Avoiding Outdoor Activities in Polluted Areas Paper Example

Question 1: The Pathogenesis Causing the Clinical Manifestations With Which Jackson Smith Presented With

The clinical manifestations that Jackson Smith is presented with indicate the presence of Acute Severe Asthma. The pathogenesis of this disease is complex, interactive, and involves the interplay of two factors, which include host factors and environmental exposures. One of the host factors is genetics. The disease has some inheritable component to the form in which it is expressed. In essence, several genes are involved in the presence of Acute Severe Asthma and its features. However, there is complexity in the involvement of these genes due to linkages to particular phenotypic characteristics but not the clinical picture of the disease itself (Carson, Usmani, & Smith, 2014). Genetics plays a role in airway hyperresponsiveness, as well as dysfunctional regulation of the production of inflammatory mediators. These mediators comprise of growth factors, chemokines and cytokines. Innate immunity is another host factor that might have led to the development of Acute Severe Asthma. Due an imbalance between Th1 and Th2 cytokines, there is the likelihood of one suffering from allergic diseases like asthma. In this case, air inflammation in the disease would cause loss of normal balance between the Th lymphocyte populations. These are the Th1 and Th2 lymphocytes. The Th1 cells initiate the production of interferon-Y and IL-2 that provide defense to the cells in response to a given infection. On the other hand, Th2 produces a family of cytokines that include IL-4, -5, -6, -9, and -13) (Chang et al., 2017). The cytokines can help in mediating an allergic inflammation. Ideally, environmental stimuli like infections would activate Th1 responses while bringing about a balance in the relationship of Th1 and Th2. Cytokine imbalance would occur because of the type of infections in the life of an individual and exposure to allergens repeatedly. In the subpopulations of cytokines, Th1 cytokine can inhibit the production of Th2. Allergic inflammation would lead to excessive expression of the Th2 cytokines.

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Considerately, cytokine dysregulation where Th1 activity in asthma becomes diminished leads to the loss of immune balance. In the development, severity and persistence of Acute Severe Asthma, environmental factors play a critical role. In susceptible host and at the time of development, allergens and respiratory infections would depict a significant influence on the development of the disease. The exposure to cockroach allergen like an allergen in inner-city dwellings leads to allergen sensitization, which would consequently cause Acute Severe Asthma. Allergen exposure also promotes airway inflammation persistence and the possibility of an exacerbation. When one is exposed to house-dust mite, they would be infected with the disease. Additionally, respiratory infections during the early stages of development lead to the inception of acute severe asthma. These infections include parainfluenza virus and respiratory syncytial virus (RSV) (Arulparithi et al., 2015).

In essence, symptomatic rhinovirus infections experience early in life would result into recurrent wheezing, which is evident in the case of Jackson Smith. The influence of these infection depends on the interaction with atopy. Atopic state of an individual tends to enhance lower airway response to the respiratory infections. The airway interactions would occur in situations where people are exposed to viruses and allergens simultaneously. Concisely, air pollution, tobacco smoke, as well as the dietary intakes of a person are associated with increased risk for Acute Severe Asthma onset. Exposure to tobacco smoke facilitates the severity of the disease and brings forth decreased responsiveness to the inhaled corticosteroids (Cook & Saglani, 2016). Heavy exercise outdoors within communities, which have high ozone concentrations might cause asthma manifestations. An increase in pollution levels increases the exacerbations of the disease. Low intake of omega-3 fatty acids and antioxidants may cause airway dysfunction hence leading to asthma as unique inflammatory mediators are generated. Due to mucus plugging of the airways, air may be trapped that cause severe asthma exacerbations. Mucus secretion and hyperplasia can cause mucus plugging in the case of asthma. The mediators that trigger secretion of mucus are leukotrienes, neutrophil elastase, and eosinophil cationic protein.

Question 2: Two high priority nursing strategies to manage Jackson and evidence-based rationales for these strategies

One of the nursing strategies that can be used to manage the condition of Jackson is the administration of systemic corticosteroids based on their prescription. Corticosteroids are crucial as they help in the suppression of airway inflammation. They lead to reduced airway hypersensitivity, edema, as well as secretions. Since Jackson has been diagnosed with Acute Severe Asthma, systemic corticosteroids would be vital in the first-line medication of the patient. Some of these corticosteroids that would be prescribed include prednisolone, dexamethasone, methylprednisolone, and hydrocortisone. The corticosteroids should be administered for between three and ten days. However, the need to reduce dose or duration of the therapy would depend on the severity of asthma. Ideally, to prevent Jackson's relapse, he should be given a five to ten days oral systematic corticosteroids course when he is being discharged (Oczypok et al., 2015). The strategy will be essential as it reduces swelling and the production of mucus in the airways. As such, the airways will be less inflamed hence enabling Jackson to have a better control over his life.

Another vital strategy would be administering non-invasive positive-pressure ventilation (NPPV) appropriately. The NPPV will enhance alveolar ventilation and improves the process of gas exchange. It also leads to a decreased need for endotracheal intubation, as well as mechanical ventilation. When extrinsic positive end-expiratory pressure is applied with the NPPV, the work of breathing will be reduced significantly. As such, the fatigued respiratory muscles of Jackson will rest adequately. The NPPV would be administered through nasal or facial masks. In the process, positive airway pressure may be applicable. The NPPV should be set appropriately to avoid worsening the patient's hyperinflation (Neame et al., 2015).

Question 3: a. The mechanism of action of these drugs, and relate to the underlying pathogenesis of an Acute Severe Asthma

nebulised Salbutamol is taken through inhalation as an aerosol. The drug acts at beta 2- adrenoreceptors that are found on the smooth muscle and envelope the bronchi. Once the drug unbinds from the receptors, blood carries it around the body. In the body, it acts on various beta 2- receptors before its inactivation in the stomach and liver. Nebulised Ipratropium bromide acts as an anticholinergic agent hence blocking muscarinic acetylcholine receptors. The drug inhibits reflexes that have been mediated vagally through antagonization of acetylcholine action (Pallin et al., 2015). Anticholinergics will prevent any increase in intracellular cyclic guanosine monophosphate concentration. These result from the nature of interaction between acetylcholine and the muscarinic receptors found in bronchial smooth muscles. IV Hydrocortisone is used in the case of Jackson for treatment of inflammation. The drug is similar to cortisol, which is a natural hormone that adrenal glands produce. It has potent anti-inflammatory action, which enables it to suppress immune response. The drug is given as an injection.

b. The nursing implications (monitoring for and responding to adverse effects, and evaluating therapeutic effect) when administering these drugs to a patient with an Acute Severe Asthma

When administering these drugs, the care practitioners should assess the severity of the condition. In essence, through this, they will come up with proper prescriptions that would not bring forth any adverse outcomes to the patient. Proper dosage will be given to the patients and advised on how they should use the drugs. Complete observations should also be ensured based on the clinical priorities. However, when administering corticosteroids, the process should be conducted within the first hour of treatment. The patient should be observed for at least one hour after the severe dyspnoea. There would also be the need to provide post-acute care and arrange follow up (Sandrock & Norris, 2015).

References

Arulparithi, C. S., Babu, T. A., Ravichandran, C., Santhanam, I., Sathyamurthi, B., Parivathini, S., & Hemachitra, J. (2015). Efficacy of nebulised budesonide versus oral prednisolone in acute severe asthma. The Indian Journal of Pediatrics, 82(4), 328-332.

Bruijnzeel, P. L., Uddin, M., & Koenderman, L. (2015). Targeting neutrophilic inflammation in severe neutrophilic asthma: can we target the diseaserelevant neutrophil phenotype?. Journal of leukocyte biology, 98(4), 549-556.

Carson, K. V., Usmani, Z. A., & Smith, B. J. (2014). Noninvasive ventilation in acute severe asthma: current evidence and future perspectives. Current opinion in pulmonary medicine, 20(1), 118-123.

Chang, X., Chen, J., Shuzhen, B. I., Qing, L. I., & Song, Y. (2017). Application of compound ipratropium bromide combined with budesonide in acute severe asthma. Chinese Journal of Primary Medicine and Pharmacy, 24(21), 3254-3257.

Cook, J., & Saglani, S. (2016). Pathogenesis and prevention strategies of severe asthma exacerbations in children. Current opinion in pulmonary medicine, 22(1), 25-31.

Lefebvre, P., Duh, M. S., Lafeuille, M. H., Gozalo, L., Desai, U., Robitaille, M. N., ... & Lin, X. (2015). Acute and chronic systemic corticosteroid-related complications in patients with severe asthma. Journal of Allergy and Clinical Immunology, 136(6), 1488-1495.

Neame, M., Aragon, O., Fernandes, R. M., & Sinha, I. (2015). Salbutamol or aminophylline for acute severe asthma: how to choose which one, when and why?. Archives of Disease in Childhood-Education and Practice, 100(4), 215-222.

Oczypok, E. A., Milutinovic, P. S., Alcorn, J. F., Khare, A., Crum, L. T., Manni, M. L., ... & Oury, T. D. (2015). Pulmonary receptor for advanced glycation end-products promotes asthma pathogenesis through IL-33 and accumulation of group 2 innate lymphoid cells. Journal of Allergy and Clinical Immunology, 136(3), 747-756.

Pallin, M., Hew, M., & Naughton, M. T. (2015). Is noninvasive ventilation safe in acute severe asthma?. Respirology, 20(2), 251-257.

Sandrock, C. E., & Norris, A. (2015). Infection in severe asthma exacerbations and critical asthma syndrome. Clinical reviews in allergy & immunology, 48(1), 104-113.