Changes in the phalanges occur due to impaired nutrition of the periosteum
Swollen veins in the neck indicate the formation of stagnation at the level of the veins of the systemic circulation, more pronounced at the height of inspiration
Doppler study allows you to quantify the pressure in pulmonary artery, measure the reverse flow of blood (regurgitation) from the right ventricle into the atrium
Oxygen supply can reduce all symptoms of the disease caused by hypoxia
To indicate the underlying disease, use an additional code, if necessary.
Excludes: Eisenmenger’s defect (Q21.8)
Chronic heart disease of pulmonary origin
Cor pulmonale (chronic) NOS
In Russia, the International Classification of Diseases, 10th revision (ICD-10) has been adopted as a single normative document for recording morbidity, reasons for the population's visits to medical institutions of all departments, and causes of death.
ICD-10 was introduced into healthcare practice throughout the Russian Federation in 1999 by order of the Russian Ministry of Health dated May 27, 1997. No. 170
The release of a new revision (ICD-11) is planned by WHO in 2017-2018.
With changes and additions from WHO.
Processing and translation of changes © mkb-10.com
Coronary heart disease is a pathology of the heart muscle associated with a lack of blood supply and increasing hypoxia. The myocardium receives blood from the coronary (coronary) vessels of the heart. In diseases of the coronary vessels, the heart muscle lacks blood and the oxygen it carries. Cardiac ischemia occurs when oxygen demand exceeds oxygen availability. In this case, the heart vessels usually have atherosclerotic changes.
The diagnosis of IHD is common among people over 50 years of age. With increasing age, pathology occurs more often.
Ischemic disease is classified according to the degree of clinical manifestations, susceptibility to vasodilating (vasodilating) drugs, and resistance to physical exercise. Forms of IHD:
It also has several subspecies:
According to the international classification 10 (ICD-10), angiospastic angina (Prinzmetal's angina, variant) corresponds to 20.1 (Angina with confirmed spasm). Angina pectoris - ICD code 20.8. Unspecified angina was assigned code 20.9.
According to the international classification of the 10th revision, acute infarction corresponds to code I21, its varieties are distinguished: acute extensive infarction of the lower wall, anterior wall and other localizations, unspecified localization. The diagnosis of “recurrent myocardial infarction” was assigned code I22.
Other forms of IHD - codes I24-I25:
ICD-10 code I24.0 is assigned to coronary thrombosis without infarction.
ICD code I24.1 - post-infarction Dressler syndrome.
Code I24.8 according to the 10th revision of the ICD - coronary insufficiency.
Code I25 according to ICD-10 - chronic ischemic disease; includes:
The tendency to ischemia is increased with the following factors risk of ischemic heart disease:
Men over 50 and women during menopause are most likely to suffer from angina and heart attacks.
Risk factors for coronary heart disease that aggravate the course of coronary heart disease: uremia, diabetes mellitus, pulmonary failure. IHD is aggravated by disturbances in the conduction system of the heart (blockade of the sinoatrial node, atrioventricular node, bundle branches).
The modern classification of coronary artery disease allows doctors to correctly assess the patient’s condition and take the right measures to treat it. For each form that has a code in the ICD, its own diagnostic and treatment algorithms have been developed. Only by freely navigating the varieties of this disease can the doctor effectively help the patient.
Hemorrhagic vasculitis is considered a disease that is a type of immune vasculitis of small vessels and is characterized by advanced education immune complexes, increased permeability of vascular walls. This pathology may develop 2-3 weeks after acute tonsillitis, flu or scarlet fever. Hemorrhagic vasculitis is more common in children than in adults. Children aged 4 to 12 years are especially susceptible to the disease. Boys get sick 2 times more often than girls.
Hemorrhagic vasculitis ICD 10 (according to the international classification of diseases, tenth revision) is included in the group of diseases under the code D69.0 Allergic purpura. For most photos hemorrhagic vasculitis It is clear that the main symptom of the disease is an allergic rash.
The causes of hemorrhagic vasculitis in adults and children are divided into several types:
The most common causes of hemorrhagic vasculitis are associated with the influence of infectious agents.
The principle of the mechanism of formation of the disease is the formation of immune complexes, which, circulating through the bloodstream, can remain on the inner surface of the vascular walls. After this, immune complexes gradually destroy the walls of small vessels, which causes an inflammatory process of an aseptic nature and a decrease in the elasticity of the capillaries. As a result, this contributes to increased permeability of the vessel walls and the formation of lumens, which lead to the formation of blood clots and fibrin deposits. Therefore, it is believed that the main symptom of vasculitis is hemorrhagic syndrome and microthrombosis.
Most photos of hemorrhagic vasculitis in children show that the disease begins with ordinary skin rashes. The rash is most often small-spotted in nature, located in a symmetrical order and does not disappear with pressure. The rash usually appears around the joint surfaces, in the area of extension of the limbs and in the buttock area. A rash on the face, trunk, feet, or palms is quite rare. The intensity of the rash can vary - from rare and small elements to multiple ones that tend to merge. After the rashes disappear, pigmentation and severe peeling may remain in their place.
70 percent of patients exhibit symptoms of hemorrhagic vasculitis such as damage to the articular surfaces. This sign often occurs along with rashes in the first week of the disease. Damage to joints can be minor and cause short-term pain, but it can also be more extensive, when not only large (ankle and knee) but also small articular surfaces are affected. Swelling occurs and shape changes articular surface, and painful sensations can last from 2 hours to 5 days. However, the disease does not cause severe deformation of the articular surfaces.
The third most common symptom is moderate abdominal pain, which may go away on its own within 24 hours. Typically, pain occurs at the very beginning of the disease, before rashes and joint disorders. For some, pain in the abdomen occurs suddenly in the form of intestinal colic, the location of which is difficult to determine. Painful sensations may appear several times throughout the day. In parallel with the pain, dyspeptic disorders appear - vomiting, nausea, diarrhea. In some cases, the temperature rises to 37.5 degrees. To more rare signs Vasculitis may include kidney damage in the form of glomerulonephritis and pulmonary syndrome, which is manifested by cough and shortness of breath.
When the disease occurs in a child, a functional systolic murmur may be heard in the heart. Also often due to inflammatory processes in the vessels of the brain, the central nervous system is affected. Children may complain of headache, weakness, dizziness, nausea and irritability. Sometimes boys experience testicular damage (mostly bilateral), which causes swelling and tenderness of the tissue.
Treatment of hemorrhagic vasculitis begins with hospitalization, which lasts at least 20 days, and mandatory bed rest.
First of all, a strict diet is prescribed, which prevents the development of allergies in patients. The diet for hemorrhagic vasculitis excludes the consumption of chocolate, cocoa, citrus fruits, strong black tea and coffee, red fruits and berries. Recommended consumption vegetable purees, olive oil, butter, low-fat dairy products, stewed or boiled meat and fish, cereal soups and stews, dry white bread, fruits, green tea with milk, jelly, juices, puddings. The duration of the diet for hemorrhagic vasculitis reaches 1-2 years to prevent relapse of the disease.
Drug treatment includes the use of the following drugs:
Since the disease worsens under emotional stress and excitement, it is necessary to exclude stressful situations or use sedatives and tranquilizers that improve the outcome of complex treatment.
Treatment of hemorrhagic vasculitis in children is carried out over a long period of time - at least two years. It is imperative to register a sick child with a dispensary and visit a doctor every month for the first six months. Then once every 3 months or once every six months, depending on the condition. Preventive measures consist of treating foci of chronic infection, systematically taking tests to detect helminth eggs. During treatment, it is forbidden to engage in sports, be long time in the sun and do physiotherapy.
According to most forums, hemorrhagic vasculitis has a positive prognosis, since 95 percent of sick children recover within months.
Treatment of hemorrhagic vasculitis with folk remedies consists of preparing infusions, ointments and teas based on plant materials. Folk remedies used both externally and internally.
To the most useful and effective means The following recipes include:
If the diagnosis of the disease is confirmed, then before using the above recipes you should carefully read the ingredients in order to exclude allergenic products or herbs to which individual intolerance occurs. It is also necessary to consult a doctor and not self-medicate.
The term “chronic cor pulmonale” refers to changes in the heart muscle caused by lung diseases. This excludes cases of pathology complicating diseases of the heart and large vessels (mitral stenosis, cardiosclerosis after a heart attack, congenital defects, dilated cardiomyopathy).
In diagnosis, an indispensable condition should be primary disorder structure of lung tissue and its functions. The prevalence of the recorded pathology among the adult population allows us to place it in third place after ischemic and hypertension diseases.
In the International Classification of Diseases (ICD-10), types of chronic pulmonary heart disease are included in the general class of cardiovascular diseases. Codes I26, I27, I28 are different etiological factors. All cases are united by the gradual formation of overload of the right heart due to the development of high blood pressure in the pulmonary circulation.
Depending on the causes, the WHO Expert Committee has developed a classification of chronic pulmonary heart disease. Diseases are divided into 3 groups:
All risk factors for underlying disease accelerate and negatively affect the heart.
In patients of groups 1 and 2, all changes develop due to spasm of small arterioles in the lung tissue as a reaction to insufficient oxygen supply. In group 3, in addition to spasm, there is a narrowing or blockage of the vascular bed. The pathogenesis of the disease is associated with the following mechanisms.
All taken together leads to increased load on the right ventricle, hypertrophy, and then failure of the right heart. Enlarged right atrioventricular orifice contributes to insufficient closure tricuspid valve.
Soviet pulmonologists B. Votchal and N. Palev proposed a clinical description of the stages of development of the pulmonary heart:
At the early stage of the disease, the manifestations of chronic pulmonary heart disease do not differ from the typical symptoms of major pulmonary diseases. They intensify with exacerbation and are treatable.
Shortness of breath is a consequence of oxygen deficiency, but it also accompanies inflammation of the lung tissue, emphysema. The intensity does not always correspond to the degree of hypoxia.
Tachycardia is a nonspecific symptom; the heart rate increases in various diseases that are associated with activated sympathetic nervous system and increased release of adrenaline.
Chest pain is not similar to angina. They are believed to be caused by insufficiency of the coronary vessels, which have to feed the thickened muscle of the right ventricle. Spasm of the arteries of the heart and intoxication of the myocardium with inflammatory products are also important.
Increased fatigue and weakness occur when the shock capacity of the heart decreases. Peripheral tissues of various organs, including the brain, lack blood supply.
Heaviness in the legs, swelling - in addition to myocardial weakness, an increase in the permeability of the vascular wall plays a role. Swelling occurs on the feet and legs. They intensify in the evening and subside during the night. In the third stage, they spread to the thighs.
The feeling of heaviness and pain in the right hypochondrium is caused by an enlarged liver and stretching of its capsule. In a severe form of the disease, ascites simultaneously appears and the abdomen “grows” rapidly. This symptom is more pronounced in elderly patients with concomitant atherosclerosis of the abdominal arteries.
A cough with a small amount of sputum is more associated with the underlying pathology of the lungs.
Manifestations of encephalopathy - chronic lack of oxygen and excess carbon dioxide cause pathological disorders in the brain, disrupt vascular permeability, and promote edema. Patients have 2 possible symptoms:
At severe course seizures occur with loss of consciousness or dizziness, cold sweat and decreased blood pressure.
In people with chronic pulmonary heart The diagnosis can be suspected by its appearance: in the compensation stage, dilated skin vessels appear in the cheek area (blush) and on the conjunctivae (“rabbit eyes”). Cyanosis is found on the lips, tip of the tongue, nose, and ears.
When examining the fingers, changes in the nail phalanges are visible: they become flat and widened (“ drumsticks"). Unlike heart failure, the arms and legs remain warm to the touch.
When auscultating the heart, the doctor hears:
The x-ray reveals a typical bulging of the contours of the pulmonary artery, an enhanced tissue pattern, and an expansion of the zone of lymphatic vessels. This indicates an increase in pressure in the pulmonary circle. In the decompensation stage, the heart shadow expands to the right.
Echocardiography assesses the strength of the right ventricle, the degree of dilatation, and overload. From high blood pressure the wall of the interventricular septum bends to the left.
Respiratory functions are measured with special devices, and the spirogram is deciphered by a doctor in the functional diagnostics office.
The study of pressure in the pulmonary artery is carried out in complex diagnostic cases. A reliable sign Hypertension in the pulmonary circle is considered to be a resting pressure of 25 mm Hg. Art. and higher, and with load - over 35.
During the examination, it is necessary to establish the functional class of manifestations of cor pulmonale.
Treatment of chronic pulmonary heart disease should begin with the prevention of exacerbations of respiratory diseases, especially colds and flu, with the timely use of antiviral and antibacterial treatment.
Patients are advised to limit physical activity. Do not visit mountainous areas, because in high altitude conditions even healthy person experiencing oxygen deficiency. And in patients with pulmonary diseases, a reflex vascular spasm occurs and the degree of tissue hypoxia deepens.
Women should be aware of the negative effects of birth control pills.
It is necessary to stop smoking and even staying in a smoky room.
All treatment methods are aimed at eliminating or weakening the existing mechanisms of pathology, these include:
Oxygen is supplied in a humidified form through a mask, cannulas in the nasal passages, and some clinics use oxygen tents with special air saturation conditions. For a therapeutic effect on chronic pulmonary heart disease, the oxygen level in the inhaled air must be at least 60%.
Therapy is carried out for an hour up to 5 times a day and more often.
To reduce pressure in the pulmonary artery, medications of different groups are used:
The drugs Heparin and Pentoxifylline are necessary to improve blood flow and antithrombotic action.
In case of severe heart failure, cardiac glycosides are prescribed very carefully.
Patients with symptoms of decompensation are treated in a hospital. Observation and clinical examination are carried out by a local therapist and pulmonologist.
The mortality rate of patients from chronic pulmonary heart disease remains at high level: 45% of patients survive the decompensation stage for about two years. Even with intensive care their life expectancy is predicted to be no more than four years.
Lung transplantation gives 60% of patients survival over the next two years.
The disease is very difficult to treat. Any person has the opportunity to rid himself of bad habits, take care of your health in time. The appearance of cough, shortness of breath and other symptoms requires immediate medical attention.
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Pulmonary heart (cor pulmonale) is dilatation of the right ventricle secondary to lung diseases, which are accompanied by the development of pulmonary artery hypertension. Right ventricular failure develops. Clinical manifestations include peripheral edema, jugular venous distension, hepatomegaly, and sternal bulge. Diagnosis is made clinically and echocardiographically. Treatment involves eliminating the cause.
Corpulmonale develops as a result of lung diseases. This condition does not include right ventricular (RV) dilatation secondary to left ventricular failure, congenital heart disease, or acquired valvular disease. Cor pulmonale usually occurs chronic condition, but can be acute and reversible.
I26-I28 Cor pulmonale and pulmonary circulation disorders
Acute cor pulmonale usually develops with massive pulmonary embolism or artificial ventilation lungs, used for acute respiratory distress syndrome.
Chronic cor pulmonale usually develops with COPD (chronic bronchitis, emphysema), less often with extensive loss of lung tissue due to surgical intervention or injury, chronic pulmonary embolism, pulmonary veno-occlusive disease, scleroderma, interstitial pulmonary fibrosis, kyphoscoliosis, obesity with alveolar hypoventilation, neuromuscular disorders involving the respiratory muscles, or idiopathic alveolar hypoventilation. U patients with COPD a severe exacerbation or pulmonary infection may cause right ventricular overload. With chronic cor pulmonale, the risk of venous thromboembolism increases.
Lung diseases cause pulmonary arterial hypertension through several mechanisms:
Pulmonary hypertension increases right ventricular afterload, leading to the same cascade of events that occurs in heart failure, including increased end-diastolic and central venous pressure, ventricular hypertrophy, and dilatation. The load on the right ventricle may increase with increased blood viscosity due to hypoxia-induced polycythemia. Sometimes right ventricular failure leads to left ventricular pathology when interventricular septum bulges into the left ventricular cavity, preventing filling of the left ventricle, thereby creating diastolic dysfunction.
The presence of clinical, laboratory and instrumental symptoms of chronic obstructive and other lung diseases indicated in the article “Pulmonary heart - Causes and pathogenesis” already suggests a diagnosis of chronic pulmonary heart disease.
Cor pulmonale is initially asymptomatic, although patients usually have significant manifestations of the underlying lung disease (eg, shortness of breath, fatigue on exercise). Later, as pressure builds into the right ventricle, physical symptoms typically include systolic pulsation in the sternum, a loud pulmonary component of the second heart sound (S2), and murmurs of tricuspid and pulmonary valve insufficiency. Later, the gallop rhythm of the right ventricle (III and IV heart sounds), intensifying with inspiration, swelling of the jugular veins (with a dominant wave a, if there is no blood regurgitation due to tricuspid valve insufficiency), hepatomegaly and edema of the lower extremities are added.
The classification of pulmonary hypertension in COPD by N. R. Paleev successfully complements the classification of cor pulmonale by B. E. Votchal.
An examination to diagnose cor pulmonale should be carried out in all patients who have at least one of the reasons for its possible development. Chest radiographs demonstrate right ventricular enlargement and proximal pulmonary artery dilatation with distal attenuation of the vascular pattern. ECG signs of right ventricular hypertrophy (for example, deviation electrical axis right, cog QR in lead V and dominant wave R in leads V1-V3) correlate well with the degree pulmonary hypertension. However, because pulmonary hyperventilation and bullae in COPD lead to cardiac remodeling, physical examination, radiography, and ECG may be relatively insensitive. Cardiac imaging using echocardiography or radionuclide scanning is necessary to assess left and right ventricular function. Echocardiography helps assess right ventricular systolic pressure, but is often technically limited in pulmonary disease. Right heart catheterization may be required to confirm the diagnosis.
This condition is difficult to treat. The main importance is to eliminate the cause, especially to reduce or slow the progression of hypoxia.
In the presence of peripheral edema, diuretics may be indicated, but they are effective only in the presence of simultaneous left ventricular failure and fluid overload of the lungs. Diuretics may worsen the condition, since even a small decrease in preload often worsens the manifestations of cor pulmonale. Pulmonary vasodilators (eg, hydralazine, blockers calcium channels, dinitrogen oxide, prostacyclin), effective for primary pulmonary hypertension, do not give results in cor pulmonale. Digoxin is effective only in the presence of concomitant left ventricular dysfunction. This drug should be prescribed with caution because patients with COPD are very sensitive to the effects of digoxin. In case of hypoxic cor pulmonale, it was proposed to perform a venotomy, but the effect of reducing blood viscosity can hardly be neutralized negative consequences reduction in the volume of blood carrying oxygen, except in cases of significant polycythemia. In patients with chronic cor pulmonale long-term use anticoagulants reduces the risk of venous thromboembolism.
Thrombosis of arteries and veins of the intestine is called “mesenteric” after the name of the vessels. Most often it is a complication of acute myocardial infarction, an attack atrial fibrillation, slow sepsis. Mesenteric thrombosis usually affects the superior mesenteric artery. Much less often it is found in the inferior artery and mesenteric veins.
Thrombosis in veins is less common than in mesenteric arteries. The mixed form, in which blockage of both veins and arteries occurs, is rarely observed in very advanced cases.
The disease is difficult to diagnose. 1/10 of deaths from intestinal infarction occur in people under 40 years of age. Women are more susceptible to this type of pathology than men.
In the International Classification of Diseases (ICD-10) embolism and thrombosis iliac artery coded I 74.5 and included in the zonal pathology group abdominal aorta. Venous mesenteric thrombosis is a component of acute vascular diseases of the intestine and has code K55.0.
The intestinal loops are in a “suspended” state and are secured in place by a dense mesenteric ligament. Arterial and venous vessels. They are located almost parallel. The arteries (superior and inferior mesenteric) arise from the abdominal aorta and divide the blood supply into sections:
Between the main arteries there are “spare” collateral vessels. Their task is to help blood supply to the damaged area. A feature of intestinal collaterals is that they pump blood in only one direction: from the area superior artery into the inferior mesenteric. Therefore, in the case of upper-level thrombosis, no help can be expected from anastomoses.
Venous drainage from the intestine goes to the portal vein. Difficulty occurs when it narrows due to liver disease. Collateral circulation is formed by a group of portocaval anastomoses between the portal and vena cava. The small intestine is in the worst position. It does not have a developed collateral network.
By arterial system The embolus can reach the mesentery:
Venous blood, having the opposite direction and a tendency to decrease speed and increase viscosity, is more susceptible to the formation of its own thrombotic masses. The formation of blood clots in the veins is caused by:
Pathology classification includes different sides mechanism of injury.
The reasons are distinguished:
Depending on the degree of blood flow disturbance, stages are distinguished:
The pathological consequences of thrombosis can be:
In surgery, there is a stage of functional acute obstruction of the mesenteric vessels, in which there is no organic damage, and the pathology is caused by a temporary spasm.
The maximum damaging factor is abdominal trauma. Compensation does not have time to fully develop. Protective mechanisms increase blood clotting are activated, which aggravates the patient’s condition.
During operations on the aorta (narrowing of the isthmus, change in position for congenital defects, replacement of a site of an aneurysm with a graft), doctors know the possible mechanism of thrombosis of the mesenteric vessels: restored full blood circulation leads to a high flow rate through thoracic aorta into the abdominal area and the femoral artery to the legs. In this case, partial “robbing” of the mesenteric vessels occurs due to the additional suction action of the jet. Small blood clots may form in the capillaries supplying the intestinal wall.
Any circulatory disorders cause intestinal ischemia.
In the compensated stage, the damaged lumen of the vessel is completely replaced by the flow of blood through collaterals. This form is typical for chronic ischemia with a gradual course of the disease.
Subcompensation also depends on collaterals, but has clinical manifestations.
During decompensation, the entire period is divided into 2 phases:
Symptoms of manifestation acute thrombosis mesenteric vessels are determined by the level of circulatory blockage and the form of ischemia.
Signs of pre-thombosis caused by arterial insufficiency can be identified by questioning and clarifying the patient’s complaints:
Thrombosis of mesenteric veins is milder and slower. More often it is a chronic process.
In order to make a correct diagnosis, it is important for the doctor to get answers to questions about the initial manifestations, duration of pain, and characteristics of the stool.
The decisive method is diagnostic laparoscopy, which allows you to examine the intestines and clarify the stage of ischemic changes and the localization of the area.
Leukocytosis with a shift of the formula to the left does not provide certain information, since it is characteristic of many diseases. Increased level lactate dehydrogenase enzyme indicates the presence of necrotic tissue.
Ultrasound of the abdomen and fluoroscopy can provide some assistance in differential diagnosis. Preparing the patient and wasting time on angiography is not rational.
If laparoscopy is not possible, doctors proceed to laparotomy - an operation with a large incision in the midline of the abdomen:
For vein thrombosis, fibrinolytic therapy is indicated in the first 6 hours.
During the operation, the doctor must find ways to:
Restoring blood supply is carried out in the following way:
IN postoperative period The patient is prescribed large doses of Heparin to thin the blood.
The chronic form of thrombosis should be considered in patients with heart failure complicated by myocardial infarction. The clinic distinguishes 4 stages:
Mesenteric thrombosis, according to clinical trials, is observed much more often than diagnosed cases are registered. This pathology is masked by various acute conditions: cholecystitis, renal colic, appendicitis. The limited time for diagnosis does not always allow the disease to be detected.
Fatal cases, according to pathologists, are 1–2.5% of hospital mortality. These are thrombosis in the stage of infarction and diffuse peritonitis. Late surgery (after 12 hours) means high mortality (up to 90%).
A good prognosis for recovery with surgical treatment of chronic thrombosis in the first two stages. Timely seeking surgical help for abdominal pain allows the patient to be operated on in a favorable time frame and prevent perforation of the intestinal wall.
I27.0 Primary pulmonary hypertension
Pulmonary (arterial) hypertension (idiopathic) (primary)
I27.1 Kyphoscoliotic heart disease
I27.8 Other specified forms of pulmonary heart failure
I27.9 Pulmonary heart failure, unspecified
In Russia International Classification of Diseases 10th revision ( ICD-10) was adopted as a single normative document for recording morbidity, reasons for the population’s visits to medical institutions of all departments, and causes of death.
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Chronic obstructive pulmonary disease(COPD) is a disease characterized by a partially irreversible, steadily progressive limitation of airflow caused by an abnormal inflammatory response lung tissue to damaging factors external environment. The term "COPD" means a combination chronic bronchitis and secondary pulmonary emphysema.
Classification COPD is based on the severity of the disease. Stage 0(increased risk of developing COPD): normal spirometry, chronic symptoms(cough, sputum production). Stage I(mild): FEV 1/FVC<70%. ОВФ 1 ³ 80% от должного. Наличие/отсутствие хронических симптомов (кашель, продукция мокроты) . Stage II(moderate): FEV 1 /FVC<70%. 30% £ОВФ1 £ 80%от должного (IIA 50% £ ОВФ 1 £ 80%). (IIБ 30% £ ОВФ1 £ 50%). Наличие/отсутствие хронических симптомов (кашель, продукция мокроты) . Stage III(severe): FEV 1/FVC<70%. ОВФ1 <30% от должного или ОВФ 1 <50% от должного, в сочетании с дыхательной недостаточностью (Р а О 2 менее 8,0 кПа в сочетании или без Р а СО 2 более 6,7 кПа при дыхании на уровне моря) или клиническими признаками правожелудочковой недостаточности.
Statistics. 1849.2 cases per 100,000 population over 18 years of age; 548.8 cases - 15-17 years; 307.7 cases are under 14 years of age. According to WHO, the prevalence of COPD among men is 9.34/1000, and among women - 7.33/1000. People over 40 years predominate. COPD is in 6th place among the leading causes of death in the world, in 5th place in developed countries of Europe, and 4th in the USA.
Etiology. The development of COPD is promoted by smoking, occupational hazards (dust, irritants, smoke, fumes, etc.), air pollution (at home - products of fossil fuel combustion, odors of cooked food, heating appliances). Severe respiratory infections in childhood predispose to the development of COPD throughout life. The risk of developing COPD is inversely proportional to the level of socioeconomic status.
Genetic features. COPD does not develop in all individuals who have antitrypsin defects, leading to the early development of panlobular emphysema. Emphysema due to deficiency: . a 1 - antitrypsin (*107400, mutations of the PI, AAT, 14q32.1, Â genes) - liver cirrhosis, absence of a 1 - globulin peak during electrophoresis of serum proteins, a small amount of a 1 - serum antitrypsin and panlobular (covering all sections) emphysema, more pronounced in the basal parts of the lungs. Insufficiency of a 2 - macroglobulin. (*103950, 12p13.3-p12.3, Â).
Pathogenesis. The inflammatory process is induced by various pollutants and gases. Tobacco smoke has a direct damaging effect on lung tissue and the ability to cause inflammatory changes. Chronic inflammatory process of the respiratory tract, pulmonary parenchyma and blood vessels is characterized by an increased number of macrophages, T lymphocytes and neutrophils. Activated inflammatory cells release a large number of inflammatory mediators (leukotriene B4, IL-8, TNF-a, etc.), which can damage the structure of the lungs and maintain inflammation. In addition to inflammation, an imbalance of proteolytic enzymes and antiproteinases and oxidative stress are essential in the pathogenesis of COPD. Bronchitic component... At an early stage in small bronchi (diameter<2 мм) обнаруживают бактериальное обсеменение, воспаление, закупорку слизью, перибронхиолярный фиброз и облитерацию.. При сформировавшейся патологии — гиперплазия слизистых желёз, серозное воспаление и отёк; бронхоспазм и закупорка дыхательных путей секретом приводят к бронхиальной обструкции. Emphysematous component... Destruction of the alveolar walls and supporting structures leads to the formation of significantly expanded air spaces.. An increase in the airiness of the lung tissue leads to a narrowing of the airways during dynamic collapse during exhalation (expiratory bronchial collapse).. Destruction of the alveolar-capillary membrane reduces the diffusion capacity of the lungs.
Pathomorphology. Pathological changes in large and peripheral bronchi, pulmonary parenchyma and pulmonary vessels. In the trachea, bronchi and bronchioles with a diameter of more than 2-4 mm, inflammatory cells infiltrate the surface epithelium. Hypersecretion of mucus is also observed. Damage and restoration of the bronchial wall are repeated cyclically, its structural remodeling occurs, the collagen content increases and the formation of scar tissue narrows the lumen and leads to fixed airway obstruction. Microdestruction of the pulmonary parenchyma leads to the development of centrilobular emphysema, hence dilatation and destruction of the respiratory bronchioles. Thickening of the vascular intima is their first structural change with a further increase in the content of smooth muscle elements and infiltration of the vascular wall with inflammatory cells. As COPD progresses, the accumulation of large amounts of SMC, proteoglycans and collagen contributes to further thickening of the vascular wall.
Clinical manifestations
Complaints: epidemiological criterion for COPD is chronic productive cough lasting more than 3 months a year for 2 or more years in a row; shortness of breath of an expiratory nature, increasing over time, intensifying during an exacerbation.
Physical examination: upon examination (in later stages) the participation of accessory respiratory muscles; on auscultation - prolonged exhalation, dry scattered wheezing with quiet breathing, wheezing with forced exhalation, moist wheezing more often with exacerbation; during percussion - from a boxy tint to a distinct boxy sound. Tachycardia, accent of the second tone over the pulmonary artery.
Laboratory data: during an exacerbation, leukocytosis, increased ESR, neutrophil band shift; in severe cases - polycythemia (erythrocytosis), hypercapnia, hypoxemia, decreased content of a 1 - antitrypsin in the serum and the absence of a 1 - globulin peak in serum protein electrophoresis; bacteriological examination of sputum makes it possible to identify the causative agent of exacerbation of chronic bronchitis and exclude tuberculosis.
Instrumental data.. Spirometry is a criterion for diagnosis and severity (decrease in forced expiratory volume in 1 s (FEV 1) with a concomitant decrease in the Tiffno index, minimal dynamics of parameters (less than 15% of the original) after the introduction of bronchodilators; forced vital capacity within normal limits or decreased; increase in residual lung volume; diffusion capacity within normal limits or reduced.. ECG: increasing signs of pulmonary hypertension, hypertrophy of the right heart, chronic pulmonary heart.. EchoCG: signs of pulmonary hypertension.. Chest X-ray in COPD reveals increased and deformation of the bronchopulmonary pattern, with emphysema - a heart of normal size, increased airiness of the lung tissue, flattening of the diaphragm and bullous changes
Types of COPD. There are 2 classic types of COPD, which have different names. Emphysematous patients with shortness of breath (COPD type A) are classified as “pink puffers”, bronchitis patients with a characteristic cough (COPD type B) are referred to as “blue puffers”.
. “Pink puffers” suffer predominantly from emphysema with a slowly progressive course, more often after 60 years.. Loss of body weight.. Progressive shortness of breath on exertion.. Productive cough.. Auscultation: weakened breathing, isolated wheezing.. Hypoxemia and hypercapnia are moderate.. Diffusion lung capacity is reduced.. The respiratory function indicators improve little after inhalation of bronchodilators.
. “Blue edema” suffer predominantly from chronic bronchitis.. Productive cough.. Episodic shortness of breath.. Weight gain at a young age.. Auscultation: dry wheezing.. Cor pulmonale often develops with signs of right ventricular failure.. Severe hypoxemia and hypercapnia as a result of respiratory fatigue. muscles or decreased central stimulation of breathing.. Polycythemia.. Improved respiratory function after inhalation of bronchodilators.. The diffusion capacity of the lungs suffers slightly.
More often, mixed variants are observed, combining the signs of “pink puffs” and “blue swelling”.
Diagnostic tactics. The basis of diagnosis when contacting is to identify patients with chronic cough and exclude other causes of cough (sputum examination, radiography); optimal diagnosis is detection of FVD during a screening study (decrease in RVF 1).
Concomitant diseases. aggravating the course and worsening the prognosis of COPD: obesity, sleep apnea syndrome, heart failure, diabetes, arterial hypertension.
Treatment. General tactics: stopping exposure of the lungs to harmful factors. Regimen and diet: stay in the fresh air, avoid hypothermia, contact with patients with respiratory infections; annual anti-influenza and anti-pneumococcal vaccination; physical training programs. Drug treatment outside of exacerbation: anticholinergic bronchodilators (ipratropium bromide) or combinations with b 2 agonists (inhalation from a can, through a spacer or nebulizer), long-acting theophyllines. Inhaled GCs with the effectiveness of an initial two-week course of systemic steroids (improved respiratory function parameters). Expectorants with antioxidant properties (acetylcysteine, ambroxol). Regular use of antitussives and narcotic drugs for COPD is contraindicated. a 1 - Antitrypsin - in case of its deficiency. Long-term oxygen therapy at stage III for hypoxia (p a O 2 less than 60 mm Hg). Drug treatment for exacerbation: inhaled b2 - short-acting agonists (salbutamol) during therapy with anticholinergic drugs (ipratropium bromide), methylxanthines with caution (monitoring serum concentrations). GK IV or orally (30-40 mg 10-14 days per os). Antibiotics only in the presence of purulent sputum (aminopenicillins, cephalosporins of II - IV generations, new macrolides, pneumotropic fluoroquinolones of III - IV generations). In stage III, oxygen therapy is supplemented with assisted ventilation. Surgical treatment: bullectomy, surgical correction of lung volume, lung transplantation. Features of treatment in old age are determined by the presence of concomitant diseases (limitation of xanthines, sympathomimetics, combination with cardiovascular drugs). Features of the management of pregnant and lactating women are associated with increasing hypoxemia in COPD (oxygenation control) and the possible teratogenicity of the drugs used.
Complications and their treatment. Frequent infections (antibacterial therapy); secondary pulmonary hypertension and cor pulmonale (oxygenotheria, decreased pulmonary pressure); secondary polycythemia (oxygen therapy); acute or chronic respiratory failure.
Prevention. Fighting smoking, improving production and the environment.
Course and prognosis of the disease. The course is steadily progressing. The prognosis depends on the rate of decline in FEV 1 .
Synonyms: chronic obstructive bronchitis, obstructive emphysema.
Abbreviations FEF 1 - forced expiratory volume in the first second. FVC - forced vital capacity.
ICD-10. J43 Emphysema. J44 Other chronic obstructive pulmonary disease
Pharmacological group(s) of the drug.
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