| Chronic obstructive pulmonary disease (COPD) occurs when the flow of air through the lungs is restricted due to underlying chronic bronchitis and/or emphysema. COPD due to chronic bronchitis is characterized by enlarged, inflamed mucus glands that block the airways (bronchioles) with excessive mucus, resulting in a frequent, productive cough. COPD secondary to emphysema is caused by damaged lung capillaries and the destruction of air sacs (lung alveoli) where oxygen exchange occurs, resulting in shortness of breath and an infrequent, nonproductive cough. Since chronic bronchitis and emphysema often occur together and overlap, some experts prefer the name chronic obstructive pulmonary disease (COPD) rather than either chronic bronchitis or emphysema. Asthma, although not considered a true form of COPD, is another obstructive pulmonary disease in which chronically inflamed airways become sensitized to certain triggers (pollution, smoke, stress, exertion, allergens), temporarily blocking air flow. However, unlike COPD, inflammation and muscle spasms (bronchospasm) that occur with asthma are reversible.
Airway obstruction from COPD is generally permanent and progressive. Due to the similarity of COPD and asthma symptoms, certain individuals with COPD may be able to partially reverse airway obstruction with medication that enlarges constricted airways (bronchodilators), similar to that used by asthmatics. Conversely, those with asthma may develop true COPD if repeated airway inflammation leads to scarring and permanent airway constriction.
Although the most common cause of COPD is smoking, another well-established cause of COPD is the deficiency of a liver protein called alpha-1 antitrypsin (AAT). AAT deficiency is an inherited disorder that accounts for less than 5% of COPD in the US ("Chronic"). Normal lung function is dependent on elastic fibers surrounding the airways and within the walls of lung alveoli where gas exchange takes place. These elastic fibers are composed of a protein called elastin. In normal individuals, AAT protects lung elastin from breakdown by the enzyme elastase, which typically functions to digest and remove old or damaged cells from the lung. With AAT deficiency, AAT does not fully release from the liver, which may allow elastase to destroy lung tissues.Risk: The most common cause of COPD is smoking. Smokers experience more frequent respiratory symptoms such as coughing and shortness of breath, and more deterioration in lung function than ex-smokers or nonsmokers. Effects of passive smoking or second-hand smoke on the lungs are not well quantified. Smoking is responsible for 90% of COPD in the US. Although not all cigarette smokers develop COPD, an estimated 15% will. Current smokers with COPD have higher death rates than ex-smokers with COPD. Individuals who smoke are 10 times more likely to die from COPD than nonsmokers ("Chronic").
Air pollution can cause problems for individuals with lung disease, but it is unclear whether air pollution contributes to the development of COPD. Some occupational pollutants such as cadmium and silica do increase the risk of COPD. Individuals at risk for this type of occupational pollution include coal miners, construction workers, metal workers, and cotton workers. Exposure to occupational pollutants is responsible for 19% of COPD cases ("Chronic").
Alpha-1 antitrypsin (AAT) protein deficiency accounts for up to 5% of cases of emphysema in the US, with an onset between the ages of 20 and 40 ("Chronic").
COPD occurs predominantly in individuals older than 40. Older men with a low body mass index (BMI) have increased risk for COPD, and individuals with a high BMI have a lower risk (Harik-Khan). Females have nearly twice the rate of chronic bronchitis than males, with 7.5 million females and 3.7 million males affected ("Chronic"). Conversely, of the affected population, 57% of males compared to 43% of females suffer from emphysema; however, incidence is increasing in women probably in response to the increased incidence of female smokers ("Chronic"). Incidence and Prevalence: Currently, COPD affects at least 32 million Americans with more than 100,000 deaths annually. It is the fourth leading cause of death in the US. Approximately 11 million individuals have chronic bronchitis, 2 million have emphysema and between 50,000 and 100,000 Americans have chronic lung disease due to AAT deficiency ("Chronic"). |
Source: Medical Disability Advisor
| History: Individuals with COPD present with a combination of signs and symptoms of chronic bronchitis, emphysema, and asthma. Symptoms include worsening shortness of breath with exertion (dyspnea), cough, wheezing, and frequent colds. Physical exam: The exam for individuals with emphysema usually reveals a chest resembling the shape of a barrel (barrel chest), rapid and labored breathing, rapid heart rate (tachycardia), and normal skin color. Breath sounds are faint. Individuals with chronic bronchitis have less distressed breathing, but the skin may appear blue. Unique breath sounds with a musical-type pitch indicate secretions or inflammation in the airways (rhonchi). Tests: Chronic obstructive pulmonary disease is specifically diagnosed by pulmonary function tests (PFTs). Simple measurement of air flow (spirometry) can be done in the doctor's office to confirm COPD. The diagnosis, classification of severity, prognosis, and guidance of treatment are determined by a complete PFT done in a standardized PFT laboratory. Blood gas analysis is another indicator of severity of disease. A chest x-ray can also provide information on the severity of COPD. Serum chemistry and a complete blood count (CBC) may also be performed. |
Source: Medical Disability Advisor
| The general treatment goals for COPD are to optimize lung function, slow down or stop disease progression, prevent acute flare-ups and complications, and maintain quality of life. Specific treatment includes smoking cessation, bronchodilators, antibiotics, supplemental oxygen, and occasionally corticosteroids. Certain treatments may be long term and others may be added only during acute episodes. A few individuals may be candidates for surgical removal (wedge resection) of large bubble-like structures (bullae) in the lung, or for lung transplantation.
Most individuals with COPD experience one to two exacerbations per year that require either outpatient medical treatment or hospitalization (Blanchard). |
Source: Medical Disability Advisor
| If smoking is stopped during the early stages of COPD, some of the damaged small airways may return to normal. Individuals with mild COPD treated early may be free of disability. Individuals with severe COPD will continue to have progressively deteriorating lung function despite treatment and usually become permanently disabled.
The individual's age and postbronchodilator forced expiratory volume in 1 second (FEV1) are the most important predictors of prognosis. Young age and FEV1 greater than 50% have a good prognosis. Older individuals and those with more severe lung disease do more poorly. Supplemental oxygen (when indicated) has been shown to increase survival. Smoking cessation improves prognosis. Increase in size (hypertrophy) of the right ventricle in the heart (cor pulmonale), abnormally increased arterial carbon dioxide tension (hypercapnia), rapid heartbeat (tachycardia), and malnutrition indicate a poor prognosis. |
Source: Medical Disability Advisor
| Pulmonary rehabilitation combines exercise training with behavioral and educational programs designed to help individuals with COPD control symptoms and improve day-to-day activities. It is a team approach with individuals working closely with their doctors; nurses; respiratory, physical, and occupational therapists; psychologists; exercise specialists; and dietitians. The main goals of pulmonary rehabilitation are to help individuals improve their day-to-day lives and restore their ability to function independently. Pulmonary rehabilitation can help reduce the number and length of hospital stays and increase the chances of living longer. Pulmonary rehabilitation involves exercise training of the lower body, the upper body, and ventilatory muscle training. It also includes psychosocial support and educational programs.
Since smoking is well known to be the primary risk factor for the onset and progression of COPD, many pulmonary rehabilitation programs provide educational sessions and counseling to help individuals stop smoking. |
Source: Medical Disability Advisor
| The two most serious complications of COPD are right-sided heart failure (cor pulmonale) and respiratory failure. If the impairment is severe enough, the individual may succumb to respiratory failure. Most COPD individuals recover from their first few episodes of respiratory failure. However, increasing frequency of respiratory failure episodes is a sign of the last stages of this chronic disease.
Some COPD individuals develop single or multiple large, irregular-shaped air spaces in the lungs called bullae. These bullae can be large enough to compromise good portions of the lung by crowding and compressing them. They can also break, causing an accumulation of air in the chest cavity (pneumothorax) that further compromises pulmonary function. Increased blood pressure in the lung (pulmonary hypertension) and malnutrition are sometimes complications of COPD.
Decreased bone mineralization and increased fracture risk is linked to COPD, with osteopenia present in 35% to 72% of individuals, and osteoporosis present in 36% to 60% of individuals with COPD. This decrease in bone mass is probably secondary to the use of oral and inhaled corticosteroid therapy (Biskobing). |
Source: Medical Disability Advisor
| Individuals with COPD should avoid inhaled irritants in the workplace such as gases, fumes, and dust. Very cold or hot air temperatures should also be avoided. Work at higher altitudes may be discouraged with moderate or severe COPD. Tolerance for physical exertion may be limited with COPD. If individuals with an asthmatic component to their COPD have an acute attack while working, they should be given time to take inhaled medication and rest, and then be evaluated for ability to continue working. |
Source: Medical Disability Advisor
| If an individual fails to recover within the expected maximum duration period, the reader may wish to consider the following questions to better understand the specifics of an individual's medical case. Regarding diagnosis:
- Does individual have a history of smoking? If so, how much has individual smoked and for how long?
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Was individual exposed to cadmium or silica including occupations such as coal mining, construction work, or metal or cotton work?
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Although rare, does individual have a deficiency of the protein alpha-1 antitrypsin (AAT)?
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Does individual complain of shortness of breath with exertion (dyspnea), progressive exercise limitation, or alteration in mental status? Is there coughing, wheezing, or frequent mucus production?
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Does individual have a barrel-shaped chest?
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Were pulmonary function tests (PFTs) and/or spirometry done? Were arterial blood gases (ABGs), blood chemistry, and a complete blood count (CBC) performed? Was a chest x-ray obtained? What did all test results reveal?
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Was diagnosis of COPD confirmed?
Regarding treatment:
- Has individual completely stopped smoking? If not, was individual urged to participate in a smoking cessation program?
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Has individual participated in a pulmonary rehabilitation program?
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Were bronchodilators, antibiotics, supplemental oxygen, and corticosteroids administered, as needed?
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Is individual compliant with the medication regimen?
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Is individual a candidate for surgical removal (wedge resection) of large bubble-like structures (bullae)?
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Is individual a candidate for lung surgery or transplantation? Would individual benefit from consultation with a specialist (transplant surgeon)?
Regarding prognosis:
- How advanced is the disease?
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Has individual completely stopped smoking? Was smoking stopped and treatment begun during the early stages of COPD?
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Is individual's postbronchodilator forced expiratory volume in 1 second (FEV1) better, worse, or the same?
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Has individual developed right-sided heart failure (cor pulmonale), abnormally increased arterial carbon dioxide tension (hypercapnia), malnutrition, or respiratory failure?
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Is this the first episode of respiratory failure or is it a recurrence, suggesting late stage disease?
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Has pneumothorax occurred, further compromising pulmonary function? How severely is pulmonary function compromised? How will this affect the ability of individual to function?
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Has individual developed increased blood pressure in the lung (pulmonary hypertension)?
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Source: Medical Disability Advisor
| Biskobing, D. M. "COPD and Osteoporosis." Chest 121 2 (2002): 609-620. MD Consult. Elsevier, Inc. 16 Dec. 2004 <http://home.mdconsult.com/das/journal/view/43307764-2/N/12216913?sid=287184853&source=MI>.Blanchard, A. R. "Treatment of Acute Exacerbations of COPD." Clinical Cornerstone 5 1 (2003): 28-36. MD Consult. Elsevier, Inc. 16 Dec. 2004 <http://home.mdconsult.com/das/journal/view/43307764-2/N/13361736?sid=287184853&source=MI>. "Chronic Obstructive Pulmonary Disease (COPD) Fact Sheet." American Lung Association. Oct. 2003. 22 Oct. 2004 <http://www.lungusa.org/site/pp.asp?c=dvLUK9O0E&b=35020>. Harik-Khan, R. I., J. L. Fleg, and R. A. Wise. "Body Mass Index and the Risk of COPD." Chest 121 2 (2002): 370-376. MD Consult. Elsevier, Inc. 16 Dec. 2004 <http://home.mdconsult.com/das/journal/view/43307764-2/N/12216880?sid=287184853&source=MI>. |
Source: Medical Disability Advisor
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