Analysis of controversial issues in the differential diagnosis of pneumoconiosis and pulmonary tuberculosis

08tkacheva.qxd 05/22/2009 16:22 Page 8 Lectures Differential diagnosis of pneumoconiosis with other diffusely disseminated lung diseases ✑ V.N. Tkachev Course of Occupational Diseases at the Department of Faculty Therapy of the Faculty of Pediatrics of the Russian State Medical University Diffusely disseminated lung diseases include diseases in which fibrosis and focal dissemination develop in the lung tissue. In professional pathology, these are pneumoconiosis - diseases that arise under the influence of the dust factor. In terms of prevalence, pneumoconiosis occupies a leading place among occupational diseases. This is due to the fact that at enterprises in many industries there are still a large number of production processes accompanied by the formation and release of dust. Most often, these are processes associated with rock drilling, crushing, grinding, sifting, processing and processing of quartz, granite, fibrous materials, electric welding and gas cutting of metals, processing and finishing of metal surfaces. Industrial dust varies in its chemical composition, leading to various types of pneumoconiosis. The most common pneumoconiosis is silicosis caused by exposure to silica dust. Brief characteristics of pneumoconiosis To understand the mechanism of development of pneumoconiosis, it is necessary to analyze the pathogenesis of silicosis. Dust containing silicon dioxide penetrates into the small respiratory tract and directly into the alveoli. Respirable particles penetrate here, the size of which does not exceed 5 microns (medium non-disperse dust). Dust particles are captured by alveolar macrophages, which are then destroyed and secrete fibrogenic factor (mucoprotein). In this case, activation of fibroblasts occurs, followed by excessive formation of collagen and the development of pneumofibrosis. When inhaling dust with a high content of silicon dioxide, a nodular process most often develops, usually bilateral. Nodules are concentrically or vortex-shaped bundles of connective tissue, partially hyalinized, with quartz particles inside, which can then transform into nodular formations. Great importance In the pathogenesis of silicosis, local immunity is impaired, since macrophages are involved in signal transfer from T lymphocytes to B lymphocytes, which produce immunoglobulins. With silicosis, a large number of macrophages die and Tkillers are activated, which contribute to even greater development of fibrosis. Complaints with silicosis are usually scanty (shortness of breath, possible cough and chest pain), there are no changes in blood tests, and therefore the diagnosis of pneumoconiosis (silicosis) is based on radiological manifestations. There are three radiological forms of pneumoconiosis (International Classification of 1971, amended in 1976), the letter designations within each of these forms indicate the severity of the process in the lungs: 08tkacheva.qxd 05/22/2009 16:22 Page 9 Differential diagnosis of pneumoconiosis nodular (p, q, r): bilateral strengthening and deformation of the pulmonary pattern with focal formations up to 1.5 mm in size (p), nodules measuring 1.5–3 mm (q), nodules measuring 3–10 mm ( r); interstitial (s, t, u): bilateral linear and mesh changes (s), severe changes (t), severe changes (u); nodular (A, B, C): small nodular – the largest diameter of the nodes is 1–5 cm (A); large-nodular – node diameter 5–10 cm (B); massive – the diameter of the nodes is more than 10 cm (C). The staged process (stages I, II, III) in pneumoconiosis is characterized by an increase in fibrosis, the appearance of pleurodiaphragmatic and pleurocostal adhesions, the fusion of nodules and their calcification, the formation of nodes, and shell-like calcification of lymph nodes (LNs). In parallel with the worsening of these changes, the patient’s shortness of breath increases. Impairments in external respiration function (ERF) in pneumoconiosis, as in other diffusely disseminated processes in the lungs, are predominantly restrictive. At stage III of silicosis, complications may occur: pulmonary emphysema, bullous emphysema, pneumothorax, mid-lobe syndrome, cavities, cor pulmonale. Pulmonary tuberculosis is the most common and severe complication of silicosis, which dramatically changes its course. Most frequent form, aggravating silicosis, is focal tuberculosis (usually the foci are localized in upper sections lungs); infiltrative and disseminated forms are less common. In stage III silicosis, infiltrative tuberculous opacities can be distinguished from silicotic fibrous fields by the “path” connecting the infiltrative opacities with the root of the lung. According to the course, pneumoconiosis is divided into rapidly progressive, slowly progressive and regressive (occurs in some cases). In the treatment of silicosis, polyvinylpyrrolidone (to preserve the macrophage membrane), non-steroidal anti-inflammatory drugs (effect on fibroblasts), novocaine inhalation (to remove dust particles from the bronchial tree), antihistamines, B vitamins, ascorutin, gluten cocorticosteroids (GCS) with a rapidly progressing course. Differential diagnosis pneumoconiosis is carried out with the following diseases: disseminated pulmonary tuberculosis; sarcoidosis; exogenous allergic alveolitis (EAA); idiopathic fibrosing alveolitis (IFA); lymphogranulomatosis. Considering the similarity of the radiological manifestations of these diseases, important reference points for establishing a diagnosis are the clinical features and course of the disease, the results of the study of sputum and bronchoalveolar lavage fluid, as well as the analysis of the patient’s X-ray archive, which makes it possible to establish the evolution of radiological changes. Establishing a diagnosis of any type of pneumoconiosis is impossible without taking into account the professional route (work experience in dust production conditions) and the sanitary and hygienic characteristics of working conditions (type of dust and its concentration in the workplace). The first manifestations of pneumoconiosis can develop during work or many years after cessation of contact with dust (“late pneumoconiosis”). Approaches to the differential diagnosis of pneumoconiosis (silicosis) with some diffusely disseminated processes are summarized in the table. General Medicine 2.2006 9 Clinical manifestations 10 General Medicine 2.2006 Lymphogra nulematosis ELISA Obstructive type of disorders In the acute stage - obstructive changes, with chronicity - restrictive Progression of restrictive type of disorders, emphysema Restrictive and obstructive disorders of varying severity Mixed type of disorders depending on the severity of the process Polymorphic shadows . There may be interstitial changes and an increase in lymph nodes Increased ESR, lymphopenia, eosinophilia Fluctuations from normal values ​​to severe disorders Leukocytosis, shift of the leukocyte formula to the left, increase in ESR Absolute lymphopenia Leukocytosis, lymphocytosis and monocytosis, increase in ESR Absent Changes in the peripheral blood Granulomas, Berezovsky cells –Sternberg Consolidation and thickening of interalveolar septa, obliteration of alveoli and capillaries by fibrous tissue Epithelioid cell granulomas Tuberculous tubercles consisting of cells: epithelioid, lymphoid, Pirogov-Langhans, with caseosis Epithelioid cell granuloma (all cells of the tuberculous tubercle without caseosis) semolina with dust particles (SiO2) inside and fibrous rings around Morphological signs 16:22 EAA Increase in restrictive type of FVD disorders Diffuse interstitial fibrosis, nodular or nodular process. Monomorphic shadows X-ray picture 05/22/2009 Enlargement of hilar lymph nodes, less often parabronchial, tracheo-bronchial. The appearance of a large-spotted pattern in the basal and small-spotted patterns in the middle zones, as well as small focal shadows Chills, increased Intensification of the pulmonary pattern of body temperature, due to interstitial shortness of breath, cough, pain component, the summation of these in the chest, shadows creates a picture of the muscles, joints of miliary foci Dyspnea in acute pro Intensification and deformation of the progressive course, pulmonary pattern, interstitial fever, weight loss, algal fibrosis, “honeycomb lung” chest pain, arthralgia, rarely hemoptysis General malaise, enlargement of the mediastinal lymph nodes, fever more often with the formation of conglomerates. There are interstitial and infiltrative changes in the lung tissue. Shortness of breath, cough, chest pain, lymph nodes are not enlarged. Slowly progressive course of Dissemini Intoxication syndrome. There may be cough, tuberculosis, sputum production (MBT), hemoptysis, chest pain Sarcoidosis More often asymptomatic onset, with progression the appearance of low-grade fever, weakness, aching pain in the chest Pneumoconiosis (silicosis) Disease Differential diagnosis of pneumoconiosis (silicosis) with some diffusely disseminated processes 08tkacheva.qxd Page 10 Lectures 08tkacheva.qxd 05/22/2009 16:22 Page 11 Differential diagnosis of pneumoconiosis Disseminated pulmonary tuberculosis When a diffusely disseminated process in the lungs is detected (for example, during a periodic medical examination), the patient is usually referred to an anti-tuberculosis dispensary panser. The phthisiatrician rejects the diagnosis of disseminated pulmonary tuberculosis if monomorphic foci are identified on the radiograph, since in tuberculosis the tubercles are at different stages of morphological development and differ in density - shadow polymorphism. With tuberculosis, it is also possible to damage intrathoracic lymph nodes, most often in the form of their slight enlargement, which appears mainly on tomograms. At late development In silicosis, calcification of the lymph nodes of the roots of the lungs like an “eggshell” and the silicotic nodules themselves often occurs. When tuberculosis is associated with silicosis, the localization of radiological changes is of particular importance: tuberculosis foci are located in the upper parts of the lungs, and silicotic nodules are located in the middle and lower parts. Symptoms of intoxication characteristic of the tuberculosis process, changes in peripheral blood (leukocytosis, lymphocytosis and monocytosis, increased ESR), results of sputum testing for Mycobacterium tuberculosis (MBT), and bronchoscopy data are taken into account. In silicosis, there is a discrepancy between the poor clinical picture and the usually clear radiographic changes. With specific treatment of tuberculosis, significant positive dynamics are achieved, while therapy for silicosis does not give positive changes and is aimed only at stabilizing the process. nisms (mainly helper activity) leads to the formation of epithelial cell granulomas, which contain Pirogov–Langhans cells, but they lack (unlike tuberculous granulomas) cheesy necrosis. Sarcoidosis begins with damage to the intrathoracic lymph nodes; sometimes, along with intrathoracic lymph nodes, peripheral lymph nodes also enlarge. In addition to the lungs, other internal organs may also be involved in the process of sarcoidosis. In the acute form of the disease, arthralgia, erythema nodosum, increased body temperature, and weight loss are noted. With pneumoconiosis, there are no symptoms of intoxication and no increase in any groups of lymph nodes. Radiologically, in sarcoidosis, along with lymph node enlargement, a finely spotted pattern is observed in the middle and subcortical zones with small focal shadows in the middle and lower sections, which resembles the nodular form of pneumoconiosis (p). The diagnosis of sarcoidosis is confirmed by histological examination of material obtained from bronchoscopy, mediastinoscopy, skin biopsy or peripheral lymph node, where epithelioid cell granulomas with Pirogov-Langhans giant cells without caseosis are found. The main treatment method for sarcoidosis is the use of corticosteroids. Due to the possibility of spontaneous regression of the disease (in 20–30% of cases), treatment with prednisolone can be abstained in the asymptomatic course of newly diagnosed sarcoidosis of intrathoracic lymph nodes. Other medications used include cytostatics (methotrexate), but after its discontinuation, relapses often occur. Exogenous allergic alveolitis Sarcoidosis Sarcoidosis is a disease of unknown etiology. The decrease in the immune system of EAA has an acute onset and occurs with symptoms of intoxication - high temperature, chills, chest pain, shortness of breath. The disease is caused by inhalation of a certain antigen of bacterial, fungal, animal or plant origin into the patient’s body. Among them are whey proteins and excrement of chickens, pigeons and other birds, cattle, pigs; various dusts - fish, wheat flour, animal wool, cotton, flax, oak, maple, cedar sawdust, etc. The onset of the disease may not be so acute if the doses of the antigen are small, but with repeated and prolonged contact (often of a professional nature), fibrosis forms in the lung tissue, accompanied by increasing shortness of breath. X-rays reveal interstitial and small-focal changes in the lungs in acute alveolitis, and interstitial fibrosis in chronic alveolitis. At FVD study Basically, progressive restrictive disorders are noted. Transbronchial lung biopsy reveals predominantly lymphocytic infiltration between the alveolar septa and alveoli, as well as sarcoid-like granulomas. The effectiveness of therapeutic measures for acute course EAA depends on the timing of cessation of contact with the etiological factor. GCS are often prescribed, the dose of which and the scheme for reducing it depend on the speed of reverse development of clinical and radiological symptoms. When the pathological process transitions to the stage of interstitial fibrosis, treatment measures are the same as for ELISA. Idiopathic fibrosing alveolitis is known, although there is a hypothesis about its occurrence in conditions of autoimmune aggression (as a kind of collagenosis). It is possible that a qualitative change in the composition of collagen molecules during ELISA is associated with radiation, allergic or toxicoallergic factors. The gradual onset of the disease is characterized by gradually occurring shortness of breath, dry cough, and increased fatigue. The acute form is manifested by fever, weight loss, progressive shortness of breath, chest pain with deep inspiration; hemoptysis is rare, arthralgia is quite common. Changes in the hemogram, blood protein fractions and immunological parameters during ELISA are nonspecific and have no significance for diagnosis. Radiologically, at the stage of interstitial edema, there is an increase and deformation of the pulmonary pattern in the lower fields of both lungs. The roots of the lungs lose their structure, and septal lines (Kerley lines) appear. As the disease progresses, the deformation of the pulmonary pattern intensifies and becomes rough, leading to the appearance of a “honeycomb lung.” The transparency of the lung fields decreases according to the “frosted glass” type, and widespread bilateral darkening of an infiltrative nature appears. Differential diagnosis of ELISA is carried out with both interstitial and nodular forms of silicosis, and analysis of the work history is of great importance. In the treatment of ELISA, the drugs of choice are corticosteroids and cytostatics, Dpenicillamine. The average life expectancy of patients with IFA is 3–4 years. IFA is characterized by progressive interstitial pneumofibrosis with the formation of a “honeycomb lung”, leading to increasing respiratory failure. The cause of the disease is not Lymphogranulomatosis (Hodgkin's disease) - a primary tumor disease of lymphoid tissue. Significantly more often they affect young and middle-aged people than older people. Clinical and radiological manifestations depend on the stage of the disease (I–IV). Clinical signs of lymphogranic nulomatosis are general malaise, undulating fever, and enlarged lymph nodes. Peripheral lymph nodes are dense, elastic, often not fused to each other, and increase with any banal inflammation (tumor lymphadenitis). Mediastinal lymph nodes reach significant sizes and can be massive conglomerates that displace the mediastinum, trachea, and esophagus. LNs are rarely located asymmetrically. Changes in lung tissue such as thickening of the interalveolar septa and infiltration are more often one-sided. Not only the mediastinal lymph nodes and lungs are affected, but also other organs. The respiratory function is disturbed more by the obstructive type. An increase in ESR, lymphocytopenia and eosinophilia observed in some cases in blood tests are nonspecific. The diagnosis is established on the basis of histological examination of the LN biopsy material. Morphologically, granulomas, erased structure of the node, and Berezovsky–Sternberg cells are determined. Since interstitial and infiltrative changes occur in the lung tissue, the differential diagnosis is made with both interstitial and nodular forms of silicosis. Treatment of lymphogranulomatosis is carried out according to schemes depending on the stage of the disease. Cycles of polychemotherapy are carried out, and then radical radiation therapy of the main groups of lymph nodes, both changed and not changed. The main goal of therapy in stages I–III of lymphogranulomatosis is cure, and in stage IV – to achieve long-term remission. Subscription to the scientific and practical journal “Atmosphere” continues. Cardiology” Subscription can be issued at any post office in Russia and the CIS. The magazine is published 4 times a year. The cost of a six-month subscription according to the Rospechat agency catalog is 60 rubles, for one issue – 30 rubles. Subscription index 81609. Subscription to the scientific and practical journal “Atmosphere” continues. Nervous diseases” Subscription can be issued at any post office in Russia and the CIS. The magazine is published 4 times a year. The cost of a six-month subscription according to the Rospechat agency catalog is 60 rubles, for one issue – 30 rubles. Subscription index 81610. General medicine 2.2006 13

1. Disseminated pulmonary tuberculosis.

2. Sarcoidosis of the respiratory system.

3.Histiocytosis X.

4.Bronchoalveolar cancer.

5.Carcinomatous lymphangitis.

6. Wegener's granulomatosis.

7. Idiopathic fibrosing alveolitis.

1. Warm alkaline inhalations and salt-alkaline inhalations - activate the function of the epithelium of the respiratory mucosa. Pathways, liquefies mucus, which partially leads to the removal of dust. 2% solution of Na bicarbonate - once a day for 5-7 minutes, a course of 15-20 sessions.

2. Physiotherapy - ultraviolet irradiation course of 18-20 sessions in winter, 1 time per day.

3. A set of gymnastic exercises.

Medical and social examination for pneumoconiosis

The rule when determining the ability to work of patients with pneumoconiosis is the following: the presence of pneumoconiosis is considered absolute contraindication to continue working in contact with dust. The patient is recognized as partially incapacitated, permanently disabled in his profession, and in need of constant rational employment. When employed with reduced qualifications and wages the patient is sent to the bureau of medical and social examination to determine the percentage (degree) of loss of general and professional ability to work and group III disability for an occupational disease for the period of retraining (approximately 1 year). With I and more often with stage III pneumoconiosis, permanent complete loss of ability to work is possible. The patient is recognized as having completely lost his general and professional ability to work, incapacitated for work outside his profession, and in need of referral to a bureau medical and social examination to determine II, less often I group of disability for occupational disease and the percentage of general and professional loss of ability to work.

Rehabilitation of patients with pneumoconiosis includes:

1) medical rehabilitation(inpatient, outpatient, sanatorium-resort treatment and health improvement in a dispensary, rest home, boarding house, health group);

2) social rehabilitation(material compensation for damage to health by disability group and percentage of loss of professional and general ability to work, material provision of benefits for professional patients, etc.);

3) labor rehabilitation (temporary and permanent rational employment, free training or retraining for a new profession).

3) Intoxication with organophosphate pesticides. Pathogenesis. Clinic. Diagnostics. Treatment. Prevention. Issues of examination of work ability.

Answer: Etiology

Many FOS are active multifunctional additives for lubricating oils. They are used in industry for ore flotation, polymerization, production of solvents, fireproof plastics, etc.

FOS are highly toxic and have high biological activity. They are not durable and decompose in soil and water within a month. Phosphates found in products are quickly destroyed during heat treatment.

FOS enter the body through the respiratory system, gastrointestinal tract and intact skin without causing local changes.

Some of these compounds are capable of being converted into more active substances in the body.

Pathogenesis

The leading link in the mechanism of action of FOS on the human body is a violation of the catalytic function of cholinesterase enzymes. As a result, a disorder of acetylcholine metabolism occurs, expressed in characteristic changes in the central and autonomic nervous system, as well as in violations of activity internal organs and skeletal muscles.

Acetylcholine (ACh) is a mediator of the central nervous system, involved in the transmission of impulses from motor nerves to muscles, in all ganglia (parasympathetic and sympathetic), in the transmission of excitation from postganglionic parasympathetic fibers to effector cells, as well as from postganglionic sympathetic fibers innervating the sweat glands. ACh accumulates in the endings of nerve fibers and, under the influence of nerve impulses, causes depolarization of membranes, changes in their permeability, and redistribution of K + and Na + ions, which underlie the transmission of nerve impulses. These processes are implemented within a fraction of a millisecond. Their intermittency is due to the rapid hydrolysis of acetylcholine by cholinesterase enzymes (ChE). Acetylcholinesterase (AChE) plays a leading role in the hydrolysis of ACh. ChE can be located on the parasympathetic and postsympathetic membrane (extracellular ChE, which plays a major role). Inside the cells there is ChE, which plays the role of an enzyme reserve. When ChE interacts with ACh, an acetylated enzyme is formed - a fragile compound that quickly undergoes hydrolysis, as a result of which the active centers of ChE are freed for new reactions with ACh. When ChE interacts with FOS, a phosphorelated enzyme, resistant to hydrolysis, is formed, which is unable to interact with ACh molecules and has lost its main catalytic function.

The toxic effect of FOS on the nervous system is regarded as muscarinic-like, nicotine-like, curare-like and central. Noncholinergic mechanisms of action of FOS include their ability to phosphorelate certain proteins, affect proteolytic enzymes, change the picture of peripheral blood, affect the liver, etc.

Clinical picture.

The muscarinic-like effect is associated with stimulation of M-cholinergic receptors and is manifested by profuse sweating, salivation, bronchorrhea, spasm of the smooth muscles of the bronchi, intestines, and muscles of the iris with the development of miosis. The nicotine-like effect associated with the excitation of H-cholinergic receptors is manifested by hyperkinesis of the choreic and myoclonic type. The curare-like effect is the development of peripheral paralysis. Central action manifested by the appearance of clonic and tonic convulsions, mental disorders, disorders of consciousness up to a coma.

Acute poisoning:

The first signs of intoxication appear after latent period, the duration of which depends on the dose of the toxic substance and the route of its entry into the body. With inhalation poisoning, signs of intoxication appear after a few minutes, with oral poisoning after 15-60 minutes, and with skin contact - after 2-3 hours.

Mild form of acute intoxication:

General weakness, headache, slight dizziness, nausea, increased sweating, and hypersalivation appear. There is pallor of the skin, bradycardia, and isolated dry rales in the lungs. The pupils are constricted, fibrillation of the tongue and eyelids is observed. All these phenomena persist for several hours, maximum days.

Acute intoxication of moderate severity: the above-described symptoms are accompanied by severe central nervous system disorders. Depression, apathy, speech impairment, increased threshold of excitability of analyzers (vision, smell, taste), fibrillation of the muscles of the face and limbs are noted. There may be crises of a diencephalic nature, schizophrenia-like psychoses with hallucinations. Myocardial dystrophy, liver enlargement and tenderness, slight proteinuria and microhematuria are observed. The duration of clinical phenomena in moderate poisoning ranges from several hours to several days.

Acute severe OP intoxication goes through three stages: excitation, convulsive and paralytic.

In the stage of excitement, anxiety, fear, dizziness, profuse salivation and sweating, nausea, vomiting, abdominal pain, blurred vision, and lacrimation are observed.

In the convulsive stage, against the background of sharp asthenia and twilight consciousness, attacks of tonic-clonic convulsions develop. Attacks of convulsions alternate with complete relaxation. The condition becomes more serious due to disorders of the central nervous system, cardiovascular system, liver, and kidneys.

In the paralytic stage, coma occurs, breathing occurs

there is a smell of pesticides. Salivation and bronchorrhea are intensely expressed (the patient “drowns” in his own fluid). Signs appear respiratory failure: shortness of breath, cyanosis. Laryngo- and bronchospasm and suffocation may be observed. Pneumonia and pulmonary edema may develop. Paralysis of the entire striated muscles develops with a drop in muscle tone and the disappearance of reflexes. Severe myocardial dystrophy develops, dysfunction of the liver and kidneys worsens (increase in liver size, urobilinuria, proteinuria, microhematuria). The temperature rises from low-grade to febrile with coma.

Thus, muscarinic-like symptoms tend to appear first, followed by nicotine-like symptoms, and then curare-like and central ones.

In patients who have suffered acute OP poisoning, long time the phenomena of asthenic syndrome in combination with vegetative disorders persist.

Chronic intoxication:

Develops with prolonged contact with small doses of FOS. Functional cumulation is observed, due to the action of repeated contacts with FOS, in the intervals between which there is no time for complete restoration of ChE to occur. This leads to a progressive decrease in enzyme activity.

One of the main signs is the development of astheno-vegetative syndrome. IN initial stages headache, dizziness, a feeling of heaviness in the head, a burning sensation in the temples, memory loss, sleep disturbances, and loss of appetite are noted. With more pronounced phenomena, disorientation and impaired consciousness are observed. May be noted vascular disorders, changes emotional sphere. In rare cases, focal symptoms from the nervous system: nystagmus, smoothness of the nasolabial fold, deviation of the tongue, tremor of the fingers, pyramidal signs, decreased corneal reflex. During this period, persistent red dermographism, bradycardia, arterial hypertension, ECG shows signs of diffuse changes in the myocardium. An enlarged liver may occur. In peripheral blood, erythrocytosis, leukocytosis, decreased ESR. In severe cases, toxic encephalopathy is detected, manifested by persistent headaches, dizziness, memory loss, and sleep disturbances (insomnia or dreams with scary dreams). Hallucinations and fear appear. There are constant muscle twitching, hand tremors, paresthesia, constriction of the pupils, the appearance of horizontal nystagmus, and intellectual impairment.

Stage II – therapeutic dose of dipyroxime

administration of additional smaller doses of atropine. Daily doses for maintenance treatment: 1 tbsp. – 4-6 mg, in 2 tbsp. – 30-50 mg, in 3 tbsp. – 100-150 mg.

4) Prevention of occupational diseases. Preliminary and periodic preventive medical examinations, procedure. Rehabilitation and medical examination for occupational diseases.

Answer: Activities aimed at preventing occupational diseases:

1) Engineering and technical measures aimed at primary prevention:

Replacing toxic substances with less toxic ones,

Sealing of technological processes,

Improvement of technology,

Creating effective ventilation.

2) Hygienic measures:

Providing personal protective equipment,

The use of protective ointments and pastes,

Correct lighting workplace,

Compliance drinking regime,

Hygienic control of the workplace.

3) Medical and biological measures:

Inhalator device,

Sanitation of microtraumas,

The use of vitamin complexes,

The use of adaptogens when working with vibration, noise, ultrasound,

The use of pectins when working with heavy metals,

Creation of psychological relief rooms.

The main task of preventive examinations– identifying early signs of exposure unfavorable factors production environment for the purpose of further implementation of therapeutic, health-improving and preventive measures.

Preliminary medical examinations are aimed at preventing persons with certain deviations in the condition of organs and systems most susceptible to the influence of this unfavorable factor from working.

Purpose of periodic medical examinations– identification of the earliest signs of exposure to industrial hazardous factors, as well as common diseases, which are contraindications for continuing this professional activity. As a result of periodic medical examinations, a medical report is issued, which indicates the diagnosis of the identified disease, as well as an assessment of professional suitability and the necessary recommendations for prevention and treatment

Order No. 90 of March 14, 1996 “On the procedure for conducting preliminary and periodic medical examinations of workers and medical regulations for admission to the profession”

Order No. 555 of September 29, 1989 “On improving the system of medical examinations of workers and drivers of individual vehicles.”

5) Occupational diseases associated with physical overload and overexertion individual organs and systems. Diseases of the musculoskeletal system. Production factors. Stenosing ligamentosis, styloidosis (ulnar and shoulder), epicondylosis. Pathogenesis, clinic.

Answer: Main indicators of the severity of the labor process:

Weight of load lifted and moved manually

Stereotypical labor movements

Working posture

Body tilts

Moving in space

Main indicators of the intensity of the labor process:

Monotone

Operating mode

Causes of illness from functional overstrain: static or dynamic loads on local or regional muscle groups, frequently repeated movements of the same type - at a fast pace, with high coordination, uneven rhythm of work, forced uncomfortable working posture, external or internal pressure on tissues or organs, macrotraumatization of tissues due to pressure or friction tools or products, irrational work practices.

Specific damage to occupational diseases from functional overstrain: musculoskeletal system, nervous system, vocal apparatus, visual analyzer.

Industries with a high prevalence of musculoskeletal diseases: mining, coal, mechanical engineering, electrical engineering, logging, construction, and agriculture.

Among the diseases of the musculoskeletal system, the most common are diseases of the muscles, ligaments and joints. upper limbs: myositis, crepitating tenosynovitis of the forearm, stenosing ligamentitis (stenosing tenosynovitis), epicondylitis of the shoulder, bursitis, deforming osteoarthritis, periarthrosis of the shoulder joint, osteochondrosis of the spine (discogenic lumbosacral radiculitis). Diseases develop subacutely, have a recurrent or chronic course.

A hazardous production factor (HPF) is a production factor whose impact on a worker under certain conditions leads to injury or other sudden sharp deterioration health. Trauma is damage to body tissues and disruption of its functions. external influence. An injury is the result of an industrial accident, which is understood as a case of exposure to a hazardous production factor on a worker while performing his job duties or tasks of a work manager.

A harmful production factor (HPF) is a production factor whose impact on a worker under certain conditions leads to illness or decreased ability to work.

STENOSIS LIGAMENTOSIS is a disease characterized by damage to the annular ligament surrounding the deep flexor tendon of the finger, with its scarring and stenosis, blocking the extension of the finger. Clinically manifested by pain that occurs primarily. with repeated monotonous movements, later a typical picture of the so-called appears. snapping finger: when blocked, the finger can be extended passively with a clicking sound. In the early stage, local injections of non-steroidal anti-inflammatory drugs and resorption therapy are effective; in the later stage, surgical treatment is effective.

Ulnar styloiditis is tenosynovitis of the extensor carpi ulnaris, or stenosing ligamentitis of the sixth canal of the dorsal carpal ligament. Its essence lies in the narrowing of the VI canal due to fibrous changes in the tendons of the extensor carpi ulnaris, its sheath and the ligaments that form the canal. The cause of the disease is trauma to this area or its long-term professional microtraumas (for seamstresses, typists, polishers, etc.). Spontaneous pain appears in the area of ​​the styloid process ulna, intensifying with radial abduction of the hand and radiating to the IV and V fingers. On palpation, there is tenderness over the styloid process of the ulna, and sometimes slight swelling in this area. In some cases, x-rays reveal thickening of the soft tissues above the styloid process.

Epicondylosis of the shoulder is a common disease of the working arm. It occurs due to overstrain and microtrauma of the muscles attached to the epicondyles of the shoulder. External epicondylosis of the shoulder is more common. Develops in people whose work involves prolonged and intense pronation and supination of the forearm with simultaneous frequent flexion and extension at the elbow joint (choppers, cutters, mechanics, masons, painters, milkmaids for manual milking, machine operators). The disease is based on microtraumatization of the periosteal tissue of the epicondyle as a result of overstrain of the muscles extending from the external and internal epicondyle. Aseptic inflammation develops with changes in the periosteum, fascia, ligaments, and muscles. Aching, nagging pain appears in the area of ​​the epicondyle. They disappear only at rest or when the arm is slightly bent at the elbow. Characteristic and constant symptoms are Thomsen (sharp pain in the area of ​​the lateral epicondyle when extending the hand) and Welsh (pain when quickly and vigorously straightening an arm bent at the elbow).

6) Intoxication with carbamic acid derivatives (carbamates). Diagnostics. Treatment. Prevention. Issues of examination of work ability. Medical and social rehabilitation.

Answer: Derivatives of carbamic acids are used as means of protecting fruits, vegetables, melons, grains and industrial crops from pests, diseases and weeds. Most of the currently used pesticides in this group belong to herbicides, but they also include fungicides, insecticides, nematicides, zoocides, etc.

Most derivatives of carbamipic acids have low and moderate toxicity, as well as weakly expressed cumulative properties. Along with this, among them there are highly toxic compounds and drugs with pronounced cumulative properties. Carbamates are unstable to external influences.

The main routes of entry into the body are through the respiratory system, skin, and gastrointestinal tract.

Pathogenesis. Main pathogenetic mechanism The development of intoxication with carbamates is their ability to inhibit cholinesterase activity and have a muscarinic and nicotine-like effect. In this regard, a disruption of enzymochemical processes in tissues occurs. In the genesis of carbamate poisoning, disruption of redox and metabolic processes, in particular the metabolism of nucleic acids, is also of significant importance. Defeat is characteristic parenchymal organs, hematopoiesis, endocrine glands and central nervous system. All these pesticides have an allergenic effect. A specific feature of their action (for example, sevin) is a pronounced effect on the generative function.

Pathological picture. Degeneration of parenchymal organs, severe vascular disorders, and pulmonary edema are noted. At lower doses of pesticides, irritation of the mucous membrane of the gastrointestinal tract is found in experimental animals. Histologically, focal amyloidosis is detected in the liver and spleen, and a focal non-purulent interstitial inflammatory process is detected in the kidneys.

Clinical picture. Acute intoxication. Characterized by rapid development. Main symptoms: severe weakness, headache, irritation of the mucous membranes of the nose, eyes, nausea, vomiting, drooling, increased sweating, abdominal pain, diarrhea. Pallor of the skin, constriction of the pupils with spasms of accommodation, bradycardia, and angina are observed. Fibrillar muscle twitching is possible. Sometimes bronchospasm and pulmonary edema are noted. Often all these phenomena are accompanied by confusion and convulsions. Of great importance is the reduction in cholinesterase activity and alkaline phosphatase in blood. In case of TMTD poisoning, symptoms of irritation of the mucous membranes and skin come to the fore. This drug may have the most allergenic effect. Therefore, in the clinical picture of poisoning, the development of allergic dermatosis is possible. In addition, TMTD has the ability to increase a person’s sensitivity to alcohol, which can manifest itself in collaptoid poisoning.

Chronic intoxication. Symptoms develop gradually and are scant. Characteristic of this intoxication is irritation of the mucous membranes of the upper respiratory tract and bronchi, which is manifested by subatrophic nasopharyngitis, tracheitis and chronic obstructive bronchitis. Subsequently, symptoms of vegetative-vascular dystonia, myocardiopathy and neurasthenic syndrome develop. Often, signs of polyneuritis of the extremities are observed. Neuroendocrine disorders are possible. Sometimes symptoms of damage to the digestive glands are noted: gastroduodenitis, colitis and even rectal polyposis. Changes in peripheral blood are manifested by moderately severe hypochromic anemia, leukopenia and thrombocytopenia.

Diagnostics - determine the activity of cholinesterase, carry out a diagnostic minimum.

Treatment. In case of acute intoxication, emergency care is indicated. Antidote and symptomatic therapy are required. Anticholinergic drugs, in particular atropine, are recommended as an antidote. For mild poisoning, 1-2 ml of a 0.1% atropine sulfate solution is administered intramuscularly; for more severe forms, the dose can be increased to 5 ml. Injections must be repeated every 5-6 minutes until bronchorrhea, miosis or signs of atropine overdose appear (dry mucous membranes, temporary visual impairment). Subcutaneous administration of a 0.05% solution of proserin and oral tropacin tablets (0.01 g) are also indicated. Further symptomatic therapy is recommended: intravenous administration glucose - 20 ml of 40% solution, 5% ascorbic acid solution, B vitamins. Cardiac medications are prescribed - 1 ml of 10% caffeine solution, 2 ml of 25% cordiamine solution; oxygen, carbogen.

For chronic intoxication antidote therapy Anticholinergic drugs must be combined with vitamin therapy, sedatives and physiotherapy. Timely assistance and active treatment lead to the reverse development of the pathological process.

Prevention - observe the work and rest schedule, use personal protective equipment, preventive and periodic medical examinations.

When carrying out an examination of work ability in cases of occupational poisoning with pesticides, it is necessary to: clarify and confirm the diagnosis of poisoning, establish occupational etiology, clarify the nature of the poisoning, the degree of severity, determine the degree of decrease in professional work ability, and determine rehabilitation measures.

7) The concept of occupational diseases, the structure of occupational diseases, classification. List of occupational diseases, application in the work of a doctor. General principles of classification, diagnosis and therapy of occupational diseases.

Answer: Occupational diseases- appear as a result of damage to the body by harmful production factors.

Harmful production factors - interaction on a worker in production conditions, which, depending on the nature and degree of severity, can lead to a decrease in working capacity, the occurrence of occupational diseases and poisoning, an increase in morbidity with temporary loss of ability to work, negative consequences in the long term for the workers themselves or their children.

Classification:

I. 1) Physical factor: microclimate of the working area, vibration, noise, ultrasound, infrasound, ionizing

2) Chemical factor

3) Exposure to dust

4) Biological factor: microorganisms, protein preparations, antibiotics

5) Severity of labor: movement in space, the mass of the lifting load, stereotypical working movements, static load, physical and dynamic load, body tilt, working posture.

6).Labor intensity: duration of concentrated observation, number of production facilities at the same time, load on the auditory analyzer, work with optical instruments, load on the vocal apparatus.

II. By type of exposure to harmful factors:

–complex impact- when factors arrive simultaneously, but in different ways (blood, gastrointestinal tract, lungs)

-combined effect- one and the same route of entry of several substances

-combined effect-simultaneous or sequential action on the body of factors of different nature (chemical, biological, physical factors)

III. With the flow:

Chronic

Deferred

IV . The nature:

Annoying,

Mainly affecting: blood, organ parenchyma

Sensitizing effect

Long-term effect

8) Occupational dust and toxic bronchitis: hazardous industries, classification, clinical picture, diagnosis, treatment, prevention.

Answer:Dust bronchitis characterized by diffuse inflammation of the trachea and bronchi, which occurs in persons exposed to industrial aerosols for a long time elevated concentrations. Spheres of production: non-ferrous metallurgy, coal industry, production of mineral fertilizers.

Pathogenesis: Stage I formation of pathology, the duration of which is up to 10 years of dust exposure, due to chronic irritation the number of goblet cells increases (morphological hypertrophy of the mucosa), which leads to hypersecretion. But this process is not accompanied by activation of dust removal, since due to a change in the sol/gel ratio, the movement of the cilia becomes ineffective. Dust accumulates with sputum in the bronchi, and a periodic cough appears (mucociliary insufficiency is formed).

Stage II characterized by the development of catarrhal and atrophic changes in the bronchial mucosa. The epithelium is desquamated, replaced by a functionally defective regenerative one, which leads to an increase in mucociliary insufficiency and an even more pronounced disruption of the dust elimination process. The protective properties of immunoglobulins A decrease, and a deficiency of nonspecific protective factors develops. Against the background of the clinical and morphological picture of endobronchitis, the addition of infection causes the development of a symptom complex characteristic of chronic dust bronchitis.

Classification:

I. by etiology:

a) dust (inorganic and organic aerosols),

b) toxic dust (chemical irritants and inorganic aerosols),

c) toxic (chemical irritants).

II. According to the development mechanism:

a) bronchitis irritants (inorganic dust and chemical irritants),

b) allergic (organic dusts and allergens),

c) mixed form.

III. Functional characteristics:

a) simple,

b) obstructive.

IV. By The nature of changes in the bronchial mucosa:

a) hypertrophic endobronchitis,

b) atrophic endobronchitis,

c) purulent endobronchitis,

d) catarrhal endobronchitis.

V. By Level of damage:

a) proximal,

b) distal.

VI.By Gravity process A:

a) mild course,

b) moderate severity,

c) severe course.

VII. Disease phase:

a) exacerbation,

b) subsiding exacerbation,

c) remission.

VIII Complications: pneumosclerosis, pulmonary emphysema, pneumonia, bronchial asthma, central lung cancer, cor pulmonale.

IX. Degree of respiratory failure: 1, 2, 3 tbsp.

Clinical picture: Simple bronchitis: imperceptible, gradual onset, rare exacerbations, cough with mucous sputum in the morning. During an exacerbation, the temperature rises, the cough with mucous sputum intensifies, and a small amount of dry wheezing is heard. Fiberoptic bronchoscopy shows a picture of catarrhal endobronchitis. External respiration functions are within normal limits.

Obstructive bronchitis: obstruction develops when the distal bronchi are involved. Shortness of breath during physical activity and an unproductive cough appear, which intensifies when exposed to cold air, irritants and physical activity. Auscultation of breathing is weakened, whistling dry rales are heard. X-rays show peribronchial sclerosis and pulmonary emphysema. When studying the respiratory function, obstructive changes and a decrease in vital capacity of the lungs are revealed. Fiberoptic bronchoscopy shows a picture of diffuse endobronchitis, possible signs of catarrhal inflammation, dust spots (impregnation).

Purulent dust bronchitis is characterized by a cough with purulent sputum, severe shortness of breath, loss of body weight, changes in the terminal phalanges of the fingers (“drum sticks”), and cyanosis. Developing nephrotic syndrome. On auscultation, small and medium-sized wheezing sounds are heard. X-ray examination reveals severe pneumosclerosis and emphysema. When studying the respiratory function, there are pronounced obstructive changes, a sharp decrease in vital capacity. During an exacerbation, there is an increase in temperature, an increase in the amount of wheezing in the lungs, a sharp increase in shortness of breath and the amount of purulent sputum.

Diagnostics

1. Compliance of the diagnosis with WHO criteria: duration of cough with sputum for more than 3 months per year for at least two years.

2. Study of the professional route, sanitary and hygienic characteristics of working conditions, data from preliminary and periodic medical examinations (must confirm the presence of a long period of work in dusty conditions, exceeding the maximum permissible concentration, the nature of the dust, the absence of other etiological factors in the development of chronic bronchitis).

3.Fibrobronchoscopy.

4.X-ray chest.

5. Study of external respiration function.

6. Study of blood gas composition.

7. Study of general blood count and general sputum analysis.

The diagnostic process thus takes place in two stages:

a) establishing a diagnosis of chronic bronchitis,

b) resolving the issue of the connection between the disease and the profession.

Differential diagnosis is carried out with:

Primary pulmonary emphysema,

Pneumoconiosis,

Bronchial asthma,

Exogenous allergic alveolitis.

Treatment:

1. Activation of regeneration processes of the elastic framework of the lungs by inhalation of drugs with natural protease inhibitors. (contriked 5000 ATRE once a day for a month).

2. Reducing bronchial obstruction (anticholinergic drugs - Atrovent, Troventol, if necessary, sympathomimetics and theophylline preparations.

3. Anti-inflammatory therapy using corticosteroids, immunomodulators, antibiotics (as indicated).

4. Improving sputum drainage (mucolytics and mucokinetics).

5. For chronic hypoxemia - long-term oxygen therapy.

6. According to indications - bronchoalveolar lavage.

7. Inhalation of a 2% solution of sodium chloride, sodium bicarbonate with the addition of bronchodilators, essential oils.

8. Laser therapy (reduces the tone of the pulmonary vessels, has anti-inflammatory, immunomodulatory effects, increases the activity of antioxidant enzymes).

9. UHF on the roots of the lungs.

10. Chest massage, physical therapy.

9) Vibration disease from exposure general vibration, reasons, potentially hazardous industries, classification, clinic. Diagnostics. Treatment, Prevention. Issues of examination of work ability. Medical and social rehabilitation (MSR).

Answer: Vibration disease is an occupational disease, the main etiological factor of which is vibration in production (mechanization equipment, agricultural machinery, road machines, tools, railway transport, air transport).

General vibration is transmitted while sitting through the buttocks or while standing through the soles of the feet.

Pathogenesis: Contact with sources of vibration leads to irritation of skin, muscle receptors, receptors of the vascular bed, periosteum in the contact zone and along the path of vibration registration. Afferent impulses cause responses reflex reactions at various levels of the central nervous system. The regional circulatory system is affected and vasospasms occur. The changes are dystrophic in nature and manifest themselves as angiotrophoneurosis.

The entire human body is exposed to general vibration through supporting surfaces, vibration of the working surface: drivers of heavy vehicles, agricultural machine operators, excavator operators, drilling rig operators.

Classification:

I degree – initial manifestations:

1. Angiodystonic syndrome (cerebral or peripheral)

2. Vegetative-vestibular syndrome

3. Syndrome of sensory (vegetative-sensory) polyneuropathy of the lower extremities

II degree – moderately expressed manifestations:

1. Cerebro-peripheral angiodystonic syndrome

2. Syndrome of sensory (vegetative-sensory) polyneuropathy in combination with

Polyradicular disorders (polyradiculoneuropathy syndrome)

Secondary lumbosacral radicular syndrome (a consequence of osteochondrosis of the lumbar spine)

Functional disorders of the nervous system (neurasthenia syndrome)

III degree – pronounced manifestations:

1. sensory-motor polyneuropathy syndrome

2. discirculatory encephalopathy syndrome in combination with peripheral polyneuropathy (encephalopathy syndrome).

Diagnostics based on professional route, working conditions, objective and paraclinical data.

ETM: acrohypothermia up to 18-20 0C, cold test, capillaroscopy, aldesiometry, pallesthesiometry, dynamometry, ENMG, rheovasography, thermal imaging, EEG.

Treatment: etiological - elimination of contact with vibration, pathogenetic - improvement of microcirculation, elimination of trophic disorders, relief of pain, restoration of musculoskeletal function.

Examination of working capacity: assessment of severity, clinical syndromes, concomitant diseases, age, work experience, presence of other specialties.

VB I degree – professional ability to work is preserved, treatment, temporary transition to light work

VB II degree – employment without contact with vibration

III degree VD - limited ability to work, disability of 2 or 3 groups due to an occupational or general disease.

10) The influence of professional and production factors on the specific functions of the female body, on the fetus and newborn. Characteristics of action chemical substances on reproductive function men.

Answer: The influence of unfavorable professional factors can affect the so-called specific functions of the female body - ovarian-menstrual and childbearing, as well as the offspring.

Of the specific functions of the female body, the most sensitive to harmful toxic effects is the ovarian-menstrual function. Its violations occur most often and are usually the earliest. In short-term workers who have contact with toxic substances, hypermenstrual syndrome (menorrhagia, increased frequency of menstruation) is observed predominantly, while in workers with extensive experience, hypomenorrhea and other symptoms of decline of ovarian function more often occur. This pattern reflects a certain phase of exposure to toxic substances: promotion functional ovarian activity, observable in the first phase of intoxication, is replaced period of imaginary normalization, after which they gradually develop degenerative changes in the ovaries, leading to the extinction of their functions. It is important to emphasize that menstrual dysfunction is sometimes observed when exposed to low concentrations of toxic substances; they may not be accompanied by a general picture of intoxication, representing in these cases the only and earliest manifestation of toxic effects.

The adverse effects of toxic substances on reproductive function can manifest themselves in various forms. Development infertility described in cases of intoxication lead, mercury, arsenic, those working in contact with gasoline, benzene, phthalic anhydride, chlorinated hydrocarbons.

Pathological course of pregnancy and childbirth(toxicosis of pregnant women, threatened miscarriages, premature or rapid labor, premature rupture of water and vice versa - weakness labor activity, uterine atony leading to bleeding in the third stage of labor) is observed with a significantly increased frequency in workers with lead, mercury, arsenic, benzene, gasoline, styrene, carbon disulfide, trichlorethylene, as well as among production workers nylon fiber, synthetic rubber, from electric welders.

The adverse effect on the fetus is due to the penetration of a toxic substance through the placental barrier. The possibility of such penetration has been proven for lead, mercury, phosphorus, fluorides, benzene, trinitrotoluene, nicotine, carbon monoxide, gasoline, cadmium, antimony, carbon disulfide, chloroprene, and a number of pesticides. The result may be an increased frequency of stillbirths, the birth of non-viable children (increased infant mortality in the first days or weeks after birth), and deformities. In addition, for a number of toxic substances (lead, mercury, fluorides, arsenic, antimony, gasoline, carbon disulfide, mercury and organochlorine compounds, etc.), the possibility of their penetration into milk has been proven, which adversely affects the function of lactation (shortening its duration, reducing the amount milk and a change in its quality and taste, causing the child to refuse the breast) and on the child’s condition.

The possibility of disruption of embryogenesis when exposed to even small doses of toxic substances that are harmless to the mother (formaldehyde, manganese, chloroprene, pesticides) has been experimentally proven.

Of the many physical factors that can be influenced in production conditions, the most pronounced adverse effect on the female genital area is ionizing radiation(especially internal exposure). Various disturbances of ovarian-menstrual function are found in working women under the influence of even relatively small doses of ionizing radiation (menstrual cycle disorders, menorrhagia). The degree of their persistence depends on the dose and duration of exposure to the latter (if exposed to large doses, irreversible sterility may occur).

The unfavorable effect of ionizing radiation on the fetus (the occurrence of developmental abnormalities and a decrease in fetal viability) is due, on the one hand, to its effect on a woman during pregnancy (irradiation is especially dangerous in its early stages), on the other hand, to the retention of radioactive substances in the body of a pregnant woman, which can pass through the placenta into the fetus (internal exposure).

Vibration- both high-frequency and low-frequency - adversely affects the female genital area. Experimental studies confirm the adverse effects of vibration on the ovaries and uterus(development degenerative changes in them). An increased incidence of prolapse and prolapse of the genital organs has been noted in women exposed to low-frequency jolt-like vibration (truck drivers, railway car attendants, electric welders).

Overheating e in production conditions leads to frequent development menstrual irregularities(mostly like hypomenstrual syndrome), to an increase in late toxicosis in pregnant women and especially to birth disorders(weakness of labor, fetal asphyxia), as well as high mortality of newborns in the first days of life.

In women exposed to electromagnetic fields of radio frequencies, especially Microwave, are observed menstrual irregularities(menorrhagia, increased menstruation), as well as frequent complications of labor(weakness of labor, bleeding, aggravated arterial hypotension, typical for this impact). The microwave field adversely affects lactation.

Lifting and carrying heavy loads adversely affect ovarian-menstrual function, as well as reproductive function (increased incidence of pregnancy complications, spontaneous miscarriages) and the level of gynecological morbidity, contribute to the development of prolapse of the internal genital organs and retroflexion of the uterus.

Substances causing predominant damage reproductive organs men

Target Toxicant

Spermatogonia Bisulfan, procarbazine

Spermatocytes 2-methoxyethanol, procarbazine

Spermatids Methyl Chloride

Sertoli cells Dinitrobenzene, hexanedione

Leydig cells Ethane dimethyl sulfonate

Epididymocytes Chlohydrin, methyl chloride, ethane dimethyl sulfonate

Accessory sex glands Imidazole

11) Acute and chronic benzene intoxication: potentially hazardous industries, potentially dangerous professions. Pathogenesis, classification, clinical picture, diagnosis, treatment, prevention. Benzene leukemia.

Answer: Etiology. Benzene is a liquid with a specific aromatic odor, easily soluble in alcohol, ether, fats, lipids and sparingly soluble in water. Benzene is widely used in various organic synthesis reactions. It is a valuable raw material for the manufacture of synthetic products; it is found in some types of petroleum and motor fuel; it is found in small quantities in technical combustible gases, in petroleum solvent gasolines; it can be found as an impurity in its homologues (toluene, xylene) and other organic solvents. .

The maximum permissible concentration of benzene (MPC) is 5 mg/m 3 of air.

Under industrial conditions, the penetration of benzene and many of its compounds into the human body is possible through the lungs in the form of vapors and through intact skin. When exposed to benzene, the development of both acute and chronic intoxication is possible. Acute poisoning occurs as a result of short-term inhalation of large concentrations of benzene vapor due to accidental leakage indoors or while working in confined spaces (cleaning benzene tanks, etc.). Chronic intoxication develops with prolonged inhalation of small concentrations of benzene vapor and with systematic contact with the skin. At acute intoxications benzene can be found in blood, brain, liver, adrenal glands. At chronic intoxications most of it is determined in adipose tissue and bone marrow. A significant portion of benzene is excreted from the body in exhaled air and urine. Another part of benzene is oxidized to form phenol, diphenols, which are excreted in the urine in the form of glucuronic acid and sulfur compounds.

Pathogenesis. The mechanisms of development of toxic hemodepression are diverse and complex. They include as possible direct cytotoxic effect on the earliest cells of hematopoiesis precursors - pluripotent stem cells, and on microenvironment the latter (stromal cells of the bone marrow and other hematopoietic organs, non-cellular elements). The consequence of this action is a decrease in the number of stem cells (“narrowing of the bridgehead of hematopoiesis”), disruption of their proliferation and differentiation.

Cytokinetic studies of the bone marrow, even at low levels of benzene exposure, noted inhibition of the proliferation of neutrophil and erythrocyte precursor cells, as well as compensatory activation of hematopoiesis, which for a long time prevents the development of peripheral cytopenia.

The impact of toxic substances - hemosuppressants on the morphofunctional state of hematopoietic cells, caused by interference in the processes of lipid peroxidation, DNA synthesis, and oxidative phosphorelation, should be taken into account. The consequence of this is a defect in production and a reduction in cell survival, primarily for granulocytes.

The role of autoimmune mechanisms in the development of hemodepression, associated with a violation of the antigen-recognition properties of T-lymphocytes and their depressive effect on myelopoiesis, has also been established.

The balance of some vitamins is disrupted: the content of B vitamins (primarily pyridoxine and cyanocobolamin), involved in the process of bone marrow hematopoiesis, decreases, as well as ascorbic acid, which takes part in the regulation of blood clotting and normalization of the permeability of capillary walls.

Benzene acts directly on the central nervous system, causing development neurodystrophic symptom complex.

The severity of depression of erythro-, leuko-, and thrombocytopoiesis caused by a toxic substance can be different. It depends on the intensity and duration of action of the etiological factor, the individual sensitivity of the body to its action, the state of endogenous factors affecting hematopoiesis, especially in women (iron deficiency, dysfunction of the thymus, thyroid glands, ovaries, etc.).

Clinical picture

Acute intoxication. Benzene poisoning is accompanied by damage to the central nervous system with symptoms of cerebral disorders, which can also be observed during intoxication with poisons that have narcotic properties.

At mild degree acute benzene intoxication, victims are in a state of mild euphoria. General weakness, dizziness, tinnitus, headache, nausea, vomiting appear, staggering when walking.

All of these phenomena are unstable and completely disappear within a few hours, without causing any disturbances in other organs.

In case of acute intoxication moderate severity general weakness, headache intensify, inappropriate behavior, anxiety are noted, skin becomes pale, body temperature decreases, breathing quickens, frustration is observed cardiovascular activity: frequent, weak pulse, drop in blood pressure. Marked muscle twitching, tonic and clonic seizures, pupil dilation. Possible total loss consciousness, coma . In patients who have suffered acute intoxication of moderate severity, after some time a complete recovery may occur; sometimes they remain persistent functional disorders of the nervous system in the form of asthenovegetative syndrome.

Severe degree acute benzene intoxication is characterized by almost immediate loss of consciousness, development of toxic coma, accompanied by respiratory arrest due to paralysis of the respiratory center. In such conditions, death often occurs. Changes in the blood appear only in the form of moderate short-term leukocytosis due to a violation of the central regulation of hematopoiesis. No deep lesions of bone marrow hematopoiesis are observed during acute benzene intoxication.

Chronic intoxication. This form of intoxication is characterized primarily by damage to bone marrow hematopoiesis. The clinical picture consists of a set of hematological symptoms, which are combined with changes in other organs and systems.

If in the clinical picture the leading one is anemic syndrome, then general weakness, fatigue, frequent dizziness, often headache, a feeling of spots before the eyes, and shortness of breath during physical exertion predominate. Skin in patients, the mucous membranes are pale, as are the visible mucous membranes, there is a shift in the boundaries of relative cardiac dullness to the left, and a systolic murmur is often heard above the apex and in the area of ​​the projection of the pulmonary artery. The lymph nodes and spleen are not enlarged.

In cases where it prevails thrombocytosis depression, various clinical manifestations hemorrhagic syndrome (bleeding gums, skin hemorrhages, menorrhagia, nosebleeds). The severity of hemorrhagic syndrome is determined by the severity of hematopoietic damage. Hemocoagulation disorders and structural changes play a role in the origin of hemorrhages. vascular wall stromal cells up to the development of “bone marrow fibrosis” with subsequent ruptures of blood vessels.

Changes in peripheral blood when exposed to hemotoxic substances are characterized by cytopenias, mainly mild. Sometimes cytostatic reactions are transient. Most often, the first hematological symptom is leukopenia, which can be transient. Diagnostic value has a persistent decrease in the number of leukocytes - less than 4.0. 10 /l. Leukopenia, as a rule, is formed due to a decrease in the content of neutrophils, which leads to relative lymphocytosis. Qualitative changes in leukocytes occur: an increase in the content of neutrophils with pathological granularity, their hyperpigmentation, rejuvenation of the leukogram with a shift to the left. Along with leukopenia, moderate thrombocytopenia (less than 180 10 /l) and mild erythropenia may be observed. The content of reticulocytes is either normal or slightly increased (> 12%).

In cases where depression of erythropoiesis predominates, changes in the peripheral blood are mainly found in red blood: the hemoglobin content decreases (< 115г/л у женщин и < 132г/л у мужчин) и количества эритроцитов

(< 3,7 10 /л у женщин и < 4,0 10 /л у мужчин). Анемия обычно умеренная, нормохромная. При глубокой депрессии кроветворения в крови обнаруживается выраженная панцитопения. При этом резко ускорена СОЭ, удлинено время кровотечения (>6–10 minutes).

The picture of sternal punctures is different. With moderate cytopenia of peripheral blood, it is characterized by signs of a mild hypoplastic state (decrease in segmented neutrophils with a decrease in the number of young forms of the myeloid series), unstable reticulocytosis. The presence of the latter along with hyperplasia of the erythroid lineage and increased mitotic activity of myeloid cells indicates activation

regenerative processes and is regarded as a compensatory reaction to the influence of a hemotoxic factor.

A typical representative of such poisons is benzene. The picture of acute intoxication was outlined above.

Chronic benzene intoxication occurs with predominant defeat hematopoiesis and the nervous system, as well as changes in other organs and systems.

Prolonged contact with benzene leads to the development of chronic benzene intoxication (mild, moderate and severe) and leukemia (acute and chronic).

To establish a diagnosis of pneumoconiosis, it is first of all necessary that the patient’s work history contains contact with the relevant types of industrial dust. Differential diagnosis is helped by: anamnestic data; objective examination data; data from laboratory, instrumental and functional studies, such as bronchofibroscopy, biopsy of the bronchial mucosa, transbronchial biopsy of lung tissue, puncture of the lymph nodes of the roots of the lungs, examination of bronchoalveolar lavage fluid, special sputum studies, special allergy tests, features of the clinical picture of pneumoconiosis, data from consultations with specialists ; document data (professional history, sanitary and hygienic characteristics of working conditions, outpatient card, medical examination cards).

In the clinical and radiological picture of various types of pneumoconiosis, there are many common features. At the same time, depending on the composition of the inhaled dust, they also have some differences (see the clinical picture of silicosis, silicosis, carboconiosis and other types of pneumoconiosis). This concerns the timing of their development, the form of the fibrotic process in the lungs, its tendency to progression and complications. For example, silicosis occurs with a shorter period of work in contact with dust than other types of pneumoconiosis, is characterized primarily by the presence of a nodular form of pneumofibrosis, usually has a more pronounced tendency to progress and is much more often combined with pulmonary tuberculosis. With asbestosis, mainly an interstitial form of pneumofibrosis develops, which is often observed in combination with chronic bronchitis, and sometimes with bronchogenic cancer. Therefore, if we take into account the “dust” work experience, the composition of industrial dust and the characteristics of the clinical and radiological picture of the disease, the differential diagnosis of various types of pneumoconiosis does not present any difficulties.

In cases where a disseminated process in the lungs is detected in people who work for a long time in conditions of exposure to dust, it is necessary to keep in mind the possibility of developing not only pneumoconiosis, but also some other non-occupational diseases: disseminated pulmonary tuberculosis (mediastinal-pulmonary form of sarcoidosis), diffuse fibrosing alveolitis, lung carcinomatosis. For differential diagnosis, it is important to take into account the clinical symptoms of the corresponding diseases.

Pneumoconiosis sometimes has to be differentiated from some forms of systemic diseases: rheumatoid arthritis, Wegener's granulomatosis, lupus pulmonary vasculitis, etc. In these cases, it is especially important to take into account the uniqueness of the clinical picture of these diseases.

Literature:
Pulmonologist's Handbook / V.V. Kosarev, S.A. Babanov. – Rostov n/d: Phoenix, 2011. – 445, p.

1. Differential diagnosis / Andrew T. Raftery, Eric Lim; translated from English – M.: MEDpress-inform, 2005. – P. 290.

2. Makhonko M.N., Zaitseva M.R., Shelekhova T.V., Kurnosov S.V. Clinical case stages of diagnostic search for occupational lung disease. Materials of the XI international scientific and practical conference “Science and technology: a step into the future - 2015”. – 02/27/2015-03/05/2015 – Sat. scientific works - Czech Republic, Prague). – Volume 14. – pp. 31-41.

3. Rational pharmacotherapy of respiratory diseases: Hand. for practicing doctors / A.G. Chuchalin, S.N. Avdeev, V.V. Arkhipov, S.L. Babak and others. Under general. ed. A.G. Chuchalina. – M.: Litterra, 2004. – 874 p.) – (Rational pharmacotherapy: Serial manual for practicing physicians; T. 5).

4. Shmelev E.I. Differential diagnosis of disseminated lung diseases of non-tumor nature DOCX. - RMJ. – 2001. – No. 21. – P. 919-922.

Currently, occupational pathologists still often have to make a differential diagnosis between pneumoconiosis (PZ), especially silicosis, and pulmonary tuberculosis (PT). The clinic of occupational pathology and hematology of the Saratov State Medical University often receives patients with suspected disseminated lung disease (DLD), primarily PD, after undergoing treatment in an anti-tuberculosis dispensary. This is explained by the fact that with ignorance of professional history and the absence of TL, it is difficult to recognize PP. Our institution also treats patients with established diagnosis silicotuberculosis, the prognosis of which mainly depends on the form of TL.

PZ is a group of chronic occupational lung diseases caused by prolonged inhalation of industrial dust and characterized by sclerotic changes in the lung tissue. Tuberculosis is a chronic infectious disease caused by Mycobacterium tuberculosis, which is characterized by the development of specific inflammatory granulomas in organs and tissues (mainly in the lungs) and a polymorphic clinical picture. TL is one of the most ancient and widespread diseases, which is a social disaster and problem. The work of many authors has revealed that at the moment this pathology affects socially active, wealthy people, and not just disadvantaged people.

A number of publications have established that the features of the clinical course of a specific disease without intoxication syndrome, the x-ray picture and localization of x-ray changes, the detection of coal dust particles, asbestos bodies and other elements of the working environment in the biosubstrate, negative results of tuberculin tests, lack of response to chemotherapy help in differential diagnosis with TL. Although some scientists note that positive tuberculin tests often occur in uncomplicated silicosis. In this matter, it is important to carefully collect professional, epidemiological, and life history (contact with harmful dust production factors, contact with a tuberculosis patient, nature and duration of contact, living conditions). If tuberculosis is suspected, repeated cultures of sputum, urine, wash water from the bronchi or during repeated bronchological examinations, a lung biopsy is performed. The diagnostic algorithm when working with patients with DLD should consist of three mandatory components: a thorough study of the history and clinical symptoms of the disease; performing a computed tomogram (CT); examination of biopsy material. Clinicians have determined that the final diagnosis of PD is established on the basis of several diagnostic criteria: professional history data; assessment of dust content in the working area; X-ray picture at the time of examination and over several years; indicators of external respiration function. A large number of specialists in domestic and foreign literature emphasize that in patients with silicosis, impaired blood and lymph circulation in the lungs, tension in regulatory processes, and functional inferiority of the B-system of immunity predispose them to the development of TL. According to the order of the Ministry of Health and social development dated April 27, 2012 No. 417n “On approval of the list of occupational diseases” included pneumoconiosis complicated by tuberculosis: silicotuberculosis, coniotuberculosis, anthracosilicotuberculosis (J 65 - disease code according to ICD-10). Considerable attention is paid to the similarity of clinical and radiological data, the similarity of morphological characteristics, immunological changes, the combination of silicosis and tuberculosis, their close relationship, which are the source of many studies and serious difficulties in carrying out differential diagnosis. It is known that the rate of development, course, and progression of PD depend on hygienic working conditions, living conditions, the reactivity of the body, concomitant pathology and complications.

Thus, issues of differential diagnosis of PZ and TL continue to be resolved taking into account the occupational route, sanitary and hygienic characteristics of the specific patient’s workplace, life history, epidemiological history, clinical, physical, radiological and biopsy materials. Differential diagnosis of DLD, especially PZ, is helped by: features of the clinical picture; anamnestic data (profanamnesis); objective examination indicators; data from laboratory, functional, instrumental (radiography, CT, biopsy of lung tissue), physical examinations; information about consultations with narrow specialists; document data: copies of the work record book, sanitary and hygienic characteristics of working conditions, extracts from medical records of outpatient and inpatient patients, cards of preliminary and periodic medical examinations. In the prevention of PH and THB today, the main tasks are still to improve medical care and working conditions, living conditions of individuals, the use of personal protective equipment, high-quality medical examinations, the presence of good nutrition, compliance with personal hygiene rules, the availability of cleanliness, light and fresh air .

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