Asthma: Clinical Disease of Chronic Airway Soreness
Write a 2- to 3-page paper that addresses the following:
Describe the pathophysiological mechanisms of chronic asthma and acute asthma exacerbation. Be sure to explain the changes in the arterial blood gas patterns during an exacerbation.
Explain how the factor you selected might impact the pathophysiology of both disorders. Describe how you would diagnose and prescribe treatment for a patient based on the factor you selected.
Construct two mind maps—one for chronic asthma and one for acute asthma exacerbation. Include the epidemiology, pathophysiology, and clinical presentation, as well as the diagnosis and treatment you explained in your paper.
The School requires that all papers submitted include a title page, introduction, summary, and references.
Asthma
Student’s Name
Institutional affiliation
Asthma
Asthma refers to a complicated clinical disease of chronic airway soreness and inflammation characterized by, reversible, recurrent, airway blockades. Airway swelling also triggers airway hyperactivity that causes the airways to thin in response to several stimuli. In other words the respiratory inner organs becomes swollen and sore, making them sensitive and reactive to things that patient find irritating or allergic. The common symptoms include wheezing, chest lightness shortness, dyspnea as well as morning cough. Therefore, the paper seeks to describe the pathophysiological mechanisms of chronic asthma and acute asthma exacerbation, particularly explaining he changes in the arterial blood gas patterns during an exacerbation.
Pathophysiology of Asthma
The illness is characterized by involuntary airways narrowing, hence increasing the vulnerability of airways organs as they become more responsive to inhaled spasmogens, and an eosinophilic inflammatory infiltrate (Barnes, Rodger, & Thomson, 2013). Over the past two decades, the US has seen an increase in prevalence morbidity and mortality rates. The factors has managed the process (Barnes, Rodger, & Thomson, 2013) According to CDC, the observed increase is due to the genetic influences such as air pollution, diet, and lifestyle modernization, and parental atopy, allergen exposure as well as viral or bacterial exposure in in early childhood(Barnes, Rodger, & Thomson, 2013)
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Physiologically, physicians have employ the decreasing of brachial airflow after bronchoprovocation with either histamine or methacholine to document the bronchial. Other causative urgent that aggravate airway hindrance include viral upper respiratory infection, cigarette smoke, respiratory allergens and cold air and exercise (Barnes, Rodger, & Thomson, 2013). When the allergen provokes the bronchial, an early phase immunoglobulin E (igE), thus triggering a decrease in bronchial airflow (K, Sumangalip.P, & Subash.Y.E, 2013). In this situations, patients experiences a forced expiratory volume in 1 second, followed by late phase, igE-mediated reaction that lasts for 4 to 8 hours (K, Sumangalip.P, & Subash.Y.E, 2013). In addition, based on the gross asthmatic airways reveals hyperinflation of the lungs, thickening of lamina, sloughing of epithelial cell, cilia cell distribution, smooth muscle hypertrophy and hypesecretion of mucus gland (K, Sumangalip.P, & Subash.Y.E, 2013).
Asthma Exacerbation.
Asthma exacerbation arises when the symptoms flare up and worsen progressively. During an exacerbation, airways inflammation occurs such that the muscle bronchial tube get narrow and the muscle contracts) (Weinberger, Cockrill, & Mandel, 2013). This makes the breathing process to become more difficult. An acute exacerbation of asthma is dreadful and life-threatening even a patient does not seek fails to contact the doctor) (Weinberger, Cockrill, & Mandel, 2013). That is why attempting to identify the symptoms early is essential and to take appropriate action. The major symptoms for an acute exacerbation tend to vary from one victim to another as it ranges from mild to severe during an exacerba...
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