Amy Parsons Case Study Asthma

Amy Parsons’, a 16-year-old female competitive swimmer, chief complaint is periods of severe coughing during the recent summer months. Her cough is described as dry, hacking, and non-productive. It occurs when swimming in the community pool and is accompanied with shortness of breath and wheezing. It was significantly worse last summer after swimming in the lake at her grandmother’s rural house. The cough seems better when in the pool but worse when out. Amy had three episodes of otitis media before she was eighteen months old, four upper respiratory infections between ages two and ten, and currently gets four to five colds per year. Amy had eczema as a child. Her vital signs are within defined limits and her peak expiratory flow rates are

Asthma is diagnosed with a history, physical exam, laboratory findings, and pulmonary function studies. The strongest risk factor for developing asthma is a genetic predisposition to immunoglobulin E-mediated response to common allergens. Damage to bronchial epithelium and airway inflammation contributes to the pathogenesis. T2 helper cells respond to allergens by stimulating B cells to differentiate into immunoglobulin E producing plasma cells. T2 helper cells also stimulate growth factors for mast cells and activate eosinophils. Cytokines have a big role in chronic inflammation and the associated complications. Tumor necrosis factor alpha, an inflammatory cytokine stored and released from mast cells, increases movement and stimulation of inflammatory cells leading to airway remodeling and mucous cell hyperplasia. The stimulation of neutrophils, eosinophils, lymphocytes, and mast cells cause epithelium injury increasing airway inflammation and decreasing airflow. The inflammatory process causes airway obstruction leading to wheezing, breathlessness, chest tightness, and cough (Grossman,