1 Brittany Wickware Walden University NURS 6501: Advanced Pathophysiology October 9, 2016 Week 6 Assignment
2 Introduction Asthma effects approximately 34 million people in the United States with half of those developing the disease in childhood (Huether & McCance, 2012). Under diagnosis usually re- sults from respiratory infection diagnosis and can progress during childhood causing chronic air- way changes. Asthma causes a chronic inflammatory disorder of the airway that results in hyper- responsiveness reactions of the bronchioles, airflow limitation, inflammatory respiratory symp- toms, and disease chronicity. The disease can present as an acute exacerbation and can become severely chronic if early interventions are not taken to decrease severity of the disease. All ages, not just children, can be present with asthma symptoms and a thorough history is needed to help diagnose the disease (National Asthma Education, 2007). Treatment is based on the diagnosis of an acute exacerbation, chronic long term disease, severity of damage and if infection is present. Asthma Pathophysioloy The pathophysiology of asthma involves the bronchial mucosa ’ s hyper-responsiveness to an allergen and constriction of the airway (Heuther & McCance, 2012). Mast cells, eosinophils, basophils, macrophages, neutrophils, and lymphocytes release inflammatory mediators that in- crease capillary permeability and constrict smooth muscle causing thus narrowing the airway and obstructing airflow. Early activation of B cells, also referred to as plasma cells, produces antigen specific IgE that bind the surface of mast cells causing degranulation and release of histamine, bradykinins, and other mediators. These mediators cause even worsening reactions such as va- sodilation, mucous secretion, bronchospasm and mucosal edema.
3 An acute exacerbation of asthma can start suddenly and progress to airway obstruction quickly. Arterial blood gasses are one of the first tests done to show oxygenation status and how the respiratory system is tolerating the attack (Padmavathi, 2013). Air trapping in the lungs leads to increased alveolar gas pressure and decreased perfusion to alveoli. Hyperventilation follows the increased ling volume and results in early hypoxemia without CO2 retention. If the treatment is not initiated, the hypoxemia will further increase hyperventilation and cause a decrease in PaCO2 resulting in respiratory alkalosis. Respiratory failure is seen when airway obstruction
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