Chronic Obstructive Pulmonary Disease (COPD)

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Questions to Ask Your Doctor about COPD
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Causes

Smoking tobacco causes 80% to 90% of COPD cases. An agent in tobacco smoke stimulates inflammation in the lungs, leading to destruction of the alveoli and narrowing of the airways. While smoking is related to most cases of emphysema, only 15% to 20% of smokers develop the disease. What other factors contribute to the development of "smokers emphysema" remains unclear.

Familial emphysema, or alpha1-antitrypsin (AAT) deficiency-related emphysema, is caused by the hereditary deficiency of a protein called alpha1-antitrypsin. This deficiency leads to uncontrolled destruction of the alveoli and emphysema. Occupational exposure to dust, fumes, and gases appears to contribute slightly to lung function decline and chronic bronchitis. The role of air pollution in COPD remains controversial.

Emphysema
In the lung there are millions of tiny, thin-walled, elastic air sacs called alveoli (see Anatomy of the Respiratory System). These tiny sacs perform the crucial task of replenishing the blood with oxygen (via inhalation) and ridding the body of carbon dioxide (CO2) in exhalation.

Emphysema is the enlargement of the alveoli accompanied by destruction of their walls. In "smokers emphysema" an agent in cigarette smoke sets off a self-perpetuating, low-grade inflammation that causes the release of enzymes (elastase) from inflammatory cells that break down collagen and elastin — substances that maintain the structure and elasticity of alveoli — in the alveolar walls. The NHLBI (National Heart, Lung and Blood Institute) reports that this creates an imbalance between the elastin-degrading enzymes and their inhibitors. They also found that oxidants in cigarette smoke inactivate a significant number of elastase inhibitors, thereby decreasing the amount of active antielastase available to protect the lung and further upsetting the elastase-antielastase balance.

This disruption of the alveolar walls and elastin leads to a decrease in the elastic recoil of the lungs, limiting the ability of the alveoli to passively shrink and to exhale. This accounts for the main limitation to exhalation seen in severe COPD. The disruption of the alveolar walls also leads to their increase in size, making the lungs larger and placing the chest at a mechanical disadvantage. Disruption of the alveolar walls also makes exchange of oxygen from the alveoli to the capillaries and carbon dioxide from the capillaries to the alveoli more difficult. Collapse of the bronchial walls occurs when the cartilage in the bronchial walls has been weakened.

Familial emphysema
People with familial emphysema have a hereditary deficiency of alpha-1-protease inhibitor, also called alpha1-antitrypsin (AAT). When there is a genetic deficiency of AAT, the activity of elastase—an enzyme that breaks down elastin—is not inhibited and elastin degradation occurs unchecked. Individuals with a severe genetic deficiency of AAT usually have symptoms by the time they reach early middle age. It is critical that people with this deficiency never smoke.

Destruction of alveolar walls, capillaries, and attachments between alveoli and bronchioles causes (1) susceptibility of airways to compression and collapse, impeding airflow out of the lungs; (2) entrapment of air in the alveoli; (3) poor air-gas exchange, that is, reduced ability to inhale oxygen and exhale carbon dioxide (CO2), resulting in increased levels of CO2 in the blood; (4) the development of bullae (areas of lung extensively destroyed so that they become large dilated air sacs); and (5) enlarged lungs.

Chronic Bronchitis
Chronic bronchitis is the presence of cough productive of sputum for 3 months per year, in 2 consecutive years. In chronic bronchitis, tobacco smoke causes inflammatory cells (neutrophils and leukocytes) to arrive in the bronchi. These cells worsen airway obstruction by causing inflammation and thickening of the airways. Also, mucus-producing glands deep within the lining of the airways become enlarged (hypertrophy) and increase in number (hyperplasia), and the number of surface cells that produce mucus (goblet cells) increases, resulting in excessive secretion of mucus in the lungs. The resulting chronic cough and expectoration affects the central conducting airway (see Anatomy of the Respiratory System).

The function of mucus in the lungs is to trap and clear particles, to dilute harmful substances, to lubricate the airways, and to humidify inspired air. In chronic bronchitis, (1) the hyperplasia and hypertrophy of the submucosal glands (mucus-producing glands deep within bronchial walls) thicken the airway walls; (2) the resulting increased volume of mucus that occurs plugs the airways; (3) columnar cells (cells that line the surface of the airways) undergo changes that result in the destruction of cilia — delicate hairlike structures on columnar cells lining the airways that sweep mucus with offending agents up and out of the lungs. The loss of cilia and the inability to clear bacteria predispose the patient to lung infections.

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