and its compounds, hydrocyanic acid, dichloroethane, carbon tetrachloride, benzene. V agriculture insecticides and pesticides are widely used, which can also be sources of intoxication. Organophosphate insecticides (thiophos, etc.) are especially dangerous for humans.

Pathological anatomy. Changes in poisoning with chemical industrial poisons are varied. They are described in detail in textbooks of toxicology, forensic medicine, dermatology. However, it should be noted that each group of chemicals with severe intoxication has its own characteristics in the pathological picture, characteristic only for this intoxication, i.e. under the influence of each group of chemicals, there is its own preferential localization of the process, its own target organs. So, with intoxication with chlorinated hydrocarbons, the liver is mainly affected, with intoxication with substances that have a benzene ring in their structure, the hematopoietic organs, with intoxication with drugs - the nervous system and liver, with intoxication with mercury and its derivatives - the nervous system and kidneys.

Occupational diseases caused by exposure to industrial dust (pneumoconiosis)

Pneumoconiosis(from lat. pneumon- lungs, conia- dust) - dust lung diseases. The term "pneumoconiosis" was proposed in 1867 by Zenker.

Industrial dust called the smallest particles of solid matter formed during the production process, which, entering the air, are in suspension in it for a more or less long time.

Distinguish between inorganic and organic dust. TO inorganic dust include quartz (97-99% composed of free silicon dioxide - SiO 2), silicate, metal, to organic- vegetable (flour, wood, cotton, tobacco, etc.) and animal (woolen, fur, hair, etc.). There are mixed dust, for example, containing in various proportions coal, silica and silicate dust, or iron ore dust, consisting of iron and silica dust. Industrial dust particles are classified into visible (more than 10 microns in diameter), microscopic (from 0.25 to 10 microns) and ultramicroscopic (less than 0.25 microns), detected using an electron microscope.

The greatest danger is posed by particles less than 5 microns in size, penetrating into the deep parts of the pulmonary parenchyma. The shape, consistency of dust particles and their solubility in tissue fluids are of great importance. Dust particles with sharp, serrated edges injure the mucous membrane of the respiratory tract. Fibrous dust particles of animal and plant origin cause chronic rhinitis, laryngitis, tracheitis, bronchitis, pneumonia, pneumonitis. When dust particles dissolve, chemical compounds appear that have an irritating, toxic and histopathogenic effect and have the ability to cause the development of connective tissue in the lungs, i.e. pneumosclerosis.

Classification. Among pneumoconiosis, silicosis, silicatoses, metalloconiosis, carboconiosis, pneumoconiosis from mixed dust, pneumoconiosis from organic dust are distinguished.

Silicosis

Silicosis(from lat. silicium- silicon), or chalicosis(from the Greek. chalix- limestone), caused by prolonged inhalation of dust containing free silicon dioxide - SiO 2 (Fig. 337).

Pathogenesis. Currently, the development of silicosis is associated with chemical, physical and immune processes that occur when a dust particle interacts with tissues. This does not exclude the importance of the mechanical factor.

According to toxic-chemical theory, crystalline silicon dioxide in tissue fluids slowly dissolves to form a colloidal solution of silicic acid (H 2 SiO 3), which damages tissue and causes a fibrotic process. However, this theory cannot be

Rice. 337. Silicosis. Quartz dust particles. Electron diffraction pattern: a - x10,000; b - x20,000

clarify complex mechanism the development of connective tissue in silicosis. Physicochemical theories allow explaining the mechanism of action of quartz particles by a violation of the structure of its crystal lattice, as a result of which favorable conditions are created for an active chemical reaction between a quartz particle and the surrounding tissue. When silica particles dissolve slowly, silicic acid is formed. high degree polymerization, which has toxic properties and causes the development of connective tissue, and this acid, like glycosaminoglycans, takes part in the construction of collagen fibers. According to immunological theory, when exposed to silicon dioxide on tissues and cells, when they disintegrate, autoantigens appear, which leads to autoimmunization. The immune complex arising from the interaction of antigen and antibodies has a pathogenic effect on the connective tissue of the lungs, as a result of which a silicotic nodule is formed. However, no specific antibodies have been found in silicosis.

It has been established that the primary reaction in the pathogenesis of silicosis is damage to pulmonary macrophages by silica dust. The absorbed quartz particles damage the membranes of the phagolysosomes in which they are located, disrupting their permeability. As a result of increased membrane permeability, hydrolytic enzymes of macrophages enter the cytoplasm from phagolysosomes, which leads to autolysis and death of the latter. According to this theory, we are talking about the leading role in the pathogenesis of silicotic fibrosis death of coniophages followed by stimulation of fibroblasts decay products of macrophages.

Pathological anatomy. Atrophy and sclerosis are found in the mucous membrane and in the submucosa of the nasal concha, larynx, trachea. Lungs with silicosis are enlarged in volume, dense due to widespread sclerosis and a sharply increased content of silicon dioxide (in the dry matter of healthy lungs it is 0.04-0.73%, with silicosis - 4.7-12.35%). In the lungs, silicosis manifests itself in two main forms: nodular and diffuse-sclerotic (or interstitial).

At nodular form in the lungs, a significant number of silicotic nodules and nodes are found (Fig. 338), which are miliary and larger sclerotic areas of a round, oval or irregular shape, gray or gray-black in color. In severe silicosis, the nodules merge into large silicotic nodules that occupy most of the lobe or even the whole lobe. In such cases, they talk about tumor-like silicosis of the lungs (Fig. 339). The nodular form occurs when the dust contains high free silicon dioxide and when exposed to dust for a long time.

At diffuse sclerotic form typical silicotic nodules in the lungs are absent or very few, they are often found in bifurcation lymph nodes... This form is observed upon inhalation of industrial dust with a low content of free dioxide.

silicon. In recent years, in connection with the use of various measures for the prevention of silicosis, the diffuse-sclerotic form of silicosis is more common. With this form, numerous thin bands of connective tissue and sclerosis around the bronchi and blood vessels are visible in the lungs. Connective tissue grows in the alveolar septa, peribronchial and perivascular. Widespread emphysema, deformation of the bronchi, narrowing and expansion of their lumen develop (bronchiectasis),various forms bronchiolitis, bronchitis (more often catarrhal-desquamative, less often purulent). Sometimes find mixed form silicosis of the lungs.

Silicotic nodules can be typical and atypical. Structure typical silicotic nodules are twofold: some are formed from concentrically located hyalinized bundles of connective tissue and therefore have a rounded shape, others do not have a round shape and consist of bundles of connective tissue, whirling in different directions (Fig. 340). Atypical silicotic nodules have irregular outlines, they lack concentric and vortex-like arrangement of bundles of connective tissue. All nodules contain many dust particles lying free or in macrophages, which are called dust cells or coniophages(fig. 341).

Silicotic nodules develop into alveolar lumen and alveolar passages, as well as at the site of the lymphatic vessels. Alveolar

Rice. 340. Typical silicotic nodules:

a - a nodule with a concentric arrangement of collagen bundles; b - a knot with a vortex-like arrangement of beams

histiocytes phagocytose dust particles and turn into coniophages. With prolonged and strong dusting, not all dust cells are removed, therefore, their accumulations form in the lumens of the alveoli and alveolar passages. Collagen fibers appear between the cells, cellular fibrous nodule. Gradually, dust cells die, the number of fibers increases - a typical fibrous nodule. Similarly, a silicotic nodule is built at the site of the lymphatic vessel.

With silicosis in the center of large silicotic nodes, connective tissue breaks down to form silicotic caverns. Decay occurs due to changes in the blood vessels and the nervous apparatus of the lungs, as well as as a result of instability of the connective

Rice. 341. Silicosis. Alveolar macrophage (coniophage); conglomerates and individual particles of quartz crystals (Quartz) in the cytoplasm of the macrophage; I am the core; M - mitochondrion; Lz - lysosome. Electronogram. x25,000 (according to Policar)

Noah tissue of silicotic nodules and knots, which differ in biochemical composition from normal connective tissue. Silicotic connective tissue is less resistant to collagenase than normal.

V lymph nodes (bifurcation, basal, less often in peri-tracheal, cervical, supraclavicular) show a lot of silica dust, widespread sclerosis and silicotic nodules. Rarely, silicotic nodules are found in the spleen, liver, bone marrow... The right half of the heart is often hypertrophied, up to the development of a typical pulmonary heart.

Tuberculosis is often associated with silicosis. Then talk about silicotuberculosis, in which, in addition to silicotic nodules and tuberculous changes, the so-called silicotuberculosis foci.

Flow chronic silicosis. It is divided into three stages (silicosis I, II, III). Rarely found "Acute" silicosis, characterized by the development of the disease and the onset of death after a short period of time (1-2 years). This silicosis develops when there is a very high content of free silica in the dust. Late silicosis refers to a disease that occurs in workers a few years after they leave the profession associated with exposure to dust.

Silicatoses

Silicatoses- pneumoconiosis caused by dust, which does not contain free silicon dioxide, but silicates (in them it is in a bound state with other elements - magnesium, aluminum, iron, etc.). Silicates are widespread in nature and have a variety of industrial applications.

Among silicatoses, asbestosis, talcosis, kaolinosis, cementosis, mica pneumoconiosis, etc. are distinguished. Highest value have asbestosis, talc and mica pneumoconiosis.

Asbestosis

Asbestosis- pneumoconiosis, which develops upon prolonged contact with asbestos dust. The course of the disease is chronic with progressive shortness of breath, cough, pulmonary heart failure.

Asbestos (mountain flax) is a mineral of fibrous structure. In terms of chemical composition, it is hydrous magnesium silicate (3Mgx2SiO 2x2H2O). Asbestos fibers have a length of 2-5 and even 125-150 microns, their thickness is 10-60 microns. Asbestos is widely used in industry.

Pathological anatomy. At autopsy, a permanent finding is catarrhal-desquamative, less often purulent bronchitis, broncho- and bronchioectasis with hyperplasia of the mucous glands, dystrophic changes in cartilage and their calcification. The defeat of the bronchi in asbestosis, apparently, is associated with the form of asbestos particles, long sharp dust grains of which, getting stuck in the lumen of the bronchi and bronchioles, constantly

injure and irritate their mucous membrane. In the chest cavity, common pleural adhesions, pleura is considerably thickened. Lungs are compacted due to the proliferation of connective tissue in the interalveolar septa, between the lobules, around the bronchi and blood vessels. Unlike silicosis, asbestosis does not produce well-defined sclerotic nodules and nodules. In the overgrown connective tissue, significant accumulations of dust and small infiltrates from histiocytes, lymphoid cells are found. The presence of asbestos bodies, representing light or dark yellow formations 15-150 nm long, 1-5 nm thick, with clavate ends, as if consisting of separate segments; their shape and size are different (Fig. 342). In severe cases, interstitial sclerosis reaches a sharp degree, the lumens of the alveoli become barely visible or they are completely invisible.

The lymph nodes tracheal bifurcations, basal slightly enlarged, dense, they contain a lot of dust. Hyperplasia of cells of the reticuloendothelium, focal or diffuse sclerosis, but without the development of nodules is noted. On the fingers and toes, palms, soles, less often on the shins, so-called asbestos warts, characterized by severe hyperkeratosis and acanthosis. In the horny masses of warts, fibers are found - asbestos crystals; in the prickly and basal layers, cells with division figures and giant multinucleated cells are found foreign bodies.

Death with asbestosis occurs from associated pneumonia, pulmonary heart disease due to emphysema and tuberculosis. When asbestosis is combined with tuberculosis, they talk about asbestos-tuberculosis. Deaths from asbestosis often have mesothelioma and lungs' cancer.

Rice. 342. Asbestos bodies in the lung: a, b - various forms of bodies

Talc

Talc- pneumoconiosis caused by talc. The course of the disease is chronic.

Talc is a magnesian silicate (3MgOх4SiO 2 xH 2 O) containing 29.8-63.5% silicon dioxide; does not dissolve in water. Talc is used in rubber, ceramic, paper, textile, perfumery, paint and varnish industries.

Pathological anatomy. The deceased are found to have widespread pleural adhesions. V lungs find diffuse interstitial sclerosis with thickening of interalveolar septa, peribronchial and perivascular sclerosis, talcum dust deposits located in dust cells and outside them. The overgrown connective tissue looks like thick strands, in which the lumens of compressed alveoli are barely visible. There are miliary or larger sclerotic areas that do not resemble typical silicotic nodules. Sometimes the so-called talc bodies(fig. 343). Bronchiectasis, pulmonary emphysema are constantly found.

In bifurcation and root lymph nodes find a large amount of talcum dust and severe sclerosis. Often, tuberculosis joins talcosis, there is talcotuberculosis.

Talc used for dusting surgical rubber gloves can get into abdominal cavity on the wound surface, peritoneum and cause inflammation with the subsequent formation of adhesions and nodules - granulomas. In such cases, they talk about surgical talcosis. Granulomas microscopically resemble tuberculous, but giant cells have the character of foreign body cells. Between the granuloma cells and in the giant cells, talcum dust particles are visible in the form of needle crystals and plates, which also distinguishes these granulomas from tuberculous ones.

Rice. 343. Talcous body. Electronogram

Mica pneumoconiosis

Mica pneumoconiosis- pneumoconiosis from mica dust - is rare, has a chronic, relatively benign course.

Mica is a mineral, aluminosilicate containing water. The main representatives of mica are muscovite, biotite, phlogonite. The content of bound silicon dioxide, aluminum and other compounds in different micas is not the same.

Pathological anatomy. As a rule, they find a catarrhal-desquamative bronchitis, mild bronchiectasis, moderate emphysema. V lungs find widespread interstitial sclerosis, and the development of connective tissue is noted in the interalveolar septa, around the bronchi and blood vessels, mica dust and "mica bodies", similar to asbestos. In the lymph nodes, dust deposits, sclerosis are found.

Metalloconioses

Among metalloconiosis, siderosis, aluminosis, beryllium disease, titanosis, baritosis, stanyosis, etc. are distinguished. siderosis, aluminosis and beryllium disease.

Siderosis

Siderosis (pneumoconiosis siderotica)- pneumoconiosis, which occurs in miners who extract hematite (red iron ore, natural iron oxide Fe 2 O 3), in foundry workers, polishers of metal products, nail workers, engravers, electric welders.

Pathogenesis. It was believed that lung fibrosis is caused not by iron dust, but by an admixture of silicon dioxide, therefore such cases were considered as silicosiderosis. Currently, the harmlessness of iron-containing dust is denied, since it causes pulmonary fibrosis. However, this fibrosis is weaker than in silicosis and silicosis, which leads to a long and benign course of the pulmonary process. Apparently, the benign course of pneumosclerosis in siderosis is due to the fact that iron dust is non-toxic and is well excreted by macrophages through the bronchial tree.

Pathological anatomy. Distinguish between red and black siderosis. Red siderosis caused by dust containing iron oxides. At the same time, the lungs are enlarged in volume, yellowish-brownish-red in color. Black siderosis arises from dust with ferrous oxide or carbonic and phosphate compounds. The lungs turn black and resemble anthracosis lungs.

At find mild interstitial sclerosis, submiliary and miliary nodules(Fig. 344), consisting of clusters of dust cells filled with particles of iron dust (the reaction to iron is positive). Few collagen fibers are found between dust cells. V lymph nodes find a lot of dust and significant diffuse sclerosis.

Rice. 344. Lung siderosis:

a - submiliary nodules; b - miliary nodules

Aluminosis

Aluminosis("Aluminum lungs") - pneumoconiosis, which develops as a result of inhalation of vapors and dust of metallic aluminum and its compounds.

Aluminum is used to obtain alloys - aluminum bronze, brass, duralumin - for aircraft construction, the manufacture of various products, dishes, pyrotechnic powder and powder for dyes. Aluminum alum is used in the textile industry.

Severe aluminosis occurs in workers involved in spraying aluminum dye, making pyrotechnic aluminum powder, obtaining aluminum from bauxite by electrolysis, in the production of artificial abrasives. In some patients, the disease proceeds very quickly and severe changes in the lungs develop after 1-2 years of work at the enterprise.

Pathological anatomy. V lungs reveal a widespread interstitial sclerosis with the proliferation of connective tissue in the interalveolar septa, around the bronchi and blood vessels with the formation of sclerosis areas of various sizes. There are few cells in the connective tissue, only in places infiltrates from lymphoid and plasma cells are visible. The lumens of the preserved alveoli are filled with dust cells containing aluminum particles. Frequent bronchiectasis changes, focal emphysema, especially around the edges of the lungs. The lymph nodes bifurcations of the trachea are moderately enlarged, dense, gray-black, with bands of connective tissue of gray-white color. Heart enlarged, the wall of the right ventricle is hypertrophied.

Beryllium

Beryllium lung disease- pneumoconiosis caused by dust or vapors of metallic beryllium (Be) and its compounds - oxide (BeO), beryllium fluoride (BeF 2), etc., which are highly toxic.

Beryllium is more common among workers in the production of beryllium from ore or its alloys. Alloys of beryllium with magnesium, copper, and aluminum are used for the manufacture of particularly hard parts that do not spark during friction; therefore, beryllium is widely used in instrument making and aviation technology. Beryllium serves as a source of neutrons, which it emits under the influence of α-particles and γ-rays.

Pathogenesis. The action of beryllium on the body is based on a change in protein metabolism, leading to the development of an autoimmune process. Sensitization of the body with beryllium compounds with haptenic properties plays a significant role in the pathogenesis of the disease, which explains the development of granulomatosis.

Pathological anatomy. There are two forms of beryllium disease - acute and chronic.

At acute form find pneumonia with exudate containing many cells of the alveolar epithelium, lymphoid and plasma cells, neutrophils and erythrocytes. In later phases, miliary nodules appear in the interalveolar septa and alveoli - beryllium granulomas. In the early stages, granulomas consist of histiocytes, epithelioid cells, a small number of lymphoid, plasma and giant cells of the Langhans type or cells of foreign bodies; in the later stages, argyrophilic and collagen fibers appear in the granulomas and the nodule turns into a sclerotic one.

In granulomas, there are formations that give a positive reaction to iron, the so-called conchoidal (shell-shaped) bodies(Fig. 345) with a diameter of up to 100 microns.

At chronic form beryllium infection is observed interstitial sclerosis of the lungs, the development of miliary granulomas (chronic beryllium granulomatosis). Sometimes there are many granulomas (miliary beryllium disease), they merge with each other, forming nodules of a grayish-white color, up to 2 mm in diameter and larger ones up to 1.5 cm. Nodules are found in the lumens of the alveoli, alveolar passages, in the bronchioles and small bronchi, which leads to obliterating bronchiolitis.

The lymph nodes bifurcations of the trachea and gate of the lungs, cervical are white-gray, yellowish or black with characteristic granulomas, but without necrosis and lime deposits. Granulomas are found in liver and spleen. When beryllium particles enter through damaged skin, they appear in the subcutaneous tissue, where tuberculosis-like tubercles are formed, since necrosis can be observed in their center.

Carboconiosis

Anthracosis and graphitosis are most common among carboconiosis. We will focus only on anthracose.

Anthracosis

Anthracosis- pneumoconiosis, which develops with prolonged inhalation of coal dust. Carbon pigment causes the development of sclerosis, the degree of which depends on the nature of the coal and the composition of the rock in which the coal seams lie. So, inhalation of anthracite dust leads to the development of more pronounced sclerosis of the lungs than the action of bituminous coal dust. Charcoal dust almost does not cause sclerosis.

According to a number of researchers, pulmonary sclerosis in anthracosis is largely or even entirely associated with the action of silicon dioxide, contained in varying amounts in coal seams, and coal dust itself does not have a sclerosing property. Domestic researchers believe that coal dust leads to the development of sclerosis, but much less pronounced than quartz dust.

As a rule, pure anthracosis flows longer and more benign than silicosis, because coal dust is well excreted by macrophages through the bronchial tree and lymphatic drainage of the lungs. Sclerosis is more pronounced if the dust contains a significant admixture of silicon dioxide. In such cases, we are talking about mixed pneumoconiosis - anthracosilicosis or silicoantracosis.

Pathological anatomy. Sclerosis in anthracosis is characterized by the development of connective tissue in places of coal dust deposits - interalveolar septa, around the vessels and bronchi. Dust is located in numerous dust cells (Fig. 346) and outside them. With anthracosis, areas of newly formed connective tissue with dust cells are called anthracotic foci. When small anthracotic foci merge, large anthracotic nodes.

Rice. 346. Anthracosis. Alveolar macrophage. Phagocytosed particles of coal (U) in the cytoplasm; expansion of the tubules of the endoplasmic reticulum (ES). I am the nucleus of a macrophage. х14,000 (according to Policar)

At diffuse anthracotic pneumosclerosis significant areas of the lungs are airless, dense, gray-black, slate, and therefore the changes are called slate, or anthracotic, induration of the lungs.

With anthracosis, chronic bronchitis and recurrent focal pneumonia develop. Emphysema is usually pronounced. Due to circulatory disorders and direct exposure to a significant amount of coal dust, lung tissue can undergo necrosis and softening with the formation of cavities of an irregular or round shape, with crumbling black walls and tiny black contents. These forms of anthracosis, accompanied by hemoptysis and resembling pulmonary tuberculosis, are called black consumption.

The lymph nodes with a sharp anthracosis, they are soldered to the wall of the trachea or bronchi, while a breakthrough of coal masses into the lumen of the bronchial tree is possible, followed by aspiration into the lungs and the development of pneumonia, abscess and gangrene of the lungs. With significant pneumosclerosis and pulmonary emphysema, there is hypertrophy of the right heart.

Pneumoconiosis from mixed dust

This group includes anthracosilicosis, siderosilicosis, siderosilicosis, pneumoconiosis of electric welders and etc.

The most important among them is anthracosilicosis, or silicoanthracosis (see. Anthracosis).

Pneumoconiosis from organic dust

Among organic dust, the importance of various bacteria and fungi (especially the spores of thermophilic actinomycetes), dust containing antigens of animal and plant origin, medications. Pneumoconiosis occurs in people employed in agriculture ("farmer's lung"), poultry ("poultry farmer's lung"), animal husbandry, as well as cotton processing, textile (byssinosis - from the Greek. byssos- flax) and the pharmaceutical industry.

Pathogenesis. In the development of bronchial and pulmonary changes in pneumoconiosis from organic dust, allergic and immunopathological processes are of great importance. These are atopic reactions and reactions of immediate anaphylaxis, characteristic of bronchial asthma, as well as immunocomplex reactions with damage to the microvasculature of the lungs and the development of pneumonitis.

Pathological anatomy. Farmer's lung, like the poultry farmer's lung, is based on the morphology exogenous allergic alveolitis(see chapter Interstitial diseases lungs). Byssinosis is characterized by chronic obstructive bronchitis and bronchial asthma(cm. Chronic nonspecific lung disease).

Occupational diseases caused by physical factors

Among these diseases, the greatest clinical interest are: decompression sickness, diseases due to exposure to industrial noise (noise sickness), vibrations (vibration sickness), sickness due to exposure to electromagnetic waves of radio frequencies, as well as ionizing radiation (radiation sickness).

Decompression sickness

Decompression sickness occurs during a rapid transition from high blood pressure to normal. It is found in workers in caissons during the construction of bridges, dams, docks, tunnels, etc. Under the influence of increased pressure in the caisson, the nitrogen of the inhaled air is excessively absorbed by tissues and blood. With a rapid transition to an atmosphere with normal pressure (decompression), nitrogen released from tissues does not have time to be released through the lungs and accumulates in tissues, blood and lymphatic vessels in the form of bubbles that clog the lumen of blood vessels (decompression sickness). This causes disorders of blood circulation and tissue nutrition. Death can occur immediately, several hours or several (1-20) days after leaving the caisson chamber.

Pathological anatomy. At rapid onset of death severe rigor mortis is often noted. When pressing on the skin, crepitus is observed due to the accumulation of gas in the subcutaneous tissue and the development of emphysema, sometimes covering the face. In places

the skin, as a result of the uneven distribution of blood in the vessels, has a marbled appearance. Due to the resulting asphyxia, the blood of most of the deceased remains liquid. Crepitation is found in many organs. At microscopic examination gas bubbles are found in the dilated cavities of the right heart and coronary vessels, the inferior vena cava, the vessels of the lungs, brain and spinal cord, their membranes, the vessels of the liver, spleen, and small intestine. They are clearly visible in large blood vessels, especially veins: the blood in the vessels takes on a foamy appearance. Severe tissue and organ anemia is noted. V lungs find edema, hemorrhages, interstitial emphysema. Cavities hearts slightly expanded. V liver the phenomena of fatty degeneration are observed. In the head and spinal cord disorders of blood and lymph circulation lead to dystrophic changes in nerve cells and the appearance of ischemic foci of softening of the brain tissue, followed by the development of cysts in these areas. Purulent cystitis and ascending purulent pyelonephritis can be a consequence of changes in the spinal cord, paresis of the pelvic organs.

At long-term exposure high atmospheric pressure due to circulatory disorders occurring in the long bones, mainly lower limbs, find foci of rarefaction surrounded by a zone of sclerosis, as well as foci of aseptic necrosis of bone tissue, sometimes with secondary osteomyelitis. In the joints, cartilage atrophy occurs with the development of deforming osteoarthritis, arthritis.

Diseases due to occupational noise (noise sickness)

Under the influence of industrial noise, workers in a number of professions (boiler makers, riveters, etc.) develop persistent morphological changes in the organ of hearing. They are the basis of the so-called noise sickness.

Pathological anatomy. In the peripheral part of the cochlear nerve (n. cochlear s) dystrophic changes are noted, similar to those observed when exposed to various toxic substances... Changes are found in the nerve cells of the spiral node, as well as in the myelin nerve fibers, which are the peripheral processes of the bipolar cells of the spiral node, heading to the organ of Corti.

With a strong degree of deafness, there is atrophy of the spiral (Corti's) organ in all the curls of the snail; in its place, a flat cord of cubic cells appears, with which the vestibular membrane merges. The preserved nerve fibers are found in the upper curls of the cochlea, partially or completely atrophied in the middle and main curls. In this regard, atrophic changes occur in the spiral node, where only individual nerve cells are preserved. Changes in the auditory nerve and the terminal apparatus of the vestibular nerve

may be absent. Stiffness occurs in the joints of the auditory ossicles. Under the action of super-powerful noises and sounds, damage and death of the organ of Corti, rupture of the tympanic membranes, accompanied by bleeding from the ears, occur.

Vibration Disease (Vibration Disease)

Vibration sickness found in workers dealing with vibration technology. It includes pneumatic hammers for drilling and breaking ore and coal, for minting and cutting off metal products, as well as installations for grinding and polishing metal and wood products, installations for compacting concrete, asphalt pavement of roads, for driving piles, etc.

Vibration sickness is based on a peculiar vibrational angiotrophoneurosis, one of the main symptoms of which is a spasm of not only small, but also larger blood vessels. In addition to vasospasm, their atony is sometimes observed.

Pathological anatomy. Based on the study of biopsies taken from persons working with riveting hammers, it was found that due to spasm in the vessels, changes of the type appear. obliterating endarteritis(fig. 347). Due to the presence of vascular changes, trophic changes appear in the skin and nails, gangrene of the fingers and feet develops. Prolonged pressure on the muscles of the instruments, changes in the spinal cord and in the corresponding peripheral nerves lead to atrophy of the muscles of the forearm, suprascapular region, deltoid and rhomboid muscles. In the osteoarticular apparatus - elbow and shoulder joints, the bones of the hand - they reveal damage to the tendons, muscles,

Rice. 347. Vibration disease. Vascular changes such as obliterating endarteritis

joint capsules, cartilage, articular ends and adjacent areas of bones with deposition of calcium salts in the tendons and the formation of bone tissue. In the bones, there are cystic foci of rarefaction, foci of sclerosis, also with the deposition of calcium salts in them. They are more often located in the heads of the bones of the wrist and in the distal epiphyses of the radius and ulna. In the bones of the wrist, foci of sclerosis and cysts are more often localized in the lunate, capitate and scaphoid bones. In the presence of cysts, a pathological bone fracture can occur. Development of deforming arthrosis is possible.

Osteoarticular changes are caused by a violation of the dispersion of tissue colloids, i.e. a change in the physicochemical properties of tissues, as a result of which bone tissue loses its ability to bind calcium salts.

Diseases due to exposure to radio frequency electromagnetic waves

Over the past decades, various ranges of electromagnetic radio frequencies (EMW) have been widely used in many industries. They occupy a section of the electromagnetic spectrum with a wavelength from several millimeters to tens of thousands of meters. The higher the vibration frequency, the shorter the wavelength. Therefore, the terms "ultra-short waves" (VHF) and "ultra-high-frequency waves" (UHF) are interchangeable. The shortest-wave part of the electromagnetic spectrum is made up of ultra-high-frequency waves (UHF), which are also called microwaves (MW) and cover the range from 1 mm to 1 m.VHF - UHF, which have a wavelength of 1 to 10 m, are directly adjacent to it, and then follow KB - HF, which have a wavelength of 10 to 1000 m and more.

MKV, VHF and KB have found wide application in the field of radar, radio navigation, radio astronomy, radio meteorology, radio line communications, broadcasting, television and physiotherapy. The widespread use in many industries of various radio frequency ranges requires the study of their biological effect on the body. There are no acute deaths among people exposed to electromagnetic waves of radio frequencies; therefore, only changes in the organs of animals under the action of EME of high intensity are described.

Pathological anatomy. At fatal as a result of exposure to EME, overheating phenomena are characteristic. At autopsy, they find a sharp rigor mortis, plethora of the brain and all internal organs, numerous hemorrhages in the brain, serous membranes and internal organs... The myocardium has a boiled look. Microscopic examination in the myocardium revealed coagulation necrosis of muscle fibers, in the liver - small-droplet fatty degeneration of hepatocytes, in the kidneys - protein degeneration of the epithelium of the convoluted tubules. Sometimes there are foci of necrosis in the liver and kidneys. In the testes, necrosis of the germinal epithelium is observed, in the ovaries - the death of primordial follicles.

fishing, in nervous system- a sharp vacuolization of the cytoplasm and lysis of neurons predominantly of the vegetative sections (thalamo-hypothalamic region and autonomic centers of the medulla oblongata).

Chronic exposure low intensity EME of radio frequencies of various ranges, which is found in industry, causes dysfunctions of the nervous, cardiovascular systems and gonads. The most dramatic morphological changes are found in the nervous system, especially in its thin formations - synapses and sensitive nerve fibers of the receptor zones of the skin and internal organs. Significant changes are detected in the hypothalamic region, where the neurosecretory function of neurons is impaired, which is accompanied by a persistent drop in blood pressure. Fatty degeneration of muscle fibers is found in the myocardium. Dystrophy and necrosis of the germinal epithelium occur in the testes. Changes in other internal organs are minimal. The same directionality of the main morphological changes remains for the entire range of radio waves. However, the severity of the pathological process decreases as the EMW of radio frequencies lengthens.

Illness due to exposure to ionizing radiation (radiation sickness)

At present, the use of ionizing radiation has become widespread. In this regard, the contingent of persons who have contact with various sources of radiation has significantly expanded.

Sources of ionizing radiation can be nuclear power plants and reactors, nuclear engines on ships and submarines, X-ray and γ-installations in medical institutions, radioactive isotopes used in scientific research, industry, agriculture and medicine. In addition, humans have to deal with radiation in space. When the body is exposed to ionizing radiation, it is possible to develop clinical syndrome defined as radiation sickness.

The severity of the biological effect of ionizing radiation largely depends on: a) the depth of penetration of radiation; b) ionization density, which is understood as the number of ions formed per unit path of particles. The penetration depth and ionization density are different for different types of radiation. γ-rays, X-rays and neutrons have the highest penetrating power, α- and β-rays at high density are characterized by low penetrating power. Cosmic rays (heavy particles) are very penetrating. The biological effect of ionizing radiation can occur under the influence of external sources of radiation (γ-rays, X-rays, neutrons, cosmic rays), as well as as a result of internal radiation when radioactive substances enter the body. The severity of the biological

the effect of ionizing radiation during internal irradiation depends on: 1) the nature of the distribution of the radioactive substance in the body; 2) ways and speed of its removal; 3) the period of radioactive decay.

Biological action ionizing radiation is determined by some features of the primary interaction of radiation energy and the reaction of body tissues. The starting point is the effect of ionization and excitation of atoms in the structures of organs and tissues of the body. Following the primary physical effect of irradiation, intense radiochemical transformations occur in the environment, which characterize the second phase of the processes developing during irradiation: these phenomena are a general biological form of reactions inherent in various organs and systems. During irradiation, great importance is attached to the ionization of water, which is rich in all living tissues, which leads to the formation of products unusual for them in the tissues of the body in the form of active radicals and strong oxidants. The duration of the existence of free radicals in tissues is very short (calculated in thousandths of a second), but a chain reaction in tissues has already begun. It has been established that elementary biochemical processes are disturbed during irradiation. There are changes in the dispersity and viscosity of colloidal solutions (hyaluronidase - hyaluronic acid system). At higher doses, denaturation of proteins is observed, at lower doses, shifts in a number of enzyme systems are revealed. The activity of enzymes that regulate the exchange of nucleic acids, proteins and carbohydrates, the synthesis of saturated and unsaturated fatty acids in the bone marrow are disrupted. There is evidence that the products of water radiolysis convert active sulfhydryl groups of enzymes into inactive disulfide groups. Changes are also observed in other enzyme systems of cells that play an important role in their life. Inactivation of enzyme systems also leads to the cessation of mitotic cell division. Consequently, regeneration processes are disrupted.

Suppression of mitotic activity can be considered as one of the specific manifestations of the biological effect of ionizing radiation, therefore, organs are more vulnerable, the renewal of their structures under conditions of physiological and reparative regeneration occurs due to cellular regeneration. This includes the hematopoietic organs, sex glands, skin and epithelium of the digestive tract. The severity of the biological effect of ionizing radiation depends on their dose. Light forms radiation sickness is observed with general X-ray irradiation at a dose of 258x10 -4 -516x10 -4 C / kg 1 (100-200 R), medium - at a dose of 516x10 -4 x10 -4 -774x10 -4 C / kg (200-300 R) , severe - at a dose of 774x10 -4 -1290x10 -4 C / kg (300-500 R), lethal - at a dose of 1290x10 -4 C / kg (500 R) and above.

1 According to the SI system, the unit of the exposure dose of radiation (X-ray and γ-radiation) instead of X-ray is the coulomb per kilogram (C / kg) ■ 1 P = 2.58 ■ 10 -4 C / kg.

Classification. Distinguish between acute and chronic radiation sickness. The picture of radiation sickness manifests itself most typically in cases of its acute course. Chronic forms are very diverse.

Acute radiation sickness. The literature describes cases of radiation sickness with total massive exposure to X-rays with therapeutic purpose... Mass cases of acute radiation sickness were recorded during the explosions of atomic bombs in Hiroshima and Nagasaki in 1945.

Pathological anatomy. In acute radiation sickness, the main changes are observed in the hematopoietic system. In the bone marrow, there is a rapidly progressive devastation and at the height of the disease there is almost no normal hematopoietic tissue (panmyeloftiz). Only a small number of highly resistant reticular cells remain. Anemia, leukopenia, thrombocytopenia occur. In the lymph nodes, spleen and the lymphatic apparatus of the gastrointestinal tract, the disintegration of lymphocytes and the suppression of their neoplasm are noted. With the predominance of changes in hematopoiesis, they talk about bone marrow form radiation sickness.

Along with changes in the hematopoietic system, acute radiation sickness is characterized by circulatory disorders and hemorrhagic syndrome. The appearance of hemorrhages is associated with deep structural changes in the walls of the vessels of the microvasculature, a sharp increase in their permeability, as well as thrombocytopenia. Circulatory disorders, hemorrhages, edema can be found in various organs and tissues. They can prevail in the brain, which is typical for nervous (cerebral) form acute radiation sickness. Hemorrhages can be pronounced in the gastrointestinal tract. In this regard, necrosis and ulceration of the mucous membrane occur in it. Ulcerative necrotic processes in the digestive tract, especially in the small intestine, are also due to death integumentary epithelium its mucous membrane, which, as already noted, is highly sensitive to the action of ionizing radiation. When these changes dominate, talk about intestinal form acute radiation sickness.

Due to the multiplicity of hemorrhages, and most importantly, with a decrease in natural immunity in relation to its own microflora inhabiting the oral cavity and intestines, there are autoinfectious processes: putrid or gangrenous stomatitis, glossitis, tonsillitis and enterocolitis. Toxemia often develops, which underlies toxemic (toxic) form acute radiation sickness.

Inflammatory process in acute radiation sickness has some features. Despite the presence of necrosis with numerous colonies of microbes, the leukocyte reaction is completely absent in the underlying living tissues and no granulation tissue is formed.

V skin with irradiation, erythema and blisters are observed, turning into long-term non-healing ulcers, also without the participation of neutrophils. Hair loss (epilation), up to complete baldness, is very typical.

When irradiated from long distances, hyperpigmentation can develop on the skin, and when irradiated from a short distance, depigmentation can develop. V lungs hemorrhages, necrotic and autoinfectious processes are found. The so-called aleukocytic pneumonia. Serous-fibrinous-hemorrhagic exudate appears in the alveoli of the lungs, massive necrosis and significant microbism develop, but there is no leukocyte reaction. The endocrine glands are especially hard to damage sex glands and pituitary. In the testes, the germinal epithelium is affected, in the ovaries, the eggs. In men, spermatogenesis is suppressed, against the background of which giant cells appear in the testes as a manifestation of impaired regeneration. Sterilization sets in, which lasts for many years. The so-called castrate cells appear in the anterior lobe of the pituitary gland. These are vacuolated basophilic cells, apparently related to the gonadotropic cells of the pituitary gland. The appearance of castrate cells, apparently, is associated with damage to the gonads during radiation sickness.

Causes of death patients with acute radiation sickness: shock (at high doses), anemia (due to suppression of hematopoiesis), hemorrhages in vital organs, internal bleeding, infectious complications.

Chronic radiation sickness. Chronic radiation sickness can develop as a result of an acute injury, which has left persistent changes in the body, excluding the possibility of complete regeneration of the hematopoietic organs, or with repeated exposure to radiation in low doses.

Depending on the depth of the lesion of the hematopoietic system, varying degrees chronic radiation sickness.

Pathological anatomy. The manifestations of chronic radiation sickness are varied. In some cases, there are aplastic anemia and leukopenia, due to the extinction of regeneration processes in the bone marrow with a weakening of immunity, the addition of infectious complications and hemorrhages. In other cases, they develop leukemia. Their occurrence is associated with the perversion of the regeneration process in the hematopoietic tissue, while the proliferation of undifferentiated cells of the hematopoietic tissues with the absence of their differentiation and maturation is noted. Chronic radiation sickness can lead to the development tumors.

So, after prolonged exposure to X-rays, skin cancer is often observed. The experiment showed that the strontium radioisotope, which is selectively deposited in the bones and stored there for a long time, can lead to the development osteosarcoma. A single irradiation of animals with γ-rays after 10-12 months can lead to the formation of tumors in various organs.

Occupational diseases caused by overvoltage

Stress disorders affect a wide variety of professions. They can be conditionally divided into 4 groups: 1) diseases of peripheral nerves and muscles; 2) diseases of the musculoskeletal system; 3) diseases of the veins of the lower extremities; 4) diseases of the vocal apparatus.

Diseases first group represented by neuritis, cervicobrachial plexitis, cervicothoracic and lumbosacral radiculitis, myositis, myofascitis and neuromyofasciitis of the hands. Second group are tenosynovitis, styloiditis, "carpal tunnel syndrome" and "snap finger syndrome", chronic arthritis and arthrosis, osteochondrosis of various parts of the spine, etc. Third group diseases of occupational overvoltage are varicose veins and thrombophlebitis of the lower extremities. Fourth group represented by chronic laryngitis, nodules of the vocal cords ("singer's nodules"), contact ulcers of these ligaments.

Occupational diseases caused by exposure to biological factors

Dust occupational diseases of the lungs are one of the most severe and widespread types of occupational diseases in the world, the fight against which is of great social importance.

The main occupational dust diseases are pneumoconiosis, chronic bronchitis, and upper respiratory tract diseases.

Neoplasms of the respiratory system are among the extremely rare dust diseases.

Pneumoconiosis- chronic occupational dust lung disease, characterized by the development of fibrotic changes as a result of prolonged inhalation action of fibrogenic industrial aerosols.

In accordance with the classification adopted in the USSR in 1976, the following types of pneumoconiosis were identified according to the etiological principle.

1. Silicosis - pneumoconiosis caused by inhalation of silica dust containing free silicon dioxide, ie, silica and its crystalline modifications: quartz, cristobalite, tridymite. The most common is the crystalline variety of silica - quartz, containing 97 - 99% free SiO 2. The effect of quartz-containing dust on the body is associated with the extraction of minerals, since about 60% of all rocks are composed of silica.

2. Silicatosis - pneumoconiosis arising from the inhalation of dust of minerals containing silicon dioxide in a bound state with various elements: aluminum, magnesium, iron, calcium, etc. (kaolinosis, asbestosis, talcosis; cement, mica, nopheline pneumoconiosis, etc.).

3. Metalloconiosis - pneumoconiosis from exposure to metal dust: iron, aluminum, barium, tin, manganese, etc. (siderosis, aluminosis, baritosis, stanyosis, manganoconiosis, etc.).

4. Pneumoconiosis from mixed dust: a) with a significant content of free silicon dioxide - more than 10%; b) not containing free silicon dioxide or with its content up to 10%.

5. Pneumoconiosis from organic dust: vegetable - byssinosis (from cotton and flax dust), bagasse (from sugarcane dust), farm lung (from agricultural dust containing fungi), synthetic (plastic dust), as well as from exposure to soot - industrial carbon.

Silicosis- the most severe form of pneumoconiosis. This form of pneumoconiosis is the most common among coal miners, it is also found among workers in the mining industry, especially among drillers, woodcutters. Known diseases of silicosis in ceramic, pottery, mica industries, when grinding on sandstone stones and other works associated with the formation of dust containing crystalline silicon dioxide.

Silicosis develops in different periods of work under dusty conditions. The prevalence, rate of development of the disease and the degree of its severity depend on working conditions, dispersion, concentration of quartz dust.

The severity of silicosis increases with an increase in the content of free SiO 2 in the dust. At old enterprises with a high dust content, silicosis among miners developed with an experience of 3 - 10 years, among molding cutters - 1 - 4 years, among porcelain workers - 10 - 30 years. At present, such conditions practically do not occur and cases of silicosis are found mainly only in persons with long experience who have previously been exposed to high concentrations of dust.

For the pneumoconiotic process in silicosis, the development of nodular fibrosis is characteristic, as well as the growth of fibrous tissue along the bronchi, blood vessels, near the alveoli and lobules. Pathological phenomena, as a rule, grow slowly, clinical symptoms do not always correspond to the severity of the pulmonary fibrotic process, therefore, X-ray data are of primary importance for the diagnosis and determination of the stage of the disease. There are interstitial, diffuse sclerotic, nodular or mixed forms of fibrosis. Depending on the clinical course, the nature and severity of changes in the lung tissue distinguish 3 degrees of the disease.

Silicosis is a general disease of the body, in which, along with impaired respiratory function (subjectively - shortness of breath, cough, chest pain), the development of emphysema, chronic bronchitis, pulmonary heart disease is observed. Changes in immunological reactivity, metabolic processes, disturbances in the activity of the central and autonomic nervous systems are recorded.

With the development of the silicotic process, asthmoid bronchitis, bronchiectasis occur, and the most common complication is tuberculosis. A characteristic feature of silicosis is that it progresses even after stopping work in the dusty profession.

Silicatose. Specific fibrosclerotic lung diseases develop from inhalation of dust containing silicon dioxide in a state bound to other elements (Mg, Ca, A1, Fe, etc.). Many minerals are referred to silicates: asbestos, talc, kaolin, nepheline, opein, etc .; artificial compounds: mica, cement, fiberglass, etc. Dust causing silicatoses is found in many industries: chamotte-dinas, rubber, cement, etc.

Danger to health is posed by the extraction, processing, loosening, mixing, transportation of minerals. Silicatosis develops at a later date than silicosis, and is often combined with silicosis (silicosilicatosis). The action of silicate dust is weaker than quartz. The most aggressive is the dust of magnesium silicate 3MgO 2SiO 2 2H 2 O - chrysotile asbestos - a fibrous mineral.

When asbestos dust is inhaled in the lungs, there is generalized fibrosis, secreted in a special form called asbestosis. Clinical and morphological features of this disease are determined by the fibrous structure of asbestos. Asbestos fibers in the overwhelming majority of cases are not phagocytosed, it is difficult to remove them by lymph due to the needle-like nature of the dust particles. They penetrate the bronchi, injure mucous membranes, and cause an inflammatory reaction. There is also a mechanical effect of asbestos dust. The development of asbestosis occurs depending on the concentration of dust at different times - from 3 to 11 years. Characteristic is the presence in the sputum of asbestos bodies 30 - 70 microns long, pale yellow in color, having the form of fibers with clavate extensions at the ends.

Clinically, asbestosis is accompanied by shortness of breath, cough, at first dry, and then with phlegm. There are emphysema of the lungs, chronic bronchitis, a decrease in the vital capacity of the lungs, changes from of cardio-vascular system... There are 3 stages of asbestosis. Often, asbestosis is complicated by chronic pneumonia, tuberculosis, and lung cancer.

Talcosis also belongs to silicatoses, which develops among workers in textile, rubber, paper, perfumery, ceramic and other industries in contact with talc for 15 - 20 years. The course of talcosis is benign. Pneumosclerosis - interstitial, in a pronounced stage - diffuse interstitial fibrosis with small nodular shadows. Talcosis is often complicated by emphysema and chronic bronchitis.

Pneumoconiosis can also be caused by other types of dusts that do not contain silicon dioxide. These are, for example, siderosis, aluminosis, apatitosis, baritosis, manganoconiosis, anthradosis, graphitosis, pneumoconiosis from grinding dust, etc. Metalloconiosis and carboconiosis are more benign and develop 15 to 20 years after starting work in the profession. Often there is a combination of a mild fibrotic process with chronic bronchitis, which, as a rule, is decisive in the clinic of diseases.

Among metalloconiosis, beryllium disease (pneumoconiosis from inhalation of beryllium dust and its compounds), which is particularly aggressive, and manganoconiosis (manganese pneumoconiosis) should be noted. Manganoconiosis develops upon inhalation of aerosols of disintegration and condensation of manganese and its compounds. Manganese oxides and salts are found in the extraction of manganese ores, the smelting of high-quality steels and alloys, in arc welding, submerged arc welding, etc.

The first signs of manganoconiosis appear after 4 - 5 years of work. Mangaioconiosis, in contrast to beryllium disease, is accompanied by a benign course, but is combined with chronic manganese poisoning, which manifests itself in a predominant lesion of the nervous system.

Byssinosis("Byssos" - textile fiber) - an occupational disease that develops as a result of prolonged exposure to dust from cotton, flax, hemp, jute, kenaf among workers of cotton ginning and cotton spinning factories, flax mills, etc. Dust generated during production operations with coarse, low-grade raw materials, may be contaminated with bacteria and fungi.

The main symptom in the clinical picture of byssinosis is a violation of bronchial patency, developing under the influence of bronchoconstrictor agents contained in cotton, flax and other types of plant dust. In addition, fungal and bacterial contamination of organic plant dust is a source of protein substances that have a sensitizing effect. The main complaints are chest tightness, difficulty breathing, shortness of breath on exertion, cough, weakness. Initially, these symptoms are noted only when performing work after a break - "symptom of Monday", and later they become permanent, complicated by persistent disorders of the bronchopulmonary apparatus and pulmonary heart disease.

Pneumoconiosis caused by organic dust (byssinosis, etc.) is rare.

Pneumoconiosis from mixed dusts. Pneumoconiosis of this type includes electric welding pneumoconiosis, pneumoconiosis of gas cutters, refractory workers, steel makers, grinders, emery machines, etc.

Electric welding pneumoconiosis develops in electric welders during prolonged work in poorly ventilated rooms, when a high concentration of welding aerosol containing iron oxide, manganese or fluorine compounds is created. Pneumoconiosis is favorable. Complaints of shortness of breath with significant physical exertion, dry cough. There is a diffuse increase and deformation of the pulmonary pattern with numerous small focal seals. In the 2nd stage of the disease, chronic bronchitis and emphysema join.

In all cases of development of pneumoconiosis, the severity of the pneumofibrotic process depends on the structure and composition of the exposed dust. For example, anthracite dust is more coniotic than soft brown coal and shale. An admixture of silica increases the coniosity hazard.

Pneumoconiosis in severe stages is often complicated by pulmonary tuberculosis. This combination is called coniotuberculosis. There are the following types of coniotuberculosis: silicotuberculosis, anthracotuberculosis, siderotuberculosis, etc. Taking into account the peculiarities of the clinic, they are considered as independent nosological forms of the disease.

The state system of measures to combat silicosis has led to a significant improvement in working conditions and a decrease in the level of dustiness in the air at the enterprises of the mining, metallurgical, machine-building and other industries. As a result, the incidence of pneumoconiosis, including its most severe type, silicosis, has decreased.

Industrial dust can lead to the development of occupational bronchitis, pneumonia, asthmatic rhinitis and bronchial asthma. Some of the dust settles on the mucous membrane of the nose and bronchi. Depending on the nature and concentration in the air, it causes a different reaction in the nasal mucosa. Hypertrophic and atrophic rhinitis... Chromium compounds and nickel sulfate cause ulcerative-necrotic lesions of the mucous membrane and even perforation of the nasal septum. Dust lingers in respiratory tract causing local processes: bronchitis, bronchiolitis.

Dust bronchitis become the most common types of pathology. As the dust level decreases, the incidence of pneumoconiosis and bronchial asthma decreases, and small dust concentrations cause dust bronchitis. Dust bronchitis occurs when inhaling moderately aggressive mixed dust of coarse dispersion (metal, vegetable, cement, etc.). The prevalence and timing of the development of the disease depend on the concentration and chemical composition dust, more often bronchitis develops after 8 - 10 years of work at the relevant enterprise.

Bronchitis from allergenic dusts is accompanied by bronchospasm and is complicated by asthma. Plant dust - cotton, linseed, jute causes bronchitis of an asthmatic nature with exacerbations after a day off. In the future, they are complicated by emphysema and pneumosclerosis. Bronchial asthma is caused by ursolic and some other types of dust that have an allergenic effect.

Dust and pneumonia. Slag pneumonia occurs in the fertilizer industry among workers grinding waste containing phosphorus salts. There are indications of the severity of such pneumonia with a high percentage of emphysema, sometimes fatal.

Lipoid pneumonia develops in workers exposed to high concentrations of highly dispersed oil aerosols (oil mists).

Pathogenesis of dust lung diseases. There are several theories of the mechanism of dust action, and the main ones are mechanical, toxic-chemical and biological. Mechanical proponents tried to explain the development of fibrosis physical properties dust, considering that the harder the dust particles and the sharper its edges, the more aggressive they are. However, carboreside dust, being more hard than quartz, does not cause pneumoconiosis. The toxic-chemical theory explained the fibrogenic properties of silica dust by its solubility in the body's media, toxic effect... But there is no direct relationship between the degree of quartz solubility and the degree of fibrogenicity. The solubility of amorphous silicon is approximately 2 times greater than the solubility of crystalline quartz and tridymite, but tridymite has the greatest fibrogenicity, then crystalline quartz and the least - amorphous silicon.

B.T. Velichkovsky put forward a hypothesis about the relationship of the fibrogenic properties of silicon dioxide with the microstructure of the surface of quartz particles and the formation of silanol groups on it. In case of mechanical damage to the quartz crystal lattice on the surface of the silica fracture in the presence of water vapor contained in the air, active chemical radicals SiOH and silanol groups are formed. The latter, reacting with tissue proteins, cause their destruction and the development of fibrotic changes.

At present, it is generally accepted that the leading role in the development of silicosis is played by macrophages phagocytosing silica dust particles. The death of macrophages is considered the first stage in the development of other pneumoconiosis, as well as chronic dust bronchitis.

It has been established that dust, even quartz, does not have a direct fibrogenic effect without a sequential change in the processes of phagocytosis, death, decay of coniophages. For the manifestation of the fibrogenic properties of dust, direct contact of dust particles with the membrane of the phagocytic cell is required. The content of dead macrophages activates fibroblasts, inducing the development of fibrosis in the lungs. The effect of fibrogenic dust on a macrophage is due to the cytotoxic effect, which consists in the rapid destruction of phagolysosomes containing particles absorbed by the cell. The further development of dust pathology is associated with the products of destruction of coniophages, which affect the body in three directions: mobilize an additional number of cells necessary for the processes of self-cleaning of the lungs from dust, cause immunological changes, stimulate fibroblasts and the formation of collagen.

From the standpoint of this theory, it is possible to most convincingly link clinical manifestations dust diseases of the lungs with quantitative indicators of dust content, their chemical structure and physicochemical properties of dust.

Modern dusty pathology of the respiratory system is defined as a combination of numerous reactions of the body to dust, such as interstitial fibrosis, emphysema, reflex bronchospasm, chronic astmoid bronchitis, etc.

Large dust particles with a size of 5 - 7 microns and more, due to their size, penetrate the bronchial tree, exerting a mechanical traumatic effect on the alveolar wall and causing the development of dust bronchitis. Dust particles with a size of 0.5 - 2 microns penetrate the alveoli and exhibit a cytotoxic effect, and also contribute to the development of nodular forms of pneumoconiosis. Fine dust, with a grain size of 0.3 - 0.02 microns, for a long time getting into the lungs, accumulate 7 - 10 in macrophages and only then show a cytotoxic effect as the effect of decompensation of hypertrophied coniophages. Such dust contributes to the formation of diffuse sclerotic changes in the lung tissue. This can explain the mechanism of action of dusts with low cytotoxicity, for example, anthracosis.

The place of formation of dust nodules depends on the fibrogenicity of dust and the level of dust. So, for high concentration quartz dust enhanced disintegration of microphages with dust is observed in the cavity of the alveoli, around which silicotic nodules are formed, with a decrease in dust content - in the pulmonary parenchyma in the area of ​​peribronchial and perivascular lymphatic follicles. With a low content of dust in the air, nodules are formed in regional lymph nodes, and diffuse sclerotic changes prevail in the lungs.

Viral infection, other reasons that reduce the immunobiological reactivity of the body, inhibit the activity of macrophages, inhibit the self-cleaning of the lungs from dust and thus contribute to the earlier development of dust diseases.

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-1.jpg" alt = "(! LANG:> PROFESSIONAL DISEASES Dust diseases lungs Prof, MD Solovyova I. ">

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-2.jpg" alt = "(! LANG:> Non-inflammatory diseases of the respiratory system silicosis; silicosis (asbestosis, talc, cementum ,"> Невоспалительные заболевания дыхательной системы силикоз; силикатозы (асбестоз, талькоз, цементный, слюдяной, нефелиновый, ОЛИВИНОВЫЙ каолиноз); металлокониозы (бериллиоз, сидероз, алюминоз, баритоз, манганокониоз, пневмокониозы, обусловленные пылью редкоземельных твердых и тяжелых сплавов); карбокониозы (антракоз, графитоз, сажевыйпневмокониоз); пневмокониозы, обусловленные вдыханием смешанной пыли (антракосиликоз, сидеросили коз, силикосиликатоз); пневмокониозы, обусловленные вдыханием органической пыли (хлопковый, зерновой, пробковый, тростниковый). !}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-3.jpg" alt = "(! LANG:> In 1996 GU"> В 1996 г. ГУ "НИИ медицины труда" РАМН предложили новую класси фикацию пневмокониозов, изло женную в методических указаниях № 95/235 Министерства здравоохране ния и медицинской промышленности !} Russian Federation... 1) Developing from exposure to moderate and highly fibrogenic dust (with a free silicon dioxide content of more than 10%) - silicosis, anthracosilicosis, silicosiderosis, silicosilicatosis. These pneumoconioses are most common among sandblaster, chopper, tunneller, farmer, barn worker, refractory worker, and ceramic workers. They are prone to the progression of the fibrous process and complication of tuberculosis infection.

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-4.jpg" alt = "(! LANG:> pneumoconiosis is characterized by moderate fibrosis, benign and slow progressing,"> пневмокониозы характеризуется умеренно выраженным пневмофиброзом, доброкачественным и медленнопрогрессирующим течением, нередко осложняются неспецифической инфекцией, хроническим бронхитом, что в основном определяет тяжесть заболевания. 2) Развивающиеся от воздействия слабофиброгенной пыли (с содержанием свободного диоксида кремния меньше 10 % или не содержащей его) – силикатозы (асбестоз, талькоз, каолиноз, оливиноз, нефелиноз, пневмокониоз от воздействия цементной пыли), карбокониозы (антракоз, графитоз, сажевый пневмокониоз и др.), пневмокониоз шлифовальщиков и наждачников, метал локониозы или пневмокониозы от рентгеноконтрастных видов пыли (сидероз, в т. ч. от аэрозоля при электросварке или газорезке железных изделий, баритоз, станиоз, мангано кониоз и др.).!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-5.jpg" alt = "(! LANG:> 3) Developing from exposure to aerosols of toxic allergic action (dust containing"> 3) Развивающиеся от воздействия аэрозолей токсико аллергического действия (пыль, содержащая металлы аллергены, компоненты пластмасс и других полимерных материалов, органические пыли и др.) бериллиоз, алюминоз, легкое фермера и другие гиперчувствительные пневмониты. В !} initial stages diseases are characterized by the clinical picture of chronic bronchiolitis, alveolitis of a progressive course with an outcome in fibrosis. The concentration of dust is not decisive in the development of this group of pneumoconiosis. The disease occurs with minor, but prolonged and constant contact with the allergen.

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-6.jpg" alt = "(! LANG:> groups of factors affecting the nature and severity of the response of lung tissue to"> группы факторов, влияющих на характер и степень выраженности реакции легочной ткани на минеральную пыль Концентрация пыли, интенсивность ее экспонирования, длительность контакта (стажа работы). Индивидуальная чувствительность к пыли и наличие факторов, предрасполагающих к развитию фиброза. Характер пыли, геометрические размеры частиц и аэродинамические свойства.!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-7.jpg" alt = "(! LANG:> Immunological theory of pneumoconiosis silicosis develops in quartz particle phagocytosis"> Иммунологическая теория пневмокониозов силикоз развивается при фагоцитозе кварцевых частиц макрофагами. Скорость гибели макрофагов пропорциональна фиброгенной агрессивности пыли. Гибель макрофагов первый и обязательный этап в образовании силикотического узелка. Протеолитические энзимы, такие как металлопротеиназы и эластаза, высвобождающиеся из поврежденных макрофагов, в свою очередь также способствуют разрушению легочных структур.!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-8.jpg" alt = "(! LANG:> Immunological theory of pneumoconiosis The inflammation phase is accompanied by reparative processes,"> Иммунологическая теория пневмокониозов Фаза воспаления сопровождается репаративными процессами, при которых факторы роста стимулируют выработку и пролиферацию мезенхимальных клеток, регулируют образование новых сосудов и эпителия в поврежденных тканях. Неконтролируемые механизмы неоваскуляризацин и эпителизации могут легко привести к развитию фиброза. Фиброгенные частицы пыли самостоятельно активируют провоспалительные цитокины (Ил 1 и ФНО). Обнаружена связь силикоза с системой HLA, возможно определяющей харак тер иммунного ответа.!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-9.jpg" alt = "(! LANG:> SILICOSIS cough, phlegm and shortness of breath with physical activity... With "> SILICOSIS, cough, sputum and shortness of breath during exercise. With the formation of large fibrous nodes and changes in the pleura, complaints of pain in the chest, tingling under the shoulder blades appear. The percussion sound is shortened, and with the formation of emphysema, a box shade appears. hard breathing, which is replaced by weakened breathing as emphysema grows, wheezing appears.The leading diagnostic method is standard radiography of the lungs.

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-10.jpg" alt = "(! LANG:> Development of emphysema A - norm B - emphysema - expansion of alveolar"> Развитие эмфиземы А – норма Б – эмфизема – расширение альвеолярных ходов, уплощение альвео!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-11.jpg" alt = "(! LANG:> Emphysema. Dr. H. O. van der Zalm, 1976 Centriacinar,"> Эмфизема легких. Dr. H. O. van der Zalm, 1976 Центриацинарная, Диффузная эмфизема буллезная эмфизема!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-12.jpg" alt = "(! LANG:> Emphysema of the lungs">!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-13.jpg" alt = "(! LANG:> Emphysema of the lungs">!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-14.jpg" alt = "(! LANG:> Pulmonary emphysema, uneven elasticity of the alveolar frame, vascular changes">!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-15.jpg" alt = "(! LANG:> Long-term development of silicosis With relatively short exposure to large"> Отдаленные сроки развития силикоза При относительно непродолжительном воздействии больших концентраций кварцсодержащей пыли может иметь место запоздалая реакция на нее с формированием т. н. позднего силикоза. Это особая форма болезни, развивающаяся спустя 10 20 и более лет после прекращения работы с пылью. Стаж работы у этих больных обычно не превышает 4- 5 лет.!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-16.jpg" alt = "(! LANG:> Asbestosis The most dangerous and severe pneumoconiosis downstream"> Асбестоз Самым опасным и тяжелым по течению пневмокониозом является асбестоз, вызванный вдыханием пыли асбеста волокнистого бесструктурного гидросиликата, стойкого к воздействию высоких температур. амфиболовый асбест, отличается от хризотилового большейтоксичностью, фиброгенностью и канцерогенностью.!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-17.jpg" alt = "(! LANG:> Where can you find asbestos? The main materials made from asbestos are :"> Где можно встретить асбест? Основными материалами, изготовленными из асбеста, являются: арматура труб, кровельные покрытия, клепальные изделия, панели для стен и полов, гофрированные и формовые листы, асбестовая бумага для изоляции проводов и труб, тормозные накладки и накладки для сцепления, синтетиче ская пряжа, шнур, веревки и т. д.!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-18.jpg" alt = "(! LANG:> MPC for asbestos According to international standards, the maximum permissible concentration of asbestos"> ПДК асбеста Согласно международным стандартам, предельно допустимой концентрацией асбеста в зоне дыхания рабочего считается одно фиброволокно на 1 см 3 воздуха. Санитарно гигиенический регламент США допу скает не более 0, 1 фиброволокна/см 3. Решающим для подтверждения наличия асбестоза как !} occupational disease is the detection of asbestos fibers in the workplace, as well as the identification of specific asbestos (glandular) bodies in biological media and body tissues.

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-19.jpg" alt = "(! LANG:> Limestone dolomite pneumoconiosis A pathological process caused by limestone dolomite dust,"> Известняково доломитовый пневмокониоз Патологический процесс, вызываемый известняково доломитовой пылью, развивается в респираторных и бронхиальных структурах легких и в дальнейшем траснформируется в интерстициальный пневмосклероз и атрофический бронхит. Пневмосклеретические изменения в легких, носящие интерстициальный характер, а клинически - фарингиты, бронхиты и эмфизему!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-20.jpg" alt = "(! LANG:> Metalloconioses are caused by inhalation of metal dust: beryllium"> Металлокониозы обусловлены вдыханием металлической пыли: бериллия (бериллиоз), железа (сидероз), алюминия (алюминоз), бария (баритоз) и т. д. Наиболее распространенным является сидероз, который развивается у горнорабочих при добыче железа и его переработке, у сталеплавильщиков, газо и электросварщиков при работе в замкнутых пространствах и других лиц, имеющих контакт с пылью железа при сварке, нарезке и обработке изделий!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-21.jpg" alt = "(! LANG:> Onset of metalloconiosis The manifestation of the disease is the appearance of fine-spotted shadows on the radiograph"> Начало металлокониозов Манифестацией заболевания считается появление на рентгенограмме мелкопятнистых теней повышенной плотности, разбросанных по всем легочным полям без образования конгломератов. Несоответствие скудных !} clinical symptoms distinct changes in the X-ray diffraction pattern are explained by the impermeability of the electric welding aerosol for x-rays... With the termination of work in contact with iron dust or welding aerosol, all X-ray logical changes can disappear (regressive pneumoconiosis).

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-22.jpg" alt = "(! LANG:>"> Карбокониозы Развиваются при длительном контакте с углеродсодержащеи пылью (уголь, графит, сажа). Характерным для них является умеренновыраженный мелкоочаговый и интерстициальный фиброз легких. Одним из распространенных заболеваний этой группы является антракоз, вызванный вдыханием дисперсной угольной пыли!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-23.jpg" alt = "(! LANG:> PZL diagnostics study of respiratory function"> Диагностика ПЗЛ исследование функции внешнего дыхания (ФВД), проведение фибробронхоскопии, стандартной рентгенографии легких, рентгеновской томографии, компьютерной и магнитно резонансной томографии (при подозрении на сосудистый генез изменений в легких), специфических лабораторных исследований. биопсия легочной ткани и внутригрудных лимфатических узлов.!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-24.jpg" alt = "(! LANG:> Radiography of the lungs I. Small opacities are characterized by shape, size, profusion"> Рентгенография легких I. Малые затемнения характеризуются формой, размерами, профузией (численной плотностью на 1 см 2) и распространением по зонам правого и левого легкого: а) округлые (узелковые): р 1, 5 мм; q- 1, 5 3, 0 мм; r до 10, 0 мм; б) линейные (интерстициальные): s тонкие линейные до 1, 5 мм шириной; t средние линейные до 3, 0 мм шириной; u грубые, пятнистые, неправильные до 10, 0 мм.!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-25.jpg" alt = "(! LANG:> Radiography of the lungs Small round-shaped opacities have clear contours, medium"> Рентгенография легких Малые затемнения округлой формы имеют четкие контуры, среднюю интенсивность, мономорфные, диффузно располагаются преимущественно в верхних и средних отделах легких. Малые линейные неправильной формы затемнения, отражающие перибронхиальный, периваскулярный и межуточный фиброзы, имеют сетчатую, ячеистую или тяжисто ячеистую форму, располагаются преимущественно в средних и нижних отделах легких. Символы записываются дважды: (р/р, q/q, r/r)или(р/u, q/t, p/s).!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-26.jpg" alt = "(! LANG:> Saturation density or concentration of small opacities per 1 cm 2 of the pulmonary field"> Плотность насыщения или концентрация малых затемнений на 1 см 2 легочного поля шифруется арабскими цифрами: 1 - единичные, легочный бронхо сосудистый рисунок прослеживается; 2 немногочисленные мелкие тени, легочный бронхо сосудистый рисунок дифференцируется частично; 3 множественные малые затемнения, легочный бронхо сосудистый рисунок не дифференцируется. Например, 0/0, 0/1, 1/0, 3/3 и т. д. Числитель основные формы, знаменатель другие. II. Большие затемнения (результат слияния округлых затемнений на месте ателектазов, пневмонических фокусов, при осложнении туберкулезом): А до 50 мм; В до 100 мм; С более 100 мм.!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-27.jpg" alt = "(! LANG:> Based on the radiological characteristics, interstitial pneumoconiosis forms are distinguished,"> Исходя из рентгенологической характеристики выделяют формы пневмокониозов интерстициальную, узелковую узловую!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-28.jpg" alt = "(! LANG:> Bronchodilator test FEV 1 spirometry must be measured (at least twice, difference"> Бронходилаторный тест Спирометрия ОФВ 1 должно быть измерено (минимум дважды, разница в 5%) до ингаляции бронходилататора. Бронходилататор должен быть ингалирован посредством устройства MDI (баллончик) + спейсер или через небулайзер, чтобы быть убежденным что вещество поступило в легкие Доза бронходилататора должна быть выбрана максимальной для пациента (в зависимости от кривой потока)!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-29.jpg" alt = "(! LANG:> Bronchodilator test Spirometry Possible doses of substances: ü 400"> Бронходилаторный тест Спирометрия Возможные дозы веществ: ü 400 µg β 2 -агониста, или ü 80 -160 µg антихолинергика, или ü комбинация двух веществ ОФВ 1 должно быть измерено снова: ü 10 -15 минут после β 2 -агониста ü 30 -45 минут после антихолинергика или комбинации!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-30.jpg" alt = "(! LANG:> Bronchodilator test Results Any increase in FEV 1 greater than / equal to 200 ml and 12%"> Бронходилаторный тест Результаты Любое повышение ОФВ 1 которое более/равно 200 мл и 12% прироста от исходного показателя ОФВ 1 расценивается как достоверное (тест положительный). Обычно полезным для клинической интерпретации является указание как абсолютных изменений в мл от исходного, так и % прироста от базовой линии.!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-31.jpg" alt = "(! LANG:> TREATMENT OF PZD There is no specific pathogenetic therapy for pneumoconiosis."> ЛЕЧЕНИЕ ПЗЛ Специфической патогенетической терапии пневмокониозов не существует. Больным проводят лечение, направленное на снижение воспаления в ткани легкого, улучшение дренажной функции бронхов и элиминацию пылевых частиц!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-32.jpg" alt = "(! LANG:> Labor recommendation for dust bronchitis For uncomplicated cases of dust bronchitis"> Трудовые рекомендации при пылевом бронхите При неосложненных случаях пылевого бронхита больному противопоказан труд с воздействием: пыли, неблагоприятных факторов микро и макроклимата, веществ раздражающего органы дыхания действия, физического перенапряжения.!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-33.jpg" alt = "(! LANG:> Treatment of Specific, pathogenetic therapy of pneumoconiosis, chronic dust"> Лечение Специфической, патогенетической терапии пневмокониозов, хронического пылевого бронхита и биссиноза не существует. Больным проводят лечение, направленное на снижение воспаления в ткани легкого, улучшение дренажной функции бронхов и элиминацию пылевых частиц!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-34.jpg" alt = "(! LANG:> TREATMENT Basic therapy is formed by bronchodilators, since it is bronchial"> ЛЕЧЕНИЕ Базисную терапию формируют бронходилататоры, поскольку именно бронхиальная обструкция наряду с прогрессированием пневмосклероза играет первостепенную роль в патогенезе и прогрессировании. β 2–агонисты быстро воздействуют на бронхиальную обструкцию, улучшая самочувствие больных в короткие сроки. При !} long-term useβ 2 - agonists develop resistance to them, after a break in taking drugs, their bronchodilator effect is restored.

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-35.jpg" alt = "(! LANG:> Classification of bronchodilators Duration 2 - Agonists Anticholinergic blockers of Salbutamo action"> Классификация бронхолитиков Длительность 2 -Агонисты Холиноблокаторы действия Сальбутамо л Ипратропия Короткого бромид действия Фенотерол Окситропиум Тербуталин Сальметеро л Тиотропия Длительного действия бромид Формотерол Препараты теофиллина Резервные медленного высвобождения; препараты!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-36.jpg" alt = "(! LANG:> Treatment of exacerbations of BRONCHOLITICS"> Лечение обострений БРОНХОЛИТИКИ Анти- Метилксантины β 2 -Агонисты холинергические (теофиллин) препараты Быстрый и сильный Продолжительный Слабый бронхолитический эффект эффект Расслабляют гладкую Снижение холинергического Высокая токсичность мускулатуру бронхов тонуса ветвей блуждающего Возможна дозозависимая нерва кардиотоксичночть Отсутствие кардиотоксичности!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-37.jpg" alt = "(! LANG:> BERODUAL N Composition" two in one "ONE AND UNIQUE COMBINED BRONCHOLITION"> БЕРОДУАЛ Н Состав «два в одном» ЕДИНСТВЕННЫЙ И УНИКАЛЬНЫЙ КОМБИНИРОВАННЫЙ БРОНХОЛИТИК (не содержит гормональный компонент) СИЛА ДЛИТЕЛЬНОСТЬ β 2 агониста Антихолинергика Фенотерол 50 мкг Ипратропиум 20 мкг БЕРОДУАЛ Н!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-38.jpg" alt = "(! LANG:> Safety and dosing regimen Does not contain hormone component"> Безопасность и режим дозирования Не содержит гормональный компонент Безопасность Лечение приступов Низкая доза β 2 агониста 2 ингаляции (через 5 мин. повторные 2 ингаляции) Возможность применения у пациентов с сердечно Длительная терапия сосудистыми заболеваниями Опыт применения в России более По 1 2 ингаляции 3 раза в сутки (до 20 лет 8 ингаляций в сутки)!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-39.jpg" alt = "(! LANG:> Berodual For mild to moderate attacks in many cases"> Беродуал При легких и умеренных приступах во многих случаях рекомендуется 1 мл (20 капель). В особенно тяжелых случаях, например у пациентов, находящихся в отделениях интенсивной терапии, при неэффективности доз, указанных выше, могут потребоваться более высокие дозы, до 2, 5 мл (50 капель). В особо тяжелых случаях возможно применение при условии медицинского наблюдения !} maximum dose reaching 4.0 ml (80 drops). Course and long-term treatment If necessary reapplication for each injection use 1 2 ml (20 40 drops) up to 4 times a day. Maximum daily dose 8 ml. In the case of moderate bronchospasm or as an aid in the implementation of ventilation, a dose is recommended, the lower level of which is 0.5 ml (10 drops).

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-40.jpg" alt = "(! LANG:> The method of drug delivery affects the final result of treatment no less than"> Способ доставки лекарственного вещества влияет на конечный результат лечения не меньше, чем само лекарство!!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-41.jpg" alt = "(! LANG:> The main parameter of the effectiveness of the inhalation device Pulmonary aerosol deposition When used"> Основной параметр эффективности ингаляционного устройства Легочная депозиция аэрозоля При использовании ЗАВИСИТ ОТ: разных систем колеблется 1 Размера частиц аэрозоля в пределах от 4 до 85% от 2 Правильности ингаляционной техники отмеренной дозы. 3 Типа ингаляционного устройства!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-42.jpg" alt = "(! LANG:> Distribution of aerosol particles in the respiratory tract * 5-10 microns"> Распределение частиц аэрозоля в дыхательных путях* 5 -10 мкм осаждение в ротоглотке, гортани, трахее 2 -5 мкм осаждение в средних и мелких бронхах 0, 5 -2 мкм осаждение в альвеолах менее не осаждаются в легких 0, 5 мкм Респирабельная фракция – доля частиц (%) с аэродинамическим диаметром менее 5 мкм в аэрозоле. * Task Group, 1966!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-43.jpg" alt = "(! LANG:> Benefits of nebulizer therapy: Can be used in life-threatening conditions"> Преимущества небулайзерной терапии: возможность использования при жизнеугрожающих состояниях возможность использования больших доз и комбинирования препаратов возможность использования препаратов не применяемых в ДАИ и ДПИ Достаточное количество препарата попадает непосредственно в трудновентилируемые участки легких возможность применения высоких доз препаратов более быстрое начало действия лекарственного вещества меньший риск развития !} side effects can be used from the very early age and in patients who, for a number of reasons, cannot use conventional inhalers, the absence of the need for coordination of inhalation and release of the drug substance, the generation of a homogeneous highly dispersed aerosol with optimal size particles the ability to be included in the oxygen supply circuit (IVL) short duration of the treatment procedure

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-44.jpg" alt = "(! LANG:> What drugs do we sometimes prescribe for nebulizer therapy today"> Какие препараты мы иногда назначаем для небулайзерной терапии сегодня Амфотерицин B Лидокаин Магния сульфат Адреналин Опиаты Фуросемид Препараты сурфактанта Гипертонический раствор Физиологический раствор!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-45.jpg" alt = "(! LANG:> Compressor nebulizers OMRON OMRON NE-C 28 -E"> Компрессорные небулайзеры OMRON OMRON NE-C 28 -E NE-C 29 -E NE-C 30 -E КОМПАКТНЫЙ И ЛЕГКИЙ (12× 10× 5 см) к использованию ВНЕ ДОМА Предназначен для СПЕЦИАЛЬНЫЙ ОТСЕК ПОНИЖЕННЫЙ УРОВЕНЬ ШУМА(53 д. Б) домашнего для камеры и аксессуаров, работа ОТ СЕТИ и АККУМУЛЯТОРА использования РУЧКА для переноски БАТАРЕЯ НА 300 подзарядок 1 ЦИКЛ- 30 мин. ИНГАЛЯЦИИ!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-46.jpg" alt = "(! LANG:> Mesh nebulizer Omron Micro AIR U 22 High performance pocket nebulizer Unique technology"> Меш небулайзер Omron Micro AIR U 22 Высокоэффективный карманный небулайзер Уникальная технология вибрирующей сетки - мембраны - компактный - бесшумный - удобный!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-47.jpg" alt = "(! LANG:> Omron Micro AIR U 22 Nebulizer Mesh 1. For little ones"> Меш небулайзер Omron Micro AIR U 22 1. Для маленьких и грудных детей 2. Для тех, кто ведет активный образ 3. Пожилые, ослабленные или просто «ленивые» пациенты. Бесшумные ингаляции, которые можно проводить под любым углом наклона, в режиме естественного дыхания; Возможность использования малого количества лекарственного средства.!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-48.jpg" alt = "(! LANG:> Preparations for use in nebulizers Standard solutions for Compress-Ultra-Mesh -"> Препараты для применения в небулайзерах Стандартные растворы для Компрес- Ультра- Меш- небулайзерной терапии, которые сорные звуковые небулайзеры можно применять Антибиотики, антисептики: тобрамицин, амикацин, диоксидин + + Интерферон человеческий лейкоцитарный + Ингаляционные кортикостероиды: пульмикорт + Стабилизаторы мембран тучных клеток: кромогексал + н/д + Муколитики: лазолван, ацетилцистеин, пульмозим н/д!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-49.jpg" alt = "(! LANG:> SPIRIVA (tiotropium bromide) F Anticholinergic bronchodilator long acting, providing stable bronchodilation F Possesses "> SPIRIVA (tiotropium bromide) F Long-acting anticholinergic bronchodilator providing stable bronchodilation F Possesses kinetic selectivity to the M 3 subtype of cholinergic receptors located in the smooth muscles of the bronchi - time of dissociation 3 hours of dissociation - time of 34 hours - dissociation M 1 14 h F The only representative of the subgroup in Russia for basic therapy in patients with COPD

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-50.jpg" alt = "(! LANG:> SPIRIVA: indications for use of Spiriva is shown as supporting"> СПИРИВА: показания к применению Спирива показана в качестве поддерживающей терапии у пациентов с ХОБЛ, включая хронический бронхит и эмфизему (поддерживающая терапия при сохраняющейся одышке и для предупреждения обострений). 50!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-51.jpg" alt = "(! LANG:> Bronchodilators for"> Бронхорасширяющие средства для поддерживающей терапии Бронхорасширяющий препарат длительного действия Бронхорасширяющий препарат !} short acting Placebo 1.8 1.7 FEV 1 (L) 1.6 1. 5 1. 4 Time (hours) 1.3 0 0.5 1 2 4 6 7 8 10 11 12 14 16 18 19 20 21 22 24

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-52.jpg" alt = "(! LANG:> H 3 C CH 3"> H 3 C CH 3 H 3 C C 3 H 7 + CH 3 + N Br– O Br– H O H O OH O S Антихолинергические O S CH 2 OH препараты Атропин Ипратропия Тиотропия бромид начало 5 - 15 мин 3 - 30 мин 15 - 30 мин пик 1 час 1 - 2 часа 2 - 3 часа длительность 4 - 5 часа 4 - 8 часов 24 часа!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-53.jpg" alt = "(! LANG:> SPIRIVA: drug interactions Drug interactions SPIRIVA with "> SPIRIVA: drug interactions SPIRIVA drug interactions with oral or inhaled steroids and theophylline, taking into account adverse events, have not been identified. SPIRIVA can be used in combination with other drugs: sympathomimetics, methylxanthines, oral and inhaled steroids. 53

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-54.jpg" alt = "(! LANG:> Spiriva Contraindications Hypersensitivity to atropine or"> Спирива Противопоказания Повышенная чувствительностью к атропину или его производным (например, ипратропию или окситропию) или к другим компонентам препарата; в 1 й триместр беременности; дети до 18 лет. С осторожностью Закрытоугольная глаукома, гиперплазия !} prostate, obstruction of the bladder neck.

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-55.jpg" alt = "(! LANG:> Application of Spiriva Inhalation. When using Spiriva in the form of inhalation with"> Применение Спиривы Ингаляционно. При использовании Спиривы в виде ингаляций с помощью прибора Ханди. Халер® рекомендуется применять одну капсулу в сутки в одно и тоже время. Препарат не нужно глотать. Пожилые больные должны принимать Спириву в рекомендуемых дозах. Пациенты с нарушенной функцией почек могут использовать Спириву в рекомендуемых дозах. Однако необходимо тщательное наблюдение за больными с умеренной или тяжелой почечной недостаточностью получающими Спириву (как и в случае с другими препаратами, эскретирующимися в основном почками). Пациенты с печеночной недостаточностью могут принимать Спириву в рекомендуемых дозах.!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-56.jpg" alt = "(! LANG:> Spiriva">!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-57.jpg" alt = "(! LANG:> TREATMENT Methylxanthines are added to therapy with insufficient effectiveness of bronchodilators,"> ЛЕЧЕНИЕ Метилксантины присоединяют к терапии при недостаточной эффективности бронхолитиков, они уменьшают системную !} pulmonary hypertension and strengthen the work of the respiratory muscles. Mucolytics (mucoregulators, mucokinetics), antibiotic therapy shown to a very limited contingent of patients with PZL: they are prescribed for the progression of the disease, the addition of severe bronchial obstruction, productive bronchitis and the development of its infectious complications.

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-58.jpg" alt = "(! LANG:> Inhaled glucocorticosteroids ICS - have a faster clinical effect (1,"> Ингаляционные глюкокортикостероиды ИКС - оказывают более быстрый клинический эффект (1, 5 -3 ч) - прямое действие на слизистую бронхов: - сужение сосудов, - снижение бронхиального кровотока, - уменьшение экссудации плазмы и - продукции мокроты, - торможение миграции воспалительных клеток и выброса медиаторов 58!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-59.jpg" alt = "(! LANG:> Inhaled glucocorticosteroids Benacort (budesonide powder)"> Ингаляционные глюкокортикостероиды Бенакорт (будесонид в порошке) Фликсотид (флутиказона пропионат) Беклозон и беклозон «легкое дыхание» Кленил и Кленил джет и т. д.!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-60.jpg" alt = "(! LANG:> Pulmicort Suspension - - inhaled glucocorticosteroid (budesonide) in suspension for nebulizer therapy"> Пульмикорт Суспензия – - ингаляционный глюкокортикостероид (будесонид) в виде суспензии для небулайзерной терапии 0, 25 мг/мл 0, 5 мг/мл 1 небула содержит 2 мл суспензии в упаковке 20 небул единственный глюкокортикостероид, зарегистрированный в России, который можно ингалировать через небулайзер.!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-61.jpg" alt = "(! LANG:> Indications for nebulized budesonide u Bronchial asthma"> Показания к назначению небулизированного будесонида u Бронхиальная астма u Обострение бронхиальной астмы u Плановая терапия БА u Рецидивирующая ХОБЛ u Круп, острый и рецидивирующий u Бронхолегочная дисплазия u Острый бронхиолит u Облитерирующий бронхиолит u Состояние после трансплантации комплекса сердце- легкие u Экзогенный аллергический альвеолит u Саркоидоз u Муковисцидоз u Острый респираторный дисстрес синдром u Отек гортани (аллергический, постэкстубационный)!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-62.jpg" alt = "(! LANG:> Combined preparations Symbicort (budesonide + formatter) 80/4, 5; 160/4, 5;"> Комбинир. препараты Симбикорт (будесонид +форматерол) 80/4, 5; 160/4, 5; 320/9 Серетид (флутиказон пропионат + сальметерол) 25/250 50/500 50/250 Форадил комби (будесонид 200/400 мкг + форматерол 12 мкг) Фостер (беклометазон пропионат 100 мкг? + форматерол 6 мкг) Тевакомб (флутиказон пропионат + сальметерол) 25/250!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-63.jpg" alt = "(! LANG:> Budesonide and formoterol in one inhaler Symbicort Turbuhaler® 160/4. 5 mcg 60 doses and"> Будесонид и формотерол в одном ингаляторе Симбикорт Турбухалер® 160/4. 5 мкг 60 доз и 120 доз 80/4. 5 мкг 60 доз и 120 доз 320/9 мкг 60 доз!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-64.jpg" alt = "(! LANG:> FOSTER (beclomethasone propionate 100 mcg + formatterol 6 mcg">!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-65.jpg" alt = "(! LANG:> Seretide (fluticasone propionate + salmeterol) 25/250 25/125 50/500 50/250"> Серетид (флутиказон пропионат + сальметерол) 25/250 25/125 50/500 50/250 50/100!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-66.jpg" alt = "(! LANG:> Mucolytic drugs with expectorant effect Bromhexine (bisolvone, broxin, solvin, phlegamine,"> Муколитические препараты с отхаркивающим эффектом Бромгексин (бизолвон, броксин, сольвин, флегамин, фулпен) Амброксол (халиксол, амбробене, амброгексал, амбролан, лазолван) – активный метаболит бромгексина с более выраженными муколитическими и отхаркивающими эффектами!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-67.jpg" alt = "(! LANG:> Ambroxol hydrochloride Adhatoda vasica Malabar nut)"> Амброксола гидрохлорид Adhatoda vasica Malabar nut(англ.) Бромгексин (Бисольвон®) – синтетическое производное вазицина, используется в качестве секретолитического, муколитического отхаркивающего средства Амброксол (Лазолван®) является одним из двенадцати различных метаболитов бромгексина (метаболит VIII)!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-68.jpg" alt = "(! LANG:> Scope For various respiratory diseases bronchial secretion becomes more viscous, turning "> Scope of application In various respiratory diseases, bronchial secretion becomes more viscous, turning into phlegm The natural mechanism of cleansing the bronchi from foreign particles, pathogens and mucus is disrupted. is the cough Lazolvan® dilutes phlegm, cleanses and protects the bronchi, effectively curing cough 68

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-69.jpg" alt = "(! LANG:> Complex action on the pathogenesis of cough Mucolytic - thinning phlegm"> Комплексное действие на патогенез кашля Муколитик ― разжижает мокроту и уменьшает её вязкость, расщепляя связи между мукополисахаридами мокроты1 Мукорегулятор ― стимулирует секреторные клетки бронхов, нормализуя соотношение слизистого и серозного компонентов мокроты2 Моторик ― воздействует на природный механизм очищения дыхательной системы, восстанавливая активность ресничек мерцательного эпителия бронхов 3 Модулятор ― улучшает местный иммунитет, стимулируя синтез сурфактанта 4 Потенцирует действие антибиотиков 5 69!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-70.jpg" alt = "(! LANG:> Convenient release forms for all situations and ages"> Удобные формы выпуска для всех ситуаций и возрастов 1. Сироп для детей 15 мг / 5 мл 2. Сироп для взрослых 30 мг / 5 мл 4. Раствор 7, 5 мг / 1 мл 3. Таблетки для взрослых для небулайзерной ингаляционной 30 мг, 20 или 50 таблеток терапии и приема внутрь 70!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-71.jpg" alt = "(! LANG:> Combined drugs: Ascoril Expectorant Salbutamol selective ß adrenergic agonist c "> Combined preparations: Ascoril Expectorant Salbutamol selective ß adrenergic agonist with a predominant effect on ß 2 adrenergic receptors, has a bronchodilator effect. Guaifenesin - reduces surface tension and adhesive properties of phlegm. gently stimulates the secretion of the bronchial glands, has antiseptic properties, has a calming effect and reduces irritation of the mucous membrane of the respiratory tract.

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-72.jpg" alt = "(! LANG:> Combinations Jocet - (salbutamol sulfate - 1 mg, bromhexine hydrochloride"> Комбинированные препараты Джосет – (сальбутамола сульфат – 1 мг, бромгексина гидрохлорид – 2 мг, гвайфенезин – 50 мг, ментол 0, 5 мг). Оказывает бронхолитическое, отхаркивающее и муколитическое действие. Детям до 6 лет – по 1 ч. л. Х 3 раза в сутки Детям с 6 до 12 лет – по 1 2 ч. л. Х 3 раза в сутки Детям старше 12 лет и взрослым – по 2 ч. л. Х 3 раза в сутки!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-73.jpg" alt = "(! LANG:> oxygen therapy Patients with chronic respiratory failure receive continuous oxygen therapy."> кислородотерапия Больным с хронической дыхательной недостаточностью проводят постоянную кислородотерапию. Пока занием к систематической оксигенотерапии является снижение Ра. О 2 в крови до 60 мм pт. ст. , снижение Sa. O 2!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-74.jpg" alt = "(! LANG:> Comprehensive Respiratory Therapy Pulmonary Rehabilitation">!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-75.jpg" alt = "(! LANG:> Gymnastics A. N. Strelnikova Gymnastics A. N. Strelnikova - the only one in the world"> Гимнастика А. Н. Стрельниковой Гимнастика А. Н. Стрельниковой − единственная в мире, в которой короткий и резкий вдох носом делается на движениях, сжимающих грудную клетку. Упражнения активно включают в работу все части тела (руки, ноги, голову, бедерный пояс, брюшной пресс, плечевой пояс и т. д.) и вызывают общую физиологическую реакцию всего организма, повышенную потребность в кислороде. Так как все упражнения выполняются одновременно с коротким и резким вдохом через нос (при абсолютно пассивном выдохе), это усиливает внутреннее тканевое дыхание и повышает усвояемость кислорода тканями, а также раздражает ту обширную зону рецепторов на слизистой оболочке носа, которая обеспечивает рефлекторную связь полости носа почти со всеми органами!}

Src = "https://present5.com/presentation/3/4777479_234966450.pdf-img/4777479_234966450.pdf-76.jpg" alt = "(! LANG:> Thank you for your attention!">!}