Care and management of chronic obstructive airways disease Essay

C atomic number 18 and heed of continuing obstructive fashionways disease - Essay congressmanHe was advised to quit smoking by the general practitioner, but the patient was unable to do so. In view of persistent cough and worsening health condition, the patient was referred to our center for further management and counseling. otherwise health problems in John include hypertension and hemorrhoids. He has been taking amlodipine 5 mg for hypertension. Overview of the disease Chronic obstructive pulmonary disease (COPD) is one of the devastating medical conditions that exploits a colossal degree of suffering to humans (Mosenifar, 2011). It is a source of both economic and social burden (Sullivan et al, 2000 and Fromer and Cooper, 2008). It is delineate as a disease state characterized by the front man of airflow obstruction due to chronic bronchitis or emphysema (Mosenifar, 2011). There are 2 sides of coin to the disease and they are emphysema and chronic bronchitis. Chronic br onchitis refers to presence of chronic cough with no other etiology and which is productive for at least(prenominal) 3 months during each of the two consecutive years. Emphysema is a condition in which damage of the air spaces that are present distal to the terminal bronchioles occurs. The damage is irreversible, abnormal and associated with destruction of the air space walls with no obvious fibrosis (Fromer and Cooper, 2008). ... The most distressing symptom of COPD is breathlessness which is a progressive problem and the crux of sermon of COPD is management of breathlessness. Pathophysiology Understanding of the pathophysiology of the disease helps elaborate a good management plan. The most common cause of COPD is cigarette smoking. It develops in about 15 percent of chronic spaters (NICE, 2004). Thus, John developed COPD because of chronic smoking. Other risk factors for the development of COPD are air pollution especially due to solid cooking fuels, presence of airway hyperre sponsiveness (Mosenifar, 2011). The characteristic pathophysiological changes in COPD are seen in the central airways, the peripheral airways and also the lung parenchyma. Diverse mechanisms are implicated in the pathophysiology of COPD (Thurlbeck, 1990). Primary offenders like oxidative stress due to free radicals from cigarette smoke and oxidants from phagocytes and polymorphonuclear leukocytes trigger the release of certain enzymes like leukocyte elastase in such proportions that they cannot be counteracted effectively by anti-proteases, resulting in destruction of the lung tissues (Thurlbeck, 1990) leading to necrosis or apoptosis of the lung tissue. Due to these mechanisms, certain pathological changes occur in the airways and the lung tissue like inflammation and globlet cell hyperplasia in chronic bronchitis and loss of elastic recoil in emphysema. Other changes include ciliary abnormalities, airway smooth muscle hyperplasia, bronchial wall thickening and sometimes atrophy (M osenifar, 2011). These pathophysiological changes contribute to airway flow obstruction, airway hyperresponsiveness and mucus accumulation leading to poor ventilation and oxygenation, breathlessness, cough and infection. A