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  • • Cough, shortness of breath, wheezing, and chest discomfort, often in association with triggering factors.
  • • Wheezing, diminished breath sounds, hyperinflated lung fields, hyperresonance to percussion; examination can be normal.
  • • Variable degrees of airflow limitation, improvement in airflow following bronchodilator therapy, airtrapping, and airways hyperresponsiveness.

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Asthma is a chronic inflammatory condition of the lungs. It has no known distinct etiology, and there are many different clinical manifestations, making asthma a syndrome rather than a specific disease. Asthma affects approximately 7% of the U.S. population, both adults and children, resulting in 17 million people with asthma in the United States, and over 100 million worldwide. The socioeconomic burden of asthma is high, with over 11 billion dollars spent in total costs in 1998, including billions of dollars in indirect costs from lost productivity. The prevalence of asthma is increasing worldwide, having risen approximately 75% over the years 1980–1994 in the United States. The reasons for this increase are likely due, in part, to increased exposure of susceptible individuals to indoor air pollutants or allergens, and perhaps also to a changing microbiological environment that impacts immune system development. The National Institutes of Health (NIH) and World Health Organization (WHO) have issued disease management guidelines to assist in the consistent diagnosis and treatment of asthma, but dissemination of these guidelines to the medical community is incomplete.

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The inflammation involved in asthma extends throughout the respiratory tree (Figure 6–1). The clinical manifestations of asthma are a consequence of the effects of this inflammation on the airways and surrounding lung parenchyma, resulting in airway narrowing, airflow limitation, and alterations in lung mechanics.

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Figure 6–1.
Graphic Jump Location

Overview of asthma pathophysiology. A: Biology. The biology of asthma involves the release of mediators, cytokines, and other signals from activated inflammatory cells, resulting in airway smooth muscle constriction, pulmonary vascular dilation and leakage, and mucous gland secretion. Over time, these processes result in airway remodeling. Macs, macrophages; eos, eosinophils; pmns, polymorphonuclear leukocytes; lymphs, lymphocytes; TH1, TH2, T-helper cell type 1, 2. See text for details. B: Anatomy. Airway remodeling is seen by airway wall thickening from inflammatory cell infiltration, airway edema, increased mucus secretion, subepithelial fibrosis and increased smooth muscle mass. In addition, there may be a loss of the linkage between the airway wall and surrounding tethering elements of the alveoli. C: Physiology. The physiological effects of the narrowed, thickened airways are airflow limitation and gas trapping, resulting in hyperinflation. D: Symptoms. The symptoms arising from these underlying pathophysiological changes include wheezing, cough, dyspnea, and chest discomfort.

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Many patients with asthma exhibit a two-phase response when exposed to allergen, and this response pattern serves as a useful paradigm to characterize the inflammatory events that are thought to occur. Initially, upon exposure to a sensitizing stimulus in a susceptible individual, mast cells and epithelial cells within the airway are activated ...

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