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INTRODUCTION

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Asthma is a common disease characterized by airway inflammation and episodic, reversible bronchospasm with severe shortness of breath. Subsets of clinical asthma may reflect different pathogenic factors and different responsiveness to currently available therapies. Drugs useful in classic allergic 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 anti-IgE antibodies. Leukotriene antagonists play a dual role. Chronic obstructive pulmonary disease (COPD) is characterized by airflow limitation that is less reversible than in asthma and usually follows a progressive course. However, many of the drugs used in asthma are also effective in COPD.

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High-Yield Terms to Learn
Bronchial hyperreactivity Pathologic increase in the bronchoconstrictor response to antigens and irritants; caused by bronchial inflammation
IgE-mediated disease Disease caused by excessive or misdirected immune response mediated by IgE antibodies. Example: asthma
Mast cell degranulation Exocytosis of granules (vesicles) from mast cells with release of mediators of inflammation and bronchoconstriction
Phosphodiesterase (PDE) Family of enzymes that degrade cyclic nucleotides to nucleotides, for example, second messenger cAMP (active) converted to AMP (inactive) or cGMP to GMP
Tachyphylaxis Rapid loss of responsiveness to a stimulus (eg, a bronchodilator drug)

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PATHOPHYSIOLOGY OF ASTHMA AND COPD

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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, tryptase, histamine, and prostaglandin D2. These substances bring about the “early response” consisting of bronchoconstriction and increased secretions. In addition, chemotactic mediators such as LTB4 attract inflammatory cells to the airways and several cytokines, and some enzymes are released, resulting in the “late response” leading to 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.

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FIGURE 20–1

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 WM: Cholinergic pharmacology in asthma. In: Asthma: Physiology, Immunopharmacology, and Treatment. Austen KF, Lichtenstein LM, editors. Academic Press, 1974. Copyright Elsevier.

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COPD is characterized by some degree of ...

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