Chronic obstructive pulmonary disease ( COPD ) is a type of obstructive pulmonary disease characterized by long-term breathing problems and poor airflow. The main symptoms include shortness of breath and cough with sputum production. COPD is a progressive disease, which means it usually worsens over time. Daily activities, such as walking or dressing, become difficult. Chronic bronchitis and emphysema is an old term used for different types of COPD. The term "chronic bronchitis" is still used to determine the productive cough that is present for at least three months each year for two years.
Tobacco smoking is the most common cause of COPD, with factors such as air pollution and genetics playing a smaller role. In developing countries, one common source of air pollution is heating and ventilation that lacks ventilation. Long-term exposure to this irritation leads to an inflammatory response in the lungs, which results in narrowing of the small airways and damage to the lung tissue. Diagnosis is based on poor airflow measured by pulmonary function tests. Unlike asthma, airflow reduction does not increase much with the use of bronchodilators.
Most cases of COPD can be prevented by reducing exposure to risk factors. This includes reducing smoking levels and improving indoor and outdoor air quality. While treatment can slow the deterioration, there is no known cure. Treatment of COPD includes smoking cessation, vaccination, respiratory rehabilitation, and often bronchodilators and inhaled steroids. Some people may benefit from long-term oxygen therapy or lung transplantation. In those with an acute period worsening, increased use of medications and hospitalization may be necessary.
By 2015, COPD affects about 174.5 million (2.4%) of the global population. Usually occurs in people over the age of 40. Men and women are affected equally generally. By 2015, it resulted in 3.2 million deaths, up from 2.4 million deaths in 1990. More than 90% of these deaths occur in developing countries. The number of deaths is projected to rise further due to higher smoking rates in developing countries, and an aging population in many countries. This generates an estimated economic cost of $ 2.1 trillion in 2010.
Video Chronic obstructive pulmonary disease
Signs and symptoms
The most common COPD symptoms are sputum production, shortness of breath, and productive cough. These symptoms are present for long periods and usually worsen over time. It is not clear whether there is a difference in COPD type. Although previously divided into emphysema and chronic bronchitis, emphysema is only a description of lung changes rather than the disease itself, and chronic bronchitis is merely a descriptive symptom that may or may not occur with COPD.
Cough
Chronic cough is often the first symptom to develop. When it lasts for more than three months every year for at least two years, in combination with sputum production and without any other explanation, it is the definition of chronic bronchitis. This condition can occur before the COPD develops fully. The amount of sputum produced can change from hour to day. In some cases, cough can not be present or may occur only occasionally and may be unproductive. Some people with COPD associate the symptoms with a "smoker cough". Sputum can be swallowed or spattered, depending often on social and cultural factors. A severe cough can cause rib fracture or loss of consciousness for a moment. Those with COPD often have a history of "common colds" that last a long time.
Shortness of breath
Shortness of breath is often the most disturbing symptom of people. This is generally described as: "My breath takes effort," "I feel breathless," or "I can not get enough air". Different terms, however, can be used in different cultures. Usually shortness of breath is worse at long duration and worsening over time. At an advanced stage, or late stage of lung disease occurs at rest and may always be present. This is a source of anxiety and poor quality of life in people with COPD. Many people with COPD are further breathing through pursed lips and this action can increase shortness of breath in some people.
Other features
In COPD, exhale can be longer than breathing. Chest tension may occur, but it is not common and may be caused by other problems. Those with stagnant airflow may wheeze or decrease sound with air intake on chest examination with a stethoscope. Barrels are a typical sign of COPD, but they are relatively rare. Tripod positioning can occur when the disease worsens.
Advanced COPD causes high pressure on the lung arteries, which interfere with the right ventricle of the heart. This condition is referred to as pulmonale cor, and leads to the symptoms of leg swelling and neck veins. COPD is more common than other lung diseases as a cause of cor pulmonale. Pulmonale Corps have become less common since the use of additional oxygen.
COPD often occurs along with a number of other conditions, in part because of joint risk factors. These conditions include ischemic heart disease, high blood pressure, diabetes mellitus, muscle wasting, osteoporosis, lung cancer, anxiety disorders, sexual dysfunction, and depression. In those who suffer from severe illness, feeling always tired is common. Clubbing nails are not specific to COPD and should immediately conduct an investigation for underlying lung cancer.
Exacerbations
Acute exacerbations of COPD are defined as increased shortness of breath, increased sputum production, sputum color change from clear to green or yellow, or an increase in cough in a person with COPD. They may present with signs of increased respiratory work such as rapid breathing, rapid heartbeat, sweating, active use of the muscles in the neck, bluish color of the skin, and confusion or aggressive behavior in a very severe exacerbation. Crackles can also be heard in the lungs on examination with a stethoscope.
Maps Chronic obstructive pulmonary disease
Cause
The main cause of COPD is tobacco smoke, with occupational exposure and pollution from indoor fires being a significant cause in some countries. Usually, this exposure must occur for decades before symptoms develop. A person's genetic makeup also affects the risks.
Smoking
The main risk factor for COPD globally is tobacco smoking. Of those who smoke, about 20% will get COPD, and of those who smoke a lifetime, about half will have COPD. In the United States and the UK, of those with COPD, 80-95% are current or former smokers. The likelihood of developing COPD increases with total smoke exposure. In addition, women are more prone to the harmful effects of smoke than men. In non-smokers, passive smoking is the cause of about 20% of cases. Other types of smoke, such as marijuana, cigars, and pipe smoke, also pose a risk. The smoke of the water pipe seems just as dangerous as smoking. The problem of cannabis smoke may be only with heavy use. Women who smoke during pregnancy can increase the risk of COPD in their child. For the same amount of smoking, women have a higher risk of COPD than men.
Air pollution
Bad cooking fire, often fueled by coal or biomass fuel such as wood and dirt, causes indoor air pollution and is one of the most common causes of COPD in developing countries. This fire is a method of cooking and heating for nearly 3 billion people, with their health effects being greater among women due to more exposure. They are used as a primary energy source in 80% of homes in India, China and sub-Saharan Africa.
People living in big cities have higher rates of COPD than people living in rural areas. While urban air pollution is a contributing factor in exacerbations, its overall role as the cause of COPD is unclear. Areas with poor outer air quality, including from flue gas, generally have higher levels of COPD. The overall effect in relation to smoking, however, is believed to be small.
Work exposure
Intense and prolonged exposure to dust at work, chemicals, and fumes increases the risk of COPD in both smokers and non-smokers. Workplace exposure is believed to be the cause in 10-20% of cases. In the United States, they are believed to be associated with more than 30% of cases among those who never smoked and may represent a greater risk in countries without adequate regulation.
A number of industries and sources have been involved, including high levels of dust in coal mining, gold mining, and cotton textile industry, work involving cadmium and isocyanate, and smoke from welding. Working on farms is also a risk. In some professions, the risk is estimated to be equivalent to one and a half to two packs of cigarettes a day. Silica dust and exposure to fiberglass dust may also cause COPD, with unrelated risks to it for silicosis. The negative effects of exposure to dust and exposure to secondhand smoke seem to be additive or perhaps more of an additive.
Genetics
Genetics plays a role in the development of COPD. It is more common among relatives of people with COPD who smoke than unrelated smokers. At present, the only obvious inherited risk factor is alpha 1-antitrypsin deficiency (AAT). This risk is very high if a person lacking alpha 1-antitrypsin is also smoking. He is responsible for about 1-5% of cases and his condition is around three to four in 10,000 people. Other genetic factors are being investigated, which are many possibilities.
More
A number of other factors are less closely related to COPD. The risk is greater for the poor, although if this is caused by poverty itself or other poverty-related risk factors, such as air pollution and malnutrition, is unclear. Temporary evidence suggests those with asthma and airway hyperactivity have an increased risk of COPD. Birth factors such as low birth weight can also play a role, as do some infectious diseases, including HIV/AIDS and tuberculosis. Respiratory infections such as pneumonia do not appear to increase the risk of COPD, at least in adults.
Exacerbation
Acute exacerbations (symptoms that suddenly deteriorate) are generally triggered by infection or environmental pollutants, or sometimes by other factors such as inappropriate drug use. Infection appears to be the cause of 50 to 75% of cases, with bacteria in 30%, virus at 23%, and both in 25%. Environmental pollutants include poor indoor and outdoor air quality. Exposure to personal smoke and cigarette smoke increases the risk. Cold temperatures can also play a role, with exacerbations occurring more frequently in winter. Those with more severe underlying diseases have exacerbations more often: in mild disease 1.8 per year, moderate 2 to 3 per year, and 3.4 weight per year. Those with multiple exacerbations have a faster lung function deterioration rate. Pulmonary embolism (blood clots in the lungs) may aggravate symptoms in those with pre-existing COPD. The signs of PE in COPD include pleuritic chest pain and heart failure without signs of infection.
Pathophysiology
COPD is a type of obstructive lung disease in which poor air flow, perfect reversibility (limited airflow) and the inability to breathe completely (air traps) exist. Poor airflow is the result of the breakdown of lung tissue (known as emphysema) and small airway disease (known as obstructive bronchiolitis). The relative contributions of these two factors vary among people. Severe damage to small airways can lead to the formation of large air bags - known as bullae - that replace lung tissue. This form of the disease is called bullous emphysema.
COPD develops as a significant and chronic inflammatory response to inhaled irritation. Chronic bacterial infections can also add to this inflammatory state. The inflammatory cells involved include neutrophil granulocytes and macrophages, two types of white blood cells. Those who smoke also have Tc1 lymphocyte involvement and some people with COPD have eosinophil involvement similar to asthma. Part of this cell response is carried by inflammatory mediators such as the chemotactic factor. Other processes involved with lung damage include oxidative stress generated by high concentrations of free radicals in tobacco smoke and released by inflammatory cells, and breakdown of lung connective tissue by proteases that are not adequately inhibited by protease inhibitors. Damage to the connective tissue of the lungs causes emphysema, which then contributes to poor airflow, and ultimately, poor absorption and respiratory gas release. Common muscle discharges that often occur in COPD may be partly due to inflammatory mediators being released by the lungs into the blood.
Airborne constriction occurs due to inflammation and scarring in it. This contributes to the inability to breathe completely. The greatest reduction in airflow occurs when breathing out, because the pressure in the chest compresses the current airways. It can produce more air from the previous breath left in the lungs when the next breath begins, resulting in an increase in total air volume in the lungs at a given time, a process called hyperinflation or air trapping. Hyperinflation of exercise is associated with shortness of breath in COPD, because deep breathing is less comfortable when the lungs are partially filled. Hyperinflation can also worsen during exacerbations.
Some also have a respiratory rate of hyperresponsiveness to irritants similar to those found in asthma.
Low oxygen levels, and finally, high levels of carbon dioxide in the blood, can occur from poor gas exchange due to decreased ventilation from airway obstruction, hyperinflation, and decreased desire for breathing. During exacerbations, airway inflammation also increases, resulting in increased hyperinflation, reduced expiratory airflow, and worsening of gas transfer. It can also cause inadequate ventilation, and finally, low blood oxygen levels. Low oxygen levels, if present for prolonged periods, may cause narrowing of the arteries in the lungs, while emphysema causes capillary damage in the lungs. Both of these changes result in an increase in blood pressure in the pulmonary artery, which can cause cor pulmonale.
Diagnosis
The diagnosis of COPD should be considered for anyone aged 35 to 40 years who has shortness of breath, chronic cough, sputum production, or frequent winter colds and a history of exposure to risk factors for the disease. Spirometry is then used to confirm the diagnosis. Screening them without symptoms is not recommended.
Spirometry
Spirometry measures the amount of airflow obstruction present and is generally performed after the use of bronchodilators, a drug to open the airways. Two main components are measured to make the diagnosis, the forced expiratory volume in one second (FEV 1 ), which is the largest air volume that can be inhaled out in the first second of breath, and forced vital capacity (FVC), which is the largest air volume that can be inhaled in one big breath. Typically, 75-80% of FVCs go out in the first second and the FEV ratio 1 /FVC is less than 70% in someone with COPD symptoms defining a person as having the disease. Based on this measurement, spirometry will lead to over-diagnosis of COPD in the elderly. The National Institutes for Health and Care Excellence criteria also require FEV 1 less than 80% of the predictions. People with COPD also showed a decreased lung spreading capacity for carbon monoxide (D LCO ) due to decreased surface area in the alveoli, as well as damage to the capillary bed.
The evidence for using spirometry among those who have no symptoms in an attempt to diagnose a previous condition is an uncertain effect, so it is not currently recommended. The peak of expiratory flow (maximum expiration rate), commonly used in asthma, is not sufficient for the diagnosis of COPD.
Severity
A number of methods can determine how much COPD affects a particular individual. The modified British Medical Research Council questionnaire or the COPD assessment test (CAT) is a simple questionnaire that can be used to determine the severity of the symptoms. Scores in the CAT range from 0-40 with higher scores, the more severe the disease. Spirometry can help determine the severity of air flow restriction. This is usually based on FEV 1 expressed as a percentage of "normal" predictions for age, gender, height, and weight. Both American and European guidelines recommend partially based on treatment recommendations on FEV 1 . The GOLD guidelines recommend dividing people into four categories based on symptom assessment and airflow restrictions. Weight loss and muscle weakness, as well as other diseases, should also be taken into account.
More tests
Chest x-ray and full blood count may be useful to rule out other conditions at diagnosis. The characteristic signs of X-rays are the excessive lungs, flat diaphragm, increase in retrosternal air space, and bullae, while it can help rule out other lung diseases, such as pneumonia, pulmonary edema, or pneumothorax. The scanning of high-resolution computer tomography can show the distribution of emphysema throughout the lungs and can also be useful for getting rid of other lung diseases. Unless the operation is planned, however, this rarely affects management. Arterial blood analysis is used to determine the need for oxygen; this is recommended in those with less than 35% predicted sub-FEV 1 , those with peripheral oxygen saturation of less than 92%, and those with symptoms of congestive heart failure. In areas of the world where antitrypsin alpha-1 deficiency is common, people with COPD (especially those under 45 years of age and with emphysema affecting the lower part of the lung) should be considered for testing.
Differential diagnosis
COPD may need to be distinguished from other causes of shortness of breath such as congestive heart failure, pulmonary embolism, pneumonia, or pneumothorax. Many people with COPD mistakenly think they have asthma. The difference between asthma and COPD is done on the basis of symptoms, smoking history, and whether air flow restriction can be reversed with a bronchodilator in spirometry. Tuberculosis may also present with a chronic cough and should be considered at a common site. Less common conditions that may appear also include bronchopulmonary dysplasia and obliterative bronchiolitis. Chronic bronchitis can occur with normal airflow and in this situation is not classified as COPD.
Prevention
Most cases of COPD can potentially be prevented by decreasing smoke exposure and improving air quality. Annual influenza vaccinations in those with COPD reduce exacerbations, hospitalization and death. Pneumococcal vaccination may also be helpful. The non-typable vaccine Haemophilus influenzae (NTHi) when taken does not appear to reduce exacerbations in people with COPD. Eating a high-beta-carotene diet can help but take supplements does not seem.
Smoking cess
Keeping people from starting smoking is a key aspect of preventing COPD. Government policies, public health agencies, and anti-smoking organizations can reduce smoking levels by making people reluctant to start and encourage people to quit smoking. The smoking ban in public and workplaces is an important step to reduce exposure to secondhand smoke, and while many places have institutionalized the ban, more is recommended.
In those who smoke, quitting smoking is the only way shown to slow the deterioration of COPD. Even in the late stages of the disease, it can reduce the level of lung function deterioration and delay the onset of disability and death. Often, some effort is needed before long term abstinence is achieved. The 5-year effort leads to success in nearly 40% of people.
Some smokers can achieve long-term cessation of smoking through their own volition. Smoking, however, is highly addictive, and many smokers need further support. Opportunities stop increasing with social support, involvement in smoking cessation programs, and use of drugs such as nicotine replacement therapy, bupropion, or varenicline. Combining smoking cessation drugs with behavioral therapy is more than twice as likely to be effective in helping people with COPD quit smoking, compared to behavioral therapy alone.
Occupational health
A number of measures have been taken to reduce the possibility that workers in risk industries - such as coal mining, construction, and masonry - will develop COPD. Examples of such measures include public policy making, employee education and risk management, promoting quitting smoking, checking workers for early signs of COPD, use of respirators, and dust control. Effective dust control can be achieved by increasing ventilation, using water spray and by using mining techniques that minimize dust formation. If a worker develops COPD, further lung damage can be reduced by avoiding ongoing dust exposure, for example by changing job roles.
Air pollution
Both indoor and outdoor air quality can be increased, which can prevent COPD or slow the worsening of existing diseases. This can be achieved by public policy efforts, cultural change, and personal involvement.
A number of developed countries have managed to improve the quality of the outside air through regulations. This has resulted in improvements in the lung function of their populations. Those with COPD may experience fewer symptoms if they stay indoors on days when outdoor air quality is bad.
One of the main efforts is to reduce smoke exposure from cooking and heating fuel through improved home ventilation and better stoves and chimneys. The right stove can improve indoor air quality by up to 85%. Using alternative energy sources such as solar cooking and electric heaters is also effective. Using fuels such as kerosene or coal may be worse than traditional biomass such as wood or dirt.
Management
There is no known cure for COPD, but symptoms can be treated and development may be delayed. The main objectives of management are to reduce risk factors, manage stable COPD, prevent and treat acute exacerbations, and manage related illnesses. The only measures that have been shown to reduce mortality are smoking cessation and supplemental oxygen. Quitting smoking reduces the risk of death by 18%. Other recommendations include yearly influenza vaccination, pneumococcal vaccination once every five years, and reduction of environmental air pollution exposure. In those with advanced disease, palliative care may reduce symptoms, with morphine improving feeling of shortness of breath. Noninvasive ventilation can be used to support breathing. Provide people with personalized action plans, educational sessions, and support for the use of their action plans in terms of exacerbations, reducing the number of visits to hospitals and encouraging initial treatment of exacerbations. When self-management interventions, such as taking corticosteroids and using supplemental oxygen, combined with an action plan, improved health-related quality of life compared with regular care.
Exercise
Pulmonary rehabilitation is an exercise program, disease management, and counseling, coordinated to benefit individuals. In those with recent exacerbations, pulmonary rehabilitation appears to improve overall quality of life and ability to exercise. If pulmonary rehabilitation increases mortality or hospital admission rates are unclear. Pulmonary rehabilitation has been shown to increase a person's sense of control over his illness, as well as their emotions.
The optimal exercise routine, the use of non-invasive ventilation during exercise, and the intensity of exercise suggested for COPD sufferers, is unknown. Conducting arm resistance exercises improves arm movements for people with COPD, and can result in a small increase in shortness of breath. Doing arm exercises alone does not seem to improve the quality of life. Respiratory exercises in and of themselves seem to have a limited role. Scrubbing lips breathing exercises may be useful. Tai chi exercises appear to be safe to practice for people with COPD, and may be beneficial for pulmonary function and lung capacity when compared to regular care programs. Tai Chi was not found to be more effective than other intervention training programs. Inspiratory and expiratory muscle training (IMT, EMT) is an effective method for increasing daily life activities (ADL). The combination of IMT and walking exercises at home can help limit shortness of breath in severe COPD cases. In addition, the use of high speed mobilization along with low amplitude along with exercise improves lung function and exercise capacity. The goal of spinal manipulation therapy (TST) is to improve thoracic mobility in order to reduce lung work during respiration, to improve exercise capacity demonstrated by systemic medical outcomes.
Being underweight or overweight can affect symptoms, disability rates, and COPD prognosis. People with COPD who are underweight can increase their respiratory muscle strength by increasing their calorie intake. When combined with regular exercise or pulmonary rehabilitation programs, this can lead to improvement in symptoms of COPD. Additional nutrients may be useful for those who are malnourished.
Bronchodilators
Inhaled bronchodilators are the main drug used, and produce small overall benefits. The two main types are agonists and anticholinergics 2 ; both are in the form of long acting and short acting. They reduce shortness of breath, wheezing, and exercise restrictions, resulting in an improved quality of life. It is unclear whether they changed the progression of the underlying disease.
In those with mild disease, short-acting agents are recommended as needed. In those with more severe disease, long-acting agents are recommended. Long working agents partially work by improving hyperinflation. If the long-acting bronchodilator is insufficient, then an inhaled corticosteroid is usually added. With respect to long working agent, if tiotropium (anticholinergic long work) or long-acting? 2 agonist (LABA) is better not clear, and try each and continue that work best may be recommended. Both types of agents appear to reduce the risk of acute exacerbations by 15-25%. Although both can be used at the same time, any benefit is of questionable significance.
Some short-acting agonists? 2 is available, including salbutamol (albuterol) and terbutaline. They provide some symptom relief for four to six hours. PROFITS such as salmeterol, formoterol, and indacaterol are often used as maintenance therapies. Some feel limited evidence of benefits, while others see evidence of steady benefits. Long-term use appears to be safe in COPD with side effects including shaking and heart palpitations. When used with inhaled steroids, they increase the risk of pneumonia. While steroids and LABAs may work better together, it is unclear whether these little benefits outweigh increased risks. There is some evidence that the combined treatment of LABA with long-acting (OLD), anticholinergic, can lead to fewer exacerbations, less pneumonia, increased forced expiratory volume (FEV1%), and a potential increase in quality of life when compared with treatment PROFITS and inhaled corticosteroids. Indacaterol requires once-daily inhalation doses, and is as effective as other long-acting agonists 2 that require twice-daily dosing for people with stable COPD.
The two main anticholinergics are used in COPD, ipratropium and thiotropium. Ipratropium is a short-acting agent, while tiotropium is long-acting. Tiotropium is associated with decreased exacerbations and improved quality of life, and tiotropium provides better benefits than ipratropium. It does not seem to affect the overall mortality or hospitalization rate. Anticholinergics can cause dry mouth and urinary tract symptoms. They are also associated with an increased risk of heart disease and stroke. Aclidinium, another long working agent, reduces COPD-related hospitalization and improves quality of life. The LAMA umeclidinium bromide is another anticholinergic alternative. When compared with tiotropium, LAMAs aclidinium, glycopyrronium, and umeclidinium appear to have the same degree of efficacy; with the four being more effective than placebo. Further studies are needed comparing aclidinium to thiotropium.
Corticosteroids
Corticosteroids are usually used in inhalation form, but can also be used as tablets to treat and prevent acute exacerbations. While inhaled corticosteroids (ICS) have not shown benefits for people with mild COPD, they decrease acute exacerbations in those with moderate or severe disease. On their own, they have no effect on a year's overall mortality. Whether they affect the progression of the disease is unknown. When used in combination with LABA, they can decrease mortality compared to ICS or LABA alone. Inhaled steroids are associated with increased levels of pneumonia. Long-term treatment with steroid tablets is associated with significant side effects.
Other drugs
Long-term antibiotics, especially those from macrolide classes such as erythromycin, reduce the frequency of exacerbations in those who have two or more years of the year. This practice may be cost-effective in some areas of the world. Concerns include antibiotic resistance and hearing problems with azithromycin. Methylxanthines such as theophylline generally cause more harm than benefit and thus are usually not recommended, but can be used as second-line agents in those not controlled by other measures. Mucolytics can help reduce exacerbations in some people with chronic bronchitis. Cough medicine is not recommended.
For people with COPD, the use of cardioselective (heart-specific) beta-blocker therapy does not seem to interfere with respiratory function. Cardioselective beta-blocker therapy should not be contraindicated for people with COPD.
Oxygen
Supplemental oxygen is recommended in those with low oxygen levels at rest (partial oxygen pressure of less than 50-55 mmHg or oxygen saturation of less than 88%). In this group of people, it reduces the risk of heart failure and death if it is used 15 hours per day and can improve people's ability to exercise. In those with normal or somewhat low oxygen levels, oxygen supplementation may increase shortness of breath when administered during exercise, but may not increase shortness of breath during normal daily activities or affect quality of life. Fire risks and little benefit exist when those who use oxygen continue to smoke. In this situation, some recommend not to use it. During acute exacerbations, many require oxygen therapy; the use of high oxygen concentrations without taking into account the oxygen saturation of a person can lead to increased levels of carbon dioxide and worsening results. In those at high risk of high carbon dioxide levels, 88-92% oxygen saturation is recommended, whereas for those without this risk, the recommended rate is 94-98%.
Surgery
For those with very severe disease, surgery is sometimes beneficial and may include lung transplantation or lung volume reduction surgery, which involves removing the most damaged lung parts by emphysema, allowing the remaining lung, relatively well to grow and work better. It seems very effective if emphysema mainly involves the upper lobe, but this procedure increases the risk of premature death and side effects. Pulmonary transplantation is sometimes performed for very severe COPD, especially in younger individuals.
Exacerbation
Acute exacerbations are usually treated by increasing the use of short-acting bronchodilators. This usually includes a combination of short-acting beta agonist and anticholinergic. These drugs can be administered either through a measured dose inhaler with a spacer or through a nebulizer, with both appearing equally effective. Nebulisasi may be easier for the more unhealthy. Oxygen supplements can be useful. Excessive oxygen; however, can result in increased levels of CO 2 and a decreased level of consciousness.
Oral corticosteroids increase the likelihood of recovery and decrease the overall duration of symptoms. They work just as well as intravenous steroids but seem to have fewer side effects. Five days of working steroids as well as ten or fourteen. In those with severe exacerbations, antibiotics improve results. A number of different antibiotics may be used including amoxicillin, doxycycline and azithromycin; whether someone is better than the other is unclear. The FDA recommends the use of fluoroquinolone when other options are available because of the higher risk of serious side effects. There is no clear evidence for those with less severe cases.
For those with type 2 respiratory failure (increased acute CO 2 ), non-invasive positive pressure ventilation lowers the likelihood of death or intensive care needs. In addition, theophylline may have a role in those who do not respond to other actions. Less than 20% of exacerbations require hospitalization. In those who do not have acidosis of respiratory failure, home care ("home hospitals") may help avoid some acceptance.
Prognosis
COPD usually worsens over time and can eventually lead to death. It is estimated that 3% of all disabilities are related to COPD. The proportion of disabilities from COPD globally has declined from 1990 to 2010 due to improvements in indoor air quality, especially in Asia. However, the number of years living with disabilities of COPD, has increased.
The rate at which COPD worsens varies with the presence of factors predicting poor outcomes, including severe airflow obstruction, little ability to exercise, shortness of breath, weight gain or significant overweight, congestive heart failure, continued smoking, and often exacerbations. Long-term results in COPD can be estimated using a BODE index that scores zero to ten depending on FEV 1 , body mass index, walking distance in six minutes, and modified MRC dyspnea. scale. Significant weight loss is a bad sign. Spirometry results are also a good predictor of future disease progression but not as good as the BODE index.
Epidemiology
Globally, in 2010, COPD affected about 329 million people (4.8% of the population). This disease affects men and women almost the same, because there is an increased use of tobacco among women in developed countries. The increase in developing countries between 1970 and 2000 is believed to be associated with an increase in smoking levels in the region, an increase in population and aging populations due to fewer deaths from other causes such as infectious diseases. Several developed countries have experienced increased levels, some remain stable and some have seen a decrease in COPD prevalence. The global figures are expected to continue to rise as risk factors remain common and the population continues to grow older.
Between 1990 and 2010 the number of deaths from COPD fell slightly from 3.1 million to 2.9 million and was the fourth leading cause of death. In 2012 it is the third leading cause as the number of deaths increases again to 3.1 million. In some countries, the mortality rate declines in men but increases in women. This is most likely because the level of smoking in women and men becomes more similar. COPD is more common in older people; it affects 34-200 of 1,000 people older than 65 years, depending on the population being reviewed.
In the UK, about 0.84 million people (50 million) have a diagnosis of COPD; this translates into about one person in 59 receiving a diagnosis of COPD at some point in their life. In the least socioeconomic sections of the country, one in 32 people is diagnosed with COPD, compared to one in 98 in the most affluent areas. In the United States about 6.3% of the adult population, with a total of about 15 million people, have been diagnosed with COPD. 25 million people may experience COPD if a case that is currently undiagnosed is included. In 2011, there were about 730,000 hospitalizations in the United States for COPD. In the United States, COPD is thought to be the third leading cause of death in 2011.
History
The word "emphysema" comes from the Greek ??????? emphysan which means " expand " - self consists of ?? en , which means " in ", and ????? physan , which means " breath, blast " . The term chronic bronchitis began to be used in 1808 while the term COPD was believed to be first used in 1965. Previously this term has been known by a number of different names, including chronic obstructive bronchopulmonary disease, chronic obstructive respiratory diseases, chronic airflow obstruction, chronic airflow limitations , chronic obstructive pulmonary disease, non-specific chronic pulmonary disease, and diffuse diastolic lung syndrome. The terms chronic bronchitis and emphysema were formally defined in 1959 at the CIBA guest symposium and in 1962 at a meeting of the American Thoracic Society Committee on Diagnostic Standards.
The earliest descriptions of emphysema may include: in 1679 by T. Bonet from the condition of "the lungs of many" and in 1769 by Giovanni Morgagni of the "turgid lungs especially from the air". In 1721 the first image of emphysema was made by Ruysh. This was followed by a picture by Matthew Baillie in 1789 and a description of the destructive nature of the condition. In 1814 Charles Badham used "catarrh" to describe the cough and excess mucus in chronic bronchitis. Renà © à © Laennec, the physician who invented the stethoscope, used the term "emphysema" in his book A Treatise on the Diseases of the Chest and Mediate Auscultation (1837) to describe the lung that did not collapse when he opened the coffin it was during autopsy. He notes that they do not collapse as usual because they are full of air and the airways are filled with mucus. In 1842, John Hutchinson invented the spirometer, which allowed the measurement of the vital capacity of the lungs. However, the spirometer can measure only volume, not airflow. Tiffeneau and Pinelli in 1947 explain the principle of measuring airflow.
In 1953, Dr. George L. Waldbott, an American allergist, first described a new illness he named "smoker respiratory syndrome" in 1953 Journal of the American Medical Association . This is the first association between smoking tobacco and chronic respiratory diseases.
Early treatments include garlic, cinnamon and ipecac, among others. Modern treatments developed during the second half of the 20th century. Evidence supporting the use of steroids in COPD was published in the late 1950s. Bronchodilators began to be used in 1960 after promising isoprenaline trials. Further bronchodilators, such as salbutamol, developed in the 1970s, and the use of LABA began in the mid-1990s.
Society and culture
COPD has been referred to as "smokers' lungs". People with emphysema have been known as "red puffs" or "type As" because of frequent pink skin, fast breathing rates and pursed lips, and people with chronic bronchitis have been referred to as "blue bloaters" or "type B" due to skin color and lips are often bluish from low oxygen levels and swelling of their ankles. This terminology is no longer accepted as useful because most people with COPD have a combination of both emphysema and chronic bronchitis.
Many health systems have difficulty ensuring proper identification, diagnosis and care of people with COPD; The UK Department of Health has identified this as a major problem for the National Health Service and has introduced a special strategy to address this problem.
Economy
Globally, in 2010, COPD is estimated to generate an economic cost of $ 2.1 trillion, half of what happens in developing countries. Of this amount, approximately $ 1.9 trillion is a direct cost like medical care, while $ 0.2 trillion is an indirect cost such as job loss. This number is expected to double by 2030. In Europe, COPD represents 3% of health care spending. In the United States, disease costs are estimated at $ 50 billion, largely due to exacerbations. COPD is one of the most expensive conditions seen in US hospitals in 2011, for a total cost of approximately $ 5.7 billion.
Research
Infliximab, immune suppressant antibodies, have been tested in COPD; there is a possibility of harm without any helpful proof.
Roflumilast, cilomilast, and phosphodiesterase 4 inhibitors act as bronchodilators and as anti-inflammatory. They show promise in reducing the level of exacerbations, but they do not seem to change the quality of one's life. Roflumilast and cilomilast may be associated with side effects such as gastrointestinal problems and weight loss. Sleep disturbances and mood disorders associated with roflumilast have also been reported.
Several new long-acting agents are in development. Treatment with stem cells is being studied. Although there are safe tentative data, and promising animal data, there is little human data by 2017. Human data show poor results.
A procedure known as pulmonary denervation target, which involves decreasing the supply of parasympathetic lung nervous system, is being studied but lacks sufficient data to determine its use. The effectiveness of alpha-1 antitrypsin augmentation treatment for people with antitrypsin alpha-1 deficiency is unclear.
Research continues to use telehealthcare to treat people with COPD when they experience episodes of shortness of breath; treating people remotely can reduce the number of emergency room visits and improve a person's quality of life.
Other animals
Chronic obstructive pulmonary disease can occur in a number of other animals and may be caused by exposure to tobacco smoke. Most cases of illness, however, are relatively mild. The horse is known as recurrent airway obstruction, can be very severe, and most commonly associated with allergic reactions to fungi contained in straw or contaminated straw. COPD is also commonly found in older dogs.
References
Further reading
External links
- Chronic obstructive pulmonary disease in Curlie (based on DMOZ)
Source of the article : Wikipedia
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