Review Asthma? in Chapter 27 of the Huether and McCance text. Ide
Review Asthma? in Chapter 27 of the Huether and McCance text. Identify the pathophysiological mechanisms of chronic asthma and acute asthma exacerbation. Consider how these disorders are similar and different. Select a patient factor different from the one you selected in this weeks Discussion: genetics, gender, ethnicity, age, or behavior. Think about how the factor you selected might impact the pathophysiology of both disorders. Reflect on how you would diagnose and prescribe treatment of these disorders for a patient based on the factor you selected. Review the Mind maps?Dementia, Endocarditis, and Gastro-oesophageal Reflux Disease (GERD)? media in the Week 2 Learning Resources. Use the examples in the media as a guide to construct two mind maps?one for chronic asthma and one for acute asthma exacerbation. Consider the epidemiology and clinical presentation of both chronic asthma and acute asthma exacerbation. To Complete 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. Pathophysiological mechanisms of Exacerbating Acute and Chronic Asthma Asthma alludes to a pulmonary condition that results into either a chronic or acute inflammation of the respiratory tubes coupled with a tightening of the smooth muscles of the respiratory tract. In some cases, episodes of bronchoconstriction will accompany it as well. Establishing the pathophysiological mechanism of each asthma is an important step in determining its exacerbation, diagnosis and prescribing treatment for the patient. The pathophysiological exacerbation of chronic cancer is closely tied to the etiological aspect of persistent viruses and chlamydia. Viruses and other organisms play a huge part in providing the necessary conditions for asthma to thrive. The key mechanism in this exacerbation is the viral replication that results in the epithelial cells of the respiratory tract triggering cytokine release, inflammation and the eventual large mucus production. However, the viral and chlamydia has does not result into sporadic changes in the arterial blood patterns. The asthma attack takes time and so blood PaO2 of 100 mm Hg will only fall slightly to around 85 mm Hg followed by a slight rise in the PH to 7.45 from its initial 7.40 (Casale et al 2016). Despite these processes being necessary for clearance of the viral infection, they are still super-imposed over the already existing inflammatory condition in the airways that ignites symptomatology instead. Furthermore, it means that the immune system is slowed down hence making it unable to clear the viruses. As a result, there is infiltration of the pulmonary vein which exacerbates asthma inflammation. Dehydration plays a very a far wider role in acute exacerbation of asthma. Studies show that asthma has a close relation with the water levels in the body with regard to airway epithelial cells. This will from time to time contribute to a fraction of epithelial and edema damage coupled with hyper-responsiveness. However, this does not only result should it be exercised-induced asthma. According to Walsh, Sills and Arnold (2017), during asthma attack through dehydration, the arterial blood patterns exhibit very sharp changes in the blood PH which could rise to as high as 7.60 while the blood PaO2 reduces to very low levels within a short time as low as 40 mm Hg coupled with a sharp rise in PaCO2. Acute asthma can also be triggered by a period of emotional stress grief and sorrow are upheavals to asthma symptoms exacerbations. Interestingly, greater anxiety has been noted to be common to asthma patients than hepatitis B Patients. The level of oxygen in the blood reduces very fast as the patients loose instant breath while the CO2 levels climbs up along with the PH levels in almost the same proportion. For instance in a study including 230 patients, 45% scored high on depression rating taken as depressed (Gelb, Christenson & Nadel, 2016). However, the patients with depression had health related issues. Conversely, having intense emotions brings out asthma symptoms such as airway reactivity, decreased peak expiratory flow rate, increased respiratory resistance and shortness of breath. Even though asthma is a predominantly multifactorial condition, its most pressing risk factor remains as the allergies. This involves the chronic asthma in particular. Having a family history of allergic reactions can speed asthma exacerbation. In this case, an immunological response to the allergy is a triggering factor in the symptomatology of asthma. The disruption of the normal epithelial cells leads to triggering of a response which explains the commonly occurring allergic responses to the inhalant antigens particularly among those individuals exposed to these agents. Exposure to metal toxicity in the respiratory tract exacerbates chronic asthma. Zinc, cadmium, copper and aluminum results into both chronic obstructive lung disease and the acute self-limiting neutrophil alveolitis (Morris, 2016). With time, this develops into pulmonary fibrosis as well as damaging the functional impairment based on the potential of the agent to cause that damage. Metal raise the PH levels in the body as the CO2 content in the blood rises up as well with a reduction in the Oxygen content. The factors mentioned above have widespread effects on the pathophysiological disorders present in asthma. First, viruses provide conditions for damaging of the epithelial cells in the body. This comes through triggering of the cytokine release that spearheads inflammation and large mucus production. Secondly, exposure to toxic metals leads into chronic lung disease and the self-limiting neutrophil that results into pulmonary fibrosis based on the damaging extent of the metal agent (Morris, 2016). Thirdly, the emotional stress and dehydration connotes to similar effects because they both predispose patients to sudden acute asthma exacerbation that involves decreased peak expiratory flow rate, increased respiratory resistance and shortness of breath. Diagnosis of asthma follows a very specific approach as established by its exacerbation. For the case of allergy, an allergy test is performed by the doctor. During this period, medical history and breathing tests are performed establishing how well a patients lungs are working. Even though there is no cure for asthma, the allergist will recommend taking medications that avoids asthma triggers. Corticosteroids are taken daily. Dehydration test involves testing a patients water level in which if it is found out that he/she is lacking sufficient water, they are recommend to be taking more water to boost it. For case of metal toxicity, body fluids and solids are tested for any presence of toxic substances in the body including the blood stream. Based on this heavy detoxification is conducted. Lastly, cases of viruses and chlamydia can be tested through conducting epistemological tests in the body by a qualified doctor. Upon their establishment, antibiotics are administered to attack the virus and hence reduce the risk of asthma. Acute asthma mind map Diagnosis Treatment Acute asthma Emotional stress Therapy Dehydration Clinical presentation Epistemology Corticosteroids daily Water addition Anxiety Briefing tests Depression an Pathophysiological Disruption of epithelial cells Pulmonary fibrosis Chronic asthma mind map. Detoxification Viruses and chlamydia Chronic asthma Antibiotics Treatment Allergies Lung infection Disruption of epithelial cells Working lungs Mucus production Inflammation Medical history Clinical presentation Pathophysiology Epistemology Diagnosis Metal toxicity References Casale, T. B., Tashkin, D. P., Lühmann, R., Engel, M., Moroni-Zentgraf, P., & Kerstjens, H. A. (2016). Therapy Demonstrates Reduced Risk of Severe Asthma Exacerbation and Asthma Worsening in Symptomatic Asthma, Independent of IgE or Blood Eosinophil Levels. Journal of Allergy and Clinical Immunology, 137(2), AB214. Gelb, A. F., Christenson, S. A., & Nadel, J. A. (2016). Understanding the pathophysiology of the asthma?chronic obstructive pulmonary disease overlap syndrome. Current opinion in pulmonary medicine, 22(2), 100-105. Morris, M. (2016). Drugs and Diseases: Pulmonology. Medscape. Retrieved from: emedicine.medscape.com/article/296301-overview Walsh, C. G., Sills, M. R., & Arnold, D. H. (2017). Time-dependent severity change during treatment of pediatric patients hospitalized for acute asthma exacerbations. Annals of Allergy, Asthma & Immunology, 118(2), 226-227.
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