References:
1. Pathophysiology of acute asthma depends on the inflammatory symptoms and interaction of different cell types and multiple mediators due to which the physiological features are visible on the patient affected with it. In this provided case study of Jackson Smith (18) who was admitted to the emergency department of the helathcare facility after the severe breathlessness related episode (Doeing & Solway, 2013). It was informed by the family members of the patient that he was suffering from this disease since his childhood. as the patient was admitted to the emergency ward, the clinical manifestations were collected such as severe episodes of dyspnea, shortness of breath, increased heart rate up to 32 breaths per minute, increased blood pressure, elevated pulse rate up to 130 beats per minute and wheezing sound of breath which is also known as the auscultation of lungs (Gelb et al., 2015). Further to determine the lung expansion, the physicians conducted a chest x-ray that determined hyperinflation of lungs and surrounding area. Besides these the blood gas was assessed that determined 90% SO2 PaCO2: 50mmHg and HCO3: 25mEq/L and therefore, using these clinical manifestation, the pathogenesis of Jackson’s acute asthmatic syndrome could be understood (Doeing & Solway, 2013).
While discussing the pathogenesis the initiation of the inflammatory processes should be clearly understood. in this, the host factors such as particularly the genetics and environmental exposure plays an important role that make the immune system react to the environmental factors. As per Jackson’s case study, the emergence of asthma occurred at an early stage indicating towards innate immunity, genetics, allergens, respiratory infections, and other environmental factors (Nievas & Anand, 2015). In this pathogenesis related to allergic reaction is the most important. The antigen presenting cells or APCs engulfs the allergens from the environment and then presents them to the naïve T cells. Further, the the inflammatory factors then activates the respiratory epithelium that eventually releases the thymic stromal lymphopoietin as well as other inflammatory mediators that sends the leukocyte that eventually triggers the allergic reaction. Dendric cells also play an important role in increasing the allergic reaction and presenting those allergens to the naïve T cells. Further they present the t cells in two different aspects such as the T-helper 2 and Th17 cells (Alangari, 2014). These Th 2 cell induces the immunoglobulin E antibody production from the B cells using interleukin 4 and interleukin 13. These cells are important for the allergic reaction as IgE binds to the mast cell surfaces and basophiles in the presence of interleukin 4 that is the primary reason for the inflammatory reaction. These inflammatory mediators are the reason due to which the neutrophiles, macrophages, eosinophiles and others damages the airway, stimulations related to T cells, bronchoconstriction of the lungs, creating such clinical manifestation for Jackson (Doeing & Solway, 2013).
Other than these, Jackson also develops chronic inflammations due to which he started having symptoms related to shortness of breath and higher respiratory rate. These symptoms occur due to the presence of respiratory epithelium and leukocytes. Due to the presence of mediators in the inflammatory pathway the inflammatory cells are recruited to the epithelium cells and the then eventually infiltrates the lungs and then creates a cycle for chronic inflammatory symptoms leading to epithelium damage and remodeling of airway and therefore, the blood pressure as well as the respiratory rates also gets increased (Kudo, Ishigatsubo & Aoki, 2013). Further, genetics could also be responsible for the emergence of asthma in Jackson as Kaiko et al. (2013) determines that genetic sis involved in the production of IgE, airway hyper responsiveness and dysfunctional regulation of inflammatory mediators such as chemokines, cytokines, and growth factors. This leads to the production of modified genes, due to which, people with such genetic mapping develops Asthma in their lifetime and hence, Jackson also developed acute asthma related condition (Kudo, Ishigatsubo & Aoki, 2013).
2. The two nursing strategies which will be included in the care plan for Jackson will consist of pharmacological strategy and peak flow monitoring. These both management strategies are discussed below with the support of evidences from recent literatures.
As the patient, Jackson has been admitted in the emergency department of the healthcare facility and is suffering from acute asthmatic syndrome, it is important to implement immediate intervention using which the patient condition could be controlled (Price et al., 2013). This is because, due to progressive and continuous dyspnea, patient starts showing signs of increased aggressiveness, anxiety, which affects the asthma related condition. Therefore the medications which will be used for Jackson are Corticosteroids, which is primary medication if the patient develops alleviating symptoms so that it can enhance the patient’s airway function, and decreases the peak flow variability (Chung et al., 2013). Further, immunomodulators, anticholinergics, as well as short acting beta 2 could also be used in pharmacological intervention of Jackson as Chung et al. (2013) mentions that these drugs in acute asthmatic related condition helps in the reduction of prevent the binding of mast cell with basophile, decreasing the tone related issues of airway and relief the acute condition of the asthma respectively. The second strategy will be Peak flow monitoring, which is also an important intervention or strategy for patients affected with acute asthma as it helps to measure the highest airflow during a forced expiration or exhalation. Moorhead et al. (2013) also mentioned that in people with moderate and severe asthma, this intervention should be implemented. Therefore, the potential complications could be easily identified and preventive and corrective action could be taken against the disease condition. Further it also helps in the improvement of congestion and breath sounds or wheezing which is one of the primary clinical manifestations of the disease (Mebazaa et al., 2015).
3. Salbutamol: it is inhaled in the form of aerosol and therefore it acts as β2-adrenoreceptors which acts on the smooth muscles that covers the bronchi. Further, it helps in the binding to the epinephrine’s active site which in the course helps in the stabilization of the receptor which in the course makes more amount of cAMP that in the triggers the intracellular cascades to release the potassium ion (Gallenmüller et al., 2014). This decreases the intracellular calcium ion that helps in the hindrance of muscle contraction ability. Salbutamol in this place works as a other β2 receptors that helps in the relaxation of these muscles and hence, provides relief to the patient (Hahner, Burger-Stritt & Allolio, 2013). Nursing effect will be evaluated by patient observation and patient’s improvement will be used for the identification of effectiveness of drug. Further, the side effects will also be monitored and patient will be provided with pain killers and anti depressants so that anxiety, headache, and muscle cramps will be removed (Tashkin & Ferguson, 2013).
Nebulised ipratropium bromide: This drug is associated with chronic pulmonary disorder and it is used with concomitantly with inhaled beta2-agonists for the treatment of reversible obstruction of the airway (Nouira et al., 2014). This drug blocks the muscarinic receptors that associated with acetylcholine and thereby reliefs the COPD related condition of the patient. Further, to treat the dizziness, nausea, headache that will be maintained by observing the patient condition and understanding his mental and physical stability (Tashkin & Ferguson, 2013).
IV Hydrocortisone 100mg: IV Hydrocortisone 100mg: this drug is naturally occurring glucocorticoids, having saltretaining properties which is used in the replacement of adrenocorticol deficiency syndrome (Hahner, Burger-Stritt & Allolio, 2013). It helps to modify the immune response related to diverse stimuli and then increases the metabolic effects. This drug has similar side effects as the abovementioned drugs due to which the management mechanism will depend on the patient observation. Further, evaluation will be carried out after observing patient condition and improvement (Alani & Seymour, 2014).
References:
Alangari, A. A. (2014). Corticosteroids in the treatment of acute asthma. Annals of thoracic medicine, 9(4), 187.
Alani, A., & Seymour, R. (2014). Systemic medication and the inflammatory cascade. Periodontology 2000, 64(1), 198-210.
Chung, K. F., Wenzel, S. E., Brozek, J. L., Bush, A., Castro, M., Sterk, P. J., … & Boulet, L. P. (2013). International ERS/ATS guidelines on definition, evaluation and treatment of severe asthma. European Respiratory Journal, erj02020-2013.
Doeing, D. C., & Solway, J. (2013). Airway smooth muscle in the pathophysiology and treatment of asthma. Journal of applied physiology, 114(7), 834-843.
Gallenmüller, C., Müller-Felber, W., Dusl, M., Stucka, R., Guergueltcheva, V., Blaschek, A., … & Abicht, A. (2014). Salbutamol-responsive limb-girdle congenital myasthenic syndrome due to a novel missense mutation and heteroallelic deletion in MUSK. Neuromuscular Disorders, 24(1), 31-35.
Gelb, A. F., Yamamoto, A., Verbeken, E. K., & Nadel, J. A. (2015). Unraveling the pathophysiology of the asthma-COPD overlap syndrome: unsuspected mild centrilobular emphysema is responsible for loss of lung elastic recoil in never smokers with asthma with persistent expiratory airflow limitation. Chest, 148(2), 313-320.
Hahner, S., Burger-Stritt, S., & Allolio, B. (2013). Subcutaneous hydrocortisone administration for emergency use in adrenal insufficiency. European journal of endocrinology, EJE-12.
Kaiko, G. E., Loh, Z., Spann, K., Lynch, J. P., Lalwani, A., Zheng, Z., … & Diener, K. R. (2013). Toll-like receptor 7 gene deficiency and early-life Pneumovirus infection interact to predispose toward the development of asthma-like pathology in mice. Journal of Allergy and Clinical Immunology, 131(5), 1331-1339.
Kudo, M., Ishigatsubo, Y., & Aoki, I. (2013). Pathology of asthma. Frontiers in microbiology, 4, 263.
Mebazaa, A., Yilmaz, M. B., Levy, P., Ponikowski, P., Peacock, W. F., Laribi, S., … & McDonagh, T. (2015). Recommendations on pre?hospital & early hospital management of acute heart failure: a consensus paper from the Heart Failure Association of the European Society of Cardiology, the European Society of Emergency Medicine and the Society of Academic Emergency Medicine. European journal of heart failure, 17(6), 544-558.
Moorhead, S., Johnson, M., Maas, M. L., & Swanson, E. (2018). Nursing Outcomes Classification (NOC)-E-Book: Measurement of Health Outcomes. Elsevier Health Sciences.
Nievas, I. F. F., & Anand, K. J. (2013). Severe acute asthma exacerbation in children: a stepwise approach for escalating therapy in a pediatric intensive care unit. The journal of pediatric pharmacology and therapeutics, 18(2), 88-104.
Nouira, S., Bouida, W., Grissa, M. H., Beltaief, K., Trimech, M. N., Boubaker, H., … & Boukef, R. (2014). Magnesium sulfate versus ipratropium bromide in chronic obstructive pulmonary disease exacerbation: a randomized trial. American journal of therapeutics, 21(3), 152-158.
Price, D., Bosnic-Anticevich, S., Briggs, A., Chrystyn, H., Rand, C., Scheuch, G., … & Inhaler Error Steering Committee. (2013). Inhaler competence in asthma: common errors, barriers to use and recommended solutions. Respiratory medicine, 107(1), 37-46.
Tashkin, D. P., & Ferguson, G. T. (2013). Combination bronchodilator therapy in the management of chronic obstructive pulmonary disease. Respiratory research, 14(1), 49.
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