Chronic Bronchitis and Emphysema Pathophysiology Research Paper

Chronic Bronchitis and Emphysema Pathophysiology - Research Paper ExampleThe exact prevalence of these lung unsoundnesss crosswise the globe is not well known. In this article, both the diseases with be discussed by comparing and contrasting with each other. Definitions Chronic bronchitis is defined clinically as a condition in which the patient suffers from expectorant cough up for a minimum of 3 months for 2 consecutive years (Celli, 2008). The diagnosis is mainly through clinical presentation. On the other hand, emphysema is defined as a condition in which the patient has standing(prenominal) and abnormal enlargement of the air spaces distal to the terminal bronchioles and associated with destruction of the walls without any obvious fibrosis (Celli, 2008). Chest radiography and pulmonary function tests are needed to arrive at the diagnosis. Pathophysiology In inveterate bronchitis, there is ordinary inflammation of the bronchi. The endothelium is damaged because of which the mucociliary response is impaired. This leads to improper clearance of bacteria and mucus. Thus, inflammation, along with inadequate clearance of mucus contributes to obstruction in the disease. There is histopathological evidence of goblet cell hyperplasia, mucus plugging, smooth muscle hyperplasia and fibrosis. alveolar consonant attachments that are supportive are lost, the airways are deformed and the air lumens are narrowed. The capillary pulmonary slam is undamaged. In emphysema, the airspaces distal to the terminal bronchioles are enlarged permanently, because of which alveolar surface area necessary for vaunt exchange is decreased. Loss of alveolar walls leads to decreased elastic recoil property of the alveoli, causing limitations to airflow. Decrease in the alveolar limiting structure causes narrowing of the airway, causing further limitation of airflow. There are 3 characteristic patterns of morphology in emphysema and they are centriacinar, panacinar and distal acinar. In centriacinar type, destruction is mainly in the central portions of the acini. In panacinar type, entire alveolus is involved. In distal acinar type, only those acini in the distal portion of the airways in involved. (Maclay et al, 2009). Etiology and pathogenesis The most common etiological agent in both chronic bronchitis and emphysema is cigarette smoking. Smoking over a long duration of time triggers the macrophages to release chemotactic factors alike(p) elastases which destroy the tissues of the lung. Passive smoking and other environmental factors also can contribute to chronic clogging pulmonary disease. Airway hyperresponsiveness is a happen factor for chronic bronchitis. Alpha-1 antitrypsin deficiency, a genetic disorder, is an consequential risk factor for chronic pulmonary obstructive disease, especially emphysema. Intravenous drug abuse is another important risk factor for emphysema. The disease occurs because of the pulmonary vascular damage that occurs due to i nsoluble fillers present in the drugs. Immunodeficiency syndromes like HIV infection, vasculitis disorders, connective tissue disorders and Salla disease are risk factors for both chronic bronchitis and emphysema (Celli, 2008). Prognosis As far as prognosis is concerned, both the conditions are associated with significant mortality and morbidity. The prognosis is worse in emphysema because of damage to pulmonary vascular bed. Chronic obstructive pulmonary disease is infact, the fourth leading cause of mortality in the United States. Both chronic bronch