The pathophysiologic hallmark of asthma is a reduction in airway diameter caused by smooth muscle contraction, vascular congestion, bronchial wall edema, and thick secretions. These changes are reflected in pulmonary function changes, increased work of breathing, and abnormal distribution of pulmonary blood flow ( Table... 6.4-1). Both large and small airways often contain plugs composed of mucus, serum proteins, inflammatory cells, and cellular debris. On a microscopic level, airways are infiltrated with eosinophils and mononuclear cells. Evidence of microvascular leakage, epithelial disruption, and vasodilation is frequently noted. The airway smooth muscle is hypertrophied and characterized by new vessel formation, an increased number of epithelial goblets cells, and deposition of interstitial collagen beneath the epithelium.7 Subepithelial fibrosis, an increase in the thickness of the reticular layer of the basement membrane, is characteristically increased in both the large and small airways.7 Recent data collected from transbronchial biopsy, alveolar lavage, and specialized airway imaging techniques suggest that inflammation affects all bronchial pulmonary structures.8
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If you suffer with asthma, you will no doubt be familiar with the uncomfortable sensations as your bronchial tubes begin to narrow and your muscles around them start to tighten. A sticky mucus known as phlegm begins to produce and increase within your bronchial tubes and you begin to wheeze, cough and struggle to breathe.