Chronic Obstructive Pulmonary Disease (COPD) (cont.)
What is chronic asthma?
Asthma, like chronic bronchitis, is a disease of the
airways. Obstruction to the flow of air is due to inflammation of the airways as
well as spasm of
muscles surrounding the airways in asthma. The narrowing that results from spasm
of the muscles is called bronchospasm. Generally, bronchospasm in asthma is
reversible and subsides spontaneously or with the use of bronchodilators
(medications that relax the muscles surrounding the airways). We now know that a
major component of asthma is inflammation of the airways, and this inflammation
causes thickening of the walls of the airways. In many asthmatics,
anti-inflammatory medications such as inhaled steroids are required to reduce
this inflammation. In long standing asthma, this chronic inflammation can lead
to scarring and fixed airway obstruction. For more, please read the
Asthma article.
What is bronchiectasis?
Bronchiectasis is another abnormality that can be found
in patients with COPD. In bronchiectasis, serious and repeated infections of the
lung as well as abnormal development of the lung results in permanent damage to
the airways. The damaged airways become enlarged tubes or, in more severe cases, large sacs.
These segments of lung can impair clearance of secretions. The damaged,
mucus-filled airways often become infected, resulting in further inflammation
and damage to the airways. Patients with bronchiectasis often have a vigorous
cough producing large amounts of infected mucus.
What causes COPD?
Smoking is responsible for 90% of COPD in the United
States. Although not all cigarette smokers will develop COPD, it is estimated
that 15% will. Smokers with COPD have higher death rates than nonsmokers with
COPD. They also have more frequent respiratory symptoms (coughing, shortness of breath, etc.) and more
deterioration in lung function than non-smokers.
Effects of passive smoking or "second-hand smoke" on the lungs are not
well-known; however, evidence suggests that respiratory infections, asthma, and
symptoms are more common in children who live in households where adults smoke.
Cigarette smoking damages the lungs in many ways. For example, the irritating
effect of cigarette smoke attracts cells to the lungs that promote inflammation.
Cigarette smoke also stimulates these inflammatory cells to release elastase, an
enzyme that breaks down the elastic fibers in lung tissue.
Air pollution can cause problems for persons with lung disease, but it is
unclear whether outdoor air pollution contributes to the development of COPD.
However, in the non-industrialized world, the most common cause of COPD is
indoor air pollution. This is usually due to indoor stoves used for cooking.
Some occupational pollutants such as cadmium and silica do increase the
risk of COPD. Persons at risk for this type of occupational pollution include
coal miners, construction workers, metal workers, cotton workers, etc. (Most of
this risk is associated with cigarette smoking and these occupations, an issue
not well controlled for. These occupations are more often associated with
interstitial lung diseases, especially the pneumoconioses) Nevertheless, the
adverse effects of smoking cigarettes on lung function are far greater than
occupational exposure.
Another well-established cause of COPD is a deficiency of alpha-1 antitrypsin
(AAT). AAT deficiency is a rare genetic (inherited) disorder that accounts for
less than 1% of the COPD in the United States.
As discussed previously, normal function of the lung is
dependent on elastic fibers surrounding the airways and in the alveolar walls.
Elastic fibers are composed of a protein called elastin. An enzyme called elastase that is found
even in normal lungs (and is increased in cigarette smokers) can break down the
elastin and damage the airways and alveoli. Another protein called alpha-1
antitrypsin (AAT) (produced by the liver and released into the blood) is present
in normal lungs and can block the damaging effects of elastase on elastin.
The manufacture of AAT by the liver is controlled by genes which are
contained in DNA-containing chromosomes that are
inherited. Each person has two AAT genes, one inherited from each parent.
Individuals who inherit two defective AAT genes (one from each parent) have
either low amounts of AAT in the blood or AAT that does not function properly.
The reduced action of AAT in these individuals allows the destruction of tissue
in the lungs by elastase to continue unopposed. This causes emphysema by age 30
or 40. Cigarette smoking accelerates the destruction and results in an even
earlier onset of COPD.
Individuals with one normal and one defective AAT gene
have AAT levels that are lower than normal but higher than individuals with two
defective genes. These individuals MAY have an increased risk of developing COPD
if they do not smoke cigarettes; however, their risk of COPD probably is higher
than normal if they smoke. Though their Alpha-1 antitrypsin blood levels may be
in the normal range, the function of this enzyme is impaired to relative to normals.
Next: What are the symptoms of COPD? »
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