chronic obstructive pulmonary disease

cause of COPD from emedicine.com

2008-12-31T07:32:00.001-08:00

* Cigarette smoking
o The primary cause of COPD is exposure to tobacco smoke. Clinically significant COPD develops in 15% of cigarette smokers. Age of initiation of smoking, total pack-years, and current smoking status predict COPD mortality. People who smoke have a greater annual decline in FEV1. Overall, tobacco smoking accounts for as much as 90% of the risk.
o Secondhand smoke, or environmental tobacco smoke, increases the risk of respiratory infections, augments asthma symptoms, and causes a measurable reduction in pulmonary function.
* Air pollution
o Although the role of air pollution in the etiology of COPD is unclear, the effect is small when compared to cigarette smoking.
o The use of solid fuels for cooking and heating may result in high levels of indoor air pollution and the development of COPD.
* Airway hyperresponsiveness
o Airway hyperresponsiveness (ie, Dutch hypothesis) stipulates that patients who have nonspecific airway hyperreactivity and who smoke are at increased risk of developing COPD with an accelerated decline in lung function. Nonspecific airway hyperreactivity is inversely related to FEV1 and may predict a decline in lung function.
o The possible role of airway hyperresponsiveness as a risk factor for the development of COPD in people who smoke is unclear. Moreover, bronchial hyperreactivity may result from airway inflammation observed with the development of smoking-related chronic bronchitis.
* Alpha1-antitrypsin deficiency
o AAT deficiency is the only known genetic risk factor for developing COPD and accounts for less than 1% of all cases in the United States. AAT is a protease inhibitor produced by the liver that acts predominantly by inhibiting neutrophil elastase in the lungs.
o Severe AAT deficiency leads to premature emphysema at the average age of 53 years for nonsmokers and 40 years for smokers.
o PiMM phenotypes occur in 90% of people and produce serum levels within the reference range. PiZZ is the most common deficient state and accounts for 95% of people in the severely deficient category.

frequency of copd from emedicine.com

2008-12-31T07:31:00.000-08:00

United States

Approximately 14.2 million people have COPD, approximately 12.5 million have chronic bronchitis, and 1.7 million have emphysema. Since 1982, the patients diagnosed with COPD increased by 41.5%. Researchers estimate the prevalence of chronic airflow obstruction in the United States as 8-17% for men and 10-19% for women. The prevalence rates increased in women by 30% in the last decade.
International

Worldwide data are sparse, but the rates likely are higher because more than 1.2 billion humans are exposed to the ravages of smoking. A population-based epidemiologic study from Spain determined the prevalence of COPD in individuals aged 40-69 years at 9.1% (78% were men).

Based on pooled data from a number of studies, global prevalence of COPD was 7.5%, chronic bronchitis alone was 6.4%, and emphysema alone was 1.8%. The prevalence from 26 spirometric estimates was 8.9%. The most common spirometric definitions were those of the Global Initiative for Obstructive Lung Disease (GOLD). Thus, the prevalence of physiologically defined COPD in adults aged 40 years and older is approximately 9-10%.

pathophysiology of COPD from emedicine.com

2008-12-31T07:30:00.000-08:00

Pathological changes in COPD occur in the large (central) airways, the small (peripheral) bronchioles, and the lung parenchyma. The pathogenic mechanisms are not clear but most likely involve diverse mechanisms. The increased number of activated polymorphonuclear leukocytes and macrophages release elastases in a manner that cannot be counteracted effectively by antiproteases, resulting in lung destruction. The primary offender has been human leukocyte elastase, with a possible synergistic role suggested for proteinase 3 and macrophage-derived matrix proteinases, cysteine proteinases, and a plasminogen activator. Additionally, increased oxidative stress caused by free radicals in cigarette smoke, the oxidants released by phagocytes, and polymorphonuclear leukocytes all may lead to apoptosis or necrosis of exposed cells.

Chronic bronchitis

Mucous gland enlargement is the histologic hallmark of chronic bronchitis. The structural changes described in the airways include atrophy, focal squamous metaplasia, ciliary abnormalities, variable amounts of airway smooth muscle hyperplasia, inflammation, and bronchial wall thickening. Neutrophilia develops in the airway lumen, and neutrophilic infiltrates accumulate in the submucosa. The respiratory bronchioles display a mononuclear inflammatory process, lumen occlusion by mucous plugging, goblet cell metaplasia, smooth muscle hyperplasia, and distortion due to fibrosis. These changes, combined with loss of supporting alveolar attachments, cause airflow limitation by allowing airway walls to deform and narrow the airway lumen.

Emphysema

Emphysema has 3 morphologic patterns. The first type, centriacinar emphysema, is characterized by focal destruction limited to the respiratory bronchioles and the central portions of acinus. This form of emphysema is associated with cigarette smoking and is most severe in the upper lobes. The second type, panacinar emphysema, involves the entire alveolus distal to the terminal bronchiole. The panacinar type is most severe in the lower lung zones and generally develops in patients with homozygous alpha1-antitrypsin (AAT) deficiency. The third type, distal acinar emphysema or paraseptal emphysema, is the least common form and involves distal airway structures, alveolar ducts, and sacs. This form of emphysema is localized to fibrous septa or to the pleura and leads to formation of bullae. The apical bullae may cause pneumothorax. Paraseptal emphysema is not associated with airflow obstruction.

Chronic obstructive pulmonary disease

Both emphysematous destruction and small airway inflammation often are found in combination in individual patients. When emphysema is moderate or severe, loss of elastic recoil, rather than bronchiolar disease, is the mechanism of airflow limitation. By contrast, when emphysema is mild, bronchiolar abnormalities are most responsible for the deficit in lung function. Although airflow obstruction in emphysema is virtually irreversible, bronchoconstriction due to inflammation accounts for a limited amount of reversibility.

Role of inflammation in COPD

In contrast to the eosinophil, which is the most prominent inflammatory cell in asthma, the cellular composition of the airway inflammation in COPD is predominantly mediated by the neutrophils. Cigarette smoking induces macrophages to release neutrophil chemotactic factors and elastases, thus unleashing tissue destruction. Severity of airflow obstruction has correlated with greater induced sputum neutrophilia that is also more prevalent in patients with chronic cough and sputum production and is associated with an accelerated decline in lung function.

Macrophages also play an important role through macrophage-derived matrix metalloproteinases (MMPs). Cigarette smoke causes neutrophil influx and is required for the secretion of MMPs, therefore suggesting that both neutrophils and macrophages are required for the development of emphysema. Studies have also shown that T lymphocytes, particularly CD8+, in addition to the macrophages, play an important role in the pathogenesis of smoking-induced airflow limitation. To support the inflammation hypothesis further, a stepwise increase in alveolar inflammation occurs in surgical specimens from patients without COPD versus patients with mild or severe emphysema.

COPD from emedicine.com

2008-12-31T07:29:00.001-08:00

Chronic obstructive pulmonary disease (COPD) is a devastating disorder that causes a huge degree of human suffering. COPD is currently the fourth leading cause of death in the United States.

In Western Europe, Badham (1808) and Laennec (1827) made the classic description of chronic bronchitis and emphysema in the early 19th century. A British medical textbook of the 1860s described the familiar clinical picture of chronic bronchitis as an advanced disease with repeated bronchial infections that ended in right heart failure. Overall, this malady caused more than 5% of all deaths in the Middle Ages and earlier. The condition was the most common among the poor; therefore, it was attributed to "bad" living.

Developments in the 20th century include the widespread use of spirometry, recognition of airflow obstruction as a key factor in determining disability, and the improvement of pathological methods to assess emphysema. Participants of the Ciba symposium of 1958 proposed definitions of chronic bronchitis and emphysema, incorporating the concept of airflow obstruction.

COPD is defined as a disease state characterized by the presence of airflow obstruction due to chronic bronchitis or emphysema. The airflow obstruction generally is progressive, may be accompanied by airway hyperreactivity, and may be partially reversible. Chronic bronchitis is defined clinically as the presence of a chronic productive cough for 3 months during each of 2 consecutive years (other causes of cough being excluded). Emphysema is defined as an abnormal, permanent enlargement of the air spaces distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis. Chronic bronchitis is defined in clinical terms and emphysema in terms of anatomic pathology.

COPD in Wikipedia

2008-12-30T07:01:00.000-08:00

Chronic obstructive pulmonary disease (COPD) is a disease of the lungs in which the airways become narrowed. This leads to a limitation of the flow of air to and from the lungs causing shortness of breath. In contrast to asthma, the limitation of airflow is poorly reversible and usually gets progressively worse over time.
COPD is caused by noxious particles or gases, most commonly from smoking, which trigger an abnormal inflammatory response in the lung.[1][2] The inflammatory response in the larger airways is known as chronic bronchitis, which is diagnosed clinically when people regularly cough up sputum. In the alveoli, the inflammatory response causes destruction of the tissue of the lung, a process known as emphysema. The natural course of COPD is characterized by occasional sudden worsenings of symptoms called acute exacerbations, most of which are caused by infections or air pollution.
The diagnosis of COPD requires lung function tests. Important management strategies are smoking cessation, vaccinations, rehabilitation, and drug therapy (often using inhalers). Some patients go on to requiring long-term oxygen therapy or lung transplantation.[1]
Worldwide, COPD ranked sixth as the cause of death in 1990. It is projected to be the third leading cause of death worldwide by 2020 due to an increase in smoking rates and demographic changes in many countries.[1] COPD is the 4th leading cause of death in the U.S., and the economic burden of COPD in the U.S. in 2007 was $42.6 billion in health care costs and lost productivity.[3][4]
COPD is also known as chronic obstructive lung disease (COLD), chronic obstructive airway disease (COAD), chronic airflow limitation (CAL) and chronic obstructive respiratory disease.

How Can COPD Be Prevented?

2008-12-28T06:36:00.001-08:00

How Can COPD Be Prevented?

You can take steps to prevent COPD before it starts. If you already have COPD, you can take steps to prevent complications and slow the progress of the disease.
Prevent COPD Before It Starts

The best way to prevent COPD is to not start smoking or to quit smoking before you develop the disease. Smoking is the leading cause of COPD.

If you smoke, talk to your doctor about programs and products that can help you quit. Many hospitals have programs that help people quit smoking, or hospital staff can refer you to a program. The National Heart, Lung, and Blood Institute's "Your Guide to a Healthy Heart" booklet has more information about how to quit smoking.

Also, try to avoid secondhand smoke and other lung irritants that can contribute to COPD, such as air pollution, chemical fumes, and dust.
Prevent Complications and Slow the Progress of COPD

If you have COPD, the most important step you can take is to quit smoking. This can help prevent complications and slow the progress of the disease. You also should avoid exposure to the lung irritants mentioned above.

Follow your treatments for COPD exactly as your doctor prescribes. They can help you breathe easier, stay more active, and avoid or manage severe symptoms.

Talk with your doctor about whether and when you should get flu and pneumonia vaccines. These vaccines can lower your chances of getting these illnesses, which are major health risks for people who have COPD.

Living With COPD

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Living With COPD

COPD has no cure yet. However, you can take steps to manage your symptoms and slow the progress of the disease. You can:

* Avoid lung irritants
* Get ongoing care
* Manage the disease and its symptoms
* Prepare for emergencies

Avoid Lung Irritants

If you smoke, quit. Smoking is the leading cause of COPD. Talk to your doctor about programs and products that can help you quit. Many hospitals have programs that help people quit smoking, or hospital staff can refer you to a program. The National Heart, Lung, and Blood Institute's "Your Guide to a Healthy Heart" booklet has more information about how to quit smoking.

Try to avoid secondhand smoke and other lung irritants that can contribute to COPD, such as air pollution, chemical fumes, and dust. Keep these irritants out of your home. If your home is painted or sprayed for insects, have it done when you can stay away for awhile.

Keep your windows closed and stay at home (if possible) when there's a lot of air pollution or dust outside.
Get Ongoing Care

If you have COPD, it's important to get ongoing medical care. Take all of your medicines as your doctor prescribes. Make sure to refill your prescriptions before they run out. Bring all of the medicines you're taking when you have medical checkups.

Talk with your doctor about whether and when you should get flu and pneumonia vaccines. Also, ask him or her about other diseases for which COPD may increase your risk, such as heart disease, lung cancer, and pneumonia.
Manage COPD and Its Symptoms

You can do things to help manage your disease and its symptoms. Depending on how severe your disease is, you may ask your family and friends for help with daily tasks. Do activities slowly. Put items that you need often in one place that's easy to reach.

Find very simple ways to cook, clean, and do other chores. Some people find it helpful to use a small table or cart with wheels to move things around and a pole or tongs with long handles to reach things. Ask for help moving things around in your house so that you will not need to climb stairs as often.

Keep your clothes loose, and wear clothes and shoes that are easy to put on and take off.
Prepare for Emergencies

If you have COPD, knowing when and where to seek help for your symptoms is important. You should seek emergency care if you have severe symptoms, such as trouble catching your breath or talking. (For more information on severe symptoms, see "What Are the Signs and Symptoms of COPD?")

Call your doctor if you notice that your symptoms are worsening or if you have signs of an infection, such as a fever. Your doctor may change or adjust your treatments to relieve and treat symptoms.

Keep phone numbers handy for your doctor, hospital, and someone who can take you for medical care. You also should have on hand directions to the doctor's office and hospital and a list of all the medicines you're taking.

How Is COPD Treated?

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How Is COPD Treated?

COPD has no cure yet. However, treatments and lifestyle changes can help you feel better, stay more active, and slow the progress of the disease.

Quitting smoking is the most important step you can take to treat COPD. Talk to your doctor about programs and products that can help you quit. Many hospitals have programs that help people quit smoking, or hospital staff can refer you to a program. Ask your family members and friends to support you in your efforts to quit. Also, try to avoid secondhand smoke.

The National Heart, Lung, and Blood Institute's "Your Guide to a Healthy Heart" booklet has more information about how to quit smoking.

Other treatments for COPD may include medicines, vaccines, pulmonary rehabilitation (rehab), oxygen therapy, surgery, and managing complications.

The goals of COPD treatment are to:

* Relieve your symptoms
* Slow the progress of the disease
* Improve your exercise tolerance (your ability to stay active)
* Prevent and treat complications
* Improve your overall health

Specialists Involved

To assist with your treatment, your family doctor may advise you to see a pulmonologist. This is a doctor who specializes in treating people who have lung problems.
Medicines
Bronchodilators

Bronchodilators relax the muscles around your airways. This helps open your airways and makes breathing easier.

Depending on how severe your disease is, your doctor may prescribe short-acting or long-acting bronchodilators. Short-acting bronchodilators last about 4 to 6 hours and should be used only when needed. Long-acting bronchodilators last about 12 hours or more and are used every day.

Most bronchodilators are taken using a device called an inhaler. This device allows the medicine to go right to your lungs. Not all inhalers are used the same way. Ask your health care team to show you the right way to use your inhaler.

If your COPD is mild, your doctor may only prescribe a short-acting inhaled bronchodilator. In this case, you may only use the medicine when symptoms occur.

If your COPD is moderate or severe, your doctor may prescribe regular treatment with short- and long-acting bronchodilators.
Inhaled Glucocorticosteroids (Steroids)

Inhaled steroids are used for some people who have moderate or severe COPD. These medicines may reduce airway inflammation (swelling).

Your doctor may ask you to try inhaled steroids for a trial period of 6 weeks to 3 months to see whether the medicine is helping with your breathing problems.
Vaccines
Flu Shots

The flu (influenza) can cause serious problems for people who have COPD. Flu shots can reduce your risk for the flu. Talk with your doctor about getting a yearly flu shot.
Pneumococcal Vaccine

This vaccine lowers your risk for pneumococcal pneumonia (nu-MO-ne-ah) and its complications. People who have COPD are at higher risk for pneumonia than people who don't have COPD. Talk with your doctor about whether you should get this vaccine.
Pulmonary Rehabilitation

Pulmonary rehab is a medically supervised program that helps improve the health and well-being of people who have lung problems. Rehab may include an exercise program, disease management training, and nutritional and psychological counseling. The program aims to help you stay more active and carry out your day-to-day activities.

Your rehab team may include doctors, nurses, physical therapists, respiratory therapists, exercise specialists, and dietitians. These health professionals work together and with you to create a program that meets your needs.
Oxygen Therapy

If you have severe COPD and low levels of oxygen in your blood, oxygen therapy can help you breathe better. For this treatment, you're given oxygen through nasal prongs or a mask.

You may need extra oxygen all the time or just sometimes. For some people who have severe COPD, using extra oxygen for most of the day can help them:

* Do tasks or activities, while having fewer symptoms
* Protect their hearts and other organs from damage
* Sleep more during the night and improve alertness during the day
* Live longer

Surgery

In rare cases, surgery may benefit some people who have COPD. Surgery usually is a last resort for people who have severe symptoms that have not improved from taking medicines.

Surgeries for people who have COPD that's mainly related to emphysema include bullectomy (bul-EK-to-me) and lung volume reduction surgery (LVRS). A lung transplant may be done for people who have very severe COPD.
Bullectomy

When the walls of the air sacs are destroyed, larger air spaces called bullae form. These air spaces can become so large that they interfere with breathing. In a bullectomy, doctors remove one or more very large bullae from the lungs.
Lung Volume Reduction Surgery

In LVRS, surgeons remove damaged tissues from the lungs. This helps the lungs work better. In carefully selected patients, LVRS can improve breathing and quality of life.
Lung Transplant

A lung transplant may benefit some people who have very severe COPD. During a lung transplant, your damaged lung is removed and replaced with a healthy lung from a deceased donor.

A lung transplant can improve your lung function and quality of life. However, lung transplants have a high risk of complications. These include infections and death due to the body rejecting the transplanted lung.

If you have very severe COPD, talk to your doctor about whether a lung transplant is an option. Discuss with your doctor the benefits and risks of this type of surgery.
Managing Complications

COPD symptoms usually slowly worsen over time. However, they can become more severe suddenly. For instance, a cold, the flu, or a lung infection may cause your symptoms to quickly worsen. You may have a much harder time catching your breath. You also may have chest tightness, more coughing, changes in the color or amount of your sputum (spit), and a fever.

Call your doctor right away if this happens. He or she may prescribe antibiotics to treat the infection and other medicines, such as bronchodilators and glucocorticosteroids, to help with your breathing.

Some severe symptoms may require treatment in a hospital. For more information, see "What Are the Signs and Symptoms of COPD?"

What Are the Signs and Symptoms of COPD?

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What Are the Signs and Symptoms of COPD?

The signs and symptoms of COPD include:

* An ongoing cough or a cough that produces large amounts of mucus (often called "smoker's cough")
* Shortness of breath, especially with physical activity
* Wheezing (a whistling or squeaky sound when you breathe)
* Chest tightness

These symptoms often occur years before the flow of air into and out of the lungs declines. However, not everyone who has these symptoms has COPD. Likewise, not everyone who has COPD has these symptoms.

Some of the symptoms of COPD are similar to the symptoms of other diseases and conditions. Your doctor can determine if you have COPD.

If you have COPD, you may have frequent colds or flu. If your COPD is severe, you may have swelling in your ankles, feet, or legs; a bluish color on your lips due to low levels of oxygen in your blood; and shortness of breath.

COPD symptoms usually slowly worsen over time. At first, if symptoms are mild, you may not notice them, or you may adjust your lifestyle to make breathing easier. For example, you may take the elevator instead of the stairs.

Over time, symptoms may become bad enough to see a doctor. For example, you may get short of breath during physical exertion.

How severe your symptoms are depends on how much lung damage you have. If you keep smoking, the damage will occur faster than if you stop smoking. In severe COPD, you may have other symptoms, such as weight loss and lower muscle endurance.

Some severe symptoms may require treatment in a hospital. You—with the help of family members or friends, if you're unable—should seek emergency care if:

* You're having a hard time catching your breath or talking.
* Your lips or fingernails turn blue or gray. (This is a sign of a low oxygen level in your blood.)
* You're not mentally alert.
* Your heartbeat is very fast.
* The recommended treatment for symptoms that are getting worse isn't working.

How Is COPD Diagnosed?

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How Is COPD Diagnosed?

Your doctor will diagnose COPD based on your signs and symptoms, your medical and family histories, and test results.

He or she may ask whether you smoke or have had contact with lung irritants, such as air pollution, chemical fumes, or dust. If you have an ongoing cough, your doctor may ask how long you've had it, how much you cough, and how much mucus comes up when you cough. He or she also may ask whether you have a family history of COPD.

Your doctor will examine you and use a stethoscope to listen for wheezing or other abnormal chest sounds.

You also may need one or more tests to diagnose COPD.
Lung Function Tests

Lung function tests measure how much air you can breathe in and out, how fast you can breathe air out, and how well your lungs can deliver oxygen to your blood.

The main test for COPD is spirometry (spi-ROM-eh-tre). Other lung function tests, such as a lung diffusing capacity test, also may be used. (For more information, see "Types of Lung Function Tests.")
Spirometry

During this painless test, a technician will ask you to take a deep breath in and then blow as hard as you can into a tube connected to a small machine. The machine is called a spirometer.

The machine measures how much air you breathe out. It also measures how fast you can blow air out.
Your doctor may have you inhale medicine that helps open your airways and then blow into the tube again. He or she can then compare your test results before and after taking the medicine.

Spirometry can detect COPD long before its symptoms appear. Doctors also may use the results from this test to find out how severe your COPD is and to help set your treatment goals.

The test results also may help find out whether another condition, such as asthma or heart failure, is causing your symptoms.
Other Tests

Your doctor may recommend other tests. These tests include:

* A chest x ray or chest computed tomography (CT) scan. These tests create pictures of the structures inside your chest, such as your heart and lungs. The pictures can show signs of COPD. They also may show whether another condition, such as heart failure, is causing your symptoms.
* An arterial blood gas test. This blood test measures the oxygen level in your blood using a sample of blood taken from an artery. The test can help find out how severe your COPD is and whether you may need supplemental oxygen therapy.

Who Is At Risk for COPD?

2008-12-28T06:30:00.000-08:00

Who Is At Risk for COPD?

The main risk factor for COPD is smoking. Most people who have COPD smoke or used to smoke. People who have a family history of COPD are more likely to get the disease if they smoke.

Long-term exposure to other lung irritants also is a risk factor for COPD. Examples of other lung irritants include air pollution and chemical fumes and dust from the environment or workplace.

Most people who have COPD are at least 40 years old when symptoms begin. Although it isn't common, people younger than 40 can have COPD. For example, this may happen if a person has alpha-1 antitrypsin deficiency, a genetic condition.

What Causes COPD?

2008-12-28T06:29:00.001-08:00

What Causes COPD?

Most cases of COPD develop after long-term exposure to lung irritants that damage the lungs and the airways.

In the United States, the most common irritant that causes COPD is cigarette smoke. Pipe, cigar, and other types of tobacco smoke also can cause COPD, especially if the smoke is inhaled. Secondhand smoke—that is, smoke in the air from other people smoking—also can irritate the lungs and contribute to COPD.

Breathing in air pollution and chemical fumes or dust from the environment or workplace also can contribute to COPD.

In rare cases, a genetic condition called alpha-1 antitrypsin deficiency may play a role in causing COPD. People who have this condition have low levels of alpha-1 antitrypsin (AAT)—a protein made in the liver.

Having a low level of the AAT protein can lead to lung damage and COPD if you're exposed to smoke or other lung irritants. If you have this condition and smoke, COPD can worsen very quickly.

What Is COPD?

2008-12-28T06:21:00.000-08:00

What Is COPD?

COPD, or chronic obstructive pulmonary (PULL-mun-ary) disease, is a progressive disease that makes it hard to breathe. "Progressive" means the disease gets worse over time.

COPD can cause coughing that produces large amounts of mucus (a slimy substance), wheezing, shortness of breath, chest tightness, and other symptoms.

Cigarette smoking is the leading cause of COPD. Most people who have COPD smoke or used to smoke. Long-term exposure to other lung irritants, such as air pollution, chemical fumes, or dust, also may contribute to COPD.
Overview

To understand COPD, it helps to understand how the lungs work. The air that you breathe goes down your windpipe into tubes in your lungs called bronchial tubes, or airways.

The airways are shaped like an upside-down tree with many branches. At the end of the branches are tiny air sacs called alveoli (al-VEE-uhl-eye).

The airways and air sacs are elastic. When you breathe in, each air sac fills up with air like a small balloon. When you breathe out, the air sac deflates and the air goes out.

In COPD, less air flows in and out of the airways because of one or more of the following:

* The airways and air sacs lose their elastic quality.
* The walls between many of the air sacs are destroyed.
* The walls of the airways become thick and inflamed (swollen).
* The airways make more mucus than usual, which tends to clog the airways.

In the United States, the term "COPD" includes two main conditions—emphysema (em-fi-SE-ma) and chronic obstructive bronchitis (bron-KI-tis).

In emphysema, the walls between many of the air sacs are damaged, causing them to lose their shape and become floppy. This damage also can destroy the walls of the air sacs, leading to fewer and larger air sacs instead of many tiny ones.

In chronic obstructive bronchitis, the lining of the airways is constantly irritated and inflamed. This causes the lining to thicken. Lots of thick mucus forms in the airways, making it hard to breathe.

Most people who have COPD have both emphysema and chronic obstructive bronchitis. Thus, the general term "COPD" is more accurate.
Outlook

COPD is a major cause of disability, and it's the fourth leading cause of death in the United States. More than 12 million people are currently diagnosed with COPD. An additional 12 million likely have the disease and don't even know it.

COPD develops slowly. Symptoms often worsen over time and can limit your ability to do routine activities. Severe COPD may prevent you from doing even basic activities like walking, cooking, or taking care of yourself.

Most of the time, COPD is diagnosed in middle-aged or older people. The disease isn't passed from person to person—you can't catch it from someone else.

COPD has no cure yet, and doctors don't know how to reverse the damage to the airways and lungs. However, treatments and lifestyle changes can help you feel better, stay more active, and slow the progress of the disease.

Pathophysiology of COPD

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The above pathogenic mechanisms result in the pathological
changes found in COPD. These in turn result in physiological
abnormalities—mucous hypersecretion and ciliary dysfunction,
airflow obstruction and hyperinflation, gas exchange
abnormalities, pulmonary hypertension, and systemic effects.
Mucous hypersecretion and ciliary dysfunctionMucous hypersecretion results in a chronic productive cough.
This is characteristic of chronic bronchitis but not necessarily
associated with airflow obstruction, and not all patients with
COPD have symptomatic mucous hypersecretion. The
hypersecretion is due to squamous metaplasia, increased
numbers of goblet cells, and increased size of bronchial
submucosal glands in response to chronic irritation by noxious
particles and gases. Ciliary dysfunction is due to squamous
metaplasia of epithelial cells and results in an abnormal
mucociliary escalator and difficulty in expectorating.
Airflow obstruction and hyperinflation or air trappingThe main site of airflow obstruction occurs in the small
conducting airways that are < 2 mm in diameter. This is
because of inflammation and narrowing (airway remodelling)
and inflammatory exudates in the small airways. Other factors
contributing to airflow obstruction include loss of the lung
elastic recoil (due to destruction of alveolar walls) and
destruction of alveolar support (from alveolar attachments).
The airway obstruction progressively traps air during
expiration, resulting in hyperinflation at rest and dynamic
hyperinflation during exercise. Hyperinflation reduces the
inspiratory capacity and therefore the functional residual
capacity during exercise. These features result in breathlessness
and limited exercise capacity typical of COPD. The airflow
obstruction in COPD is best measured by spirometry and is a
prerequisite for its diagnosis.
Gas exchange abnormalitiesThese occur in advanced disease and are characterised by
arterial hypoxaemia with or without hypercapnia. An abnormal
distribution of ventilation:perfusion ratios—due to the
anatomical changes found in COPD—is the main mechanism
for abnormal gas exchange. The extent of impairment of
diffusing capacity for carbon monoxide per litre of alveolar
volume correlates well with the severity of emphysema.
Pulmonary hypertensionThis develops late in COPD, at the time of severe gas exchange
abnormalities. Contributing factors include pulmonary arterial
constriction (as a result of hypoxia), endothelial dysfunction,
remodelling of the pulmonary arteries (smooth muscle
hypertrophy and hyperplasia), and destruction of the
pulmonary capillary bed. Structural changes in the pulmonary
arterioles result in persistent pulmonary hypertension and right
ventricular hypertrophy or enlargement and dysfunction (cor
pulmonale).
Systemic effects of COPDSystemic inflammation and skeletal muscle wasting contribute
to limiting the exercise capacity of patients and worsen the
prognosis irrespective of degree of airflow obstruction. Patients
also have an increased risk of cardiovascular disease, which is
associated with an increase in C reactive protein.
Pathophysiology of exacerbationsExacerbations are often associated with increased neutrophilic
inflammation and, in some mild exacerbations, increased
numbers of eosinophils. Exacerbations can be caused by
infection (bacterial or viral), air pollution, and changes in
ambient temperature.
In mild exacerbations, airflow obstruction is unchanged or
only slightly increased. Severe exacerbations are associated with
worsening of pulmonary gas exchange due to increased
inequality between ventilation and perfusion and subsequent
respiratory muscle fatigue. The worsening ventilation-perfusion
relation results from airway inflammation, oedema, mucous
hypersecretion, and bronchoconstriction. These reduce
ventilation and cause hypoxic vasoconstriction of pulmonary
arterioles, which in turn impairs perfusion.
Respiratory muscle fatigue and alveolar hypoventilation can
contribute to hypoxaemia, hypercapnia, and respiratory
acidosis, and lead to severe respiratory failure and death.
Hypoxia and respiratory acidosis can induce pulmonary
vasoconstriction, which increases the load on the right ventricle
and, together with renal and hormonal changes, results in
peripheral oedema.

Pathogenesis of COPD

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Inflammation is present in the lungs, particularly the small
airways, of all people who smoke. This normal protective
response to the inhaled toxins is amplified in COPD, leading to
tissue destruction, impairment of the defence mechanisms that
limit such destruction, and disruption of the repair mechanisms.
In general, the inflammatory and structural changes in the
airways increase with disease severity and persist even after
smoking cessation. Besides inflammation, two other processes
are involved in the pathogenesis of COPD—an imbalance
between proteases and antiproteases and an imbalance between
oxidants and antioxidants (oxidative stress) in the lungs.
Inflammatory cellsCOPD is characterised by increased numbers of neutrophils,
macrophages, and T lymphocytes (CD8 more than CD4) in the
lungs. In general, the extent of the inflammation is related to
the degree of the airflow obstruction. These inflammatory cells
release a variety of cytokines and mediators that participate in
the disease process. This inflammatory pattern is markedly
different from that seen in patients with asthma.
Inflammatory mediatorsMany inflammatory mediators are increased in COPD,
including
x Leucotriene B4, a neutrophil and T cell chemoattractant which
is produced by macrophages, neutrophils, and epithelial cells
x Chemotactic factors such as the CXC chemokines interleukin
8 and growth related oncogene , which are produced by
macrophages and epithelial cells. These attract cells from the
circulation and amplify pro-inflammatory responses
x Pro-inflammatory cytokines such as tumour necrosis factor
and interleukins 1 and 6
x Growth factors such as transforming growth factor , which
may cause fibrosis in the airways either directly or through
release of another cytokine, connective tissue growth factor.
Protease and antiprotease imbalanceIncreased production (or activity) of proteases and inactivation
(or reduced production) of antiproteases results in imbalance.
Cigarette smoke, and inflammation itself, produce oxidative
stress, which primes several inflammatory cells to release a
combination of proteases and inactivates several antiproteases
by oxidation. The main proteases involved are those produced
by neutrophils (including the serine proteases elastase,
cathepsin G, and protease 3) and macrophages (cysteine
proteases and cathepsins E, A, L, and S), and various matrix
metalloproteases (MMP-8, MMP-9, and MMP-12). The main
antiproteases involved in the pathogenesis of emphysema
include 1 antitrypsin, secretory leucoprotease inhibitor, and
tissue inhibitors of metalloproteases.
Oxidative stressThe oxidative burden is increased in COPD. Sources of oxidants
include cigarette smoke and reactive oxygen and nitrogen
species released from inflammatory cells. This creates an
imbalance in oxidants and antioxidants of oxidative stress. Many
markers of oxidative stress are increased in stable COPD and
are further increased in exacerbations. Oxidative stress can lead
to inactivation of antiproteases or stimulation of mucous
production. It can also amplify inflammation by enhancing
transcription factor activation (such as nuclear factor B) and
hence gene expression of pro-inflammatory mediators.

Pathology of COPD

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Chronic obstructive pulmonary disease (COPD) is characterised
by poorly reversible airflow obstruction and an abnormal
inflammatory response in the lungs. The latter represents the
innate and adaptive immune responses to long term exposure
to noxious particles and gases, particularly cigarette smoke. All
cigarette smokers have some inflammation in their lungs, but
those who develop COPD have an enhanced or abnormal
response to inhaling toxic agents. This amplified response may
result in mucous hypersecretion (chronic bronchitis), tissue
destruction (emphysema), and disruption of normal repair and
defence mechanisms causing small airway inflammation and
fibrosis (bronchiolitis).
These pathological changes result in increased resistance to
airflow in the small conducting airways, increased compliance of
the lungs, air trapping, and progressive airflow obstruction—all
characteristic features of COPD.We have good understanding
of the cellular and molecular mechanisms underlying the
pathological changes found in COPD.

alpha1 antitrypsin deficiency

2008-12-20T06:52:00.001-08:00

The best documented genetic risk factor for COPD is
1 antitrypsin deficiency. However, this is rare and is present in
only 1-2% of patients with COPD. 1 antitrypsin is a
glycoprotein responsible for most of the antiprotease activity in
serum. Its gene is highly polymorphic, but some genotypes
(usually ZZ) are associated with low serum concentrations
(typically 10-20% of normal). Severe deficiency of 1 antitrypsin
is associated with premature and accelerated development of
COPD in smokers and non-smokers, though the rate of decline
in lung function is greatly accelerated in those who smoke.
The 1 antitrypsin status of patients with severe COPD who
are less than 40 years old should be determined since over half
of such patients have this deficiency. Detection of such cases
identifies family members who will require genetic counselling
and patients who might be suitable for future potential
treatment with 1 antitrypsin replacement.

Occupation

2008-12-20T06:51:00.002-08:00

Intense prolonged exposure to dusts and chemicals can cause
COPD independently of cigarette smoking, though smoking
seems to enhance the effects of such occupational exposure to
increase the risk of developing COPD. About 20% of diagnosed
cases of COPD are thought to be attributable to occupation; in
lifelong non-smokers this proportion increases to 30%.
Exposure to noxious gases and particles—such as grain,
isocyanates, cadmium, coal, other mineral dusts, and welding
fumes—have been implicated in the development of chronic
airflow obstruction. Thus, a full chronological occupational
history should be taken, as relevant occupational exposures are
often missed by clinicians.

Air pollution

2008-12-20T06:51:00.001-08:00

Urban air pollution may affect lung function development and
consequently be a risk factor for COPD. Cross sectional studies
have shown that higher concentrations of atmospheric air
pollution are associated with increased cough, sputum
production, and breathlessness and reduced ventilatory
function. Exposure to particulate and nitrogen dioxide air
pollution has been associated with impaired ventilatory
function in adults and reduced lung growth in children. In
developing countries indoor air pollution from biomass fuel
(used for cooking and heating) has been implicated as a risk
factor for COPD, particularly in women.

smoking

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Cigarette smoking is clearly the single most important risk
factor in the development of COPD. Current smoking is also
associated with an increased risk of death. Pipe and cigar
smoking also significantly increase morbidity and mortality
from COPD, though the risk is less than for cigarettes. Around
half of cigarette smokers develop some airflow obstruction, and
10-20% develop clinically significant COPD. Although smoking
is the most important risk factor, it is not a prerequisite: COPD
can occur in non-smokers with longstanding asthma or with
1 antitrypsin deficiency. Moreover, about 20% of COPD cases
in men are not attributable to smoking.
A more contentious issue is the possible relation between
environmental tobacco smoke and development of COPD:
several case-control studies have shown a trend towards an
increased risk of COPD with passive smoking. However, the
adverse effect of maternal smoking on childhood ventilatory
function is clearer: smoking during and after pregnancy is
associated with reduced infant, childhood, and adult ventilatory
function. Most studies have shown that the effects of antenatal
smoking are greater in magnitude than, and independent of,
the effects of postnatal exposure.

The morbidity and economic costs associated with COPD

2008-12-20T06:39:00.001-08:00

The morbidity and economic costs associated with COPD are
high, largely unrecognised, and more than twice those from
asthma. The impact on quality of life is particularly high in
patients with frequent exacerbations, and even patients with
mild COPD have an impaired quality of life.
Since the mid-1990s, emergency admissions for COPD have
increased by at least 50%, so that in 2002-3 there were 110 000
hospital admissions for an exacerbation of COPD in England,
accounting for 1.1 million bed days. At least 10% of emergency
admissions to hospital are as a consequence of COPD, and this
proportion is even greater during the winter. Most admissions
are of people older than 65 years with advanced disease, who
are often admitted repeatedly and use a disproportionate
amount of resources. About 25% of patients with COPD
diagnosed need admission to hospital, with some 15% of
patients being admitted each year.
The impact in primary care is even greater, with 86% of care
being provided exclusively by primary care. An average general
practitioner’s list will contain some 200 patients with COPD
(even more in areas of social deprivation), although not all will
have it diagnosed. On average, patients with COPD make six or
seven visits annually to their general practitioner. Each patient
costs the UK economy an estimated £1639 annually, equating
to a national burden of £982m (€1450, $1741m). For each
patient, annual direct costs to the NHS are £819, with 54% of
this being due to hospital admissions and 19% due to drug
treatment. COPD results in further costs to society in that
roughly 40% of UK patients are below retirement age, and the
disease prevents about 25% from working and reduces the
capacity to work in a further 10%. Annual indirect costs of
COPD have been estimated at £820 per patient and consist of
the cost of disability, absence from work, premature mortality,
and the time caregivers miss work.

mortality of COPD

2008-12-20T06:38:00.002-08:00

COPD is the fourth leading cause of death in the US and
Europe.With the increase in cigarette smoking in developing
countries, especially China, COPD is expected to become the
third leading cause of death worldwide by 2020. During 2003,
about 26 000 people died from COPD in the UK, accounting
for 4.9% of all deaths, with 14 000 of these deaths occurring in
men and 12 000 in women. These represent 5.4% of all male
deaths and 4.2% of all female deaths.
In the UK over the past 30 years, mortality from COPD has
fallen in men and risen in women, and the sex difference in
COPD deaths will probably disappear in the near future. In the
US, mortality from COPD in women has also risen substantially,
from 20.1 to 56.7 per 100 000 between 1980 and 2000, while in
men the increase has been more modest, from 73.0 to 82.6 per
100 000. In 2000, for the first time, more women than men died
from COPD (59 936 v 59 118). Mortality increases with age,
disease severity, and socioeconomic disadvantage. On average,
COPD reduces life expectancy by 1.8 years in the UK (76.5 v
78.3 years for controls)—mild disease reducing it by 1.1 years,
moderate disease by 1.7 years, and severe disease by 4.1 years.

prevalence of COPD

2008-12-20T06:38:00.001-08:00

Estimating and comparing the prevalence of COPD in different
countries is complicated by differences in its precise definition
and in the level of underdiagnosis. For example, in the United
Kingdom mild COPD is defined as the ratio of forced
expiratory volume in 1 second (FEV1) to the forced vital
capacity (FVC) being < 0.7 and the FEV1 being 50-80% of the
expected value. Other guidelines suggest slightly different
spirometric values (see third article in this series).
A national UK study reported an abnormally low FEV1 in
10% of men and 11% of women aged 16-65 years. Similarly, a
study in Manchester found non-reversible airflow obstruction in
11% of adults aged > 45, of whom 65% had not had COPD
diagnosed. In the United States the reported prevalence of
airflow obstruction with an FEV1 < 80% of the expected value is
6.8%, with 1.5% of the population having an FEV1 < 50% of
expected and 0.5% having more severe obstruction (FEV1 < 35%
of expected). As in the UK, about 60% of those with airflow
obstruction had not had COPD diagnosed. As much as 40-50%
of the actual prevalence of COPD, based on measurements of
ventilatory function,may be undiagnosed;many people present
relatively late with moderate or severe airflow obstruction.
In England and Wales some 900 000 people have COPD
diagnosed—so, after allowing for underdiagnosis, the true
number with COPD is likely to be about 1.5 million. The mean
age at diagnosis in the UK is roughly 67 years, and prevalence
increases with age. COPD is more common in men than
women and is associated with socioeconomic deprivation. The
prevalence of diagnosed COPD in women is increasing (from
0.8% in 1990 to 1.4% in 1997), whereas in men it seems to have
reached a plateau since the middle 1990s. Similar trends have
been reported in the US. These trends in prevalence probably
reflect sex differences in cigarette smoking since the 1970s.

definition of copd

2008-12-20T06:36:00.000-08:00

In 2004, the UK National Institute for Clinical Excellence
defined chronic obstructive pulmonary disease (COPD) as
“characterised by airflow obstruction. The airflow obstruction is
usually progressive, not fully reversible and does not change
markedly over several months. The disease is predominantly
caused by smoking.” COPD is the preferred umbrella term for
the airflow obstruction associated with the diseases of chronic
bronchitis and emphysema. These are closely related to, but not
synonymous with, COPD.
Although asthma is associated with airflow obstruction, it is
usually considered as a separate clinical entity. Some patients
with chronic asthma also develop airflow obstruction that is
relatively fixed (a consequence of airway remodelling) and often
indistinguishable from COPD. Because of the high prevalence
of asthma and COPD, these conditions coexist in many patients,
creating diagnostic uncertainty. Other conditions also associated
with poorly reversible airflow obstruction include cystic fibrosis,
bronchiectasis, and obliterative bronchiolitis. Although these
conditions need to be considered in the differential diagnosis of
obstructive airways disease, they are not conventionally covered
by the definition of COPD

copd key

2008-12-20T06:34:00.000-08:00

• Ch ronic Obstructive Pulmonar y Disease (COP D) is a
preventable and treatable disease with some significant extra-
pulmonary effects that may contribute to the severity in individual
patients. Its pulmonary component is characterized by airflow limitation
that is not fully reversible. The airflow limitation is usually progressive
and associated with an abnormal inflammatory response of the lung
to noxious particles or gases.
• Worldwide, the most commonly encountered risk factor for COPD
is cigarette smok ing. At ever y possible opportunity
individuals w ho smok e should be encouraged to quit . In
many countries, air pollution resulting from the burning of wood and
other biomass fuels has also been identified as a COPD risk factor.
• A diagnosis of COPD should be considered in any patient who has
dyspnea, chronic cough or sputum production, and/or a history of
exposure to risk factors for the disease. The diagnosis should be
confirmed by spirometry.
• A COP D m a n agement program includes four components:
assess and monitor disease, reduce risk factors, manage stable
COPD, and manage exacerbations.
• P harmacologic treatment can prevent and control symptoms,
reduce the frequency and severity of exacerbations, improve health
status, and improve exercise tolerance.
• Patient education can help improve skills, ability to cope with
illness, and health status. It is an effective way to accomplish smoking
cessation, initiate discussions and understanding of advance directives
and end-of-life issues, and improve responses to acute exacerbations.
• COPD is often associated with exacerbations of symptoms.

1 Antitrypsin Deficiency

2008-12-19T08:56:00.001-08:00

Many variants of the protease inhibitor (PI or SERPINA1) locus that encodes 1AT have been described. The common M allele is associated with normal 1AT levels. The S allele, associated with slightly reduced 1AT levels, and the Z allele, associated with markedly reduced 1AT levels, also occur with frequencies >1% in most Caucasian populations. Rare individuals inherit null alleles, which lead to the absence of any 1AT production through a heterogeneous collection of mutations. Individuals with two Z alleles or one Z and one null allele are referred to as PiZ, which is the most common form of severe 1AT deficiency.

Although only 1–2% of COPD patients are found to have severe 1AT deficiency as a contributing cause of COPD, these patients demonstrate that genetic factors can have a profound influence on the susceptibility for developing COPD. PiZ individuals often develop early-onset COPD, but the ascertainment bias in the published series of PiZ individuals—which have usually included many PiZ subjects who were tested for 1AT deficiency because they had COPD—means that the fraction of PiZ individuals who will develop COPD and the age-of-onset distribution for the development of COPD in PiZ subjects remain unknown. Approximately 1 in 3000 individuals in the United States inherits severe 1AT deficiency, but only a small minority of these individuals has been recognized. The clinical laboratory test used most frequently to screen for 1AT deficiency is measurement of the immunologic level of 1AT in serum (see "Laboratory Findings," below).

A significant percentage of the variability in pulmonary function among PiZ individuals is explained by cigarette smoking; cigarette smokers with severe 1AT deficiency are more likely to develop COPD at early ages. However, the development of COPD in PiZ subjects, even among current or ex-smokers, is not absolute. Among PiZ nonsmokers, impressive variability has been noted in the development of airflow obstruction. Other genetic and/or environmental factors likely contribute to this variability.

Specific treatment in the form of 1AT augmentation therapy is available for severe 1AT deficiency as a weekly intravenous infusion (see "Treatment," below).

The risk of lung disease in heterozygous PiMZ individuals, who have intermediate serum levels of 1AT (~60% of PiMM levels), is controversial. Although previous general population surveys have not typically shown increased rates of airflow obstruction in PiMZ compared to PiMM individuals, case-control studies that compared COPD patients to control subjects have usually found an excess of PiMZ genotypes in the COPD patient group. Several recent large population studies have suggested that PiMZ subjects are at slightly increased risk for the development of airflow obstruction, but it remains unclear if all PiMZ subjects are at slightly increased risk for COPD or if a subset of PiMZ subjects are at substantially increased risk for COPD due to other genetic or environmental factors.

Passive, or Second-Hand, Smoking Exposure

2008-12-19T08:55:00.002-08:00

Exposure of children to maternal smoking results in significantly reduced lung growth. In utero tobacco smoke exposure also contributes to significant reductions in postnatal pulmonary function. Although passive smoke exposure has been associated with reductions in pulmonary function, the importance of this risk factor in the development of the severe pulmonary function reductions in COPD remains uncertain.

Ambient Air Pollution

2008-12-19T08:55:00.001-08:00

Some investigators have reported increased respiratory symptoms in those living in urban compared to rural areas, which may relate to increased pollution in the urban settings. However, the relationship of air pollution to chronic airflow obstruction remains unproven. Prolonged exposure to smoke produced by biomass combustion—a common mode of cooking in some countries—also appears to be a significant risk factor for COPD among women in those countries. However, in most populations, ambient air pollution is a much less important risk factor for COPD than cigarette smoking.

Occupational Exposures

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Increased respiratory symptoms and airflow obstruction have been suggested as resulting from general exposure to dust at work. Several specific occupational exposures, including coal mining, gold mining, and cotton textile dust, have been suggested as risk factors for chronic airflow obstruction. However, although nonsmokers in these occupations developed some reductions in FEV1, the importance of dust exposure as a risk factor for COPD, independent of cigarette smoking, is not certain. Among workers exposed to cadmium (a specific chemical fume), FEV1, FEV1/FVC, and DLCO were significantly reduced (FVC, forced vital capacity; DLCO, carbon monoxide diffusing capacity of the lung; Chap. 246), consistent with airflow obstruction and emphysema. Although several specific occupational dusts and fumes are likely risk factors for COPD, the magnitude of these effects appears to be substantially less important than the effect of cigarette smoking.

Respiratory Infections

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These have been studied as potential risk factors for the development and progression of COPD in adults; childhood respiratory infections have also been assessed as potential predisposing factors for the eventual development of COPD. The impact of adult respiratory infections on decline in pulmonary function is controversial, but significant long-term reductions in pulmonary function are not typically seen following an episode of bronchitis or pneumonia. The impact of the effects of childhood respiratory illnesses on the subsequent development of COPD has been difficult to assess due to a lack of adequate longitudinal data. Thus, although respiratory infections are important causes of exacerbations of COPD, the association of both adult and childhood respiratory infections to the development and progression of COPD remains to be proven.

Airway Responsiveness and COPD

2008-12-19T08:53:00.001-08:00

Airway Responsiveness and COPD

A tendency for increased bronchoconstriction in response to a variety of exogenous stimuli, including methacholine and histamine, is one of the defining features of asthma . However, many patients with COPD also share this feature of airway hyperresponsiveness. The considerable overlap between persons with asthma and those with COPD in airway responsiveness, airflow obstruction, and pulmonary symptoms led to the formulation of the Dutch hypothesis. This suggests that asthma, chronic bronchitis, and emphysema are variations of the same basic disease, which is modulated by environmental and genetic factors to produce these pathologically distinct entities. The alternative British hypothesis contends that asthma and COPD are fundamentally different diseases: Asthma is viewed as largely an allergic phenomenon, while COPD results from smoking-related inflammation and damage. Determination of the validity of the Dutch hypothesis vs. the British hypothesis awaits identification of the genetic predisposing factors for asthma and/or COPD, as well as the interactions between these postulated genetic factors and environmental risk factors.

Longitudinal studies that compared airway responsiveness at the beginning of the study to subsequent decline in pulmonary function have demonstrated that increased airway responsiveness is clearly a significant predictor of subsequent decline in pulmonary function. Thus, airway hyperresponsiveness is a risk factor for COPD.

Cigarette Smoking

2008-12-19T08:50:00.000-08:00

By 1964, the Advisory Committee to the Surgeon General of the United States had concluded that cigarette smoking was a major risk factor for mortality from chronic bronchitis and emphysema. Subsequent longitudinal studies have shown accelerated decline in the volume of air exhaled within the first second of the forced expiratory maneuver (FEV1) in a dose-response relationship to the intensity of cigarette smoking, which is typically expressed as pack-years (average number of packs of cigarettes smoked per day multiplied by the total number of years of smoking). This dose-response relationship between reduced pulmonary function and cigarette smoking intensity accounts for the higher prevalence rates for COPD with increasing age. The historically higher rate of smoking among males is the likely explanation for the higher prevalence of COPD among males; however, the prevalence of COPD among females is increasing as the gender gap in smoking rates has diminished in the past 50 years.

Although the causal relationship between cigarette smoking and the development of COPD has been absolutely proved, there is considerable variability in the response to smoking. Although pack-years of cigarette smoking is the most highly significant predictor of FEV1 (Fig. 254-1), only 15% of the variability in FEV1 is explained by pack-years. This finding suggests that additional environmental and/or genetic factors contribute to the impact of smoking on the development of airflow obstruction.

Although cigar and pipe smoking may also be associated with the development of COPD, the evidence supporting such associations is less compelling, likely related to the lower dose of inhaled tobacco byproducts during cigar and pipe smoking.

copd

2008-12-19T08:49:00.001-08:00

Chronic obstructive pulmonary disease (COPD) has been defined by the Global Initiative for Chronic Obstructive Lung Disease (GOLD), an international collaborative effort to improve awareness, diagnosis, and treatment of COPD, as a disease state characterized by airflow limitation that is not fully reversible (http://www.goldcopd.com/). COPD includes emphysema, an anatomically defined condition characterized by destruction and enlargement of the lung alveoli; chronic bronchitis, a clinically defined condition with chronic cough and phlegm; and small airways disease, a condition in which small bronchioles are narrowed. COPD is present only if chronic airflow obstruction occurs; chronic bronchitis without chronic airflow obstruction is not included within COPD.

COPD is the fourth leading cause of death and affects >16 million persons in the United States. COPD is also a disease of increasing public health importance around the world. GOLD estimates suggest that COPD will rise from the sixth to the third most common cause of death worldwide by 2020.

Risk Factors of COPD

2008-12-19T08:44:00.002-08:00

The most important risk factor for the development of COPD is cigarette smoking, which is associated with 85â€“90% of all cases. Smokers exhibit a substantially greater rate of annual decline in forced expiratory volume in 1 sec (FEV1) than the normal age-related decline of 15â€“30 mL/yr. Cigar and pipe smokers are also at increased risk of developing COPD, albeit less than cigarette smokers. However, only a minority (~15%) of smokers develop clinically significant COPD, suggesting that genetic predisposition and other environmental factors may be required for the development of lung injury.
Less than 1% of COPD cases are linked to alpha1-antitrypsin deficiency, a known genetic factor associated with premature development of emphysema that is greatly accelerated by smoking. Alpha1-antitrypsin inhibits neutrophil-derived elastase, an enzyme responsible for the destruction of lung parenchyma in emphysema. Patients with alpha1-antitrypsin deficiency carry a genetic polymorphism leading to decreased alpha1-antitrypsin serum levels, which in homozygous individuals may be <10% of normal. Alpha1-antitrypsin deficiency should be considered in a patient with emphysema who has (a) a minimal smoking history, (b) early onset COPD (<45 yrs), (c) a family history of lung disease, or (d) a predominance of lower lobe emphysema on chest x-ray or CT scan.
Other risk factors for COPD include occupational exposures to dusts and chemicals; pollution (indoor and outdoor), especially the combustion products of biomass fuels; severe respiratory infections in childhood; and poor socioeconomic status (which predisposes the patient to the preceding factors).

Epidemiology for COPD

2008-12-19T08:44:00.001-08:00

In the United States, approximately 16 million persons suffer from COPD. These patients account for 500,000 hospitalizations and 18 billion dollars in direct health care costs per year. Currently, 110,000 deaths per year are attributable to COPD, making it the fourth leading cause of death in the United States after heart disease, cancer, and stroke. COPD is the only major cause of death increasing in incidence owing to its high incidence in the elderly, a portion of the American population that has dramatically increased over the last few years.

COPD

2008-12-19T08:34:00.000-08:00

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Introduction for COPD

2008-12-19T08:00:00.000-08:00

COPD is a progressive condition characterized by chronic airflow limitation that is not fully reversible. The term COPD refers primarily to the entities of emphysema and chronic bronchitis. Emphysema is defined pathologically as nonuniform enlargement of the distal airspaces with destruction of the acini, loss of lung elasticity, and absence of any fibrotic changes. Chronic bronchitis is defined clinically as cough productive of at least 2 tbsp of sputum on most days of 3 consecutive mos in 2 consecutive yrs, in the absence of other lung diseases. Although asthma, cystic fibrosis, bronchiectasis, bronchiolitis, and sarcoidosis are associated with expiratory airflow obstruction, they do not fall within the classification of COPD. The diagnosis should be considered in any patient with cough, sputum production, and/or dyspnea, and a history of exposure to risk factors for COPD. Classically, chronic bronchitis accounts for 85% of COPD cases, with the remaining 15% of COPD patients having emphysema. Some patients with COPD exhibit manifestations of both emphysema and chronic bronchitis. The chronic progression of expiratory airflow obstruction is punctuated by episodic worsening in the cough, dyspnea, and sputum production that characterize the condition. These episodes are known as acute exacerbations of COPD.