EXAM

Exam



Exam

Question No. 1

Chronic obstructive bronchitis is chronic bronchitis with airflow obstruction. Chronic bronchitis is defined as productive cough on most days of the week for at least 3 mo total duration in 2 successive years. Chronic bronchitis becomes chronic obstructive bronchitis if spirometry evidence of airflow obstruction develops. Chronic asthmatic bronchitis is a similar, overlapping condition characterized by chronic productive cough, wheezing, and partially reversible airflow obstruction; it occurs predominantly in smokers with a history of asthma. In some cases, the distinction between chronic obstructive bronchitis and chronic asthmatic bronchitis is unclear. Emphysema is destruction of lung parenchyma leading to loss of elastic recoil and loss of alveolar septa and radial airway traction, which increases the tendency for airway collapse. Lung hyperinflation, airflow limitation, and air trapping follow. Airspaces enlarge and may eventually develop bullae (Anderson, 1993).

An estimated 24 million people in the US have airflow limitation, of whom about half have COPD. COPD is the 4th leading cause of death, resulting in 122,000 deaths in 2003—compared with 52,193 deaths in 1980. From 1980 to 2000, the COPD mortality rate increased 64% . Prevalence, incidence, and mortality rates increase with age. Prevalence is higher in men, but total mortality is similar in both sexes. Incidence and mortality are generally higher in whites, blue-collar workers, and people with fewer years of formal education, probably because these groups have a higher prevalence of smoking. COPD seems to aggregate in families independent of a1-antitrypsin (a1-antiprotease inhibitor) deficiency (Anderson, 1993). COPD is increasing worldwide because of the increase in smoking in developing countries, the reduction in mortality due to infectious diseases, and the widespread use of biomass fuels. It caused an estimated 2.74 million deaths worldwide in the year 2000 and is projected to become one of the top 5 causes of disease burden globally by the year 2020 (Babakus, 1992).

Question No. 2

Mrs T with preexisting airway reactivity (defined by increased sensitivity to inhaled methacholine), even in the absence of clinical asthma, are at greater risk of developing COPD than are those without. Low body weight, childhood respiratory disorders, and exposure to passive cigarette smoke, air pollution, and occupational dust (eg, mineral dust, cotton dust) or inhaled chemicals (eg, cadmium) contribute to the risk of COPD but are of minor importance compared with cigarette smoking. Genetic factors: The best-defined causative genetic disorder is a1-antitrypsin deficiency, which is an important cause of emphysema in nonsmokers and influences susceptibility to disease in smokers (Babakus, 1992). Polymorphisms in microsomal epoxide hydrolase, vitamin D-binding protein, IL-1ß, IL-1 receptor antagonist, phospholipase A2, matrix metalloproteinase 9, and ADAM-33 genes are all associated with rapid decline in forced expiratory volume in 1 sec (FEV1) in selected populations (Bearden, 1983). Inhalational exposure: Of all inhalational exposures, cigarette smoking is the primary risk factor in most countries, although only about 15% of smokers develop clinically apparent COPD; an exposure history of 40 or more pack-years is especially predictive. Smoke from burning biomass fuels for indoor cooking and heating is an important contributing factor ...