Asthma is characterized by spastic contraction of the smooth muscle in the bronchioles, which partially obstructs the bronchioles and causes extremely diffi-cult breathing. It occurs in 3 to 5 per cent of all people at some time in life.
The usual cause of asthma is contractile hypersensi-tivity of the bronchioles in response to foreign sub-stances in the air. In about 70 per cent of patients younger than age 30 years, the asthma is caused by allergic hypersensitivity, especially sensitivity to plant pollens. In older people, the cause is almost always hypersensitivity to nonallergenic types of irritants in the air, such as irritants in smog.
The allergic reaction that occurs in the allergic type of asthma is believed to occur in the following way:The typical allergic person has a tendency to form abnor-mally large amounts of IgE antibodies, and these anti-bodies cause allergic reactions when they react with the specific antigens that have caused them to develop in the first place. In asthma, these antibodies are mainly attached to mast cells that are present in the lung interstitium in close association with the bronchioles and small bronchi. When the asth-matic person breathes in pollen to which he or she is sensitive (that is, to which the person has developed IgE antibodies), the pollen reacts with the mast cell– attached antibodies and causes the mast cells to release several different substances. Among them are (a) histamine, (b) slow-reacting substance of anaphylaxis (which is a mixture of leukotrienes), (c) eosinophilicchemotactic factor, and (d) bradykinin. The combinedeffects of all these factors, especially the slow-reacting substance of anaphylaxis, are to produce (1) localized edema in the walls of the small bronchioles, as well as secretion of thick mucus into the bronchiolar lumens, and (2) spasm of the bronchiolar smooth muscle. Therefore, the airway resistance increases greatly.
As discussed earlier, the bronchiolar diameter becomes more reduced during expiration than during inspiration in asthma, caused by bronchi-olar collapse during expiratory effort that compresses the outsides of the bronchioles. Because the bronchi-oles of the asthmatic lungs are already partially occluded, further occlusion resulting from the external pressure creates especially severe obstruction during expiration. That is, the asthmatic person often can inspire quite adequately but has great difficulty expir-ing. Clinical measurements show (1) greatly reduced maximum expiratory rate and (2) reduced timed expi-ratory volume. Also, all of this together results in dyspnea, or “air hunger,” which is discussed later.
The functional residual capacity and residual volume of the lung become especially increased during the acute asthmatic attack because of the difficulty in expiring air from the lungs. Also, over a period of years, the chest cage becomes permanently enlarged, causing a “barrel chest,” and both the functional resid-ual capacity and lung residual volume become perma-nently increased.
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