The Ministry of Health of the Republic of Uzbekistan Tashkent Medical Academy The department of internal diseases №3 of medical and pedagogical faculty
Control forms of knowledge, skills and abilities
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5. Control forms of knowledge, skills and abilities - Oral
- The decision of situational problems - Demonstration of practical skills IWS
6. The evaluation criteria of the current control
Note: The basic level of knowledge and skills - a minimum of knowledge that provides the principle of "security" for the patient. 7.Quiz
1.Classification of pneumonia. 2.Differential diagnosis of diseases associated with the syndrome of cough. 3.Emergency care in acute pneumonia. 4.Clinical management of patients with cough. 5.Outpatient treatment of patients with cough. 6.Indications for hospitalization. 7.Definition of disability of patients with diseases that occur with coughing syndrome. 8. Prevention.
The main 1. Kasalliklar testes, Sharapov UF T: Ibn Sina, 2003 2. Kasalliklar testes, Bobozhanov S. T: Yangi Asr avlod 2008 3. Internal Medicine, Volume 1 Mukhin, NA M. GEOTAR - Media 2009 5. Internal Medicine, Volume 2 Mukhin, NA M.: GEOTAR - Media 2009 7. Textbook of Internal Medicine Editor-in-Chief William N. Kelley 1997
1. Umumy amaliet vrachlar Uchun maruzalar tuples, Gad, A., T., 2012 2. General practice, Ed.F. G.Nazirova, A.G.Gadaeva.M. GEOTAR Media, 2009. 3. Directory GP. Dzh.Merta. M.: Practice, 1998. 4.Collection of practical skills for general practitioners. Gadaev A. Akhmedov Kh.S. T., 2010. 5. Umumy amaliet vrachlar Uchun Amal kunikmalar tuplyu Gadaev AG, Akhmedov, HS, 2010. 6. Therapeutic Guide Washington, Ed. M.Vudli M. Practice, 2000. 7. Umumy amaliet shifokori Uchun kullanma F.G.Nazirov, A.G.Gadaev Tahrah. M. GEOTAR-Media, 2007. 8. Diagnosis of diseases of the internal organs. AN hams All tomy.2005. 9. Treatment of diseases of the internal organs. AN hams All tomy.2005.
Theme: "Cough with expectoration. Differential diagnosis of lesions with rounded tions of the lungs.Lobular pneumonia, tuberculoma, lung abscess, lung cancer, Echinococcus le g FIR.Different etiologies of pneumonia (bacterial, viral, mycoplasma). Tactics GPs. Principles of follow-up, monitoring and rehabilitation under MRA or joint venture. The principles of prevention.The principles of teaching topics »
2. Motivation Many patients go to the doctor, unaware that they have a completely different disease etiology and excellent location, what they themselves think. This applies to many areas. But the greatest ignorance of our population demonstrated in areas such as pulmonary symptoms, the symptoms of various diseases of these organs. The most common symptoms of lung - the symptoms of inflammation. At that dominates the incidence of bronchitis. The bronchi - is the upper respiratory tract. Bronchi and trachea begin with a pass into the alveoli. When pneumonia inflammatory lesions localized in these air bubbles, which are responsible for gas exchange in the lung tissue. Such symptoms lungs, the symptoms of bronchitis, characterized by a dry cough with little phlegm, slight fever, mild symptoms of intoxication. Bronchitis, in itself is not a threat to human life. However, in the absence of adequate treatment of bronchitis may progress to bronchiectasis. Its main feature - expectoration of sputum by coughing in large numbers. Patients in the truest sense expectorant sputum in the number of whole handfuls. Such problems have to solve the doctor GPs.
Since cough occurs in diseases of the heart and blood vessels, nervous system, systemic connective tissue diseases, GPs have to face to work with cardiologists, neurologists, rheumatologists. The results obtained in the course of training knowledge will be used during the passage of the GP - internal medicine and other clinical disciplines.
On a practical lesson in the theoretical part includes analysis of the clinical features of the diagnosis of pulmonary infiltrates. When klebsielleznoy or fridlenderovskoy, P. often affects the posterior segments of the upper lobes and apical (top) of the lower segments, often the inflammation extends to the whole share, early formed cavity decay is possible dissemination process. A marked intoxication. Physical and hematological changes scarce. Pleural effusion is rare. Significantly increased the frequency caused by Klebsiella focal P. maloharakternymi with manifestations. Kolipnevmonii often complicate the course of diabetes, neoplastic processes, kidney disease, and there against the background of prolonged use of hormones, antibiotics (kolipnevmoniyu in these cases are regarded as a manifestation of Dysbacteriosis a).The capsule form of the intestinal form the most virulent and cause changes resembling lobar P. Kolipnevmonii be severe, accompanied by severe intoxication, with frequent lesions ts.ns As a rule, these AP drain, frequent bilateral, complicated by lung abscess formation. Pneumonia caused by Haemophilus influenzae, most often occurs in people with chronic lung diseases. Inflammatory changes are usually located in the lower lobes of the lung: isolated foci, quickly merging, can capture the entire lobe. Often there is a prolonged duration. Perhaps this contributes to presence of Hib antigens common with lung tissue. GP is often accompanied by laringotraheobronhitom ( Laryngotracheobronchitis acute constrictive ).Ends almost always favorable. Possible outcome in chronic pneumonia Pneumonia caused by Proteus, starts quickly, runs from mild fever, slight leukocytosis, but is often accompanied by abscess formation. Pneumonia caused by Pseudomonas aeruginosa, occurs predominantly in immunocompromised patients after cardiac surgery and lung, long-term treatment with antibiotics. Characterized by severe, a tendency to dissemination process and abscess formation, often complicated by pneumothorax. Such a course can be explained by the fact that the Pseudomonas aeruginosa exotoxin produces highly toxic and hemolysins. Primary fungal P. rare. The most common cause of Candida fungi and Aspergilius. Pulmonary disease fungus Candida (see Candidiasis ) may be focal or interstitial.Focal P. candida is usually drain, take one or two beats. The gradual onset of the disease, the fever can be hectic, low grade or of the wrong type is stored for a long time. Phlegm is scanty, viscous, sometimes mixed with blood. Physical changes and expressed varying degrees, are available. For P. sometimes recurrent migration pneumonic foci. The disease is often accompanied by an obstructive syndrome complicated by serous or hemorrhagic pleurisy. P. Aspergillus (see Aspergillosis ( aspergillosis )) begins acutely, often from the first day revealed abscess formation.Characterized by high fever, pain in the side, cough with bloody sputum. The patient's condition is very serious, marked weight loss, and anemia. Pneumonia caused by chlamydia, may develop as a distinct disease (primary chlamydial P. due to Chlamydia pneumoniae), or as a manifestation of zoonotic chlamydiosis, such as Psittacosis th, which is the causative agent of Chlarnydia psittaci.They are characterized by a variety of flow. The expressed more often scant signs of intoxication and non-permanent physical changes and distinct radiographic signs. Initially dominated by changes in the interstitial tissue, and then the process involves the parenchyma. An important symptom is enlargement of the liver and spleen. Characterized by a very high erythrocyte sedimentation rate - up to 60 mm in 1 hr. Legionella P. - see Legionnaires' disease , P., caused by mycoplasma and Pneumocystis - seeMycoplasma infection , pneumocystis . Stagnant AP more often localized in the lower lobes of the lungs, predominantly in the right lung, often develop against hydrothorax. During their lingering, lingering, with no overt signs of intoxication and a high fever. Physical signs in the background of stagnant changes in the lungs is difficult to identify, and decisive diagnostic method is the X-ray. Clinical presentation There are clinical manifestations of lobar and focal P. Clinical picture of lobar pneumonia, which in modern medical practice is rare, corresponds to inflammatory changes in the lung tissue. The disease begins acutely, roughly, there are pronounced signs of intoxication, high fever since the early days of the disease, reaching in a short period of maximum digits, chills, flank pain, dry cough. Characteristic of the patient's face - haggard, with feverish flush, cyanotic lips, nostrils flaring in breathing, often around the nose and lips cold sores appear. One side of the chest behind when breathing, the patient is spared her, holds the hand. Percussion sound over the lesion may first have tympanic shade, due to an increase in the share or segment and a decrease in the elastic properties of the lung tissue. As the amount of fluid tympanic shade is replaced by toning. Breathing in the early days of vesicular disease, but may appear weak because of involvement in patients with pleural and limitations of respiratory movements. By the end of 1-2-day illness at the height of inspiration you can listen to and sometimes crepitus mixed wet and dry rales (see Souffles ) in a limited area.At this stage, enhanced by holding the chest whisper of speech, which can be determined by auscultation (bronhofoniya) or palpation ( voice tremor ).Later, as the accumulation of alveolar fibrin becomes more intense blunting pulmonary sound. At the same time the edges of the tour is limited to the lung, bronchial breathing appears, disappears crepitus, amplified bronhofoniya and voice tremor may auscultated pleural friction rub. With the onset of thinning fluid decreases the intensity of the sound deadening Perk tor, it disappears tympanic shade, bronchial breathing becomes less pronounced and reappears crepitus, but rougher than at the beginning of the disease. As the resorption of fluid breathing becomes hard, then vesicular, often in this period sonorous rales are heard. Initially dry cough, accompanied by a sharp pain in his chest. On the second day of the disease appears scant glassy viscous sputum streaked with blood. Then sputum can be uniformly painted with blood, buying a brown-red color ("rusty sputum"), the number of its increases, the viscosity decreases. Body temperature, reaching higher numbers becomes constant. In most cases the decrease in body temperature is analytically. Approximately one third of patients is critically reduced, which may be accompanied by acute circulatory failure (see Collapse ).The average duration of the febrile period of 10-11 days. When focal P. inflammatory lesions in the affected segments are in various stages of development, this can be explained by the gradual (in some cases) the development of the disease, its undulating course with the change of periods of improvement and deterioration of the patient's fever variability, variability of physical changes and their mosaicism due presence near the affected areas normally functioning lung tissue or emphysematous. With the defeat of the upper lobes of the lungs process often engages the rear, the apical and reed bronchopulmonary segments. In the lower lobes are involved more often apex (top), lateral basal and posterior basal segments. When the location of infectious foci at a depth of 4 cm from the surface of the lung and in the center of their location can not be determined dullness and amplification of voice shaking.The most constant symptoms of focal P. are hard breathing, rales (usually finely, sonorous). For more permanent focal P. symptoms of bronchial tree: dry and wet (medium and krupnopuzyrchatye) wheezing. The pleura is not always involved in the process. Tuberculosis of respiratory infectious disease characterized by the formation of lesions in the affected tissues of specific inflammation and expressed the general reaction of the organism.In many developed countries, particularly in Russia, have significantly decreased the incidence of tuberculosis and mortality. The most pronounced of these epidemiological shifts among children, adolescents and women, to a lesser extent - in men, particularly the elderly. Nevertheless, tuberculosis remains a common disease. Etiology. Pathogen - Mycobacterium tuberculosis (MT), mostly human, bovine, and rarely, in exceptional cases, the type of bird. The main source of infection - the sick people or domestic animals, mostly cows. Aerogenic usually become infected by breathing in air emissions sick tiny droplets of sputum, which contain MT. In addition, the possible penetration into the body of infection in the use of milk, meat and eggs from infected animals and birds. In these cases, the germs are entered in the lungs or of the pharyngeal tonsils, or lymph and blood from the intestines of ways. The vast majority of newly diagnosed sputum detect MT-sensitive, and in 5-10% - resistant to a variety of anti-TB drugs. In the latter case, contamination occurs from the patients who are treated ineffectively specific drug resistant strains and the isolated MT. For a special study in the sputum and in the bodies of patients is sometimes possible to detect Lformy MT, has a relatively low virulence and patogennostyo but capable, under certain conditions, to turn into a typical microbial form. Pathogenesis, symptoms. flow.For the first time penetrated into the body MT apply it in different ways - lymphatic, hematogenous, bronchopulmonary. Thus in various organs, mainly in lymph nodes and lungs, or may be formed separate multiple tubercles or larger lesions, which are characterized by the presence of epithelioid and giant cells, as well as elements tyromatosis. At the same time there is a positive reaction to tuberculin, the so-called tuberculin turn, established by intradermal Mantoux test. There may be a low-grade temperature of the body, hyperplasia of the lymph nodes, moderate lymphopenia and leukocyte shift to the left, often changing the ESR and serum protein fractions. With sufficient resistance to infection, and a small amount of MT tubercles and hearths resolve, scar or calcified, although MT in them long remain. All of these changes often go unnoticed or occur under the guise of various intercurrent diseases are eliminated spontaneously, they are identified only by careful observation of the dynamic newly-infected children, adolescents or adults. With a massive infection, influenced by other adverse factors (malnutrition, severe illness, leading to a decrease in the body's resistance immunobiological) developed symptomatic primary tuberculosis flowing as bronhoadenita, the primary complex, more or less extensive dissemination in the lungs and other organs, exudative pleurisy , inflammation of other serous membranes. It is often observed hypersensitivity of the body and the inclination to hyperergic reactions in the form of erythema nodosum, keratoconjunctivitis, allergic vasculitis, etc. Primary tuberculosis occurs predominantly in children, adolescents, less common in young adults and rarely in older and older who have had a previous primary infection, which ended in a biological cure. Remaining in the "healed" TB lesions and scarring in the lungs and lymph nodes of the MT can "wake up" and multiply. This is facilitated by the same conditions that favor the development of primary tuberculosis, and, in addition, re-infection (exogenous superinfection). Then around the old centers of perifocal inflammation occurs, the integrity of the capsule is broken, melted areas of caseous necrosis and infection spreads lymphatic, bronchogenic or by hematogenous. So develop secondary tuberculosis, a disease that is people who have had a primary infection and have known, though not sufficient, immunity. In these patients, the process proceeds with diverse clinical and pathologic changes, most chronically. Over the past. Now increased TB disease in elderly and senile age. The clinical picture of the disease, they often atypical.Even the evolutionary process in the form of a long term can proceed quickly, but sometimes have similarities with malignant diseases or chronic non-specific inflammation of the respiratory system. This leads to a delayed diagnosis of disease. A number of patients in this age group are observed miliary tuberculosis and extrapulmonary lesions (meningitis, tuberculosis, bone, adrenal glands, etc.). TB can develop as a complication of corticosteroid treatment. This "steroid" tuberculosis tend to progress, often mistakenly regard as a feature of the underlying disease. According to the classification adopted in 1974, are the following forms of pulmonary tuberculosis: 1) the primary tuberculosis complex, and 2) Tuberculosis of intrathoracic lymph nodes, and 3) disseminated pulmonary tuberculosis, 4) focal pulmonary tuberculosis, 5). infiltrative pulmonary tuberculosis, 6) tuberculoma of the lungs; 7) cavernous pulmonary tuberculosis, 8) fibroziokavernozny pulmonary tuberculosis, 9) cirrhotic pulmonary tuberculosis, 10) tuberculous pleurisy (including empyema), 11), tuberculosis, upper respiratory tract, trachea, bronchi, 12 ) pulmonary tuberculosis, combined with pneumoconiosis.In addition, a process characterized by its localization in different lobes and segments of the lung, the phases of development (resolution, compression, scarring, calcification, decay, infiltration, colonization), the presence of bacteria. Take into account the most important complications (pulmonary hemorrhage, atelectasis, amyloidosis, renal failure, legochnoserdechnaya failure, bronchial fistula, thoracic, etc.), as well as the residual changes in the lungs after cured of tuberculosis (fibrous, fibroznoochagovye, plevropnevmoskleroz, etc.). Primary tuberculosis complex - the most common form of primary tuberculosis - is found in the now relatively rare: in the lung lesions are determined by specific inflammation (primary affect) and regional bronhoadenit. Sometimes the disease is hidden, but more often begins subacute and appears subfebrile body temperature, sweating, fatigue, slight dry cough. At the beginning of the acute illness at first takes place under the guise of non-specific pneumonia with high fever, cough, chest pain, shortness of breath sometimes, a moderate leukocytosis with a shift to the left leukocyte counts, increased erythrocyte sedimentation rate. With a small amount of primary affect physical changes in the lungs are usually undetectable. At a massive inflammation marked areas deadened tone vezikulyarnobronhialnoe breath, wet finely wheezing. Some patients often grow outside the lymph nodes. Tuberculin test in 30-50% is well expressed. In the absence of the collapse of the lung tissue in the sputum and bronchial washing waters MT usually do not show. In these cases, the traheobronhoskopii find no specific changes in the bronchi, but they are present in the formation of cavities in the lungs or spread of the process of intrathoracic lymph nodes and bronhogeshyum colonization. At the same time possible to detect MT. X-ray picture is characterized by the appearance of the symptoms of bipolar as a small focal segmental or lobular, lobar pneumonia and a rare group of hilar lymph nodes at the root of the lung. Even with a favorable course of the process and the application of modern methods of treatment of primary complex heals slowly. Only a few months, sometimes only after 12 years after the identification and early treatment comes resorption or encapsulation, and calcification of the primary elements of the complex to form the hearth Gon. Complications of the disease are able to decompose the primary tumor in the lung and the formation of cavities. Sometimes there is a pleural effusion. Perhaps lymphohematogenous MT distribution and the formation of lesions in the bones, kidneys, meninges, etc. The most common form of primary TB - tuberculosis of intrathoracic lymph nodes. Clinical manifestations depend on the reactivity of the organism, the prevalence of lymph nodes.If they are formed and some small pockets of cheesy necrosis without inflammations, and the overall reactivity of the reduced mild, such a "minor" form of the process can take place with little hidden or intoxication. In more massive or infiltrative tumor-bronhoadenite there is a high fever, weakness, sweating, reduced work capacity, increased excitability. Frequent symptom - dry cough. In infants and young children due to compression of the large bronchi and enlarged mediastinal lymph nodes cough is ringing, bitonal or Whooping. In adults, this symptom is rare. On physical examination, especially of adult patients, it is difficult or even impossible to determine the hilar lymph nodes. Sometimes interscapulum with percussion can be noted triangular plot of blunting, and auscultation - changed breath and a small amount of dry, wet rarely finely wheezing. In both adults and children in cases of enlarged cervical and axillary lymph, nodes. Tuberculin reaction is relatively often, but not always sharply defined. The number of leukocytes in the blood of normal or somewhat increased with a leftward shift, ESR is increased. MT detect rare. Radiographically define the extension of the root of one, rarely both lungs, his shadow malostrukturna, deformed, especially in massive inflammations are, as is typical of infiltrative bronhoadenita. With the dramatic increase in bronchopulmonary and other groups of lymph nodes of the root contours become polycyclic character (Tumor bronhoadenit). Symptoms of intoxication, increased erythrocyte sedimentation rate, hyperergic that berkulinovye reactions may persist for a long time, even against the background of an energetic specific treatment. Inflammations are gradually resorbed around the roots of the lungs and is their seal. \ Only after February 1 of the year after the onset of the disease and the treatment of the lymph nodes there are sites of calcification. Caseous foci of calcification occurs more rapidly in children, slower in adults. The disease is often complicated by the specific lesions of the bronchial
Pneumoconiosis occupational lung diseases caused by prolonged inhalation of dust and characterized by the development of diffuse interstitial fibrosis.Mogutvstrechatsya the workers mining, coal, asbestos, engineering and other industries. The development of pneumoconiosis depends on the physical and chemical characteristics of respirable dust. The clinical picture of pneumoconiosis has a number of similarities: the slow, chronic course with a tendency to progression, often resulting in impaired work capacity; resistant sclerotic changes in the lungs.Are general principles of prevention and pneumoconiosis, particularly the implementation of technical and sanitary-hygienic measures aimed at maximum reduction of airborne dust workrooms, conducting preliminary (at entry) and periodic medical examinations. So, contraindications to employment associated with the impact of the silicon dust, are pulmonary tuberculosis, a number of diseases of the upper respiratory tract and bronchi, chronic anterior segment of the eye, the skin, allergic disease. It is mandatory periodic medical examinations two times a year, or 1 every 2 years, depending on the potential hazard of production. Inspections carried out a therapist, audiologist with radiography of the chest cavity, the study of respiratory function. Biological methods of prevention are aimed at improving the reactivity of the second acceleration removing it from dust. Recommended total ultraviolet irradiation, the use of alkaline inhalations, general and breathing exercises, organized a special meal, aimed at normalizing the protein metabolism and inhibition konioticheskogo process. There are the following main types of pneumoconiosis: silicosis and silikatozy, metallokoniozy, karbokoniozy, pnevmokoiiozy ached from the mixed (antrakosplikoz, siderosilikoz, etc.), from organic dust pneumoconiosis. Silicosis - the most common and severe form ppevmokonioza, is caused by prolonged inhalation of dust containing free silica.Most common among miners of various mines (drillers, cullers, timberers, etc.), operating foundries (sandblasters, obrubschiki, sterzhenschiki, etc.), workers of refractory materials and ceramic products. It is a chronic disease, severity, and those whose development may be different and are directly dependent on the aggressiveness as respirable dust (dust concentration, the amount of free silica in it, dispersion, etc.) and on the duration of exposure and the dust factor individual characteristics of the organism. Pathogenesis.Gradual atrophy of ciliated airway epithelium drastically reduces the natural secretion ached from respiratory and contributes to its retention in the alveoli. In iiterstitsialnoy lung tissue develops primary reactive sclerosis with steadily progressive course. The most aggressive particles have a size of 12 microns, are able to penetrate into the deeper ramifications of the bronchial tree, reaching the pulmonary parenchyma and stopping it. Mechanical plays a role, as well as damage to lung tissue toksikohimicheskoe but dust activity depends mainly on the crystal structure and the ability of the crystals to adsorb proteins, due to the presence on their surfaces silanol groups (SiOH). It causes the death of most of phagocytes to release natural substances lipoprotein (antigens) and the formation of antibodies reactive precipitation, which is the basis of forming silikoticheskogo nodule. The progression of fibrotic process entails a breach of the blood supply, lymphostasis and further growth of connective tissue. All this, together with inflammatory and atrophic processes in the bronchi leads to emphysema, pulmonary heart and respiratory insufficiency. Symptoms within. The disease develops gradually, usually with long experience in dust. Initial clinical symptoms are scanty: shortness of breath on exertion, chest pain of uncertain character, a rare dry cough. The direct examination often shows no pathology. However, even in the initial stages can be identified early symptoms of emphysema, developing advantage dominantly in the inferolateral parts of the chest, a box shade of percussion sound, reducing the mobility of lung edge and chest and respiratory depression. Joining changes in the bronchi seen breathing hard, sometimes dry wheezing. In severe forms of the disease are concerned dyspnea even at rest, chest pain intensifies, there is a feeling of pressure in the chest, cough becomes more constant and is accompanied by phlegm, increases the severity of percussion and auscultation changes, key in the diagnosis of silicosis is an X-ray examination. In the initial stage of the x-ray marked enhancement and distortion of lung pattern, the appearance of cellularity and reticulation, the occurrence of single shadows silikoticheskih nodes seal interlobar pleura, changes are usually symmetrical, sometimes more pronounced in the right lung preferentially localized in the middle and lower regions. Further increases bronchial deformation pattern, there are numerous melkopyatnistye irregular shadows with ranging between sylikoticheskimi rounded nodules with clear margins (picture "blizzard" or "shot" of light - II stage disease). In the transition process in step III shadows merge into large conglomerates with tumor formation in some cases cavities often in combination with tuberculosis expressed symptoms of emphysema. According to the release клиникорентгенологическими features 3 forms of silicosis: nodular, interstitial and tumor (nodal). The possibility of the return of the initial silikoticheskih changes are resolved. At the same time a tendency to silicosis different progression even after termination of the exposure conditions in ached comprising silica. Under unfavorable combination of factors (high dispersion and concentration, great content in the dust-free silicon dioxide, difficult working conditions, etc.) silicosis may develop after several months of work ("early silicosis"), which is extremely rare. Complications: pulmonary heart, legochnoserdechnaya failure, \ pneumonia, obstructive bronchitis, bronchial asthma, rarely broihoektaticheskaya disease.Silicosis is often complicated by tuberculosis, which leads to a mixed company of the disease - tuberculosilicosis. In the differential diagnosis of silicosis and pulmonary tuberculosis are important in the absence of silicosis symptoms of intoxication, the relative severity of complaints and physical symptoms, a characteristic X-ray pattern. Tumorous form of silicosis, lung cancer is different from the slow evolution of the shadows and relatively good Pulmonary infarction - A disease caused by thrombosis or embolism, pulmonary artery branches (primarily assessed and smaller arteries).It is believed that pulmonary infarction develops in 10-25% of cases of pulmonary embolism (PE). The etiology and pathogenesis.The disease is most often venous thrombosis of the systemic circulation (the lower extremities, pelvis, iliac, inferior vena cava, etc.), much less - thrombosis of the right heart chambers. By the development of peripheral phlebothrombosis predispose surgery, postpartum, chronic heart failure, fractures of the long bones, malignancy, prolonged immobilization (eg, bed rest). Thrombosis and pulmonary vascular congestion and delay are the blood flow in the lungs, stable pulmonary hypertension, pulmonary vasculitis. Obturaiiya vessel reflex spasm in the pulmonary arteries and vasoconstriction due to the evolution of platelet biologically active substances (serotonin, thromboxane, histamine) lead to acute pulmonary hypertension and right heart overload. There are a violation of diffusion and arterial hypoxemia, compounded iedookislennoy shunting of blood through arteriovenous anastomoses in the lungs and cross-system anastomoses. Pulmonary infarction often occurs against a background of already existing venous congestion and is usually hemorrhagic in nature due to the outpouring of the bronchial arteries in the lung tissue of blood flowing through intersystem anastomoses, as well as the return flow of blood from the pulmonary vein. Pulmonary infarction formed a day after obstruction of pulmonary vessels; complete its development is completed by the 7th day. Myocardial infection leads to the development of lung peryfokalnyh pneumonia (bacterial, kaididoznyh) often with abscess formation, with subpleural location or heart attack occurs more often hemorrhagic fibrinous pleurisy. Symptoms, course of the gauge, the localization and the number of vessels obturated, state compensatory mechanisms underlying pathology of the lungs and heart. The most common symptoms: shortness of breath suddenly emerged (or suddenly intensified), chest pain (acute, resembling angina at the time of embolism, aggravated by breathing and coughing with pleurisy), with an ashen pallor complexion, rarely cyanosis, tachycardia with a heart rate of more than 100 in 1 minute, sometimes - irregular heart rhythm (beats, less atrial fibrillation), arterial giiotenziya until the collapse, brain disorders (syncope, seizures, coma), fever, cough with mucus or bloody sputum, hemoptysis in the formation of pulmonary infarction. At the time of embolism is often marked discrepancy between dyspnea and sparse pattern in lung auscultation, with the formation of pulmonary infarction can be detected dullness, decreased breath sounds, friction noise plevrt tch fine moist rales in a limited area, one-sided pleural effusion. Occasionally there is abdominal syndrome, manifested acute pain in the right upper quadrant of the intestine paresis, pseudo symptoms of peritoneal irritation, leukocytosis, persistent hiccups, vomiting syndrome (caused by pleural lesions diafragmalyyuy, sharp swelling of the liver). Signs of acute pulmonary hypertension and right heart overload (increased heart push outward shift right border of the heart, pulsation in the second left intercostal space, focus and splitting II sound, systolic murmur in the pulmonary artery, the symptoms of right heart failure) are observed only in the obstruction of large pulmonary artery trunk . The possible source of pulmonary embolism may indicate signs of peripheral phlebothrombosis. There are many possible combinations of the above symptoms, varying degrees of severity, which makes the diagnosis of pulmonary embolism and pulmonary infarction sometimes difficult. Diagnosis helps to identify the ECG signs of acute right heart overload (high peaked P wave in leads II, III, aVF, a sign of Mack Gina-White - a deep tooth 5 in standard lead I, deep Q wave in lead III, incomplete blockade of the right bundle-branch block). When X-ray may be determined by the expansion of lint lung, and lopped his deformity, depletion of the vessels of the lung tissue section (Westermark sign), darkening of the triangular shape (because of infiltration of the surrounding myocardial tissue can easily take a rounded, irregular shape), the presence of pleural effusion, and signs of acute pulmonary heart disease - the expansion of the superior vena cava, heart shadow to the right of the cone bulging pulmonary trunk. Doppler ultrasound study of veins of the lower extremities to diagnose deep vein thrombosis of the lower limbs, echocardiography shows signs of right ventricular overload. A decisive role in the diagnosis of pulmonary embolism play radioizotoinoe lung scan, allowing you to detect specific areas to reduce lung perfusion (method of choice) and angiography which reveals vnutriarterialpye filling defects or obstruction ("open") branches of the pulmonary artery. The prognosis depends on the underlying disease, the values of a heart attack. Treatment. For suspected pulmonary embolism shows emergency hospitalization. Prehospital administered heparin (10,000 units). Heparin s dissolves the clot, but suspends the thrombotic process and prevents the buildup of thrombus proximal and distal emboli. Weakening the vasoconstrictor and bronhospaticheskoe torombotsitarnogo action of serotonin and histamine, heparin reduces the spasm of the pulmonary arterioles and bronchioles. Favorably affecting phlebothrombosis for the most common cause of thromboembolism, heparin is used to prevent a recurrence of pulmonary embolism. When expressed pain syndrome, as well as for unloading the pulmonary circulation and reduce breathlessness using narcotic analgesics (eg, 1 ml of a 1% solution of morphine in / fractional), which allows s only effectively arrest the pain, but also to reduce shortness of breath characteristic of pulmonary embolism. With the development of infarction pneumonia, chest pain may be of pleural character, and if it is linked with the breath, cough, body position more appropriate use of non-narcotic analgesics (eg, in / in a 2 ml of 50% sodium dipyrone). When complications of the disease of right heart failure, shock therapy is carried out vasopressors (dopamine, dobutamine). In cases of bronchospasm and stable blood pressure (systolic or above 100 mm Hg. Cent.) Is shown in / slow (jet or drip) injection of 10 mL of 2.4% solution of aminophylline.In addition to the bronchodilatory action, aminophylline reduces the pressure in the pulmonary arteries, has antiaggregatory properties in the hospital continue heparin (daily dose - 30 000 units) under the control of the activated partial thromboplastin time (aPTT) is possible to use low molecular weight heparin (daltepariia, enoksaiarina, Fraksiparina). Heparin was carried out for 7-10 days. Long-term treatment with indirect anticoagulants is indicated for recurrent course phlebothrombosis and pulmonary embolism, in which case a few days before the incidents patient is on therapy fenilinom under the control of prothrombin time. Duration of therapy with indirect anticoagulants for recurrent pulmonary embolism or re-development phlebothrombosis from 3 to 1.2 months, the criterion of cancellation - the disappearance or reduction of the potential threat of thrombosis and thromboembolism. In the case of thromboembolism of small branches of the pulmonary arteries and the absence of sufficient recurrent pulmonary embolism and more secure in comparison with indirect anticoagulants is 1erapiya antiplatelet prophylaxis. For this purpose, use aspirin, tiklonidin (tiklid) Trental. With the development of infarction pneumonia antibiotics are added to the therapy. After confirming the diagnosis of massive pulmonary embolism, right ventricular hypokinesis and persistent hypotension used thrombolytic agents (streptokinase, etc.), according to testimony surgical treatment (thrombectomy, install a filter in the inferior vena cava, etc.). Yüklə 1,24 Mb. Dostları ilə paylaş:
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