Chronic obstructive pulmonary disease

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(Redirected from Chronic Obstructive Pulmonary Disease)

Chronic obstructive pulmonary disease (COPD) is an umbrella term for a group of respiratory tract diseases that are characterized by airflow obstruction or limitation. It is usually caused by tobacco smoking but can also be caused by coal dust.

Conditions included in this umbrella term are:

1 Other names
2 Working definition
3 Causes
4 Progression
5 Acute exacerbations
6 Diagnosis
7 Management
8 References

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Other names

COPD is also known as CORD, COAD, COLD which respectively stand for chronic obstructive respiratory, airways, or lung disease. COPD has been referred to as CAL which stands for chronic airway limitation.

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Working definition

COPD is a chronic, progressive disorder related to tobacco abuse and characterized by airway obstruction (FEV1 <80% predicted and FEV1 / FVC ratio <70%).

The Global Initiative for Chronic Obstructive Lung Disease (GOLD) defines COPD as "a disease state characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and associated with abnormal inflammatory response of the lungs to noxious particles or gases."

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Causes

The main risk factor in the development of COPD is smoking. Approximately 15% of all chronic smokers will develop the disease. In susceptible people, this causes chronic inflammation of the bronchi and eventual airway obstruction. Other etiologies include alpha 1-antitrypsin deficiency (augmented by smoking), byssinosis, and idiopathic disease.

COPD can also be caused by prolonged exposure to certain dusty environments. For example, many people develop COPD after working in the coal mining industry and being exposed to high levels of respirable coal dust.

Among people over 70 who have never smoked, women make up 85 percent of those with COPD. This appears to be tied to decreases in estrogen as women age. Female mice that had their ovaries removed to deprive them of estrogen lost 45 percent of their working alveoli from their lungs. Upon receiving estrogen, the mice recovered full lung function. Two proteins that are activated by estrogen play distinct roles in breathing. One protein builds new alveoli, the other stimulates the alveoli to expel carbon dioxide. Loss of estrogen hampered both functions in the test mice. (Massaro & Massaro, 2004).

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Progression

COPD is a progressive disease. Obstructive changes in spirometry and decreases in diffusion capacity are typically seen before symptoms occur. Early signs and symptoms are shortness of breath on exertion, recurrent respiratory infections or a morning cough. As the disease continues, the symptoms are seen with increased frequency and severity. In the late stages, the patient often experiences severe cough, constant wheezing, and shortness of breath with minimal exertion or rest. At this late stage, progression to respiratory failure and death is common. Progression is typically caused by the patient's continued exposure to tobacco smoke. Although medications often decrease symptoms, it is not believed that they prevent the progression if the patient continues to smoke.

Early data has suggested that the drug tiotropium may slow the progression of the disease. A multicenter randomized controlled trial is currently underway to determine whether this is in fact true.

The Global Initiative for Chronic Obstructive Lung Disease has characterized the stages of COPD as follows:

0: At risk (normal spirometry, chronic symptoms such as cough or sputum expectoration)
I: Mild(FEV₁/FVC < 70%; FEV₁ < 80% predicted, with or without chronic symptoms (cough, sputum)
II: Moderate (FEV₁/FVC < 70%; 50% < FEV₁ < 80% predicted, with or without chronic symptoms such as cough, sputum, dyspnea)
III: Severe (FEV₁/FVC < 70%; 30% < FEV₁ < 50% predicted, with or without chronic symptoms such as cough, sputum, dyspnea)
IV: Very severe (FEV₁/FVC < 70%; FEV₁ < 30% predicted or FEV₁ < 50% predicted plus chronic [respiratory failure])

It should be noted that in severe and very severe COPD not only FEV1 and the FEV1/FVC ratio decrease but also FVC.

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Acute exacerbations

COPD is also characterized by exacerbations which typically present with a rapid progression of the chronic symptoms. Classically, an exacerbation is notable by increased shortness of breath, wheezing, and sputum production. Hypoxia is common as well. Exacerbations are most commonly brought on by infectious agents. Bronchodilators, antibiotics, and oral or intravenous steroids are used to treat these episodes. Exacerbations can lead to respiratory failure; if this occurs, a patient is treated with noninvasive positive pressure ventilation or standard mechanical ventilation until the lung function improves.

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Diagnosis

The diagnosis of COPD is usually suggested by symptoms; it is a clinical diagnosis and no one test is definitive. A comprehensive history from the patient, physical examination, and confirmation of airflow obstruction using spirometry are all vital in establishing the diagnosis.

The FEV₁/FVC ratio is decreased with COPD, meaning a person can not force out as much air as predicted from their lungs in one second. (Normally someone can expire about 80% of their vital capacity in one second; however, this is typically reduced in COPD). With this condition there may be air-trapping as documented by an increased residual volume (the amount of air left in the lungs after a full breath out), or hyperinflation as documented by an increased total lung capacity (the amount of air in the lungs after a full inhalation).

Reversibility testing is a technique used to evaluate the bronchoconstriction component of COPD. It is done by lung function testing before and after administration of a bronchodilator drug such as a beta-agonist.

The inflammatory component of the disease can be modified with the use of steroid drugs (usually administered by inhalation in order to avoid any systemic effect) but several weeks of treatment must be given before the effect can be evaluated.

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Management

COPD is not curable. Medicines are often used to control symptoms or to reverse acute exacerbations. COPD in all forms typically progresses if the patient continues to smoke. Therefore, smoking cessation is one of the most important factors in slowing down the progression of COPD.

The use of bronchodilators, nebulisers and corticosteroids has been shown to be effective. Patients with chronic disease and significant lung function impairment (FEV₁ < 50% predicted) may also benefit from the regular use of inhaled steroids. Oxygen therapy is the only current medical intervention that is proven to prolong the lives of patients with this disease process. Oxygen is only indicated in patients with severe hypoxia documented by a physician. Oxygen should be administered with caution to patients with COPD due to a risk of carbon dioxide retention.

Surgical management includes single or double lung transplant, and lung volume reduction surgery (LVRS), which is currently being evaluated in a large, national trial in the UK.

Many patients with COPD should be considered for pulmonary rehabilitation. The American Thoracic Society Consensus is an excellent reference.

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