SWS: TB/HIV co- infection SPECIALTY: GENERAL MEDICINE. DEPARTMENT: PATHOLOGY OF ORGANS AND SYSTEMS PREPARED: DUZIKENOVA ZHADYRA 341 GM CHECKED: SHAKIROVA. - презентация

1 SWS: TB/HIV co- infection SPECIALTY: GENERAL MEDICINE. DEPARTMENT: PATHOLOGY OF ORGANS AND SYSTEMS PREPARED: DUZIKENOVA ZHADYRA 341 GM CHECKED: SHAKIROVA M.E.

2 -Introduction -Etiology -Classification -Clinical manifestations -Pathogenesis -Treatment -Conclusion

3 Increased airiness of the lung tissue, or emphysema, is a pathological condition characterized by the expansion of the air spaces of the lungs located distal to the terminal bronchioles, and resulting from a decrease in the elastic properties of the lung tissue.

4 There are two groups of causes leading to the development of pulmonary emphysema: The first group includes factors that violate the elasticity and strength of lung structure elements: pathological microcirculation, changes in the properties of surfactant, congenital deficiency of alpha-1- antitrypsin, gaseous substances (cadmium compounds, nitrogen oxides, etc.), as well as tobacco smoke, dust particles inhaled air. These causes can lead to the development of primary, always diffuse emphysema.

5 At the basis of its pathogenesis is pathological restructuring of the entire respiratory department of the lung; weakening of the elastic properties of the lung leads to the fact that during exhalation and, consequently, an increase in intrathoracic pressure, the small bronchi, which do not have their cartilage skeleton and lack the elastic traction of the lung, passively fall off, increasing this bronchial resistance on the exhale and increasing pressure in the alveoli. Bronchial patency during inhalation during primary emphysema is not impaired.

6 Factors of the second group contribute to an increase in pressure in the respiratory department of the lungs and increase the stretching of the alveoli, alveolar passages and respiratory bronchioles. The greatest value among them is the obstruction of the respiratory tract that occurs in chronic obstructive bronchitis. Immediately with it, conditions are created for the formation of the valve mechanism of overstretching of the alveoli. So, lowering intrathoracic pressure during inhalation, causing passive stretching of the bronchial lumen, reduces the degree of existing bronchial obstruction; positive intrathoracic pressure during expiration causes additional compression of the bronchial branches and, aggravating the already existing bronchial obstruction, contributes to the retention of the inspired air in the alveoli and their overstretching and destruction.

7 Pulmonary emphysema acute chronic Occurs when a sudden violation of the patency of the bronchi (an attack of bronchospasm). When this happens, they are partially obstructed, resistance to air flow increases, especially during expiration, the intraalveolar pressure increases, which leads to a sharp expansion of the alveoli. Acute emphysema passes after the elimination of its cause and does not lead to anatomical changes. It usually occurs in patients with obstructive diseases (chronic bronchitis, bronchial asthma), in those who play wind musical instruments, glassblowers, in old age, when the alveoli naturally lose elasticity. In chronic emphysema due to thinning due to overdistension, the alveolar septa can collapse, forming large blisters (bullous emphysema).

8 Pathogenetic form primary secondary diffuse localized Morphological features Panlobular Centrolobular Periacinary Bullous

9 Air spaces in the center of the lobule are affected. This type is most common in smokers, but its mild degree can occur with anthracosis. Most often it is localized in the upper lobe. Often centroacinar emphysema is combined with bronchiolitis and chronic bronchitis. Macrophages filled with dust particles and cells of chronic inflammation are often found in the enlarged spaces. Although the pathogenesis is not fully understood, it is assumed that the cause is inflammation of the respiratory bronchioles, which leads to a local disruption of the structure of the walls of the bronchioles and nearby elastin in the interstitium.

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11 All airway cavities distal to the terminal bronchioles are affected. Usually affects the lower lobes of the lungs, and the basal sections - much stronger. Macroscopically, the lungs appear to be overstretched. The etiology and pathogenesis are poorly understood, but 70-80% of patients with a1- antitrypsin deficiency develop this type of emphysema by the age of 50 years. a1-antitrypsin is an serum acute-phase protein that inhibits the activity of collagenase, elastase, and other proteases, including trypsin. This protein also inhibits enzymes released after neutrophil and macrophage death. Any adverse effects, such as smoking, which lead to an increase in the number of inflammatory cells in the lungs, lead to the destruction of the alveolar wall in these people. The deficiency of this enzyme is inherited in an autosomal dominant manner.

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13 1. Disruption of the normal protease ratio / α1 – antitrypsin and oxidants / antioxidants towards the prevalence of proteolytic enzymes and oxidants (free radicals) damaging the wall of the alveoli; These factors contribute to the violation of the strength and elasticity of the structure of the lungs. Primary diffuse emphysema develops. A pathological restructuring of the entire respiratory part of the lung occurs. During exhalation, when the intrathoracic pressure rises, the small bronchi passively subside, the bronchial resistance increases, and, consequently, the pressure in the alveoli increases. This occurs as a consequence of the weakening of the elastic properties of the lungs due to diffuse emphysema, because the small bronchi initially do not have a cartilage skeleton.

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15 2. violation of the synthesis and function of surfactant; 3. dysfunction of fibroblasts. Fibroblasts play an important role in the repair of lung tissue. It is known that the structuring and restructuring of the lung tissue is carried out by the interstitium and its two main components - fibroblasts and the extracellular matrix. The extracellular matrix is synthesized by fibroblasts; it binds the bronchi, vessels, nerves, and alveoli into a single functional unit.Fibroblasts interact with cells of the immune system and the extracellular matrix through the synthesis of cytokines. The main components of the extracellular matrix are collagen and elastin. The first and third types of collagen stabilize interstitial tissue, the fourth type of collagen is part of the basement membrane. Elastin provides the elastic properties of lung tissue.

16 In pulmonary emphysema, pulmonary volumes and pulmonary ventilation function change, the ratio between ventilation and blood circulation is disturbed, and pressure in the pulmonary artery increase The main complaint of patients with emphysema is dyspnea, which at the beginning of the disease can appear only during physical exertion, and then at rest. When examining a patient with emphysema of the lungs, face puffiness, acrocyanosis, cyanosis of mucous membranes, cheeks, nose and earlobes, gray- earthy skin color attracts attention. Often marked almond-shaped nails, which become claw-shaped, and then formed nails such as watch glasses. Fingers in the form of drumsticks are usually the last stage of these changes. With a long course of the disease, the chest becomes barrel-shaped. The supraclavicular fossa is usually flattened or protruding; protrusion is also noted under the collarbone Poor voice jitter. Uniform weakening of vesicular respiration. Auscultative signs of bronchial obstruction (mostly dry rales, prolonged exhalation).

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18 The main symptom of emphysema is an increase in residual lung volume in absolute terms and as a percentage of the total volume. Normally, according to Bolt (W. Bolt), the residual volume is 25% of the total. With mild emphysema of the lungs - 35%, with emphysema of the lungs of moderate severity 35– 45%, with severe emphysema - 45–55%, with severe - over 55% of the total.

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22 Treatment of patients with COPD (Chronic Obstructive Pulmonary Disease) includes the following principles. Combating the factors that caused chronic bronchitis or pulmonary emphysema. Cessation of smoking. Active treatment of infections. Relief of bronchospasm. Exercise aimed at improving exercise tolerance and training respiratory muscles. Postural drainage (in the presence of bronchiectasis). With the development of pulmonary heart - oxygen therapy. Adequate hydration.

23 First of all, to prevent emphysema, it is necessary to prevent the development of bronchitis, timely and completely treat viral respiratory diseases and tuberculosis. The categorical exclusion of smoking and other harmful ones, including occupational, effects on lung tissue, restriction of physical activity, rational employment.

24 Volozhin A.I., Orderin G.V. Pathophysiology (in three volumes) // Moscow: Academy ; 255; 301 Zayko N.N., Bytsa Yu.V. Pathological physiology. / / Medpress-inform Efremov A.V., Samsonova E.N., Nacharov Yu.V. Pathophysiology. Basic concepts: textbook. - M., p. Litvitsky P.F. Pathophysiology: textbook + diabetes. - 4th ed. - M., p. Pathophysiology: a textbook in 2 tons. / Ed. V.V. Novitsky, E.D. Goldberg, O.I.Urazova. - 4th ed. reclaiming and add. - M., Mukhin N.A., Moiseev B.C. Propedeutics of internal diseases. - M.: GEOTARMED, 2002, p A.V.Strutynsky, A.P. Baranov, G.E.Roytberg, Yu.P.Gaponenkov / Fundamentals of semiotics of diseases of internal organs / MEDpressinform 2013

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