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MINISTRY OF HEALTH OF REPUBLIC OF UZBEKISTAN TASHKENT MEDICAL ACADEMY DEPARTMENT OF DEPARTMENT OF INTERNAL DISEASES № 3 OF MEDICAL AND PEDAGOGICAL FACULTY LECTURE TOPIC: «DIFFERENTIAL DIAGNOSIS OF NONCORONARY PAINS IN THE CHEST. DIFFERENTIAL DIAGNOSIS. TACTICS OF GENERAL PRACTITIONER » (for the students of medical-pedagogical faculty) TASHKENT – 2016 MINISTRY OF HEALTH OF REPUBLIC OF UZBEKISTAN TASHKENT MEDICAL ACADEMY DEPARTMENT OF DEPARTMENT OF INTERNAL DISEASES № 3 OF MEDICAL AND PEDAGOGICAL FACULTY «APPROVED» Dean of medical-pedagogical faculty, professor Khamraev A.A. ___________________ ____ _____________ 2016 y LECTURE TOPIC: «DIFFERENTIAL DIAGNOSIS OF NONCORONARY PAINS IN THE CHEST. DIFFERENTIAL DIAGNOSIS. TACTICS OF GENERAL PRACTITIONER » (for the students of medical-pedagogical faculty) LECTURER: professor Gadaev A.G. TASHKENT – 2016 TECHNOLOGY OF THE EDUCATION Amount student Time - 2 hours Form of the scholastic occupation Lecture - a visualization Plan to lectures 1. Anatomical construction of heart, circles blood current 2. Main diseases, being accompanied with non coronary pain in thorax, threatening lifes sick 3. Heart diseases, being accompanied pain in thorax (aneurysm, perikarditis, cаrdiomiopatys) 4. Diseases of belly intestine tract, being accompanied pain in thorax esophagitis, other pathology of the gullet) diagnostics diseases being accompanied with pain in thorax 5. Diseases of the nervious system, being accompanied pain in thorax 6. The diagnostics of the diseases, being accompanied pain in thorax. Principles of the treatment, preventive maintenances and dispanserisation sick with non coronary pain of the thorax Purpose of the scholastic occupation: acquaint student with этиологией, патогенезом of the diseases, being accompanied non coronary pain in thorax, train principle of the diagnostics, treatments, preventive maintenances and dispanserisation of the diseases, being accompanied non coronary pain in thorax The Pedagogical problems 1. Consolidate and deepen knowledge’s a student about disease, being accompanied non coronary pain in thorax 2. Teach student it is correct to install diagnosis in accordance with modern The results of the scholastic process: the general practitioner must know: 1. Diseases, being accompanied pain in thorax, threatening lifes 2. Principles of the differential diagnostics of the diseases, being accompanied non coronary pain in thorax 3. Tactician of conduct, principles of the categorization of the diseases treatment sick non coronary pain in thorax 3. Train student to skill to 4. Principles of the undertaking the preventive differentiate diseases, being maintenance and dispanserisation sick with non accompanied non coronary coronary pain in thorax pain in thorax 4. Acquaint student with particularity of the current of the diseases, being accompanied pain in thorax, rendering urgent help, tactician squall 5. Train student to conduct sick with non coronary pain in thorax, treatment and this Methods of teaching Text to lectures, video film, questions, technology "yes-no" Form of the education Lazer projector, visual material, special technical equipment, show thematic sick Facilities of the education Group Conditions of the undertaking the scholastic process Auditorium PRODUCTION CHART TO LECTURES Stages, time Activity Teacher Students 1. Tells about subject of the 1 stage Introductory part lectures, her purposes and plan (5 mines) 2 stages Actualization (increasing to value ) of the knowledges (20 mines) 2.1. In purpose of increasing to actualizations (increasing to value) of the knowledge’s student will assign the questions: 1. Enumerate diseases, which can be accompanied pain in thorax 2. Enumerate diseases being accompanied pain in thorax, threatening lifes sick 3. Enumerate reasons, bring about arising the pains in thorax 4. Enumerate groups a preparation, using for treatment of the diseases, being accompanied non coronary pain in thorax 1. Listen 2.1. Answer givenned questions 2.2 Study slide 1 Conducts questioning 2.2. Showing on screen, offers to get acquainted the student with purpose and problem to lectures. Slide 1, 2 3 stages Main part (information) (55 mines) 2.3. Study slide 2 3.1. Introduces the student with 3.1. Together analyse lecture material, value of the heard lecture material, subject and principle of the shaping will assign questions intelegent cultural personality, in particular squall-teacher. In purpose of increasing to actualizations of the knowledges conducts quick questioning a student: 1. On 1 point of the plan to lectures: tell anatomical construction a heart, circles blood current 2. On 2 points of the plan to lectures: enumerate main diseases,being accompanied non coronary pain in thorax, threatenning lifes sick 3. On 3 points of the plan to lectures: heart diseases, being accompanied pain in thorax (aneurysm, perikardits, cardiomiopatys) 4. On 4 points of the plan to lectures: diseases of belly intestine tract, being accompanied pain in thorax (esophagits, other pathology of the gullet) 5. On 5 points of the plan to lectures: diseases of the nervious system, being accompanied pain in thorax Main moments write in copy-book 6. On 6 points of the plan to lectures: diagnostics of the diseases being accompanied with pain in thorax 7. On 7 points of the plan to lectures: principles of the treatment, preventive maintenances and dispanserisation sick with non coronary pain of the thorax. Sopping for important moment of the lectures offers to write main positions in copy-book 4 stages final (10 mines) 4.1. Will Assign questions: 1. Enumerate most often meeting diseases, being accompanied non coronary pain in thorax 2. enumerate diseases being 4.1. Answer questions accompanied non coronary pain in thorax, threatenning lifes sick 3. Tell main key moments of the clinical current of the different diseases being accompanied non coronary pain in thorax 4.2. Listen, write 4.Назовите cardinal principles of the treatment, preventive maintenances and rehabilitations sick with non coronary pain in thorax 4.2. Gives task for independent work student: pathology supporting-motor device, being accompanied with non coronary pain in thorax In practice, general practitioner often deal with different situations, accompanied by pains in the chest, which often require a doctor's quick, efficient care to patients. What should be the assistance in various specific situations depends on what kind of pathology in the patient - whether it threatens the life of the patient? What factor cause these pains? In this chapter we discuss some diseases that are accompanied by chest pain with noncoronary character. First, eliminate the most dangerous diseases that threaten the patient's life. Myocardial infarction Spontaneous pneumothorax PATE Dissecting aortic aneurysm Only removing them, we should look for other causes of chest pain. Acute dissecting aortic aneurysm. Aneurysm - this is a local sacciform bulging wall of the aorta, or diffuse enlargement of the entire aorta in more than 2-fold compared with the norm. The main causes: atherosclerosis, trauma, Marfan syndrome, syphilis, cystic medionekroz. Acute delamination - the most frequent of emergency conditions associated with disease of the aorta. This is more common in men. Clinicaldelamination occurs by sudden disintegration intense pain in the chest or in the back radiating to the course of the aorta. Characteristic for pain is undulating course, which indicates a further exfoliating aorta. In this context, location and irradiation of pain is changed. Status of patients is severe, resembling shock, but the blood pressure initially elevated (high blood pressure is one of the main reasons for separation of the aorta). In the propagation of delamination, may be developed gemiperikards with cardiac tamponade, aortic insufficiency due to aortic valve detachment, ischemia of various organs. Often there is an asymmetry of pulse and blood pressure at the upper and lower extremities. The diagnosis is confirmed by dynamic radiography (expanding shadow of the aorta, double loop), computed tomography, magnetic resonance imaging, echocardiography, Doppler, aortography. High diagnostic value by splitting the thoracic has transesophageal echocardiography. Sensitivity and specificity is 90%. Forms of flow separation of the aorta: acute - hours, subacute - days (rarely 2-4 weeks), and chronic - months. Without treatment, the first 2 weeks 70% of patients die, 50% of the survivors die within a year. The most common cause of death aortic rupture. Surgical treatment - emergency aortic replacement.Medication is shown immediately before the operation, and in cases of suspected acute peel. In case of high blood pressure, there is assigned beta-blockers, first intravenously and then inside. Further, it is needed sodium nitroprusside. In normal blood pressure,monotherapy of beta-blockers is conducted to reduce the contractility of the left ventricle. Cardiomyopathy (ILC) - a group of diseases of the heart muscle with unknown etiology. They are referred to as primary or idiopathic, cardiomyopathies. The secondary cardiomyopathy includes diseases, where etiology is known. This myocardial damage is in systemic diseases, alcohol poisoning, with heart diseases and other pathological conditions. There are three primary forms of cardiomyopathy: dilated, hypertrophic and restrictive. Presumably causal role for various damaging factors: toxic, metabolic, infectious. There are indications of immune disorders in dilated Commission and the hereditary nature of the disease in hypertrophic ILC with autosomal dominant inheritance. Dilated cardiomyopathy (DCM) - a disease characterized by an increase in heart size, systolic dysfunction and congestive heart failure. The clinical picture. Symptoms usually develop gradually. Sometimes the disease progresses over months and even years without symptoms, but with dilation of the left ventricle, and is found in the X-ray or echocardiogram. The first symptoms - fatigue and weakness, shortness of breath and then joined, initially with exertion, and in later cases - cardiac asthma, orthopnea. Peripheral edema and hepatomegaly - late and optional features.Very often cardialgia and much less-angina. A significant part of the clinical picture is occupied by thromboembolic complications that develop as a result of the separation of intracardiac thrombus, and the veins of the lower extremities. Sudden thromboembolism in the pulmonary artery can be the first symptom of dilated and the ILC. On examination - cold skin, alternating pulse, systolic and pulse pressure, expanding the boundaries of the heart often left, left ventricular pulse, and in later cases - right ventricle. Auscultation - a systolic murmur due to mitral or - to a lesser extent - tricuspid regurgitation, gallop rhythm, heart rhythm disturbances. In marked dilatation of the left ventricle and a significant decrease in ejection fraction, prognosis is unfavorable. The diagnosis is made on the basis of chest X-ray, ECG, echocardiography, radionuclide ventriculography, coronary angiography and myocardial biopsy. When X-rays, there is determined by the increase of the left ventricle, often cardiomegaly. There are revealed signs of venous congestion in the lungs, interstitial and alveolar edema, even, pleural effusion. On ECG - sinus tachycardia, sometimes various atrial and ventricular arrhythmias, and intraventricular and atrioventricular conduction.There can be detected abnormal tooth Q, reflecting extensive noncoronary myocardial fibrosis, and ST-segment changes and T wave. In Echocardiography, there are increase in left ventricular with rise in end-diastolic and end-systolic volumes, lower ejection fraction, mitral and tricuspid regurgitation. A characteristic is diffuse myocardial damage. Radionuclide ventriculography confirms diffuse hypokinesia wall infarction, increased volume of the heart, low ejection fraction, coronary angiography revealed normal blood vessels, it is necessary for patients with an abnormal Q wave on the electrocardiogram in the differential diagnosis of myocardial infarction. In the study of biopsy material is defined extensive interstitial and perivascular fibrosis, sometimes foci of calcifications. However, the specific diagnostic features, unique to dilated Commission, are absent. Treatment. Drug treatment is aimed at fightingagainsy heart disease. Basic principles are not different from the treatment of heart failure of any cause and they control sodium and water in the body, reducing preload and afterload, improving the pumping function of the heart. Patients are advised to limit physical activity and reduce the consumption of salt. Because of the risk of pulmonary and systemic embolism in patients with dilated cardiomyopathy with parietal thrombus in the left ventricle, as well as atrial fibrillation and reduced ejection fraction (<20%), there should be applied anticoagulation therapy such as warfarin starting dose of 10 mg / day under the constant control of prothrombin time. For the treatment of cardiac arrhythmias in DCM, it is best to use the correction of hypoxia, electrolyte disorders and acid-base balance (potassium supplements, antioxidants) and to carry out the fight against heart shortage. The use of antiarrhythmic drugs in patients with DCM did not increase life expectancy, although in recent years there are reports about beneficial effect in usingpjselective adrenergic blockers (such as metoprolol, loglresora) or p-antagonist with vasodilating properties (bucindolol or carvedilol). In addition to the antiarrhythmic action, they improve hemodynamic function. In carvedilol, there is also revealed antiaptoz effect. In cases of sustained ventricular tachycardia, and episode of syncope or sudden death, there is shown setting of automatic implantable defibrillator. If heart failure refractory to medical therapy, you need to decide on the heart transplant. Hypertrophic cardiomyopathy - a disease of the myocardium characterized by asymmetric or symmetric hypertrophy of the left ventricle with mandatory involvement in the process of hypertrophic interventricular septum.The clinical picture. The disease is more common in young age. Symtoms are variable: from asymptomatic to severe clinical symptoms and sudden death. In asymptomatic forms with prerequisite to a detailed examination of patients, there is detected sudden systolic heart murmur or ECG changes. Particularly attention is paid to the patients who have a family history of hypertrophic Commission or sudden death. One of the most common symptoms - various cardialgiae: from rare stabbing pain to typical angina. The latter is a consequence of the relative coronary insufficiency due to the mismatch of muscle perfusion and, depending on the degree of hypertrophy, or mechanical compression of the coronary arteries of the hypertrophied myocardium, as well as the diastolic filling of intramural vessels due to violation of myocardial relaxation. Second is due to frequency of occurrence of a sign - arrhythmic syndrome (30 to 70%). Extremely wide range of arrhythmias: these violations of atrioventricular conduction, and ventricular arrhythmias of various grades, including ventricular tachycardia and supraventricular arrhythmias, including atrial, although the last of the disease is not typical. Accordingly, a high frequency of arrhythmias and palpitations disruptions of the heart - a common complaint of patients with hypertrophic ILC. One of the main symptoms are fainting. Their occurrence is associated with both episodes of arrhythmia (paroxysmal ventricular and supraventricular tachycardia, complete atrioventricular block), and the syndrome of small output. The frequency of syncope and presyncope varies considerably - from single to multiple daily over a lifetime. Less frequently in patients with hypertrophic Commission, there are found signs of heart failure. Of these, most often cited dyspnea, while swelling and enlargement of the liver are very rare. On examination revealed enlargement of the heart, though not always considered to be a typical attenuation I tone at the top and the presence of systolic murmurs of different nature and intensity, often to the left edge of the sternum, in the III-IV intercostal space. It is associated with obstruction of the outflow tract of the left ventricle due to hypertrophy of the upper third of the interventricular septum with anterosystolic movement of the anterior leaflet of the mitral valve and mezosystolic cover of aortic valve. The diagnosis of hypertrophic Commission is verified using electrocardiography, echocardiography, chest X-ray. If you need to specify the extent of myocardial damage and coronary artery catheterization, there is performed heart and coronary angiography, Doppler ultrasound and biopsy endomiokarda. The presence of pathological Q waves in the ECG is a characteristic feature of hypertrophic ILC. Usually it is defined in II, III, aVF and left precordial leads, while not growing R wave in the right precordial leads. In some patients, pathologic Q wave detects from the right precordial leads, and the ventricular complex may be in the form QS - these changes are most characteristic of asymmetric septal hypertrophy. A typical ECG sign of apical hypertrophic forms of ILC are giant negative T waves in the precordial leads. Rhythm and conduction disturbances, described earlier, may not be available on a standard ECG, but are usually identified by its daily monitoring. Echocardiography - the main method of diagnosis of hypertrophic ILC. Thickening of the interventricular septum in its various departments of more than 13 mm in combination with its hypokinesia (range of motion of less than 3 mm) is considered a classic sign. There is also haracteristic of anterosystolic movement anterior mitral valve and partially cover mezosystolic aortic valve, a decrease in left ventricular diastole. X-ray of the heart reveals the typical signs of left ventricular hypertrophy, sometimes - signs of increased left atrium. But some patients radiograph is different from normal. Cardiac catheterization and coronary angiography help to clarify the nature and extent of violations of intracardiac hemodynamics (determine the pressure gradient between the left ventricle and the aorta, the increase in end-diastolic pressure in the left ventricle) and the coronary circulation. With the same purpose, there can be used radioisotope methods of research. Doppler (color Doppler scan) allows non-invasive way to get enough accurate information about the state of intracardiac hemodynamics. In biopsy endomiokarda, there are investigated five morphological characters: a) short fibers, interspersed with connective tissue, and b) a large ugly core, c) fibrosis d) with the disappearance of the degenerating muscle myofibrils, and e) a chaotic arrangement of muscle fibers with a twist. Classification. According to the localization of hypertrophy, there are the following morphological variants of hypertrophic Commission: 1. Idiopathic hypertrophic stenosis subaortalny the disproportionate hypertrophy of the interventricular septum, outflow tract obstruction of the left ventricular endocardial thickening under the aortic valve thickening and paradoxical motion of the anterior leaflet of the mitral valve to the septum in systole. 2. Asymmetric septal hypertrophy without changing the portal and the mitral valve and without outflow tract obstruction of the left ventricle. 3. Apical Hypertrophic Commission with restricted zone of apical hypertrophy. 4. Symmetrical with concentric hypertrophic Commission of left ventricular hypertrophy. Differential diagnosis is conducted with ischemic heart disease, valvular aortic stenosis, pulmonary stenosis, ventricular septal defect, mitral insufficiency, and in the beginning of the disease - and neuro dystonia. The use of these research methods eliminates the above mentioned diseases. Treatment of patients with hypertrophic Commission aims to reduce the symptoms of the cardiovascular system with medical therapy, and in the case of resistance, surgeryisindicated. Among medication, p-blockers and verapamil are most widely used in the treatment of hypertrophic Commission. Their appointment is necessary at the stage of clinical manifestations (pain, arrhythmia, shortness of breath), and in asymptomatic because of their actions on retention of disease progression by reducing the intraventricular pressure gradient and improve diastolic ventricular function. Preparations are shown in normal doses, propranolol to 120-160 mg / day, verapamil to 240-480 mg / day. There is possibility of selective p-blockers. Patients with dangerous arrhythmias justify the appointment of amiodarone. Nitrates should be avoided because of the danger and vasodilators increase obstruction of the left ventricle. Patients with atrial fibrillation should anticoagulant therapy, and it must be continued from the date of registration of the arrhythmias (aspirin or warfarin). Surgical treatment in the form of a partial muscle resection in the basal part of the interventricular septum (myotomy-miektomiya) is recommended in patients with severe clinical manifestations and in the outflow tract gradient greater than 50 mm Hg. Art., and if drug therapy is no longer having the desired effect. Restrictive cardiomyopathy - a disease characterized by diastolic dysfunction of the heart as a result of morphological changes of the endocardium, and subendokarda infarction. The dimensions of the heart is usually not enlarged, and sometimes reduced. Endomyocardial fibrosis and fibroplastic eosinophil parietal endocarditis of Leffler, previously denoted as independent entities that are now seen as the different stages of the same disease. Sometimes there is the name "endomyocardial disease." Primary for the disease is pronounced eosinophilia (sometimes called leukemia), reaching 36 to 75%. Regardless of the cause of eosinophilia in the development of heart disease, there are allocated three stages: necrotizing, thrombotic, fibrotic. As a result, developing a dramatic thickening and endocardial ventricular cavity obliteration by fibrous tissue and thrombotic masses. Often both ventricles are affected (in 50-70% of cases), but occurs isolated lesion of the right or of the left ventricle with approximately equal frequency. The clinical picture. The main symptoms of the disease are associated with heart failure, arrhythmias and embolism. The first signs of the disease are non-specific weakness, shortness of breath, decreased exercise tolerance. Pain in the heart is relatively rare. In the future, the clinical manifestations are determined with right or left ventricular failure, but even when lesions of the left and right heart combined, right ventricle symptoms usually predominate. Often there is a recurrent ascites, hepatomegaly (sometimes without peripheral edema), pronounced cyanosis of the face, swelling of the neck veins. Regardless of the prevalence of disease, there is revealed pericardial effusion, often fluid in the pleural cavity. Accordingly, heart tones are muted, usually tachycardia, low blood pressure. Often auscultated mitral insufficiency, gallop rhythm.Thromboembolic pneumonia, a frequent complication of restrictive Commission. Electrocardiography, chest X-rays, echocardiography, angiocardiography, cardiac catheterization and endocardial biopsy, blood tests - methods used to confirm the diagnosis of restrictive Commission. According to the ECG, there is revealed a low voltage QRS and T, especially with pericardial effusion, various arrhythmias, conduction block. In right ventricular endomyocardial fibrosis, 75% of patients had pathologic Q waves in leads V1-V2, negative - T-segment ST, sometimes high pravopredserdnye teeth R. During fluoroscopy in patients with right ventricular fibrosis determined marked increase in the right atrium and ventricle, reducing the blood supply pulmonary circulation, pericardial effusion in patients with left ventricular - increased left atrial stasis in the pulmonary circulation. Both forms near the top and in the outflow tract is sometimes revealed a linear calcification. Echocardiography reveals thickening of the endocardium, obliteration of the ventricular cavity, paradoxical movement of septum, pericardial effusion, often a diastolic opening of the pulmonary valve. Angiocardiography supports resizing, uneven contours of the ventricles, obliteration of the cardiac apex, increased outflow tract, reduced cardiac output. Application of endocardial biopsy justified in the differential diagnosis of sarcoidosis, myocarditis, cardiac amyloidosis. In the analysis of CROP, there is registered anemia, eosinophilia varying degrees. Differential diagnosis is conducted withwithkonstrictpericarditis, pericardial any etiology, atrial myxoma, sarcoidosis, myocarditis, cardiac amyloidosis, and other types of idiopathic cardiomyopathy. In contrast to hypertrophic and dilated restrictive KMP, KMP is not peculiar to cardiomegaly, heart size is usually small and characteristic obliteration of the cavities of the ventricles in the apical region. Most often, it should be distinguished from constrictive pericarditis. Presence indications of a history of tuberculosis, trauma (including surgeries on the heart), pericarditis, and prior systemic diseases that may involve in the process of the pericardium, makes the most likely diagnosis of constrictive pericarditis. Treatment. Effective treatment of restrictive Commission does not exist yet. It is justified to carefully use diuretics in cases of stagnation in the small and large circulation and digoxin in the case of reduction of left ventricle. Drugs with positive inotropic action isineffective, and vasodilators should be used with great caution in order to avoid the deterioration of the ventricular filling due to excessive loss of preload. To maintain adequate cardiac output during the Commission's restrictive, there is a necessity of high ventricular filling pressure. Conclusive evidence of this pathology calcium channel does not exist yet, though they may be able to increase the stretch in ventricular diastole. Alcoholic cardiomyopathy develops in years of regular alcohol abuse. In the event of a so-called "beer" heart decisive in the defeat of the myocardium is contained in beer cobalt with clinical symptoms differ from those in alcoholic heart disease. In chronic alcoholism, occurs cardiac at the subcellular level, intracellular transport of calcium is disturbed, which leads to disruption of relaxation myocardium. Clinical painting at an early stage of alcoholic cardiomyopathy is manifested with tachycardia, arrhythmia, sometimes withatrial fibrillation. There may be listened can rhythm of gallop. Identified and other signs of chronic alcoholism - hand tremors, severe sweating. In the later period, there was an increase in heart size, symptoms of cardiac decompensation. On ECG decreased or negative prong T. Treatment is aimed at the complete exclusion of alcoholic beverages, taking vitamins and other products that will improve myocardial metabolism. In heart failure, there are used cardiac glycosides, diuretics, antiarrhythmic agents. If severe heart failure is absent, there is appointed a small dose of p-blockers. Other forms of secondary cardiomyopathy in infectious and parasitic diseases, amyloidosis, etc. are discussed in the relevant chapters. Myocardiodystrophy - noncoronary group and non-rheumatic diseases infarction, characterized by impaired metabolism in the heart muscle and certain structural changes that occur under the influence of noncardiac causes. Among them, according to V. X. Vasilenko (1983) and NR Paleeva (1991), myocardial in anemia, malnutrition and obesity, vitamin deficiency, kidney damage and liver damage, violation of certain types of metabolic diseases, endocrine system diseases, intoxication, physical stress, infections . Pathophysiological mechanism is the development of energy deficit in adaptive hyperactivity infarction, designed to maintain an adequate level of functioning of the cardiovascular system in a situation of long-acting noncardiac causes. As a result, myocardial damage occurs and the picture of myocardial is developed. Changes that occur in the heart muscle, are nonspecific. When extracardiac factor actions are eliminated, changes in the heart muscle are reversible. In the development of myocardial dystrophy, there are distinguished three stages. The first stage is peculiar adaptive hyperfunction infarction, usually with hyperkinetic circulation option arising due to dysfunction of regulatory systems, increasing the effects of the sympathoadrenal and suppressing effects of parasympathetic nervous system. Stage II is characterized by the formation of the exchange-structural changes, leading to cardiac dysfunction. Stage III develops severe pathological changes in metabolism, structure and function of the heart muscle, accompanied by heart failure and heart rhythm disturbances. The clinical picture in accordance with the phasing of the development of myocardial dystrophy to a certain extent depends on its stage. In the early stages of cardiac complaints myocardiodystrophy character may be absent. Fatigue, decreased performance, poor exercise tolerance can be regarded as a manifestation of the underlying disease. Most often, patients note cardialgiae localized in the apex of the heart, long-term, no clear association with physical activity at the time of its execution, persists even after taking nitroglycerin. At the same time, both physical and emotional overload often provoke false angina in these patients, but often - after a while. Sometimes the pain can be unreasonable. In addition, many patients concerned about short of breath, dizziness, palpitations. In stage II-III of myocardiodystrophy, may appear edema, dyspnea at rest, cardiac arrhythmias and conduction. An objective examination in the early development of myocardial dystrophy, there is determined attenuation / ton over the top of the heart, a short systolic murmur, and tachycardia. Later there may be generated rhythm of gallop due to pathological III tone, often found rhythm and conduction disturbances (arrhythmias, atrial fibrillation, intraventricular and atrioventricular block); there is lack of blood circulation. Defining clinical manifestations are based on those extracardiac pathologies that led to the development of myocardial dystrophy. Thus, in myxedema,the size of the heart can significantly increase, the movement of its walls with the sluggish and slow, very early in thyrotoxicosis may develop atrial fibrillation, with symptoms of anemia can be simulated valvular heart disease - can be auscultated systolic murmur typical of mitral, tricuspid and aortic valves, with disovarialnyh diseases often patients complain of "tides", hot flashes, sweating, paresthesia in the extremities, etc. In the ECG often detected reduction and flattening of the T wave, particularly marked in the right precordial leads (V,3), rarely in Left. Sometimes shifted segment ST, disturbed intraventricular conduction. If such changes are installed on the ECG for diagnosis performed pharmacological tests (potassium, obzidanovaya). In the event of such changes in intracellular potassium deficiency ingesting 6.4 g of potassium chloride can normalize the ECG. In excess effects of catecholamine on myocardium, there is a possibility of normalization of the ECG for 1 - 1.5 h after administration of 6080 mg obzidan (Inderal, inderal). In cases where the depletion of norepinephrine in the sympathetic nerve endings of the heart, ECG can be restored after administration of p-agonists izadrina. However, it should be noted that these pharmacological tests do not need to be exaggerated. Only the combination of clinical, instrumental methods and dynamical examination can allow a diagnosis of myocardial dystrophy. Treatment should be directed towards the main process that caused degenerative changes in the myocardium. In addition to this, oral drug therapy that affects the metabolism in the heart muscle (Riboxin, mildronat, safinor, vitamins Vit. Etc.) normalizing electrolyte balance (drugs potassium, magnesium), which improves the microcirculation (dipyridamole, Teonikol, aspirin), acting on catecholamine Balance (Inderal, obzidan, Inderal). Simultaneously, there is conducted antiarrhythmic therapy, the treatment of heart failure. Pericarditis - inflammation of the pericardium sheets (epicardium and pericardium) that occurs as a complication of various diseases and is very rare for a separate disease. Currently, the main causes of pericarditis - connective tissue diseases, tuberculosis, bacterial and viral infections, postperikardiotomny syndrome associated with cardiac surgery, pericarditis with neoplastic processes, postinfarction, uremic. In 3-10% of cases, pericarditis found at autopsy, according to various authors. The frequency of pericarditis, detected clinically, is much less, since it occurs almost asymptomatic in many patients. The clinical picture. Pericardial disease usually occurs in one of three clinical forms: acute dry or swampy, swampy and chronic constrictive. At the beginning of the inflammatory process Pericarditis usually happens because DRY fibrin deposits in the exposed epicardium. The most important feature of it - chest pain, usually sharp, stabbing, but it can be a dull, oppressive. The pain is worse with deep breathing, coughing, turning the torso in the supine position and the left side is facilitated in a sitting position, and when you lean forward. It is not made easier and is not stopped taking nitroglycerin. The pain often radiates to the left supraclavicular region, neck and shoulders. The pain in most cases precedes fever (a characteristic feature of the differential diagnosis of a myocardial infarction), weakness, fatigue, myalgia. Pericardial rub - the most important objective sign of illness. Often, it is determined only by careful listening, pressing the stethoscope on the chest and the patient lying on his stomach, if the patient is based on the elbows and knees, in a deep breath, or if the patient leans forward. Pericardial friction is often transient and may disappear in a few hours after the occurrence. Sometimes pericarditis is accompanied by extrasystoles, atrial fibrillation and other arrhythmias. Pericardial effusion appears almost simultaneously with the deposition of fibrin, but in the beginning, because of severe absorptive capacity of the pericardium, it is insignificant and often accumulates gradually. Normally, heart bag contains about 25-35 ml of fluid; accumulated effusion reduces pain in the heart and leads to shortness of breath, tachycardia, and increase in jugular veins without falling down on the breath, cyanosis, and sometimes temporary disturbance of consciousness. Area of cardiac dullness is increased; apical impulse in most cases is not defined, the tones become deafer, pericardial rub vanishes. Increasing the number of exudate can lead to cardiac tamponade and the emergence of a paradoxical pulse (pulse amplitude reduction or complete disappearance on his breath); it is best felt in a carotid or femoral artery. Grow pale skin, cyanosis of the lips, nose, and ears; there is a swelling of the face and neck ("collar Stokes"). Sometimes, there are developed preferential overflow veins and swelling of one and one-hand, mostly left hand, due to compression of innominate vein fluid in the upper sinuses pericardium. Further increases and becomes harrow liver, especially the left lobe. Ascites formation and swelling in the legs and lower back. The hallmark of pericarditis that congestion in the lungs,is usually absent. The final stage of the progression of acute pericarditis can be constrictive pericarditis, but often it is developing and initially differing dramatic thickening and seal heart shirt. This leads to a decrease in elasticity of the heart and fill it with cameras followed congested peripheral veins. Stagnation in the systemic circulation - the main clinical symptom of constrictive (adhesive) pericarditis. Patients complain about shortness of breath, fatigue, weakness, rapid expansion of the neck veins. There is revealed enlargement of the liver with ascites and peripheral edema. Venous pressure sharply increases (usually more than 250 mm of water. Cent.). Muffled heart sounds are often heard extra tone after 0,1-0,12 II after a tone, sometimes systolic click, splitting / / tone due to the early closure of the aortic valve with a decrease of systolic ejection. Usually, there is determined paradoxical pulse, characteristic tachycardia, aggravated by the slightest load. Squeezes pericarditis is characterized by triad Beck: high venous pressure, ascites, a small quiet heart. Chronic constrictive pericarditis occurs with a gradual progression of heart failure. In the development of chronic constrictive pericarditis, there are 3 stages: initial, intense and dystrophic. In the initial stage, there is marked weakness, shortness of breath when walking, venous pressure rises after much pressure. Appearance of ascites is typical for the stage of pronounced symptoms. Syndrome is also characterized by a combination of hypertension in the system and the superior vena cava syndrome of hepatic and portal circulation, the ratio of which, in contrast to cases of pericardial tamponade is independent on patient's body. Dystrophic stage is characterized by the development of hypoproteinemia. At this stage of the process, along with ascites and pleural effusion, there is produced edema in the lower extremities, genitals, on the body, face, hands. This is facilitated by hypoproteinemia. In the diagnosis of pericarditis, ECG study plays an important role. On the ECG with dry pericarditis, there is found concordant ST segment position in 2 or 3 standard leads, especially in lead II and V2_6, no significant changes of the complex ORS. Subacute effects on ST segment returns to the contour with the emergence of a slight negative T wave.When the effusion occurs, voltage of complex QRSdecreases. In cases of constrictive pericarditis, it reduces more, often there is formed deep and wide tooth Q. Changes of repolarization, frequent signs of stress of the left atrium and atrial fibrillation are typical Echocardiographicallyis detected at an early stage pericardial thickening or a small amount of fluid in the pericardial cavity. In effusion pericarditis, there is clearly defined extra fluid, quantity can be installed. Constrictive pericarditis characterized by obtaining two separate echo signals corresponding to the visceral and parietal pericardium sheets of paper, restricting the movement of the rear wall of the left ventricle. Radiographically there is established increase in the heart shadow, changing its contours (smoothing of the waist), a weakening heart beating, and congestive expansion of root vessels. In cases of constrictive pericarditis, heart size normal or reduced, only the left atriumslightly increases. A typical feature pericardial calcification, sharp weakening or absence of pulsation of the heart. Pericardiocentesis not only confirm the presence of effusion of heart shirts, but also to determine its nature, to distinguish pericarditis from hydropericardium (transudate), Hilo and hemopericardium, a detailed cytological study of fluid, put bacteriological, immunological and biochemical tests. Classification. According to etiologic classification, there are distinguished three groups of pericarditis: 1. Pericarditis from exposure to the infectious agent organism (bacteria, tuberculosis, rheumatism, viral and rickettsial, fungal, protozoal for invasion). 2. Aseptic pericarditis: allergic, with connective tissue diseases (systemic lupus erythematosus, rheumatoid arthritis), trauma, autoimmune (postinfarction, postcommissurotomy, etc.), with blood diseases, cancer, metabolic disorders deep (uremic, gouty). Differential diagnosis is conducted with acute myocardial infarction, pneumonia, pleurisy, pulmonary embolism, dissecting aneurysm of the aorta, restrictive cardiomyopathy, liver cirrhosis, tricuspid valve stenosis, mitral stenosis, vena cava syndrome isrhnsymediastinal tumors. Treatment is conducted strictly differentiation depending on the etiology of the disease and its forms. With infectious pericarditis, there are appointed antibiotics including tolerability and sensitivity of the microflora. In the treatment of tuberculous pericarditis, there is usually used a combination of three drugs: rifampin - 600 mg, isoniazid and ethambutol -300 - 50 mg / kg of body weight daily. In cases of dry or exudative pericarditis with unknown etiology and no active inflammatory lesions, antibiotic therapy is usually not assigned. If a purulent pericarditis or cardiac shirt hit due to sepsis, purulent center or pneumonia, antibiotics are shown always. In this case, antibiotics should enter into the cavity of the heart shirts as possible after extraction through the catheter and washing effusion cavity. Treatment of allergic, autoimmune and recurrent pericarditis begins with the appointment of nonhormonal anti-inflammatory and antihistamine (voltaren, diclofenac, indomethacin, plaquenil, diphenhydramine, suprastin). If there is no effect, then there is shown steroid hormones, and in some cases, immunosuppressive drugs (azathioprine, colchicine). When pericarditis associated with rheumatic diseases, systemic lupus erythematosus, steroid use is justified in the very early stages of development. The same approach is also used for post-MI pericarditis (Dressler's syndrome). First, there are appointed non-steroidal anti-inflammatory drugs such as aspirin, 650 mg orally every 6-8 hours, or indomethacin 25-50 mg orally every 4-8 hours, in cases of severe clinical manifestations applied prednisolone 1 mg / kg / day by mouth with a gradual decrease dose. In cases of acute pericarditis in the initial stages macrofocal myocardial infarction should be prescribed only by aspirin. The use of other non-steroidal anti-inflammatory drugs or glyukokortikoidngh contraindicated, as they can slow scar formation and increase the probability of rupture of the myocardium. Anticoagulants in heart attack pericarditis as much as possible should be avoided because of the danger of hemorrhagic pericarditis with subsequent cardiac tamponade. In case of the neoplastic nature of pericarditis and detection of cancer cells effusion into the cavity, there is reintroduced cytostatics, preferably tyhiotepa (50 mg). In dialysis pericarditis, the number of hemodialysis increases to 6-7 weeks. If this is not successful, or there are signs of cardiac tamponade, there will be showed perikardektomiya or pericardial drainage. In cases compressing pericarditis patients should be kept under constant surveillance from retrying echocardiography to assess the effectiveness of anti-inflammatory treatment. If the volume of pericardial effusion is reduced and symptoms of cardiac tamponade disappear, then pericardiocentesis is required. If such a resolution of the disease does not occur, there are indications in the removal of fluid from the pericardial cavity. In constrictive pericarditis, there is performed surgery, the amount of which is determined by the prevalence of compressing the capsule, the degree of proliferation of connective tissue, the severity of calcium deposits. Most often, the task of surgeon is to free the surgeon from compressing the capsule from the left ventricle. During the liberation of the heart from the right ventricle, there may occur pulmonary edema intraoperative deaths. Increased surgery dramatically increases the risk of injury walled heart and large veins. For the symptomatic treatment of pericarditis, there are appointed cardiac glycosides, diuretics, angiotensin-converting enzyme. Pleurisy - an infectious or aseptic inflammation of various etiologies in pleura, accompanied by the formation on the surface fibrinous overlays and (or) the accumulation of fluid in the pleural cavity (serous, purulent, hemorrhagic, hileznogo etc.) exudate. Pleurisy may be primary and secondary. Pleurisy is considered primary in cases where the local inflammatory process and the related general reaction of the body are the main symptoms of the disease. The vast majority of pleurisy is a secondary process and occurs in the presence of inflammatory processes in the adjacent (tuberculosis, pneumonia, mediastinitis, liver abscess, subdiaphragmatic abscess, paranephritis, pancreatitis, etc.) or remote (osteomyelitis, otitis media, sinusitis, etc.) bodies and tissues. Depending on the presence or absence of effusion pleurisy, it is divided into dry (fibrinous) and effusion (exudative). Adhesions and scars in the pleural space are often referred to as an adhesive, ossificans pleurisy. However, it’s proper to consider them as an outcome of inflammation. Free pleural effusion occurs in the absence of adhesions between the sheets of the visceral and parietal pleura and can be located typically and atypically. Encysted pleurisy occurs in the presence of adhesions between the pleural leaves. Their location is very diverse. Clinical presentation and diagnosis. Symptomatic dry pleurisy usually begins with a sudden pain in one or the other side of the chest, fever and cough. There are common phenomena - fatigue, malaise, loss of appetite, night sweats, chills. On examination, while observing the patient, attention is drawn to his posture, facial expressions and character of breathing. Thus, a patient with unilateral pleurisy spares the affected side: restricts breathing movements, prefers a prone position on the patient side, motionless, hand presses the affected side while sitting or standing. Auscultation over the area of dry pleurisy, there can be listened weakened breathing and pleural friction rub, a different timbre and duration, localized or diffuse. Pleural friction rub, at first, is very soft, then gets rougher character, like the creaking of new skin or rough scrapes. The clinical picture of exudative (effusion) pleurisy usually depends on the disease, a complication which it came. In symptomatic pleural effusion, typical complaints of patients are shortness of breath, a feeling of heaviness in the chest and coughing. With the accumulation of exudate breathlessness and a feeling of heaviness in the chest expands, although a strict dependence of the complaints the amount of fluid in the pleural cavity is not marked. On examination, the patient`s typical forced position can be observed lying on the sick side. For very large effusions or phenomena of respiratory and heart failure, patients take semi-sitting position. Respiratory excursions patient side of the chest is limited (chest on the affected side behind when breathing). The increased pressure of accumulated fluid in the pleural cavity increases the amount of the relevant part of the chest, and also leads to bulging and expanding the intercostal spaces. If the number of pleural exceeds 300-500 ml, then on the affected side there are marked and deadened sound (with massive effusions chupoy pike), weakening or disappearance of voice trembling and breathing noises. Blunting area has a curved upper boundary (line Damuazo). In left-sided pleurisy,space Traube disappears. Often decisive diagnostic method is pleural puncture. There is evaluate the appearance of the pleural fluid, its cellular composition, performed biochemical and biological research. On X-ray examination in dry pleurisy, there is revealed only limited mobility of the diaphragm on the affected side, and later there is a slight darkening of diffuse pulmonary field due to pleural adhesions, Mooring. X-ray mapping of pleural effusion depends on the quantity, condition pleural cavity (eg, adhesions, Mooring, etc.) and position of the body the patient (vertical or horizontal). The x-ray light is determined by the darkening of a small to a total depending on the size of effusion. Very great diagnostic importance is thoracoscopy with pleural biopsy, which reveals tuberculous pleurisy or tumor origin. Treatment. Treatment of pleurisy should be comprehensive and aimed primarily at eliminating the main process leading to its development. Symptomatic treatment is aimed at pain relief, faster resorption of fibrin, preventing the formation of extensive adhesions and is moored in the pleural cavity. Risk of transformation of serous fluid in purulent or encysted necessitates regular pleural puncture (1-2 w), with its maximum evacuation. This tactic works best anatomical and functional outcomes as lung completely crushes and does not develop obliteration. In purulent exudate, pleurisy is evacuated; the cavity is drained and washed with antiseptic solutions, and there are introduced intrapleural antibiotics. In intoxication, dyspnea, disorders of the heart, there are used intravenously plasma-substituting solutions, inhalation of oxygen, cardiac glycosides. In order to reduce pain (especially in patients with dry pleurisy), there can be used banks, mustard, dry heat, hot compress with tight bandaging the lower parts of the chest, smearing the affected side of iodine tincture in a grid. As resorption of fluid, after the disappearance of pain, normalization of body temperature and erythrocyte sedimentation rate, and the patient should exercise therapy sessions including breathing exercises to prevent pleural adhesions. In the absence of contraindications, there are performed physiotherapy (Solux, inductothermy, electrophoresis) and spa (local motels, Southern Coast of Crimea, the Black Sea coast, etc.) treatment. Diseases of the esophagus - achalasia (undisclosed) cardio (kardiospazm, hiatospazm, functional obstruction cardio of esophagus) is a violation of the motor function of smooth muscle of the esophagus, where it becomes hypertensive lower sphincter, does not relax during swallowing and esophageal peristalsis replaced his abnormal contractions. AK - a relatively rare disease, its rate is 7 deaths per 100 thousand population. The etiology is not established. It is believed that the cause of the disease are the psycho-emotional disorders and stress, prolonged use of cold (ice) drinks and ice cream. Pathogenesis.On the base of AK, there is a violation of the innervation of the smooth muscle wall of the esophagus and the lower esophageal sphincter, which will stop the disclosure of physiological cardia in swallowing, increased tone and motility of the esophagus and the delay of food in it. The clinical picture. The main features of CA are dysphagia, regurgitation and chest pain when swallowing. Dysphagia initially episodic, in severe cases is observed at every meal, especially dry or poorly chewed, increases in sea. To facilitate the passage of food, patients drink water or milk; take a deep breath, arching body back, which helpsin some cases. Regurgitation appears with stuck in the esophagus, saliva, mucus, and food residues arising in the torso, with a packed esophagus or at night while you sleep. Nocturnal regurgitation of food into the mouth with its flowing into the airways is accompanied by symptoms of "nocturnal cough", "wet pads", "night vomiting," etc. Often, there are developed aspiration pneumonia and bronchitis. Patient has chest pain when swallowing or eating out. They disappear after regurgitation or passage of food into the stomach. A complete picture of the AK is a chronic progressive dysphagia and weight loss in a few months or years. Diagnosis.In X-ray, there is not determined air in the stomach. Levels of air and fluid in the patient standing show a delay of food in the esophagus. If barium is swallowed, there is expansion of the esophagus, and in severe cases the esophagus looks like the sigmoid colon. Peristalsis in the lower two thirds of the esophagus is abnormal, its terminal part steadfastly coracoid narrowed and presented with not weakening lower esophageal sphincter. Reception of table 1-2., nitroglycerin relaxes the esophageal sphincter and the content goes to the stomach. With the help of manometry, defined normal or increased pressure in the lower esophageal sphincter, and it is not relaxed on swallowing. In endoscopic esophageal cavity, tehre is found extensive evidence of chronic esophagitis (congestion, edema, erosion, excessive bleeding). This method eliminates the cancer of the esophagus. Complications: recurrent aspiration pneumonia and chronic bronchitis. Treatment. Drug treatment is to receive sedatives, nitrates (nitroglycerin, sustak, nitrong, nitro poppy nitrosorbid, izoket, Erin, and others), anticholinergics (gastrotsepin, metatsin, platifillin etc.) and calcium antagonists (nifedipine - on 1020 mg sublingually 20 minutes before a meal). Also, there can beappled Buscopan (1 tablet 3 times a day), nonabsorbable antacids (fosfalgagel, Maalox, almagel etc.). In failure of conservative treatment, it is resorted to cardiodiosis. With experienced specialist, this method is effective in about 85% of cases. Possible complications include perforation of the esophagus cardiodiosis and bleeding. A hiatal hernia is the displacement after hiatal in the posterior mediastinum of some abdominal organs (usually the cardia of the stomach). In frequency, it takes third place after peptic ulcer and cholecystitis. It’s found in womedslightly more often than men. Etiology and pathogenesis. In the formation of hernias is characterized by a sharp increase in the value of intra-abdominal pressure, congenital hypoplasia of the connective tissue structures, reinforcing the esophagus, or degenerative changes in the elderly, the shortening of the esophagus, the fall muscle tone, loss of fatty tissue under the diaphragm, kyphosis of the spine, and others differ axial ( sliding) hernia, in which the chest cavity out abdominal segment of the esophagus and cardia, and paraesophageal (more rare) when the abdominal segment of the esophagus and cardia remain below the diaphragm and into the chest out of the stomach or other abdominal organs. The clinical picture is determined by the symptoms of failure cardia and reflux oesophagitis: worry belching, regurgitation of gastric contents, heartburn (especially torso or lying down, sagging in vertical position); frequent dysphagia, aerophagia, fast saturation during meals, persistent hiccups, vomiting mixed with blood, iron deficiency anemia. There may be experienced shortness of breath, palpitations, angina reflex. Paraesophageal hernias often asymptomatic or may be accompanied by pain in the epigastric region and the denial. Complications: bleeding of varying intensity, causing anemia; erosion and ulcers, scars the esophagus, denial (especially paraesophageal hernia), aspiration pulmonary complications, arrhythmia and other diagnosis. Hernia in most cases allows revealing radiography in the horizontal position of the patient, with straining. With the help of esophagoscopy, there are revealed axial hernia and associated esophagitis. The reduction of pressure in the lower esophageal sphincter, identified during esophagotomokymography is considered. Treatment is mainly conservative. There are appointed a sparing diet within the extended table number 1, a binding agent (bismuth nitrate by 0.25-0.5 g 2-3 times a day, silver nitrate (0.12 g - 200 ml) 1 tbsp. Spoon 3 times a day for 15 minutes before eating) and antacids (almagel 1-2 teaspoons 3-4 times a day 30 minutes before meals vikalin on the table 1-2. 3 times a day 1 hour after meals Crushed as in 1/2 cup warm water; magnesium oxide by 0.5-1 g 3-4 times a day 1 hour after meals, etc.). If necessary, there are applied antispasmodics (no-spa on the table 1-2. 2-3 times a day, papaverine, 0.04 g 2-3 times a day) and anticholinergics (atropine sulfate and 1 table. 2-3 times a day before food platifillin 1 table. 2-3 times a day before meals, metatsin to 0.002-0.005 g 2-3 times a day). Upon accession of serious complications, there is conducted a surgical treatment, which downgrades the hernial sac into the abdominal cavity, fixing the cardia and fundoplication. It is not recommended to work which is related to the bend of the trunk and abdominal tension. Should be slept with the head of the bed elevated (23 pads), mainly on the right side. Esophageal cancer (RP) is the 5th place among all cancers in men. This tumor is with uneven rate in different countries and regions. Especially the highfrequency band it covers is Central Asia, Kazakhstan, Yakutia. In European countries, Poland is relatively rare: Men - 6, Women - 2 per 100 thousand populations. Etiology. Drinking alcoholic beverages, too hot or spicy foods, smoking, poor diet, and a small amount in the diet of fresh fruits and vegetables are the predisposing factors of this cancer. Chronic esophagitis, esophageal polyps, cicatricial stricture, achalasia cardia, Plammsra Vinson syndrome (deficiency of iron in the body) have an important role. Pathogenesis. Strong alcoholic drinks, hot food and drink injure esophageal mucosa, facilitates contact with her carcinogens. Chronic esophagitis creates the conditions for the implementation of the carcinogenic action of agents contained in tobacco smoke, and entering with food and water. Polyp of the esophagus is a real danger of transition to cancer. Scarring of the esophagus alarms in terms of their malignant transformation.Pathology.Poland - almost always the primary and located in areas of physiological restrictions.90% of cases presented with squamous cell carcinoma and 10% - adenocarcinoma. Metastasis occurs in 50% of cases and occurs with current lymph. The clinical picture. In patients, there is progressed dysphagia and they lose weight. Dysphagia starts when taking tight, then semi-liquid food. In the propagation of tumor tissue, there occursper esophageal pain in the chest. Bleeding from the tumor is usually small, but can sometimes be significant. Because of the discomfort in swallowing, patients restrict his diet and lose weight. In the case of tumor invasion into surrounding tissue, pain becomes with agonizing character and is particularly disturbs the patient at night. When involved in the pathological process of recurrent nerve, there is arisen hoarseness, and with lesions of the trachea and bronchi, there are painful cough, shortness of breath, aspiration pneumonia and lung abscess. In the propagation of the tumor in the supraclavicular region it may be determined by enlarged lymph nodes, and with lesions of the liver - an increase. Diagnosis. Patients with persistent dysphagia and (or) a decrease in body weight in a short time should be carefully examined. Esophagographyis most important for diagnosis: the expansion of the lumen of the esophagus may occur early in the disease. Ulceration of tumor formation must be distinguished from peptic ulcers in the esophagus lined with columnar epithelium. Any ulcers localized outside this zone, suspicious at the ER. In all cases of suspected RP, there is underwent endoscopy. Multiple biopsies and cytology help in the diagnosis. Computed tomography is needed to identify the tumor spreaded to the mediastinal area and about intra-aortic lymph nodes. Changes in the blood are characterized by indicators of anemia, thrombocytosis, elevated erythrocyte sedimentation rate. Bloodis determined in the stool. Treatment is carried out by oncologists. There are used surgical, radiation, drug and combined methods. Prognosis in most cases is poor. Prevention consists of smoking cessation, alcohol and hot tea, nutrition, early detection and treatment of precancerous lesions. Esophagitis - inflammation of the esophageal mucosa of various etiologies. There are acute and chronic esophagitis (reflux esophagitis). Acute esophagitis. Etiology. Acute esophagitis can be a consequence of the mucous membrane of the esophagus various damaging factors (thermal, chemical, mechanical), acute inflammatory diseases of the mouth cavity, gastrointestinal tract, infectious diseases (typhoid fever, influenza, diphtheria), allergic reactions. Pathology. Depending on the intensity of the lesions vary Bluetongue, edematous, erosive, pseudomembranous, hemorrhagic, exfoliative, and necrotic abscess forms. The lesion may be focal or diffuse. The clinical picture. Mild forms are asymptomatic. In more severe forms, there are marked burning sensation in the chest while eating, pain along the esophagus, worse when swallowing, drooling, belching, regurgitation. In erosive and hemorrhagic forms, it is possible hematemesis, melena, with exfoliative - fever. For abscess and necrotizing esophagitis is characterized by intense pain, vomiting, and severe general condition. Complications.There is possibility of bleeding, perforation, mediastinitis, stricture. Diagnosis.There is recorded medical history, the results of esophagoscopy congestion, erosion, ulceration, and necrosis. Prognosis depends on the nature and extent of lesions, associated complications. When abscess and necrotic forms poor. Treatment.Cold drinks are applied, 0.25% solution of novocaine in, vegetable oil (200 ml) anestezin (2 g) 1 tbsp. spoonful every hour. Pain syndrome is removed with subcutaneous injection of 1-2 ml of 1% solution of morphine. In order to prevent possible esophageal spasm, there made subcutaneously 1 ml of 0.1% solution of atropine and 2 mL of 2% solution of papaverine. Prophylactic antibiotics in massive doses are started. It is recommended hungry 1-2da. Subsequently, there is appointed diet number 1a, 16, 1, in severe cases - parenteral nutrition. In the case of exposure of strong alkalis or acids, stomach is washed with a weak solution of soda or acetic or citric acid. In all cases, we treat the underlying disease and athogenetic factors of esophagitisare eliminated. Osteoporosis of the spine. For that, the most important are: - few children and childless women - women with fragile body shape, early menopause, prolonged use of corticosteroids, other diseases (hyperthyroidism, Cushing's disease or syndrome, type I diabetes, liver disease and kidney disease), low body mass index <19 kg/m2. Awkwardness and discomfort in the spine. Slightly and middle incentive pain in the chest and spine. The pain intensifiesduring prolonged sitting, standing, walking. Spondylartropatiya.Characterized by a combination of chest pain with uveitis and arthralgia (including history). • age at onset 40 years • slow, gradual increase in pain • duration of pain more than 3 months • morning stiffness • reduction in pain after exercise and during movement Chest pain also occurs in lesions of bone and rib structures of the chest: Tietze's syndrome Costosternal syndrome (against bronchitis, kostosternalnayahondrodiniya) The front edge syndrome Ksifoidalgiya Chest pain at the spinal cord tumors Sudden pain or increases gradually Bilateral or unilateral pain Pain is reduced when driving, often occurs at night Sensory disorders in the area of root innervation. Herpes zoster. Shingles (herpes zoster) - sporadic disease that occurs as a result of activation of latent varicella-zoster virus. Characterized by inflammation of the posterior roots of the spinal cord and spinal ganglia. In most cases, the disease begins acutely. The body temperature can rise to 38-39 ° C, and its rise accompanies general toxic reactions (headache, malaise, chilling). In the area of innervation of one or more spinal ganglia, there appears skin rash characteristic with pain and other subjective sensations. Characterized by burning, fit-sided chest pain, which intensifies at night and often accompanies by emotional reactions. The appearance of erythematous papules and vesicles surrounded by flushing rim Psychogenic chest pain.It is a frequent variant of pain, which consists in the fact that the phenomenon of pain, as the leading in the clinical picture of the disease at some point, exists at the same time in the structure of the various affective and autonomic disorders. Psychogenic chest pain usually is localized in the zone apex, precordium and the region of the left nipple. The most common psychogenic pain in the chest marked with: - Disturbingly hypochondriacal disorders - phobic. - Disturbingly panic disorder - Depression The basic criteria of psychogenic pain: prevalence of multiple and prolonged pain. Regardless of the absence or presence of organic causes of pain complaints of the patient is much higher than those that are possible for theseorganic remains. The existence of a temporary connection between the problem and psychogenicdevelopment or increase pain of a temporary connection between the problem and the development of psychogenic or increase pain may be aching, stabbing, pressing, squeezing, burning or throbbing pain. There may be aching, stabbing, pressing, squeezing, burning or throbbing pain. Continuous.It coincides with periods of fatigue and great emotional stress. There's also a short-term pain,which is not associated with physical activity. List of the literature 1. Jeffrey Bender, Kerry Russell, Lynda Rosenfeld, Sabeen Chaudry-Oxford American Handbook of Cardiology, 2011 2. A.Zaza An introduction to cardiac electrophysiology 3.ABC of Interventional Cardiology - Ever D. Grech, 2004 4. Cardiovascular Disease in the Elderly - Wilbert S.Aronow, Jerome L.Fleg, 5.www.vidal.ru /кардиология 6.medlistok.com./infarct.asp 7.health. mail.ru /disease/infarct/ 8.мedportal.ru>…>кардиолоия 9.www.it-med.ru/library/p/heart1.htm