Asthma is a chronic respiratory condition currently prevalent and it is currently affecting millions globally. The condition is chronic, affecting the respiration process and it is characterized by airflow obstruction, airway hyper-responsiveness inflammation which manifests in symptoms like shortness of breath, coughing, wheezing, and chest tightness ( Dougherty, & Fahy, 2009 ). Asthma results in either chronic or acute inflammation of the respiratory pipes and determining the pathophysiologic mechanism of the type of asthma is important in diagnosis and therapy for the patient.
The pathophysiological exacerbation of chronic cancer is related to the causal and etiological features of viruses which help in providing environments that boost the effects of the condition. With chronic asthma, the key mechanism is viral replication which causes the epithelial cells of the respiratory tract to trigger cytokine release which then causes inflammation alongside large mucus production ( Dougherty, R. H., & Fahy, 2019 ). However, the viral effects do not erratically alter arterial blood patterns. Instead, the asthma attack takes time and the blood oxygen levels will only fall slightly and the PH will also rise slightly. When these conditions, which inhibit the clearance of the viral infection, are added to the existing inflammation of the respiratory airways, the trigger the chronic symptomatology (Casale et al 2016). This also affects the immune system that is overwhelmed and unable to fight the virus. This then results in the inflammation of the pulmonary vein which exacerbates asthma inflammation.
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Additionally, research has shown that dehydration may also cause an attack. Asthma is closely related to the body’s water levels since this affects the airway epithelial cells which could lead to edema damage and hyper-responsiveness (Walsh et al., 2017). This does not manifest if the attack was exercise-induced. The arterial blood patterns during an attack show changes in the blood PH and the oxygen levels. The PH levels rise while the blood oxygen levels become very low quickly while CO2 levels rise.
Acute asthma may be activated by the onset of emotional stress or sorrow which are cataclysmic to the exacerbations of asthma symptoms. With the inception of the attack, the oxygen levels reduce quickly and the patients have choppy breaths while the CO2 levels rise relative to the PH levels (Gelb, Christenson & Nadel, 2016). This is because intense emotional activity elicits asthma symptoms like airway reactivity, choppy breaths, elevated respiratory resistance, and reduced peak expiratory flow rates.
The most affective risk factor for asthma, despite its nature as a multifactorial condition, is allergies. This affects both the mentioned cases of asthma, although it is more prevalent in chronic asthma (ALA, 2019). A patient who has a history of allergies is more prone to asthma exacerbation, where the immune system's retaliation for the allergy might be a causal factor for the symptomatology of asthma. The epithelial cells are upset and a triggered response results in the common allergic response to the inhaled antigens which is an attack.
The diagnosis of asthma is established based on its exacerbation. For an allergic case, the practitioner would perform an allergy test, integrating the patient’s medical history and breathing test to assess the health of the lungs and the respiratory tract (Morris, 2016). The practitioner would then prescribe medications that repress asthma triggers. This may include corticosteroids which are anti-inflammatory medications taken daily (Casale et al 2016). The practitioner may also conduct dehydration tests which would help to determine if the patient has sufficient water levels in the levels, after which the practitioner may recommend taking more fluids. For the cases of viruses, these may be tested by having a qualified or specialized practitioner conduct an epistemological test, after which antiviral medications may be prescribed to reduce the risk of asthma.
References
ALA (2019). Asthma Risk Factors. [online] American Lung Association. Available at: https://www.lung.org/lung-health-and-diseases/lung-disease-lookup/asthma/asthma-symptoms-causes-risk-factors/asthma-risk-factors.html [Accessed 28 Sep. 2019].
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.
Dougherty, R. H., & Fahy, J. V. (2009). Acute exacerbations of asthma: epidemiology, biology and the exacerbation‐prone phenotype. Clinical & Experimental Allergy , 39 (2), 193-202.
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.
