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52. LUNG HEART. ETHIOLOGY, PATHOGENESIS OF ACUTE AND SUBCUTANEOUS, CHRONIC PULMONARY HEART, CLINIC, DIAGNOSTIC, TREATMENT PRINCIPLES.
Pulmonary sero-pathological condition, characterized by hypertrophy of the right ventricle caused by hypertension of the pulmonary circulation, which develops with damage to the bronchopulmonary apparatus, pulmonary vessels, chest deformity, or other diseases that impair lung function.
The acute heart lay down - a wedge is a symptom complex arising from thromboembolism of the pulmonary artery, and in case of illness, the cardiovascular and respiratory systems. Etiology: (acute heart failure with severe course)
1. Massive thromboembolism of the pulmonary artery 2. Gas, fatty, tumor embolism 3. Thrombosis of the pulmonary artery, pulmonary veins 4. Pneumothorax. Clinic: Acute development within minutes, hours, against the background of complete well-being, with frequent death. Accompanied by cardiac decompensation. There is a sharp shortness of breath, cyanosis, chest pain, agitation. Pulmonary thromboembolism quickly, within a few minutes to half an hour, leads to the development of shock and death. (Acute pulmonary heart with subacute course): 1) pulmonary artery embolism 2) pulmonary artery thrombosis with recurrent course 3) pulmonary infarction 4) valve pneumotrax 5) common acute pneumonia 6) severe course of bronchial asthma 7) pulmonary artery system disease Clinic: It develops within a few hours to several days and is accompanied by increasing shortness of breath, cyanosis and following development of a shock condition, pulmonary edema. During auscultation, a large number of wet and scattered dry rales are heard. Ripple in the 2-3 intercostal space on the left can be detected, II tone accent above the pulmonary artery. The nature of the swelling of the cervical veins, a progressive enlargement of the liver, pain on palpation. Often there is acute coronary insufficiency, accompanied by pain, rhythm disturbance, and ECG signs of myocardial ischemia. The development of this syndrome is associated with the onset of shock, compression of the vesical veins with the dilated right ventricle, and irritation of the pulmonary artery receptors. Further, the clinic of pulmonary infarction is characterized by the resumption or intensification of chest pains associated with breathing, shortness of breath, cyanosis, but less compared to the acute phase of the disease. Dry cough, or with a sparse sputum, hemoptysis, fever, tachycardia.
X-ray: a one-sided increase in the shadow of the root of the lung, increased transparency of the lung. High standing of the dome of the diaphragm, the expansion of venous vessels, an increase in the right heart. Pulmonary infarction - triangular dimming, fluid in the pleural cavity. ECG: (1-5 days of acute) deep prongs S in 1 and aVL and Q in 3, V1-V2 negative T, atrial fibrillation. In the subacute phase (1-3 weeks): negative T in 3, aVF, V1-2 leads. Diagnosis: clinical picture, ECG, x-ray, a history of thrombophlebitis of the lower extremities. Pulmonary angiography. Treatment: with the development of shock, resuscitation measures (intubation, cardiac massage, mechanical ventilation). If resuscitation is successful, an urgent operation is indicated to remove a thrombus from the trunk of the pulmonary artery and inject thrombolytic drugs into the pulmonary artery through a probe. Therapeutic relief of pain (analgesics, narcotic drugs, antipsychotics), reduction of pressure in the pulmonary artery (euphyllin, in the absence of hypotension - ganglion blockers), treatment of heart failure.
Early anticoagulant therapy is intravenous heparin with a switch to intramuscular and subcutaneous administration under the control of blood coagulation. ? -10 days, then indirect anticoagulants. (fibrolisin, streptokinase) Chronic pulmonary heart - develops over a number of years and proceeds at the beginning without heart failure, and then with decompensation of the right ventricular type. Etiology: 1) lesions in which the ventilation and respiratory function of the lungs is primarily affected (infectious inflammatory diseases of the bronchopulmonary apparatus - chronic bronchitis, chronic pneumonia, bronchiectatic disease, tuberculosis with the development of emphysema. Bronchial asthma, tumor processes, cystic degeneration of the lungs, collagenosis, silicosis, etc. ) 2) diseases that primarily affect the pulmonary vessels. (Pulmonary arteritis, primary pulmonary hypertension and thromboembolic processes in the small circle system) Pathogenesis: small hypertension circle as a result of obstructive and restrictive processes. Obstructive processes - violation of bronchial obstruction, uneven alveolar ventilation, gas diffusion is disturbed and Po2 in the alveolar air decreases - arterial hypoxia. Due to increased resistance to breathing, intrathoracic pressure was increased, which contributes to hypoventilation. Restrictive processes include a decrease in lung elasticity and resistance, a decrease in the respiratory surface and vascular tissue of the small circle. Increased blood flow through pulmonary shunts, which leads to alveolar hypoxia. Alveolus hypoxia leads to increased tone and pressure in the small circle and the development of hypertrophy of the right ventricle. Hypoxia causes an increase in the number of red blood cells, an increase in viscosity, a slowdown in blood flow, and an increase in bcc. Clinic: severe shortness of breath during physical exertion, increased fatigue, tendency to tachycardia. Sometimes pressing pain behind the sternum associated with dilatation of the pulmonary artery, dizziness, short-term episodes of loss of consciousness. The course of the disease is undulating. With an exacerbation of a chronic infection, the respiratory system due to an increase in pressure in the pulmonary artery, there is an increase in signs of heart failure with stagnation of blood in a large circle (right ventricular failure) - peripheral edema, enlargement of the liver, etc. During the examination, the appearance of a heart beat or pulsation in the epigastric region, emphasis II over the pulmonary artery. With this means the expansion of the lungs, the arteries listen to diastolic murmur (relates the insufficiency of the valve of the leg stem) in the 2 intercostal space. Acrocyanosis, expansion of the jugular veins, the appearance of signs of stagnation in a large circle are noted. Diagnosis: ECG: signs of hypertrophy and overload of the right cameras, elosy shift to the right, in lead V1-2 the R wave is enlarged, S has a small amplitude, T is negative. High P in lead II and III. X-ray: hypertrophy and dilatation of the right ventricle, signs of pulmonary hypertension. Echocardiography. Treatment: edema - diuretics. Long-term continuous oxygen therapy with oxygen cylinders.
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52. LUNG HEART. ETHIOLOGY, PATHOGENESIS OF ACUTE AND SUBCUTANEOUS, CHRONIC PULMONARY HEART, CLINIC, DIAGNOSTIC, TREATMENT PRINCIPLES.
- 74. CHRONIC GLOMERULONEPHRITIS. ETHIOLOGY, PATHOGENESIS, CLINIC, DIAGNOSTIC, TREATMENT PRINCIPLES.
kidney glomerular disease. Etiology is the outcome of OGN (? - hemolytic streptococcus), or occurs with systemic lupus erythematosus, hepatitis, and a snakebite. Pathogenesis is an autoimmune mechanism: autoAt to own kidney tissue. Clinic - Hematuric form - severe hematuria, swelling on the face, hypertension, signs of general intoxication, changes in the heart,
- Heart diseases. Coronary heart disease (CHD). Reperfusion syndrome. Hypertensive heart disease. Acute and chronic pulmonary heart.
1. IHD is 1. productive myocarditis 2. myocardial fatty degeneration 3. right ventricular failure 4. absolute coronary circulation failure 5. relative coronary insufficiency 2. Forms of acute coronary heart disease 1. myocardial infarction 2. cardiomyopathy 3. angina 4. exudative myocarditis 5 sudden coronary death 3. With angina pectoris in cardiomyocytes
- HEART DISEASES. CORONARY ARTERY DISEASE. HYPERTENSIVE HEART DISEASE. Myocardial hypertrophy. ACUTE AND CHRONIC PULMONARY HEART
HEART DISEASES. CORONARY ARTERY DISEASE. HYPERTENSIVE HEART DISEASE. Myocardial hypertrophy. ACUTE AND CHRONIC PULMONARY
- 85. GAME. ETHIOLOGY, PATHOGENESIS, CLINIC, DIAGNOSTIC, TREATMENT PRINCIPLES.
Gout - refers to the pains of metabolic “errors” and microcrystalline arthropathy, is associated with almost constant hyperuricemia (in the urine test) and the uric acid microcrystals in the tissue of the joint, kidney, vascular wall, less often the heart, eyes. Etiology - distinguish between primary (hereditary) gout - a defect in enzyme systems; secondary - leukemia during their treatment with cytostatics,
- 81. RHEUMATISM. ETHIOLOGY, PATHOGENESIS, CLINIC, DIAGNOSTICS, PRINCIPLES OF TREATMENT, PREVENTION.
Rheumatism is a systemic inflammatory obstruction of the TC, with a predominantly local path process in various membranes of the heart, developing in persons predisposed to it, mainly at the age of 7-15 years. Etiology - infection with? -Hemolytic streptococcus of group A. Pathogenesis - a connection with 2 factors: 1) the toxic effects of a number of streptococcal enzymes with their cardiotoxic d. 2) the presence of
- CHRONIC PULMONARY HEART
Chronic pulmonary heart refers to right ventricular hypertrophy against a background of a disease that affects the function or structure of the lungs, or both at the same time, except when these pulmonary changes are the result of damage to the left heart or congenital heart defects. More commonly associated with chronic bronchitis, emphysema, bronchial asthma, pulmonary fibrosis
- 51. LUNG EMPHYSIS. ETHIOLOGY, PATHOGENESIS, CLINIC, DIAGNOSTIC, TREATMENT PRINCIPLES
.Emphysema of the lungs - damage to the lungs, characterized by a decrease in the elastic properties of the lung tissue, a violation of the structure of the alveolar walls, expansion of the air spaces of the lungs distal to the terminal bronchioles with the fall of the latter on the exhale and obstruction of the airways. In most cases, panacinar pulmonary emphysema develops. Etiology - factors contributing to stretching
- 82. RHEUMATOID ARTHRITIS. ETHIOLOGY, PATHOGENESIS, CLINIC, DIAGNOSTIC, TREATMENT PRINCIPLES.
Rheumatoid arthritis is a systemic inflammatory obstruction of the connective tissue, with progressive erosive-destructive polyarthritis. Etiology - hereditary defects in the immune system. Pathogenesis - a glycosylation defect in Ig G, therefore, there will be no galactose and sialic acid, therefore conglomerates are formed from normal and abnormal Ig G, Ig M is produced on them
- 73. ACUTE DIFFUSIVE GLOMERULONEPHRITIS. ETHIOLOGY, PATHOGENESIS, CLINIC, DIAGNOSTIC, TREATMENT PRINCIPLES.
Etiology -? -Hemolytic streptococcus gr. A. Patagenesis - 3-type allergic. reactions: the formation of immune complexes, their sedimentation on the membrane of the cells of the renal glomeruli> violation of the processes of filtration of protein, salts. Clinic - the first signs of b / w 1-3 weeks. after an infectious disease. Extrarenal Syndrome - weakness, headache, nausea, lower back pain, chills, appetite, v body
- 55. SYMPTOMATIC HYPERTENSIONS ETIOLOGY, PATHOGENESIS, CLINIC, DIAGNOSTIC, TREATMENT PRINCIPLES.
processes as a symptom of other diseases are called secondary or symptomatic. Moreover, arterial hypertension often determines the severity of the underlying disease. Group Classification: 1. Hypertension caused by damage to the central nervous system. A small amount of the condition caused by traumatic brain injury, hypothalamic syndrome, Paige's diencephalic hypertensive syndrome, lesion
- 1.4. CHRONIC PULMONARY HEART (HLC)
The treatment of patients with HFS should be comprehensive and aimed at reducing pressure in the pulmonary artery (LA), improving bronchial patency and alveolar ventilation, eliminating pulmonary and heart failure, which can be achieved with adequate therapy for the underlying disease that led to the onset of HFS. 1. Bronchodilators - selective short-acting beta2-adrenostimulants
- Pulmonary heart and pulmonary circulation disorders
ICD code: (126-128) 126 Pulmonary embolism 126.0 Pulmonary embolism with reference to acute pulmonary heart 126.9 Pulmonary embolism without mention of acute pulmonary heart 127 Other forms of pulmonary heart failure 127.0 Primary pulmonary hypertension 127.1 Kyphoscoliotic heart disease 127.8 Other specified forms of pulmonary heart failure 127.9
- 80. DIFFUSIVE DISEASES OF THE CONNECTIVE TISSUE. CLASSIFICATION. ETHIOLOGY, PATHOGENESIS. Systemic lupus erythematosus. CLINIC, DIAGNOSTICS, PRINCIPLES OF TREATMENT.
Diffuse diseases of the connective tissue (DBST) - a group of nosological forms, x-systemic autoimmune and immuno-complex inflammation or excessive fibrozo formation (with systemic scleroderma) DBST includes: SLE, systemic scleroderma, dermatomyositis, Sjogren's syndrome, diffuse ectosis mixed connective tissue disease and rheumatic polymyalgia Etiology - possible
- CHRONICAL BRONCHITIS. CHRONIC PULMONARY HEART.
In recent years, due to the deteriorating environmental situation, the prevalence of smoking, and a change in the reactivity of the human body, there has been a significant increase in the incidence of chronic non-specific lung diseases (COPD). The term KNZL was adopted in 1958 in London at a symposium convened by the pharmaceutical group Ciba. He combined such diffuse diseases
- clinic, etiology, pathogenesis, treatment of acute and chronic hepatic encephalopathy
Etiology of liver failure (encephalopathy): 1. Infections: viral hepatitis, both acute and chronic - the most common cause, herpes simplex virus 2. Medications and toxins (halotane, antidepressants, mushroom poisoning, NSAIDs) 3. Ischemia ( ischemic hepatitis, surgical shock, acute Budd-Chiari syndrome) 4. Metabolic (disease