Chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease
ICD-10	J40 - J44, J47
ICD-9	490 - 496
OMIM	606963
DiseasesDB	2672
MedlinePlus	000091
eMedicine	med/373  emerg/99
MeSH	C08.381.495.389

WikiDoc Resources for Chronic obstructive pulmonary disease
Articles
Most recent articles on Chronic obstructive pulmonary disease Most cited articles on Chronic obstructive pulmonary disease Review articles on Chronic obstructive pulmonary disease Articles on Chronic obstructive pulmonary disease in N Eng J Med, Lancet, BMJ
Media
Powerpoint slides on Chronic obstructive pulmonary disease Images of Chronic obstructive pulmonary disease Photos of Chronic obstructive pulmonary disease Podcasts & MP3s on Chronic obstructive pulmonary disease Videos on Chronic obstructive pulmonary disease
Evidence Based Medicine
Cochrane Collaboration on Chronic obstructive pulmonary disease Bandolier on Chronic obstructive pulmonary disease TRIP on Chronic obstructive pulmonary disease
Clinical Trials
Ongoing Trials on Chronic obstructive pulmonary disease at Clinical Trials.gov Trial results on Chronic obstructive pulmonary disease Clinical Trials on Chronic obstructive pulmonary disease at Google
Guidelines / Policies / Govt
US National Guidelines Clearinghouse on Chronic obstructive pulmonary disease NICE Guidance on Chronic obstructive pulmonary disease NHS PRODIGY Guidance FDA on Chronic obstructive pulmonary disease CDC on Chronic obstructive pulmonary disease
Books
Books on Chronic obstructive pulmonary disease
News
Chronic obstructive pulmonary disease in the news Be alerted to news on Chronic obstructive pulmonary disease News trends on Chronic obstructive pulmonary disease
Commentary
Blogs on Chronic obstructive pulmonary disease
Definitions
Definitions of Chronic obstructive pulmonary disease
Patient Resources / Community
Patient resources on Chronic obstructive pulmonary disease Discussion groups on Chronic obstructive pulmonary disease Patient Handouts on Chronic obstructive pulmonary disease Directions to Hospitals Treating Chronic obstructive pulmonary disease Risk calculators and risk factors for Chronic obstructive pulmonary disease
Healthcare Provider Resources
Symptoms of Chronic obstructive pulmonary disease Causes & Risk Factors for Chronic obstructive pulmonary disease Diagnostic studies for Chronic obstructive pulmonary disease Treatment of Chronic obstructive pulmonary disease
Continuing Medical Education (CME)
CME Programs on Chronic obstructive pulmonary disease
International
Chronic obstructive pulmonary disease en Espanol Chronic obstructive pulmonary disease en Francais
Business
Chronic obstructive pulmonary disease in the Marketplace Patents on Chronic obstructive pulmonary disease
Experimental / Informatics
List of terms related to Chronic obstructive pulmonary disease

For patient information click here

Editor-in-Chief: Philip Marcus, M.D., M.P.H. [1], Division of Pulmonary Medicine St. Francis Hospital-The Heart Center, Roslyn, NY

Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]

Please Join in Editing This Page and Apply to be an Editor-In-Chief for this topic: There can be one or more than one Editor-In-Chief. You may also apply to be an Associate Editor-In-Chief of one of the subtopics below. Please mail us [3] to indicate your interest in serving either as an Editor-In-Chief of the entire topic or as an Associate Editor-In-Chief for a subtopic. Please be sure to attach your CV and or biographical sketch.

Overview

Chronic obstructive pulmonary disease (COPD), also known as chronic obstructive airway disease (COAD), is a group of diseases characterized by the pathological limitation of airflow in the airway that is not fully reversible. COPD is the umbrella term for chronic bronchitis, emphysema and a range of other lung disorders. It is most often due to tobacco smoking, but can be due to other airborne irritants such as coal dust, asbestos or solvents, congenital conditions such as alpha-1-antitrypsin deficiency and as well as preserved meats containing nitrites [4].

Epidemiology and Demographics

According to the World Health Organization (WHO), 80 million people suffer from moderate to severe COPD and 3 million died due to it in 2005. The WHO predicts that by 2030, it will be the 4th largest cause of mortality worldwide.

Since COPD is not diagnosed until it becomes clinically apparent, prevalence and mortality data greatly underestimate the socioeconomic burden of COPD. In the UK, COPD accounts for about 7% of all days of sickness related absence from work.

Smoking rates in the industrialized world have continued to fall, causing rates of emphysema and pulmonary neoplasms to slowly decline.

Pathophysiology and Etiology

Chronic bronchitis

Chronic bronchitis is defined in clinical terms as a cough with sputum production on most days for 3 months of a year, for 2 consecutive years.

Chronic bronchitis is hallmarked by hyperplasia (increased number) and hypertrophy (increased size) of the goblet cells (mucous gland) of the airway, resulting in an increase in secretion of mucus which contributes to the airway obstruction. Microscopically there is infiltration of the airway walls with inflammatory cells, particularly neutrophils. Inflammation is followed by scarring and remodeling that thickens the walls resulting in narrowing of the small airway. Further progression leads to metaplasia (abnormal change in the tissue) and fibrosis (further thickening and scarring) of the lower airway. The consequence of these changes is a limitation of airflow..

Emphysema

Main article: Emphysema

Emphysema is defined histologically as the enlargement of the air spaces distal to the terminal bronchioles, with destruction of their walls.

The enlarged air sacs (alveoli) of the lungs reduces the surface area available for the movement of gases during respiration. This ultimately leads to dyspnea in severe cases. The exact mechanism for the development of emphysema is not understood, although it is known to be linked with smoking and age.

Diagnosis

The diagnosis of COPD is usually suggested by symptoms; it is a clinical diagnosis and no single test is definitive. A comprehensive history from the patient is very important with regard to smoking and occupation.

Differential Diganosis of Underlying Causes

Cigarette smoking

A primary factor of COPD is chronic tobacco smoking. In the United States, around 90% of cases of COPD are due to smoking. Not all smokers will develop COPD, but continuous smokers have at least a 25% risk.

Occupational pollutants

Some occupational pollutants, such as cadmium and silica, have shown to be a contributing risk factor for COPD. The people at highest risk for these pollutants include coal workers, construction workers, metal workers and cotton workers, amongst others. However, in most cases these pollutants are combined with cigarette smoking further increasing the chance of developing COPD. These occupations are commonly associated with other respiratory diseases, particularly pneumoconiosis (black lung disease).

Air pollution

Urban air pollution may be a contributing factor for COPD as it is thought to impair the development of the lung function. In developing countries indoor air pollution, usually due to biomass fuel, has been linked to COPD, especially in women.

Genetics

Very rarely, there may be a deficiency in an enzyme known as alpha 1-antitrypsin which causes a form of COPD.

Other risk factors

Increasing age, male gender, allergy, repeated airway infection and general impaired lung function are also related to the development of COPD.

Symptoms and History

The main symptoms of COPD include dyspnea (shortness of breath) lasting for months or perhaps years, possibly accompanied by wheezing, and a persistent cough with sputum production. It is possible the sputum may contain blood (hemoptysis), usually due to damage of the blood vessels of the airways. Severe COPD could lead to cyanosis (bluish decolorization usually in the lips and fingers) caused by a lack of oxygen in the blood. In extreme cases it could lead to cor pulmonale due the extra work required by the heart to get blood to flow through the lungs.

Laboratory Studies

COPD is particularly characterised by a ratio of forced expiratory volume over 1 second (FEV₁) to forced vital capacity (FVC) being < 0.7 and the FEV₁ < 70% of the predicted value (see Spirometry). Other signs include a rapid breathing rate (tachypnea) and a wheezing sound heard through a stethoscope. Pulmonary emphysema is NOT the same as subcutaneous emphysema, which is a collection of air under the skin that may be detected by the crepitus sounds produced on palpation.

Physical examination with a plethysmograph can reveal the true extent of COPD.

The severity of COPD can be classified as follows using spirometry (see above):

Severity	Post-bronchodilator FEV1 /FVC	FEV1 % predicted
At risk	>0.7	≥80
Mild COPD	≤0.7	≥80
Moderate COPD	≤0.7	50-80
Severe COPD	≤0.7	30-50
Very Severe COPD	≤0.7	<30 or 30-50 with Chronic Respiratory Failure symptoms

Chest X Ray

Images shown below are courtesy of RadsWiki

• 
• 

Treatment

Although COPD is not curable, it can be controlled in a variety of ways. Clinical practice guidelines by Global Initiative for Chronic Obstructive Lung Disease (GOLD), a collaboration including the American National Heart, Lung, and Blood Institute and the World Health Organization, are available.

Smoking cessation

Main article: Smoking cessation

Smoking cessation is one of the most important factors in slowing down the progression of COPD. Even at a late stage of the disease it can reduce the rate of deterioration and prolong the time taken for disability and death.

Occupational change

Workers may be able to transfer to a significantly less contaminated area of the company depending on circumstances. Often however, workers may need complete occupational change.

Pharmacotherapy

Bronchodilators

There are several types of bronchodilators used clinically with varying efficacy: β₂ agonists, M₃ antimuscarinics, leukotriene antagonists, cromones and xanthines. These drugs relax the smooth muscles of the airway allowing for improved airflow. The change in FEV₁ may not be substantial, but changes in the vital capacity are significant. Many patients feel less breathless after taking bronchodilators.

β₂ agonists

There are several highly specific β₂ agonists available. Salbutamol (Ventolin) is the most widely used short acting β₂ agonist to provide rapid relief and should be prescribed as a front line therapy for all classes of patients. Other β₂ agonists are Bambuterol, Clenbuterol, Fenoterol, and Formoterol. Longer acting β₂ agonists such as Salmeterol act too slowly to be used as relief for dypsnea so these drugs should be used as a secondary therapy. An increased risk is associated with long acting β₂ agonists due to decreased sensitivity to inflammation so generally the use of a concomitant corticosteroid is indicated[5][6][7].

M₃ muscarinic antagonists (anticholinergics)

Derived from the deadly agaric Amanita muscaria, specific antimuscarinics were found to provide effective relief to COPD. Inhaled antimuscarinics have the advantage of avoiding endocrine and exocrine M₃ receptors. The quaternary M₃ muscarinic antagonist Ipratropium is widely prescribed with the β₂ agonist salbutamol. [8]. Ipratropium is offered combined with salbutamol (Combivent) and with fenoterol (Duovent). Tiotropium provides improved specificity for M₃ muscarinic receptors.

Cromones

Cromones are mast cell stabilizers that are thought to act on a chloride channel found on mast cells that help reduce the production of histamine and other inflammatory factors. Chromones are also thought to act on IgE-regulated calcium channels on mast cells. Cromoglicate and Nedocromil, which has a longer half-life, are two chromones available.

Leukotriene antagonists

More recently leukotriene antagonists block the signalling molecules used by the immune system. Montelukast, Pranlukast, Zafirlukast are some of the leukotrienes antagonists.

Xanthines

Theophylline is the prototype of the xanthine class of drug. Teas are natural sources of methylxanthines, xanthines and caffeine while chocolate is a source of theobromine. Caffeine is approximately 16% metabolized into theophylline. Nebulized theophylline is used in the EMR for treatment of dyspnea (Difficulty in breathing). Patients need continual monitoring as theophylline has a narrow therapeutic range. More aggressive EMR interventions include IV H₁ antihistamines and IV dexamethasone.

Corticosteroids

Inhaled corticosteriods (specifically glucocorticoids) act in the inflammatory cascade and may improve airway function considerably, however the long term value has not been proven. Corticosteroids are often combined with bronchodilators in a single inhaler. Some of the more common inhaled steroids in use are beclomethasone, mometasone, and fluticasone.

Salmeterol and fluticasone are combined (Advair), however the reduction in death from all causes among patients with COPD in the combination therapy group did not reach the predetermined level of statistical significance.

TNF antagonists

Tumor necrosis factor antagonists (TNF) are the most recent class of medications designed to deal with refractory cases. Tumor necrosis factor-alpha is a cachexin or cachectin and is considered a so-called biological drug. They are considerered immunosopressive with attendant risks. These rather expensive drugs include infliximab, adalimumab and etanercept.

Supplemental Oxygen

In general, long-term administration of oxygen is usually reserved for individuals with COPD who have arterial hypoxemia (PaO2 less than 55 mm Hg), or a PaO2 between 55 and 60 mm Hg with evidence of pulmonary hypertension, cor pulmonale, or secondary erythrocytosis (hematocrit >55%). In these patients, continuous home oxygen therapy (for >15 h/d) sufficient to correct hypoxemia has been shown to improve survival.

Vaccination

Patients with COPD should be routinely vaccinated against influenza, pneumococcus and other diseases to prevent illness and the possibility of death.

Pulmonary rehabilitation

Pulmonary rehabilitation is a program of disease management, counseling and exercise coordinated to benefit the individual. Pulmonary rehabilitation has been shown to relieve difficulties breathing and fatigue. It has also been shown to improve the sense of control a patient has over their disease as well as their emotions.

Diet

A recent French study conducted over 12 years with almost 43,000 men concluded that eating a Mediterranean diet "halves the risk of serious lung disease like emphysema and bronchitis". [9]

Prognosis

A good prognosis of COPD relies on an early diagnosis and prompt treatment. Most patients will have improvement in lung function once treatment is started, however eventually signs and symptoms will worsen as COPD progresses. The median survival is about 10 years if two-thirds of expected lung function was lost by diagnosis.

Bronchitis

Acute bronchitis usually resolves in 7-10 days with no underlying lung disease. Chronic bronchitis however is dependent on early recognition and smoking cessation which improves the outcome significantly.

Emphysema

The outcome is better for patients with less damage to the lung who stop smoking immediately. Still, patients with extensive lung damage may live for many years so predicting prognosis is difficult. Death may occur from respiratory failure, pneumonia, or other complications.

Asbestosis

The outcome is clouded by the many complications associated with asbestosis. Malignant mesothelioma is refractory to management affording patients with 6-12 months of life expectancy upon clinical presentation.

Pneumoconiosis

The outcome is good for patients with minimal damage to the lung. However, patients with extensive lung damage may live for many years so predicting prognosis is difficult. Death may occur from respiratory failure, pneumonia, cor pulmonale or other complications.

Pulmonary neoplasms

The stage of the tumor(s) has a major impact on neoplasm prognosis. Staging is the process of determining tumor size, growth rate, potential metastasis, lymph node involvement, treatment options and prognosis. Two-year prognosis for limited small cell pulmonary neoplasms is twenty percent and for extensive disease five percent. The average life expectancy for someone with recurrent small cell pulmonary neoplasms is two to three months.[10]

The 5-year overall survival rate for pulmonary neoplasms is 14%.

External links

• National Heart, Lung and Blood Institute - COPD U.S. NHLBI Information for Patients and the Public page.

Acknowledgements

The content on this page was first contributed by: C. Michael Gibson, M.S., M.D.

Template:WikiDoc Sources