WordNet

an impairment of health or a condition of abnormal functioning
being long-lasting and recurrent or characterized by long suffering; "chronic indigestion"; "a chronic shortage of funds"; "a chronic invalid"
of long duration; "chronic money problems" (同)continuing
habitual; "a chronic smoker" (同)inveterate
caused by or altered by or manifesting disease or pathology; "diseased tonsils"; "a morbid growth"; "pathologic tissue"; "pathological bodily processes" (同)morbid, pathologic, pathological
either of two saclike respiratory organs in the chest of vertebrates; serves to remove carbon dioxide and provide oxygen to the blood

PrepTutorEJDIC

(体の)『病気』,疾患 / (精神・道徳などの)病気,病弊
女性の話術芸人 =diseur
(病気が)長期にわたる,慢性の / 《名詞の前にのみ用いて》常習の,癖になった
病気にかかった / 病的な,不健全な(morbid)
《しばしば複数形で》『肺』,肺臓
妨害する,じゃまする;(…を)妨害する《+『of』+『名』》

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2017/12/20 05:34:01」(JST)

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Chronic obstructive pulmonary disease (COPD) is a type of obstructive lung disease characterized by long-term breathing problems and poor airflow.^[1]^[8] The main symptoms include shortness of breath and cough with sputum production.^[1] COPD is a progressive disease, meaning it typically worsens over time.^[9] Eventually everyday activities, such as walking or getting dressed, become difficult.^[3] Chronic bronchitis and emphysema are older terms used for different types of COPD.^[3]^[10] The term "chronic bronchitis" is still used to define a productive cough that is present for at least three months each year for two years.^[1]

Tobacco smoking is the most common cause of COPD, with factors such as air pollution and genetics playing a smaller role.^[2] In the developing world, one of the common sources of air pollution is poorly vented heating and cooking fires.^[3] Long-term exposure to these irritants causes an inflammatory response in the lungs, resulting in narrowing of the small airways and breakdown of lung tissue.^[5] The diagnosis is based on poor airflow as measured by lung function tests.^[4] In contrast to asthma, the airflow reduction does not improve much with the use of a bronchodilator.^[3]

Most cases of COPD can be prevented by reducing exposure to risk factors.^[11] This includes decreasing rates of smoking and improving indoor and outdoor air quality.^[3] While treatment can slow worsening, no cure is known.^[3] COPD treatments include stopping smoking, vaccinations, respiratory rehabilitation, and often inhaled bronchodilators and steroids.^[2] Some people may benefit from long-term oxygen therapy or lung transplantation.^[5] In those who have periods of acute worsening, increased use of medications and hospitalization may be needed.^[2]

As of 2015, COPD affected about 174.5 million (2.4%) of the global population.^[6] It typically occurs in people over the age of 40.^[3] Males and females are affected equally commonly.^[3] In 2015, it resulted in 3.2 million deaths, up from 2.4 million deaths in 1990.^[7]^[12] More than 90% of these deaths occur in the developing world.^[3] The number of deaths is projected to increase further because of higher smoking rates in the developing world, and an aging population in many countries.^[13] It resulted in an estimated economic cost of $2.1 trillion in 2010.^[14]

Play media

Video explanation

1 Signs and symptoms
- 1.1 Cough
- 1.2 Shortness of breath
- 1.3 Other features
- 1.4 Exacerbation
2 Cause
- 2.1 Smoking
- 2.2 Air pollution
- 2.3 Occupational exposures
- 2.4 Genetics
- 2.5 Other
- 2.6 Exacerbations
3 Pathophysiology
4 Diagnosis
- 4.1 Spirometry
- 4.2 Severity
- 4.3 Other tests
- 4.4 Differential diagnosis
5 Prevention
- 5.1 Smoking cessation
- 5.2 Occupational health
- 5.3 Air pollution
6 Management
- 6.1 Exercise
- 6.2 Bronchodilators
- 6.3 Corticosteroids
- 6.4 Other medication
- 6.5 Oxygen
- 6.6 Surgery
- 6.7 Exacerbations
7 Prognosis
8 Epidemiology
9 History
10 Society and culture
- 10.1 Economics
11 Research
12 Other animals
13 References
14 Further reading
15 External links

Signs and symptoms

Wheezing

The sound of wheezing as heard with a stethoscope.

Problems playing this file? See media help.

The most common symptoms of COPD are sputum production, shortness of breath, and a productive cough.^[15] These symptoms are present for a prolonged period of time^[16] and typically worsen over time.^[5] If different types of COPD exist is unclear.^[2] While previously divided into emphysema and chronic bronchitis, emphysema is only a description of lung changes rather than a disease itself, and chronic bronchitis is simply a descriptor of symptoms that may or may not occur with COPD.^[9]

Cough

A chronic cough is often the first symptom to develop. When it persists for more than three months each year for at least two years, in combination with sputum production and without another explanation, it is by definition chronic bronchitis. This condition can occur before COPD fully develops. The amount of sputum produced can change over hours to days. In some cases, the cough may not be present or may only occur occasionally and may not be productive. Some people with COPD attribute the symptoms to a "smoker's cough". Sputum may be swallowed or spat out, depending often on social and cultural factors. Vigorous coughing may lead to rib fractures or a brief loss of consciousness. Those with COPD often have a history of "common colds" that last a long time.^[15]

Shortness of breath

Shortness of breath is often the symptom that most bothers people.^[17] It is commonly described as: "my breathing requires effort," "I feel out of breath," or "I can't get enough air in".^[18] Different terms, however, may be used in different cultures.^[15] Typically the shortness of breath is worse on exertion of a prolonged duration and worsens over time.^[15] In the advanced stages, it occurs during rest and may be always present.^[19]^[20] It is a source of both anxiety and a poor quality of life in those with COPD.^[15] Many people with more advanced COPD breathe through pursed lips and this action can improve shortness of breath in some.^[21]^[22]

Other features

In COPD, breathing out may take longer to than breathing in.^[23] Chest tightness may occur,^[15] but is not common and may be caused by another problem.^[17] Those with obstructed airflow may have wheezing or decreased sounds with air entry on examination of the chest with a stethoscope.^[23] A barrel chest is a characteristic sign of COPD, but is relatively uncommon.^[23] Tripod positioning may occur as the disease worsens.^[16]

Advanced COPD leads to high pressure on the lung arteries, which strains the right ventricle of the heart.^[5]^[24]^[25] This situation is referred to as cor pulmonale, and leads to symptoms of leg swelling^[15] and bulging neck veins.^[5] COPD is more common than any other lung disease as a cause of cor pulmonale.^[24] Cor pulmonale has become less common since the use of supplemental oxygen.^[16]

COPD often occurs along with a number of other conditions, due in part to shared risk factors.^[2] These conditions include ischemic heart disease, high blood pressure, diabetes mellitus, muscle wasting, osteoporosis, lung cancer, anxiety disorder, sexual dysfunction, and depression.^[2]^[26] In those with severe disease, a feeling of always being tired is common.^[15] Fingernail clubbing is not specific to COPD and should prompt investigations for an underlying lung cancer.^[27]

Exacerbation

An acute exacerbation of COPD is defined as increased shortness of breath, increased sputum production, a change in the color of the sputum from clear to green or yellow, or an increase in cough in someone with COPD.^[23] This may present with signs of increased work of breathing such as fast breathing, a fast heart rate, sweating, active use of muscles in the neck, a bluish tinge to the skin, and confusion or combative behavior in very severe exacerbations.^[23]^[28] Crackles may also be heard over the lungs on examination with a stethoscope.^[29]

Cause

The primary cause of COPD is tobacco smoke, with occupational exposure and pollution from indoor fires being significant causes in some countries.^[9] Typically, these exposures must occur over several decades before symptoms develop.^[9] A person's genetic makeup also affects the risk.^[9]

Smoking

Percentage of females smoking tobacco as of the late 1990s early 2000s

Percentage of males smoking tobacco as of the late 1990s and early 2000s. Note the scales used for females and males differ.^[30]

The primary risk factor for COPD globally is tobacco smoking.^[9] Of those who smoke, about 20% will get COPD,^[31] and of those who are lifelong smokers, about half will get COPD.^[32] In the United States and United Kingdom, of those with COPD, 80–95% are either current smokers or previously smoked.^[31]^[33]^[34] The likelihood of developing COPD increases with the total smoke exposure.^[35] Additionally, women are more susceptible to the harmful effects of smoke than men.^[34] In nonsmokers, secondhand smoke is the cause of about 20% of cases.^[33] Other types of smoke, such as, marijuana, cigar, and water-pipe smoke, also confer a risk.^[9] Water-pipe smoke appears to be as harmful as smoking cigarettes.^[36] Problems from marijuana smoke may only be with heavy use.^[37] Women who smoke during pregnancy may increase the risk of COPD in their child.^[9] For the same amount of cigarette smoking, women have a higher risk of COPD than men.^[38]

Air pollution

Poorly ventilated cooking fires, often fueled by coal or biomass fuels such as wood and dung, lead to indoor air pollution and are one of the most common causes of COPD in developing countries.^[39] These fires are a method of cooking and heating for nearly 3 billion people, with their health effects being greater among women due to more exposure.^[9]^[39] They are used as the main source of energy in 80% of homes in India, China and sub-Saharan Africa.^[11]

People who live in large cities have a higher rate of COPD compared to people who live in rural areas.^[40] While urban air pollution is a contributing factor in exacerbations, its overall role as a cause of COPD is unclear.^[9] Areas with poor outdoor air quality, including that from exhaust gas, generally have higher rates of COPD.^[11] The overall effect in relation to smoking, however, is believed to be small.^[9]

Occupational exposures

Intense and prolonged exposure to workplace dusts, chemicals, and fumes increases the risk of COPD in both smokers and nonsmokers.^[41] Workplace exposures are believed to be the cause in 10–20% of cases.^[42] In the United States, they are believed to be related to more than 30% of cases among those who have never smoked and probably represent a greater risk in countries without sufficient regulations.^[9]

A number of industries and sources have been implicated, including^[11] high levels of dust in coal mining, gold mining, and the cotton textile industry, occupations involving cadmium and isocyanates, and fumes from welding.^[41] Working in agriculture is also a risk.^[11] In some professions, the risks have been estimated as equivalent to that of one-half to two packs of cigarettes a day.^[43] Silica dust and fiberglass dust exposure can also lead to COPD, with the risk unrelated to that for silicosis.^[44]^[45] The negative effects of dust exposure and cigarette smoke exposure appear to be additive or possibly more than additive.^[43]

Genetics

Genetics play a role in the development of COPD.^[9] It is more common among relatives of those with COPD who smoke than unrelated smokers.^[9] Currently, the only clearly inherited risk factor is alpha 1-antitrypsin deficiency (AAT).^[46] This risk is particularly high if someone deficient in alpha 1-antitrypsin also smokes.^[46] It is responsible for about 1–5% of cases^[46]^[47] and the condition is present in about three to four in 10,000 people.^[16] Other genetic factors are being investigated,^[46] of which many are likely.^[11]

Other

A number of other factors are less closely linked to COPD. The risk is greater in those who are poor, although if this is due to poverty itself or other risk factors associated with poverty, such as air pollution and malnutrition, is not clear.^[9] Tentative evidence indicates those with asthma and airway hyperreactivity are at increased risk of COPD.^[9] Birth factors such as low birth weight may also play a role, as do a number of infectious diseases, including HIV/AIDS and tuberculosis.^[9] Respiratory infections such as pneumonia do not appear to increase the risk of COPD, at least in adults.^[16]

Exacerbations

An acute exacerbation (a sudden worsening of symptoms)^[48] is commonly triggered by infection or environmental pollutants, or sometimes by other factors such as improper use of medications.^[49] Infections appear to be the cause of 50 to 75% of cases,^[49]^[50] with bacteria in 25%, viruses in 25%, and both in 25%.^[51] Environmental pollutants include both poor indoor and outdoor air quality.^[49] Exposure to personal smoke and secondhand smoke increases the risk.^[11] Cold temperature may also play a role, with exacerbations occurring more commonly in winter.^[52] Those with more severe underlying disease have more frequent exacerbations: in mild disease 1.8 per year, moderate 2 to 3 per year, and severe 3.4 per year.^[53] Those with many exacerbations have a faster rate of deterioration of their lung function.^[54] Pulmonary emboli (blood clots in the lungs) can worsen symptoms in those with pre-existing COPD.^[2] Signs of PE in COPD include pleuritic chest pain and heart failure without signs of infection.^[55]

Pathophysiology

On the left is a diagram of the lungs and airways with an inset showing a detailed cross-section of normal bronchioles and alveoli. On the right are lungs damaged by COPD with an inset showing a cross-section of damaged bronchioles and alveoli.

Play media

Video explanation of emphysema

COPD is a type of obstructive lung disease in which chronic, incompletely reversible poor airflow (airflow limitation) and inability to breathe out fully (air trapping) exist.^[2] The poor airflow is the result of breakdown of lung tissue (known as emphysema) and small airways disease (known as obstructive bronchiolitis). The relative contributions of these two factors vary between people.^[9] Severe destruction of small airways can lead to the formation of large air pockets—known as bullae—that replace lung tissue. This form of disease is called bullous emphysema.^[56]

COPD develops as a significant and chronic inflammatory response to inhaled irritants.^[9] Chronic bacterial infections may also add to this inflammatory state.^[54] The inflammatory cells involved include neutrophil granulocytes and macrophages, two types of white blood cells. Those who smoke additionally have Tc1 lymphocyte involvement and some people with COPD have eosinophil involvement similar to that in asthma. Part of this cell response is brought on by inflammatory mediators such as chemotactic factors. Other processes involved with lung damage include oxidative stress produced by high concentrations of free radicals in tobacco smoke and released by inflammatory cells, and breakdown of the connective tissue of the lungs by proteases that are insufficiently inhibited by protease inhibitors. The destruction of the connective tissue of the lungs leads to emphysema, which then contributes to the poor airflow, and finally, poor absorption and release of respiratory gases.^[9] General muscle wasting that often occurs in COPD may be partly due to inflammatory mediators released by the lungs into the blood.^[9]

Micrograph showing emphysema (left – large empty spaces) and lung tissue with relative preservation of the alveoli (right)

Narrowing of the airways occurs due to inflammation and scarring within them. This contributes to the inability to breathe out fully. The greatest reduction in air flow occurs when breathing out, as the pressure in the chest is compressing the airways at this time.^[57] This can result in more air from the previous breath remaining within the lungs when the next breath is started, resulting in an increase in the total volume of air in the lungs at any given time, a process called hyperinflation or air trapping.^[57]^[58] Hyperinflation from exercise is linked to shortness of breath in COPD, as breathing in is less comfortable when the lungs are already partly filled.^[59] Hyperinflation may also worsen during an exacerbation.^[60]

Some also have a degree of airway hyperresponsiveness to irritants similar to those found in asthma.^[16]

Low oxygen levels, and eventually, high carbon dioxide levels in the blood, can occur from poor gas exchange due to decreased ventilation from airway obstruction, hyperinflation, and a reduced desire to breathe.^[9] During exacerbations, airway inflammation is also increased, resulting in increased hyperinflation, reduced expiratory airflow, and worsening of gas transfer. This can also lead to insufficient ventilation, and eventually, low blood oxygen levels.^[5] Low oxygen levels, if present for a prolonged period, can result in narrowing of the arteries in the lungs, while emphysema leads to breakdown of capillaries in the lungs. Both of these changes result in increased blood pressure in the pulmonary arteries, which may cause cor pulmonale.^[9]

Diagnosis

A person blowing into a spirometer: Smaller handheld devices are available for office use.

The diagnosis of COPD should be considered in anyone over the age of 35 to 40 who has shortness of breath, a chronic cough, sputum production, or frequent winter colds and a history of exposure to risk factors for the disease.^[15]^[17] Spirometry is then used to confirm the diagnosis.^[15]^[61] Screening those without symptoms is not recommended.^[62]

Spirometry

Spirometry measures the amount of airflow obstruction present and is generally carried out after the use of a bronchodilator, a medication to open up the airways.^[61] Two main components are measured to make the diagnosis, the forced expiratory volume in one second (FEV₁), which is the greatest volume of air that can be breathed out in the first second of a breath, and the forced vital capacity (FVC), which is the greatest volume of air that can be breathed out in a single large breath.^[63] Normally, 75–80% of the FVC comes out in the first second^[63] and a FEV₁/FVC ratio less than 70% in someone with symptoms of COPD defines a person as having the disease.^[61] Based on these measurements, spirometry would lead to over-diagnosis of COPD in the elderly.^[61] The National Institute for Health and Care Excellence criteria additionally require a FEV₁ less than 80% of predicted.^[17] People with COPD also exhibit a decrease in diffusing capacity of the lung for carbon monoxide (D_LCO) due to decreased surface area in the alveoli, as well as damage to the capillary bed.^[64]

Evidence for using spirometry among those without symptoms in an effort to diagnose the condition earlier is of uncertain effect, so currently is not recommended.^[15]^[61] A peak expiratory flow (the maximum speed of expiration), commonly used in asthma, is not sufficient for the diagnosis of COPD.^[17]

Severity

MRC shortness of breath scale^[17]
Grade	Activity affected
1	Only strenuous activity
2	Vigorous walking
3	With normal walking
4	After a few minutes of walking
5	With changing clothing

GOLD grade^[15]
Severity	FEV₁ % predicted
Mild (GOLD 1)	≥80
Moderate (GOLD 2)	50–79
Severe (GOLD 3)	30–49
Very severe (GOLD 4)	<30

A number of methods can determine how much COPD is affecting a given individual.^[15] The modified British Medical Research Council questionnaire or the COPD assessment test (CAT) are simple questionnaires that may be used to determine the severity of symptoms.^[15] Scores on CAT range from 0–40 with the higher the score, the more severe the disease.^[65] Spirometry may help to determine the severity of airflow limitation.^[15] This is typically based on the FEV₁ expressed as a percentage of the predicted "normal" for the person's age, gender, height, and weight.^[15] Both the American and European guidelines recommended partly basing treatment recommendations on the FEV₁.^[61] The GOLD guidelines suggest dividing people into four categories based on symptoms assessment and airflow limitation.^[15] Weight loss and muscle weakness, as well as the presence of other diseases, should also be taken into account.^[15]

Other tests

A chest X-ray and complete blood count may be useful to exclude other conditions at the time of diagnosis.^[66] Characteristic signs on X-ray are overexpanded lungs, a flattened diaphragm, increased retrosternal airspace, and bullae, while it can help exclude other lung diseases, such as pneumonia, pulmonary edema, or a pneumothorax.^[67] A high-resolution computed tomography scan of the chest may show the distribution of emphysema throughout the lungs and can also be useful to exclude other lung diseases.^[16] Unless surgery is planned, however, this rarely affects management.^[16] An analysis of arterial blood is used to determine the need for oxygen; this is recommended in those with an FEV₁ less than 35% predicted, those with a peripheral oxygen saturation less than 92%, and those with symptoms of congestive heart failure.^[15] In areas of the world where alpha-1 antitrypsin deficiency is common, people with COPD (particularly those below the age of 45 and with emphysema affecting the lower parts of the lungs) should be considered for testing.^[15]

Chest X-ray demonstrating severe COPD: Note the small heart size in comparison to the lungs.
A lateral chest X-ray of a person with emphysema: Note the barrel chest and flat diaphragm.
Lung bulla as seen on chest X-ray in a person with severe COPD
A severe case of bullous emphysema
Axial CT image of the lung of a person with end-stage bullous emphysema
Very severe emphysema with lung cancer on the left (CT scan)

Differential diagnosis

COPD may need to be differentiated 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.^[23] The distinction between asthma and COPD is made on the basis of the symptoms, smoking history, and whether airflow limitation is reversible with bronchodilators at spirometry.^[68] Tuberculosis may also present with a chronic cough and should be considered in locations where it is common.^[15] Less common conditions that may present similarly include bronchopulmonary dysplasia and obliterative bronchiolitis.^[66] Chronic bronchitis may occur with normal airflow and in this situation it is not classified as COPD.^[16]

Prevention

Most cases of COPD are potentially preventable through decreasing exposure to smoke and improving air quality.^[11] Annual influenza vaccinations in those with COPD reduce exacerbations, hospitalizations and death.^[69]^[70] Pneumococcal vaccination may also be beneficial.^[69] The non-typable Haemophilus influenzae vaccine (NTHi) when taken by mouth does not appear to reduce exacerbations in people with COPD.^[71] Eating a diet high in beta-carotene may help but taking supplements does not seem to.^[72]

Smoking cessation

Keeping people from starting smoking is a key aspect of preventing COPD.^[73] The policies of governments, public health agencies, and antismoking organizations can reduce smoking rates by discouraging people from starting and encouraging people to stop smoking.^[74] Smoking bans in public areas and places of work are important measures to decrease exposure to secondhand smoke, and while many places have instituted bans, more are recommended.^[11]

In those who smoke, stopping smoking is the only measure shown to slow down the worsening of COPD.^[75] Even at a late stage of the disease, it can reduce the rate of worsening lung function and delay the onset of disability and death.^[76] Smoking cessation starts with the decision to stop smoking, leading to an attempt at quitting. Often, several attempts are required before long-term abstinence is achieved.^[74] Attempts over 5 years lead to success in nearly 40% of people.^[77]

Some smokers can achieve long-term smoking cessation through willpower alone. Smoking, however, is highly addictive,^[78] and many smokers need further support. The chance of quitting is improved with social support, engagement in a smoking cessation program, and the use of medications such as nicotine replacement therapy, bupropion, or varenicline.^[74]^[77] Combining smoking-cessation medication with behavioral therapy is more than twice as likely to be effective in helping people with COPD stop smoking, compared with behavioral therapy alone.^[79]

Occupational health

A number of measures have been taken to reduce the likelihood that workers in at-risk industries—such as coal mining, construction, and stonemasonry—will develop COPD.^[11] Examples of these measures include the creation of public policy,^[11] education of workers and management about the risks, promoting smoking cessation, checking workers for early signs of COPD, use of respirators, and dust control.^[80]^[81] Effective dust control can be achieved by improving ventilation, using water sprays and by using mining techniques that minimize dust generation.^[82] If a worker develops COPD, further lung damage can be reduced by avoiding ongoing dust exposure, for example by changing the work role.^[83]

Air pollution

Both indoor and outdoor air quality can be improved, which may prevent COPD or slow the worsening of existing disease.^[11] This may be achieved by public policy efforts, cultural changes, and personal involvement.^[84]

A number of developed countries have successfully improved outdoor air quality through regulations. This has resulted in improvements in the lung function of their populations.^[11] Those with COPD may experience fewer symptoms if they stay indoors on days when outdoor air quality is poor.^[5]

One key effort is to reduce exposure to smoke from cooking and heating fuels through improved ventilation of homes and better stoves and chimneys.^[84] Proper stoves may improve indoor air quality by 85%. Using alternative energy sources such as solar cooking and electrical heating is also effective. Using fuels such as kerosene or coal might be less bad than traditional biomass such as wood or dung.^[11]

Management

No cure for COPD is known, but the symptoms are treatable and its progression can be delayed.^[73] The major goals of management are to reduce risk factors, manage stable COPD, prevent and treat acute exacerbations, and manage associated illnesses.^[5] The only measures that have been shown to reduce mortality are smoking cessation and supplemental oxygen.^[85] Stopping smoking decreases the risk of death by 18%.^[2] Other recommendations include influenza vaccination once a year, pneumococcal vaccination once every five years, and reduction in exposure to environmental air pollution.^[2] In those with advanced disease, palliative care may reduce symptoms, with morphine improving the feelings of shortness of breath.^[86] Noninvasive ventilation may be used to support breathing.^[86] Providing people with a personalized action plan, an educational session, and support for use of their action plan in the event of an exacerbation, reduces the number of hospital visits and encourages early treatment of exacerbations.^[87]

Exercise

Pulmonary rehabilitation is a program of exercise, disease management, and counseling, coordinated to benefit the individual.^[88] In those who have had a recent exacerbation, pulmonary rehabilitation appears to improve the overall quality of life and the ability to exercise.^[89]^[90] If pulmonary rehabilitation improves mortality rates or hospital readmission rates is unclear.^[89] Pulmonary rehabilitation has been shown to improve the sense of control a person has over their disease, as well as their emotions.^[91]

The optimal exercise routine, use of noninvasive ventilation during exercise, and intensity of exercise suggested for people with COPD, is unknown.^[90]^[92]^[93] Performing endurance arm exercises improves arm movement for people with COPD, and may result in a small improvement in breathlessness.^[94] Performing arm exercises alone does not appear to improve quality of life.^[94] Breathing exercises in and of themselves appear to have a limited role.^[22] Pursed lip breathing exercises may be useful.^[21]^[22] Tai chi exercises appear to be safe to practice for people with COPD, and may be beneficial for pulmonary function and pulmonary capacity when compared to a regular treatment program.^[95] Tai Chi was not found to be more effective than other exercise intervention programs.^[95]

Being either underweight or overweight can affect the symptoms, degree of disability, and prognosis of COPD. People with COPD who are underweight can improve their breathing muscle strength by increasing their calorie intake.^[5] When combined with regular exercise or a pulmonary rehabilitation program, this can lead to improvements in COPD symptoms. Supplemental nutrition may be useful in those who are malnourished.^[96]

Bronchodilators

Inhaled bronchodilators are the primary medications used,^[2] and result in a small overall benefit.^[97] The two major types are β₂ agonists and anticholinergics; both exist in long-acting and short-acting forms. They reduce shortness of breath, wheeze, and exercise limitation, resulting in an improved quality of life.^[98] It is unclear if they change the progression of the underlying disease.^[2]

In those with mild disease, short-acting agents are recommended on an as needed basis.^[2] In those with more severe disease, long-acting agents are recommended.^[2] Long-acting agents partly work by improving hyperinflation.^[60] If long-acting bronchodilators are insufficient, then inhaled corticosteroids are typically added.^[2] With respect to long-acting agents, if tiotropium (a long-acting anticholinergic) or long-acting beta agonists (LABAs) are better is unclear, and trying each and continuing the one that worked best may be advisable.^[99] Both types of agent appear to reduce the risk of acute exacerbations by 15–25%.^[2] While both may be used at the same time, any benefit is of questionable significance.^[99]

Several short-acting β₂ agonists are available, including salbutamol (albuterol) and terbutaline.^[100] They provide some relief of symptoms for four to six hours.^[100] Long-acting β₂ agonists such as salmeterol, formoterol, and indacaterol are often used as maintenance therapy. Some feel the evidence of benefits is limited^[101] while others view the evidence of benefit as established.^[102]^[103]^[104] Long-term use appears safe in COPD^[105] with adverse effects include shakiness and heart palpitations.^[2] When used with inhaled steroids they increase the risk of pneumonia.^[2] While steroids and LABAs may work better together,^[101] it is unclear if this slight benefit outweighs the increased risks.^[106] Indacaterol requires an inhaled dose once a day, and is as effective as the other long-acting β₂ agonist drugs that require twice-daily dosing for people with stable COPD.^[104]

Two main anticholinergics are used in COPD, ipratropium and tiotropium. Ipratropium is a short-acting agent, while tiotropium is long-acting. Tiotropium is associated with a decrease in exacerbations and improved quality of life,^[107] and tiotropium provides those benefits better than ipratropium.^[108] It does not appear to affect mortality or the overall hospitalization rate.^[107] Anticholinergics can cause dry mouth and urinary tract symptoms.^[2] They are also associated with increased risk of heart disease and stroke.^[109]^[110] Aclidinium, another long acting agent, reduces hospitalizations associated with COPD and improves quality of life.^[111]^[112]^[113] Aclinidinium has been used as an alternative to tiotropium, but which drug is more effective is not known.^[113]

Corticosteroids

Corticosteroids are usually used in inhaled form, but may also be used as tablets to treat and prevent acute exacerbations. While inhaled corticosteroids (ICSs) have not shown benefit for people with mild COPD, they decrease acute exacerbations in those with either moderate or severe disease.^[114] By themselves, they have no effect on overall one-year mortality.^[85]^[115] Whether they affect the progression of the disease is unknown.^[2] When used in combination with a LABA, they may decrease mortality compared to either ICSs or LABA alone.^[116]^[117] Inhaled steroids are associated with increased rates of pneumonia.^[118] Long-term treatment with steroid tablets is associated with significant side effects.^[100]

Other medication

Long-term antibiotics, specifically those from the macrolide class such as erythromycin, reduce the frequency of exacerbations in those who have two or more a year.^[119]^[120] This practice may be cost effective in some areas of the world.^[121] Concerns include that of antibiotic resistance and hearing problems with azithromycin.^[120] Methylxanthines such as theophylline generally cause more harm than benefit and thus are usually not recommended,^[122] but may be used as a second-line agent in those not controlled by other measures.^[5] Mucolytics may help to reduce exacerbations in some people with chronic bronchitis.^[123] Cough medicines are not recommended.^[100]

Oxygen

Supplemental oxygen is recommended in those with low oxygen levels at rest (a partial pressure of oxygen less than 50–55 mmHg or oxygen saturations of less than 88%).^[100]^[124] In this group of people, it decreases the risk of heart failure and death if used 15 hours per day^[100]^[124] and may improve people's ability to exercise.^[125] In those with normal or mildly low oxygen levels, oxygen supplementation may improve shortness of breath when given during exercise, but may not improve breathlessness during normal daily activities or affect the quality of life.^[126] A risk of fires and little benefit exist when those on oxygen continue to smoke.^[127] In this situation, some recommend against its use.^[128] During acute exacerbations, many require oxygen therapy; the use of high concentrations of oxygen without taking into account a person's oxygen saturations may lead to increased levels of carbon dioxide and worsened outcomes.^[129]^[130] In those at high risk of high carbon dioxide levels, oxygen saturations of 88–92% are recommended, while for those without this risk, recommended levels are 94–98%.^[130]

Surgery

For those with very severe disease, surgery is sometimes helpful and may include lung transplantation or lung volume-reduction surgery,^[2] which involves removing the parts of the lung most damaged by emphysema, allowing the remaining, relatively good lung to expand and work better.^[100] It seems to be particularly effective if emphysema predominantly involves the upper lobe, but the procedure increases the risks of early death and adverse events.^[131] Lung transplantation is sometimes performed for very severe COPD, particularly in younger individuals.^[100]

Exacerbations

Acute exacerbations are typically treated by increasing the use of short-acting bronchodilators.^[2] This commonly includes a combination of a short-acting inhaled beta agonist and anticholinergic.^[48] These medications can be given either via a metered-dose inhaler with a spacer or via a nebulizer, with both appearing to be equally effective.^[48]^[132] Nebulization may be easier for those who are more unwell.^[48] Oxygen supplementation can be useful. Excessive oxygen; however, can result in increased CO₂ levels and a decreased level of consciousness.^[133]

Corticosteroids by mouth improve the chance of recovery and decrease the overall duration of symptoms.^[2]^[48] They work equally well as intravenous steroids but appear to have fewer side effects.^[134] Five days of steroids work as well as ten or fourteen.^[135] In those with a severe exacerbation, antibiotics improve outcomes.^[136] A number of different antibiotics may be used including amoxicillin, doxycycline and azithromycin; whether one is better than the others is unclear.^[69] The FDA recommends against the use of fluoroquinolones when other options are available due to higher risks of serious side effects.^[137] There is no clear evidence for those with less severe cases.^[136]

For those with type 2 respiratory failure (acutely raised CO₂ levels) non-invasive positive pressure ventilation decreases the probability of death or the need of intensive care admission.^[2] Additionally, theophylline may have a role in those who do not respond to other measures.^[2] Fewer than 20% of exacerbations require hospital admission.^[48] In those without acidosis from respiratory failure, home care ("hospital at home") may be able to help avoid some admissions.^[48]

Prognosis

Chronic obstructive pulmonary disease deaths per million persons in 2012

9–63

64–80

81–95

96–116

117–152

153–189

190–235

236–290

291–375

376–1089

Disability-adjusted life years lost to chronic obstructive pulmonary disease per 100,000 inhabitants in 2004.^[138]

no data

≤110

110–220

220–330

330–440

440–550

550–660

660–770

770–880

880–990

990–1100

1100–1350

≥1350

COPD usually gets gradually worse over time and can ultimately result in death. It is estimated that 3% of all disability is related to COPD.^[139] The proportion of disability from COPD globally has decreased from 1990 to 2010 due to improved indoor air quality primarily in Asia.^[139] The overall number of years lived with disability from COPD, however, has increased.^[140]

The rate at which COPD worsens varies with the presence of factors that predict a poor outcome, including severe airflow obstruction, little ability to exercise, shortness of breath, significantly underweight or overweight, congestive heart failure, continued smoking, and frequent exacerbations.^[5] Long-term outcomes in COPD can be estimated using the BODE index which gives a score of zero to ten depending on FEV₁, body-mass index, the distance walked in six minutes, and the modified MRC dyspnea scale.^[141] Significant weight loss is a bad sign.^[16] Results of spirometry are also a good predictor of the future progress of the disease but not as good as the BODE index.^[16]^[17]

Epidemiology

Globally, as of 2010, COPD affected approximately 329 million people (4.8% of the population).^[140] The disease affects men and women almost equally, as there has been increased tobacco use among women in the developed world.^[142] The increase in the developing world between 1970 and the 2000s is believed to be related to increasing rates of smoking in this region, an increasing population and an aging population due to fewer deaths from other causes such as infectious diseases.^[2] Some developed countries have seen increased rates, some have remained stable and some have seen a decrease in COPD prevalence.^[2] The global numbers are expected to continue increasing as risk factors remain common and the population continues to get older.^[73]

Between 1990 and 2010 the number of deaths from COPD decreased slightly from 3.1 million to 2.9 million^[143] and became the fourth leading cause of death.^[2] In 2012 it became the third leading cause as the number of deaths rose again to 3.1 million.^[144] In some countries, mortality has decreased in men but increased in women.^[145] This is most likely due to rates of smoking in women and men becoming more similar.^[16] COPD is more common in older people;^[9] it affects 34–200 out of 1000 people older than 65 years, depending on the population under review.^[9]^[67]

In England, an estimated 0.84 million people (of 50 million) have a diagnosis of COPD; this translates into approximately one person in 59 receiving a diagnosis of COPD at some point in their lives. In the most socioeconomically deprived parts of the country, one in 32 people were diagnosed with COPD, compared with one in 98 in the most affluent areas.^[146] In the United States approximately 6.3% of the adult population, totaling approximately 15 million people, have been diagnosed with COPD.^[147] 25 million people may have COPD if currently undiagnosed cases are included.^[148] In 2011, there were approximately 730,000 hospitalizations in the United States for COPD.^[149] In the United State, COPD is estimated to be the third leading cause of death in 2011.^[150]

History

Giovanni Battista Morgagni, who made one of the earliest recorded descriptions of emphysema in 1769

The word "emphysema" is derived from the Greek ἐμφυσᾶν emphysan meaning "inflate" -itself composed of ἐν en, meaning "in", and φυσᾶν physan, meaning "breath, blast".^[151] The term chronic bronchitis came into use in 1808^[152] while the term COPD is believed to have first been used in 1965.^[153] Previously it has been known by a number of different names, including chronic obstructive bronchopulmonary disease, chronic obstructive respiratory disease, chronic airflow obstruction, chronic airflow limitation, chronic obstructive lung disease, nonspecific chronic pulmonary disease, and diffuse obstructive pulmonary syndrome. The terms chronic bronchitis and emphysema were formally defined in 1959 at the CIBA guest symposium and in 1962 at the American Thoracic Society Committee meeting on Diagnostic Standards.^[153]

Early descriptions of probable emphysema include: in 1679 by T. Bonet of a condition of "voluminous lungs" and in 1769 by Giovanni Morgagni of lungs which were "turgid particularly from air".^[153]^[154] In 1721 the first drawings of emphysema were made by Ruysh.^[154] These were followed with pictures by Matthew Baillie in 1789 and descriptions of the destructive nature of the condition. In 1814 Charles Badham used "catarrh" to describe the cough and excess mucus in chronic bronchitis. René Laennec, the physician who invented the stethoscope, used the term "emphysema" in his book A Treatise on the Diseases of the Chest and of Mediate Auscultation (1837) to describe lungs that did not collapse when he opened the chest during an autopsy. He noted that they did not collapse as usual because they were full of air and the airways were filled with mucus. In 1842, John Hutchinson invented the spirometer, which allowed the measurement of vital capacity of the lungs. However, his spirometer could measure only volume, not airflow. Tiffeneau and Pinelli in 1947 described the principles of measuring airflow.^[153]

In 1953, Dr. George L. Waldbott, an American allergist, first described a new disease he named "smoker's respiratory syndrome" in the 1953 Journal of the American Medical Association. This was the first association between tobacco smoking and chronic respiratory disease.^[155]

Early treatments included garlic, cinnamon and ipecac, among others.^[152] Modern treatments were developed during the second half of the 20th century. Evidence supporting the use of steroids in COPD was published in the late 1950s. Bronchodilators came into use in the 1960s following a promising trial of isoprenaline. Further bronchodilators, such as salbutamol, were developed in the 1970s, and the use of LABAs began in the mid-1990s.^[156]

Society and culture

COPD has been referred to as "smoker's lung".^[157] People with emphysema have been known as "pink puffers" or "type A" due to their frequent pink complexion, fast respiratory rate and pursed lips,^[158]^[159] and people with chronic bronchitis have been referred to as "blue bloaters" or "type B" due to the often bluish color of the skin and lips from low oxygen levels and their ankle swelling.^[159]^[160] This terminology is no longer accepted as useful as most people with COPD have a combination of both emphysema and chronic bronchitis.^[16]^[159]

Many health systems have difficulty ensuring appropriate identification, diagnosis and care of people with COPD; Britain's Department of Health has identified this as a major issue for the National Health Service and has introduced a specific strategy to tackle these problems.^[161]

Economics

Globally, as of 2010, COPD is estimated to result in economic costs of $2.1 trillion, half of which occurring in the developing world.^[14] Of this total an estimated $1.9 trillion are direct costs such as medical care, while $0.2 trillion are indirect costs such as missed work.^[162] This is expected to more than double by the year 2030.^[14] In Europe, COPD represents 3% of healthcare spending.^[9] In the United States, costs of the disease are estimated at $50 billion, most of which is due to exacerbation.^[9] COPD was among the most expensive conditions seen in U.S. hospitals in 2011, with a total cost of about $5.7 billion.^[149]

Research

Infliximab, an immune-suppressing antibody, has been tested in COPD; there was a possibility of harm with no evidence of benefit.^[163]

Roflumilast, cilomilast, and phosphodiesterase 4 inhibitors act as a bronchodilator and as an anti-inflammatory. They show promise in decreasing the rate of exacerbations, but do not appear to change a persons quality of life.^[2]^[164] Roflumilast and cilomilast may be associated with side effects such as gastrointestinal issues and weight loss. Sleep disturbances and mood disturbances related to roflumilast have also been reported.^[164]

Several new long-acting agents are under development.^[2] Treatment with stem cells is under study.^[165] While there is tentative data that it is safe, and the animal data is promising, there is little human data as of 2017.^[166]^[167]^[168]^[169] The human data has shown poor results.^[166]^[170]

A procedure known as target lung denervation, which involves decreasing the parasympathetic nervous system supply of the lungs, is being studied but does not have sufficient data to determine its use.^[171] The effectiveness of alpha-1 antitrypsin augmentation treatment for people who have alpha-1 antitrypsin deficiency is unclear.^[172]

Research continues into the use of telehealthcare to treat people with COPD when they experience episodes of shortness of breath; treating people remotely may reduce the number of emergency-room visits and improve the person's quality of life.^[173]

Other animals

Chronic obstructive pulmonary disease may occur in a number of other animals and may be caused by exposure to tobacco smoke.^[174]^[175] Most cases of the disease, however, are relatively mild.^[176] In horses it is known as recurrent airway obstruction, can be quite severe, and most often is linked to an allergic reaction to a fungus contained in contaminated hay or straw.^[177] COPD is also commonly found in old dogs.^[178]

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^ Gøtzsche, Peter C.; Johansen, Helle Krogh (2016-09-20). "Intravenous alpha-1 antitrypsin augmentation therapy for treating patients with alpha-1 antitrypsin deficiency and lung disease". The Cochrane Database of Systematic Reviews. 9: CD007851. doi:10.1002/14651858.CD007851.pub3. ISSN 1469-493X. PMID 27644166.
^ McLean, Susannah; Nurmatov, Ulugbek; Liu, Joseph Ly; Pagliari, Claudia; Car, Josip; Sheikh, Aziz (2011-07-06). "Telehealthcare for chronic obstructive pulmonary disease". The Cochrane Database of Systematic Reviews (7): CD007718. doi:10.1002/14651858.CD007718.pub2. ISSN 1469-493X. PMID 21735417.
^ Akers, R. Michael; Denbow, D. Michael (2008). Anatomy and Physiology of Domestic Animals. Wiley. p. 852. ISBN 978-1-118-70115-7. Archived from the original on 2016-05-17.
^ Wright, JL; Churg, A (December 2002). "Animal models of cigarette smoke-induced COPD". Chest. 122 (6 Suppl): 301S–6S. doi:10.1378/chest.122.6_suppl.301S. PMID 12475805.
^ Churg, A; Wright, JL (2007). "Animal models of cigarette smoke-induced chronic obstructive lung disease". Contributions to microbiology. Contributions to Microbiology. 14: 113–25. doi:10.1159/000107058. ISBN 3-8055-8332-X. PMID 17684336.
^ Marinkovic D, Aleksic-Kovacevic S, Plamenac P (2007). "Cellular basis of chronic obstructive pulmonary disease in horses". Int. Rev. Cytol. International Review of Cytology. 257: 213–47. doi:10.1016/S0074-7696(07)57006-3. ISBN 978-0-12-373701-4. PMID 17280899.
^ Miller MS, Tilley LP, Smith FW (January 1989). "Cardiopulmonary disease in the geriatric dog and cat". Vet. Clin. North Am. Small Anim. Pract. 19 (1): 87–102. PMID 2646821.

External links

Chronic obstructive pulmonary disease at Curlie (based on DMOZ)

UpToDate Contents

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1. 慢性閉塞性肺疾患（COPD）：定義、臨床症状、診断、および病期分類 chronic obstructive pulmonary disease definition clinical manifestations diagnosis and staging
2. 安定した慢性閉塞性肺疾患（COPD）のマネージメント management of stable chronic obstructive pulmonary disease
3. 慢性閉塞性肺疾患（COPD）の増悪のマネージメント management of exacerbations of chronic obstructive pulmonary disease
4. 慢性閉塞性肺疾患（COPD）の増悪における感染のマネージメント management of infection in exacerbations of chronic obstructive pulmonary disease
5. 慢性閉塞性肺疾患（COPD）：予後因子および併存疾患 chronic obstructive pulmonary disease prognostic factors and comorbid conditions

English Journal

Cardiorespiratory responses of air filtration: A randomized crossover intervention trial in seniors living in Beijing: Beijing Indoor Air Purifier StudY, BIAPSY.

Shao D1, Du Y2, Liu S3, Brunekreef B4, Meliefste K4, Zhao Q3, Chen J3, Song X3, Wang M2, Wang J2, Xu H3, Wu R3, Wang T3, Feng B3, Lung CS5, Wang X1, He B6, Huang W7.
The Science of the total environment.Sci Total Environ.2017 Dec 15;603-604:541-549. doi: 10.1016/j.scitotenv.2017.06.095. Epub 2017 Jun 20.
PMID 28645052

Autophagy and inflammation.

Qian M1, Fang X1, Wang X2.
Clinical and translational medicine.Clin Transl Med.2017 Dec;6(1):24. doi: 10.1186/s40169-017-0154-5. Epub 2017 Jul 26.
PMID 28748360

Quantitative analysis of dynamic 18F-FDG PET/CT for measurement of lung inflammation.

Coello C1,2, Fisk M3, Mohan D4,5, Wilson FJ6, Brown AP7, Polkey MI4, Wilkinson I3,8, Tal-Singer R5, Murphy PS6, Cheriyan J3,9,8,10, Gunn RN7,11,12.
EJNMMI research.EJNMMI Res.2017 Dec;7(1):47. doi: 10.1186/s13550-017-0291-2. Epub 2017 May 25.
PMID 28547129

Japanese Journal

低線量X線CTによる肺癌検診時に併せたCOPD検診の取り組みと成果

日本呼吸器学会誌 = Annals of the Japanese Respiratory Society 5(6), 290-296, 2016-11-10
NAID 40021015690

慢性閉塞性肺疾患(COPD)患者の日常生活の実態調査 : LINQを用いて

日本呼吸ケア・リハビリテーション学会誌 = The journal of the Japan Society for Respiratory Care and Rehabilitation 26(2), 233-237, 2016-08
NAID 40020948508

疫学研究からみたCOPD合併肺癌の臨床 (特集 COPD合併肺癌 : 病因論から治療まで)

呼吸と循環 64(8), 749-754, 2016-08
NAID 40020930467

「慢性閉塞性肺疾患」

Classification	V · T · D ICD-10: J40–J44, J47; ICD-9-CM: 490–492, 494–496; OMIM: 606963; DiseasesDB: 2672;
External resources	MedlinePlus: 000091; eMedicine: med/373 emerg/99; Patient UK: Chronic obstructive pulmonary disease;

Chronic obstructive pulmonary disease
Synonyms	Chronic obstructive lung disease (COLD), chronic obstructive airway disease (COAD), chronic bronchitis, emphysema, pulmonary emphysema, others
	Gross pathology of a lung showing centrilobular-type emphysema characteristic of smoking. This close-up of the fixed, cut lung surface shows multiple cavities filled with heavy black carbon deposits.
Specialty	Pulmonology
Symptoms	Shortness of breath, cough with sputum production.
Complications	Acute exacerbation of chronic obstructive pulmonary disease
Usual onset	Over 40 years old
Duration	Long term
Causes	Tobacco smoking, air pollution, genetics
Diagnostic method	Lung function tests
Similar conditions	Asthma
Prevention	Improving indoor and outdoor air quality
Treatment	Stopping smoking, respiratory rehabilitation, lung transplantation
Medication	Vaccinations, inhaled bronchodilators and steroids, long-term oxygen therapy
Frequency	174.5 million (2015)
Deaths	3.2 million (2015)
	[edit on Wikidata]

　　[★]

英: chronic obstructive pulmonary disease, COPD
同: chronic obstructive lung disease COLD
関: 慢性気道閉塞

日本語訳としての「慢性閉塞性肺疾患」より「COPD」を使用することが勧められている

概念

1.

「COPD とは有毒な粒子やガスの吸入によって生じた肺の炎症反応に基づく進行性の気流制限を呈する疾患である．この気流制限には様々な程度の可逆性を認め、発症と経過が緩徐であり、労作性呼吸困難を生じる」疾患
完全に可逆性ではない気流制限が特徴　←　気管支喘息ではβ2受容体作動薬により気流制限の改善をみる。

2. ICU.387

慢性気管支炎や肺気腫により常に気道閉塞(一秒率:一秒量 FEV1/努力肺活量 FVC<70%)に陥っている病態で、気管支拡張薬に対する反応は乏しく、症状(呼吸困難)が恒常的・慢性的である。

疫学

患者の9割が喫煙者

病因

参考1

臨床上のリスク因子

喫煙
気道の過敏性
環境からの暴露
アトピー体質
抗酸化物質の欠乏
気管支肺低形成
結核

遺伝形式

α1アンチトリプシン欠損症は常染色体優性遺伝 AD

症状

身体所見

視診

打診上、鼓音
聴診上、呼吸音減弱、呼気延長

検査

血液ガス検査

PaO2：低下
PaCO2：上昇
A-aDO2：上昇

呼吸機能検査

%VC：軽度の肺気腫においては時に正常より増えていることがあるが、進行した肺気腫においては低下する。(093E019)
%DLCO：肺胞領域の破壊により拡散能低下

胸部単純X線写真：

肺肝境界の下降、肺の過膨張、
気管短縮(輪状軟骨上縁から胸骨上炎までが4-5cm未満に短縮していることがある、らしい)(出典不明、機序不明)

胸部CT

診断

スパイロメータの結果による

呼吸器学会ガイドライン

1. 気管支拡張薬投与後のスパイロ検査で、FEV1/FVC<70%
2. 他の気流制限を来しうる疾患を除外する

気管支拡張薬投与方法

検査は原則として急性呼吸器感染症のない臨床安定期に行う
短時間作用型気管支拡張薬は少なくとも 6 時間、長時間作用型気管支拡張薬は 24 時間中止したうえで検査を行う
検査に用いる気管支拡張薬は、通常、短時間作用型吸入用 β2刺激薬を原則とするが、抗コリン薬あるいは両者の併用であってもよい
投与方法はスペーサーを用いた β2刺激薬定量噴霧式吸入薬(MDI)吸入、ネブライザー吸入のいずれであってもよい
気管支拡張薬吸入後の検査は吸入後 30～60 分後に行うべきものとする．
気管支拡張薬吸入効果の評価は、吸入前の FEV1．0 と吸入後 FEV1．0 を比較して、200ml 以上の増加かつ前値に対して 12%以上の増加があったときに有意と判定

鑑別診断

喘息、びまん性汎細気管支炎、先天性副鼻腔気管支症候群、閉塞性細気管支炎、気管支拡張症、肺結核、塵肺症、リンパ脈管筋腫症、うっ血性心不全、間質性肺疾患、肺癌

評価法

mMRC(the Modified British Medical Research Council):日常生活に対する呼吸困難（息切れ）の影響を測定
CAT(COPD assessment test)：COPDの症状やQOLに関する8項目を0〜40点で評価
IPAG(International Primary Care Airways Group)：COPD 関連症状と危険因子を測定

BODE指数：予後評価
ADO指数：予後評価

治療

病期分類

ガイドライン1

0期：リスク群：慢性症状(咳嗽・喀痰)：(a) 禁煙、インフルエンザワクチン接種(肺炎球菌ワクチンはガイドライン上では推奨されていないが(COPD増悪予防に対する効果が証明されなかった？)、接種した方がよいとする意見がある)
I期：軽症：80%≦%FEV1：(a)。(b) 必要に応じ短時間作用型の気管支拡張薬を使用。
II期：中等症：50%≦%FEV1＜80%：(a)。(b)。(c) 呼吸リハビリテーション、長時間作用型気管支拡張薬の定期的使用
III期：重症：30%≦%FEV1＜50%：(a)。(b)。(c)。(d) 吸入ステロイド薬の考慮(増悪を繰り返す)
IV期：最重症：%FEV1＜30%または%FEV1＜50%かつ慢性呼吸不全あるいは右心不全合併：(a)。(b)。(c)。(d)。(e) 長期酸素療法、外科的治療の考慮

安定期の治療

治療のmodality：薬物療法、包括的呼吸リハビリテーション、患者教育、栄養管理、酸素療法、換気補助療法、肺容量減量手術、肺移植、在宅管理

急性増悪

COPDの急性増悪や重症度の分類には定説はない (ガイドライン1)
COPDの急性増悪とは「病態が日内変動を超えて悪化し、日常施行していた治療内容を変更せざるを得ない状態」(呼吸器疾患最新の治療2004-2006 p.267)
原因：気道感染と大気汚染が最多。1/3は原因不明。

COPDの急性増悪

定義

COPDの自然の進行の中で起きる現象で、呼吸困難、咳嗽、喀痰といった症状が日常の変動を超えて増悪したもの

入院適応

突然の安静時呼吸器困難の出現など、症状の顕著な増悪
基盤にあるCOPDが重症(III度,IV度)
新たな身体所見の発言
増悪に対する初期治療に反応しない
重大な合併症の存在
頻回の増悪
新たに発生した不整脈
診断が不確実な例
高齢者
不十分な住宅サポート

modality (ガイドライン1)

気管支拡張薬吸入の容量/回数の増加(例えば、短期間作用型β2刺激薬が用いられる)
ステロイドの全身投与(経口/静脈注射)：増悪からの回復、肺機能の回復までの時間を短縮する
(喀痰から感染症が疑われる場合)抗菌薬の投与

外来　：経口ペニシリン系薬、ニューキノロン系薬
入院例：注射用β-ラクタム系薬/β-ラクタマーゼ阻害薬、第3,4世代セフェム系薬、カルバペネム系薬、ニューキノロン系薬

病原体

三大病原体の一つがMoraxella catarrhalis

予後

参考

1. [charged] Chronic obstructive pulmonary disease: Risk factors and risk reduction - uptodate [1]

ガイドライン

1. COPD診断と治療のためのガイドライン第2版

http://www.jrs.or.jp/quicklink/glsm/guideline/nopass_pdf/copd_summary.pdf

国試

104I036、102A051

「chronic obstructive airway disease」

　　[★] 慢性閉塞性気道疾患

関: chronic airflow obstruction、chronic obstructive lung disease、chronic obstructive pulmonary disease、COAD、COPD

「COLD」

　　[★]

同: chronic obstructive lung disease, 慢性閉塞性肺疾患

「disease」

　　[★]

n.

疾患：illnessより厳密な概念。「ある臓器に明確な障害が確認され、それによって症状が出ているとはっきり説明できる場合」 (PSY.9)

特定の原因、病態生理、症状、経過、予後、病理組織所見が全てそろった場合 (PSY.9)

something that is very wrong with people's attitudes, way of life or with society.

関: ail、ailment、disease entity、disorder、ill、illness、malady、sick、sickness

注意

disease ≠ illness ≠ disorder

「obstructive」

　　[★]

adj.

閉塞性の

関: constrictive、obliterans、obliterative、occlusive、occlusively

「chronic」

　　[★]

adj.

慢性の、慢性的な、慢性型の

関: chronically、chronicity

「lung disease」

　　[★]

関: Respiratory disease

関: respiratory disease

関: respiratory disease

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リンク元	「慢性閉塞性肺疾患」「chronic obstructive airway disease」「COLD」
関連記事	「disease」「obstructive」「chronic」「lung disease」

Classification	V · T · D ICD-10: J40–J44, J47 ICD-9-CM: 490–492, 494–496 OMIM: 606963 DiseasesDB: 2672
External resources	MedlinePlus: 000091 eMedicine: med/373 emerg/99 Patient UK: Chronic obstructive pulmonary disease

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chronic obstructive lung disease

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Contents

Signs and symptoms

Cough

Shortness of breath

Other features

Exacerbation

Cause

Smoking

Air pollution

Occupational exposures

Genetics

Other

Exacerbations

Pathophysiology

Diagnosis

Spirometry

Severity

Other tests

Differential diagnosis

Prevention

Smoking cessation

Occupational health

Air pollution

Management

Exercise

Bronchodilators

Corticosteroids

Other medication

Oxygen

Surgery

Exacerbations

Prognosis

Epidemiology

History

Society and culture

Economics

Research

Other animals

References

Further reading

External links

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「慢性閉塞性肺疾患」

概念

疫学

病因

臨床上のリスク因子

遺伝形式

症状

身体所見

検査

診断

鑑別診断

評価法

治療

病期分類

安定期の治療

急性増悪

COPDの急性増悪

定義

入院適応

病原体

予後

参考

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「chronic obstructive airway disease」

「COLD」