Question 1: The case study involves a 59 years old man withchronic obstructive pulmonary disease who exhibited productive cough, dysphonia, and cyanosis. The two most common risk factors for chronic obstructive pulmonary disease include tobacco smoking and chest infection as observed in this case.Lianget al. (2018), suggested that smoking is considered as theleadingcause ofchronicobstructivepulmonarydiseasesincesmokingrepeatedly damages the air sac, airways and lining of the lungs along with lung tissues. The injury and damaged lungs failed to inhale adequate air due to the decreased number of air space and blood vessels in the lungs followed by less oxygen (Eapen et al., 2017). The patient had a history of smoking which contributed to the development of COPD. On the other hand, the chest infection enhances the development of COPD since a repeated infection of acute airway mucus glands with the pathogen resulted in the severe inflammation followed by the development of COPD (Eapen et al., 2017). As the patient frequently experience chest infection, the chest infection contributed to COPD. Pathophysiology of chronic bronchitis: Chronic bronchitis is associated with overproduction as well as hypersecretion of mucous produced from goblet cells. Due to etiological factors such as smoking, chest infection and family history of bronchitis,epithelium cell lining of the airway response to these etiological factors by secreting inflammatory molecules such as colony-stimulating factors, proinflammatory factors and interleukin 8 (Chen,Burr & McGuckin, 2018).Cook et al. (2019),suggested that during chronic bronchitis, a decrease in the secretion of regulatory substances such as angiotensin-converting enzyme as well as neutral endopeptidase was also observed. Many researchers argued that alveolar epithelium is considered as both the target
and the initiator of the inflammatory response in chronic bronchitis. During exacerbation of chronic bronchitis, the bronchial mucous membrane exhibit diminished bronchial mucociliary function and becomes hyperemic and edematous (Chen, Burr & McGuckin, 2018). This resulted in airflow impairment due to luminal obstruction observed in small airways. The airways become blocked by debris followed by increased irritation and inflammation. Therefore, the characteristic cough of bronchitis is produced by the frequent secretion of mucus in chronic bronchitis (Chang et al., 2016). Question 3: clinical manifestations common to COPD: As discussed byGalletti et al.(2016),clinical manifestations common to COPD include Shortness of breath or dysphonia especially during involving in physical activities, Frequent respiratory infections, sudden and frequent weight loss, Cyanosis of the fingertips and swelling in ankle, legs or feet. Individuals with COPD are more likely to experience frequent episodes of exacerbation (Lau, Roche & Reddel, 2017).If they left untreated then a patient experience heart problem, lung cancer, high blood pressure, and depression. Out of these clinical manifestations, the common clinical manifestations exhibited by Paul include Productivecough,Cyanosisofthefingertips,Dyspnoeaonexertion(Chen,Burr& McGuckin, 2018). All of these clinical manifestations suggested that patients experience chronic bronchitis. Question 4: As observed in this case scenario, the patient exhibited Productive cough, Cyanosis of the fingertips, Dyspnoea on exertion due to chronic Obstructive Pulmonary Disease (COPD) and history of chronic bronchitis. In this context, two interventions will beBronchodilators andPhosphodiesterase-4 inhibitors.Gerber et al. (2018),suggested that bronchodilators
usually relax muscles around the airways which in turn relieves the shortness of breath. the common mechanismof the bronchodilatorsisincludingincreasing the airway lumen, accumulative ciliary function and maximizing mucous hydration of the airway (Upham& Gleeson, 2016).Consequently, the patient experienced reduced symptoms of dysphonia or shortness of breath(Chen, Burr & McGuckin, 2018).The common bronchodilator includes ipratropium,formoterol, and salmeterol(Upham& Gleeson, 2016).. On the other hand, Phosphodiesterase-4inhibitorsarethecommondrugsusedtotreatpatientswith severechronic obstructive pulmonarydiseaseas well as chronic bronchitis (Williams et al., 2019). This drug reduces severe inflammation of the airway and relaxes the airways for adequate inhalation of breathing. The common mechanism of Phosphodiesterase-4 inhibitors is that they act at the cellular level to halt the production of an overactive enzyme which is known as PDE4. Researchers suggested that phosphodiesterase (PDEs) degrade cyclic adenosine monophosphate(Upham& Gleeson, 2016). Consequently, patients experience reduced inflammation due to the suppression effect of the drug. However, the drug has a range of side effects such as dizziness, diarrhoea, and weight loss. Therefore, in order to administrate thesemedications, the side effects of the medications are required to consider.
Paraphrase This Document
Need a fresh take? Get an instant paraphrase of this document with our AI Paraphraser
References: Chang, A. B., Upham, J. W., Masters, I. B., Redding, G. R., Gibson, P. G., Marchant, J. M., & Grimwood, K. (2016). Protracted bacterial bronchitis: the last decade and the road ahead.Pediatric pulmonology,51(3), 225-242. Chen, A. C. H., Burr, L., & McGuckin, M. A. (2018). Oxidative and endoplasmic reticulum stress in respiratory disease.Clinical & translational immunology,7(6), e1019. Cook, N. S., Kostikas, K., Oezel, B., Tatlock, S., Mycock, K., Gardner, T., ... & Gutzwiller, F. S. (2019). PP128 Quantifying The Relative Importance Of Chronic Obstructive Pulmonary Disease Symptoms To Patients.International Journal of Technology Assessment in Health Care,35(S1), 61-61. Eapen, M. S., McAlinden, K., Tan, D., Weston, S., Ward, C., Muller, H. K., ... & Sohal, S. S. (2017). Profiling cellular and inflammatory changes in the airway wall of mild to moderate COPD.Respirology,22(6), 1125-1132. Galletti,J.,Mcheileh,G.,Hahne,A.,&Lee,A.L.(2018).Theclinicaleffectsof manipulative therapy in people with chronic obstructive pulmonary disease.The Journal of Alternative and Complementary Medicine,24(7), 677-683. Gerber, A., Moynihan, C., Klim, S., Ritchie, P., & Kelly, A. M. (2018). Compliance with a COPD bundle of care in an A ustralian emergency department: A cohort study.The clinical respiratory journal,12(2), 706-711. Lau, E. M., Roche, N. A., & Reddel, H. K. (2017). Therapeutic approaches to asthma-chronic obstructive pulmonary disease overlap.Expert review of clinical immunology,13(5), 449-455.
Liang, J., Abramson, M. J., Zwar, N. A., Russell, G. M., Holland, A. E., Bonevski, B., ... & Wilson, S. (2018). Diagnosing COPD and supporting smoking cessation in general practice: evidenceâpractice gaps.Medical Journal of Australia,208(1), 29-34. Upham, J. W., & Gleeson, S. A. (2016). Combination long-acting bronchodilators for COPD.Medicine Today,17(4), 73-74. Williams, L. M., He, X., Vaid, T. M., AbdulâRidha, A., Whitehead, A. R., Gooley, P. R., ... & Scott, D. J. (2019). Diazepam is not a direct allosteric modulator of α1âadrenoceptors, but modulates receptor signaling by inhibiting phosphodiesteraseâ4.Pharmacology research & perspectives,7(1), e00455.