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Asthma is a disease characterized by airway inflammation and episodic, reversible bronchospasm. Drugs useful in asthma include bronchodilators (smooth muscle relaxants) and anti-inflammatory drugs. Bronchodilators include sympathomimetics, especially β2-selective agonists, muscarinic antagonists, methylxanthines, and leukotriene receptor blockers. Anti-inflammatory drugs used in asthma include corticosteroids, mast cell stabilizers, and an anti-IgE antibody. Leukotriene antagonists play a dual role. Chronic obstructive pulmonary disease (COPD) is characterized by airflow limitation that is less reversible than in asthma and by a progressive course. However, many of the same drugs are used.

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Bronchial hyperreactivityPathologic increase in the bronchoconstrictor response to antigens and irritants; caused by bronchial inflammation
IgE-mediated diseaseDisease caused by excessive or misdirected immune response mediated by IgE antibodies. Example: asthma
Mast cell degranulationExocytosis of granules from mast cells with release of mediators of inflammation and bronchoconstriction
Phosphodiesterase (PDE)Family of enzymes that degrade cyclic nucleotides to nucleotides, for example, cAMP (active) to AMP (inactive); various isoforms, some degrade cGMP to GMP
TachyphylaxisRapid loss of responsiveness to a stimulus (eg, a drug)
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The immediate cause of asthmatic bronchoconstriction is the release of several mediators from IgE-sensitized mast cells and other cells involved in immunologic responses (Figure 20–1). These mediators include the leukotrienes LTC4 and LTD4. In addition, chemotactic mediators such as LTB4 attract inflammatory cells to the airways. Finally, several cytokines and some enzymes are released, leading to chronic inflammation. Chronic inflammation leads to marked bronchial hyperreactivity to various inhaled substances, including antigens, histamine, muscarinic agonists, and irritants such as sulfur dioxide (SO2) and cold air. This reactivity is partially mediated by vagal reflexes. COPD is often triggered by upper respiratory infection (like asthma) but occurs in older patients (usually long-term smokers) and is poorly reversible with bronchodilators.

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Figure 20–1
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Immunologic model for the pathogenesis of asthma. Exposure to antigen causes synthesis of IgE, which binds to and sensitizes mast cells and other inflammatory cells. When such sensitized cells are challenged with antigen, a variety of mediators are released that can account for most of the signs of the early bronchoconstrictor response in asthma. LTC4, D4, leukotrienes C4 and D4; ECF-A, eosinophil chemotactic factor-A; PGD2, prostaglandin D2. (Modified and reproduced, with permission, from Gold WW: Cholinergic pharmacology in asthma. In: Asthma Physiology, Immunopharmacology, and Treatment. Austen KF, Lichtenstein LM, editors. Academic Press, 1974.)

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Acute bronchospasm must be treated promptly and effectively with bronchodilators ("reliever" drugs). Beta2 agonists, muscarinic antagonists, and theophylline and its derivatives are available for this indication. Long-term preventive treatment requires control of the inflammatory process in the airways ("controller" drugs). The most important anti-inflammatory drugs in the treatment of chronic asthma are the ...

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