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Should resting values be abnormal, then asthma, or some other chronic lung condition, is present. There is, of course, no reason why asthma and exercise-induced bronchoconstriction should not co-exist but the distinction is important because without successful treatment of underlying asthma, treatment of an exercise component will likely be ...
It is also preferred due to the former term giving the false impression that asthma is caused by exercise. In a patient with EIB, exercise initially follows the normal patterns of bronchodilation. However, by three minutes, the constriction sets in, which peaks at around 10–15 minutes, and usually resolves itself by an hour.
Additionally, the pediatric population is more susceptible to disease and complications from bronchospasm due to their airway diameter being smaller; applying Poiseuille's Law to the airways it is clear that airflow resistance through a tube is inversely related to the radius of the tube to the fourth power, therefore, decreases in airway ...
Sensitizer-induced occupational asthma is an immunologic form of asthma which occurs due to inhalation of specific substances (i.e., high-molecular-weight proteins from plants and animal origins, or low-molecular-weight agents that include chemicals, metals and wood dusts) and occurs after a latency period of several weeks to years.
Acute severe asthma, also known as status asthmaticus, is an acute exacerbation of asthma that does not respond to standard treatments of bronchodilators (inhalers) and corticosteroids. [2] Asthma is caused by multiple genes , some having protective effect, with each gene having its own tendency to be influenced by the environment although a ...
Bronchial hyperresponsiveness is a hallmark of asthma but also occurs frequently in people with chronic obstructive pulmonary disease (COPD). [2] In the Lung Health Study, bronchial hyperresponsiveness was present in approximately two-thirds of patients with non-severe COPD, and this predicted lung function decline independently of other ...
While the acronyms are similar, reactive airway disease (RAD) and reactive airways dysfunction syndrome (RADS) are not the same. [1]Reactive airways dysfunction syndrome was first identified by Stuart M. Brooks and colleagues in 1985 as an asthma-like syndrome developing after a single exposure to high levels of an irritating vapor, fume, or smoke.
The 2005 Oxford Textbook of Medicine distinguishes type 1 brittle asthma by "persistent daily chaotic variability in peak flow (usually greater than 40 per cent diurnal variation in PEFR more than 50 per cent of the time)", while type 2 is identified by "sporadic sudden falls in PEFR against a background of usually well-controlled asthma with normal or near normal lung function". [8]