Cardinal features of Asthma
is one of the most common precipitants of acute episodes of asthma. This stimulus
differs from other naturally occurring provocations such as antigen or viral infections
in that it does not evoke any long-term sequelae nor does it change airway reactivity.
When such patients are followed for sufficient periods of time, they often develop recurring episodes of airway obstruction independent of exercise, thus the onset of this problem frequently can serve as the first manifestation of the full-blown asthmatic syndrome.
There is a significant interaction among the ventilation achieved by the exercise task, the temperature among the ventilation achieved by the exercise task, the temperature, and water content of the inspired air and the magnitude of the postexertional obstruction.
Thus, for the same inspired air conditions, running will produce a more severe attack of asthma than will walking. Conversely, for a given task, the inhalation of cold air during its performance will markedly enhance the response, while warm, humid air will blunt or abolish it.
Consequently, activities such as ice hockey, cross-country skiing, or ice-skating are more provocative than is swimming in an indoor heated pool.
The mechanism by which exercise produces obstruction may be related to a thermally produced hyperemia and engorgement of the microvasculature of the bronchial wall and does not appear to involve smooth muscle contraction.
Abundant objective data exist which demonstrate that psychological factors can interact with the asthmatic diathesis to worsen or ameliorate the disease process.
The pathways and nature of the interactions are complex but have been shown to be operational to some extent in almost half the patients studied. Changes in airway caliber seem to be mediated through modification of vagal efferent activity, but endorphins also may play a role.
The most frequently studied variable has been that of suggestion, and the weight of current evidence is that it can be quite an important influence in selected asthmatics.
When physically responsive individuals are given the appropriate suggestion, they can actually decrease or increase the pharmacologic effects of adrenergic and cholinergic stimuli on their airways.
The extent to which psychological factors participate in the induction and / or continuation of any given acute exacerbation is unknown but probably varies from patient to patient and in the same patient from episode to episode.
Respiratory infections are the most common of the stimuli that evoke acute exacerbations of asthma. Well-controlled investigations have demonstrated that respiratory viruses and not bacteria or allergy are the major etiologic factors.
In young children, the most infectious agents are respiratory syncytal virus and parainfluenza virus. In older children and adults, rhinovirus and influenza virus predominate as pathogens.
Simple colonization of the trachebronchial tree is insufficient to evoke acute episodes of the bronchospasm, and attacks of asthma occur only when symptoms of an ongoing respiratory tract infection are, or have been, present.
The mechanism by which viruses induce asthma is unknown, but it is probably that the resulting inflammatory changes in the airway mucosa alter host defenses and make the tracheobronchial tree more susceptible to exogenous stimuli.
Supporting evidence for this concept is derived from the fact that the airway responsiveness of even normal (no asthmatic) subjects to nonspecific stimuli.
Supporting evidence for this concept is derived from the fact that the airway responsiveness of even normal (no asthmatic) subjects to nonspecific stimuli is transiently increased after a cough and rarely wheezing, can last from 2 8 weeks after the infection in both normal individuals and asthmatics.
With occupational exposures, other than those which given an immediate and dual Immunologic reaction, the patients give a characteristic cyclic history.
They are well when they arrive at work, and symptoms develop toward the end of the shift, progress after leaving the work site, and then regress.
from work during weekends or vacation periods brings about a remission. Frequently,
there are similar symptoms in fellow employees. Work related irritant substances,
in still other cases, directly or reflexly stimulate the airways of either latent
or frank asthmatics.
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