chronic obstructive pulmonary disease (COPD) Flashcards

1
Q

what is COPD? what are the two diseases that are encompassed by COPD?

A

Chronic obstructive pulmonary disease (COPD) is a general term for pulmonary disorders characterized by chronic air ow limitation from the lungs that is not fully reversible. COPD encompasses two main diseases: chronic bronchitis and emphysema. Chronic bronchitis is defined as a condition associated with excessive tra- cheobronchial mucus production (at the bronchial level) sufficient to cause a chronic cough with sputum produc- tion for at least 3 months in at least 2 consecutive years in a patient in whom other causes of productive chronic cough have been excluded. Emphysema is defined as the presence of permanent enlargement of the air spaces distal to the terminal bronchioles accompanied by destruction of alveolar walls or septa (at the acinar level) without obvious brosis.1 These conditions are related, often represent the progression of disease, and may have overlapping symptoms, making differentiation difficult. Accordingly, experts have recommended use of the des- ignation COPD over the traditional terms chronic bron- chitis and emphysema. COPD currently is diagnosed on the basis of the presence of cough, sputum production, and dyspnea, together with an abnormal measurement of lung function.2

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2
Q

wht is the most important cause of COPD? what are some other causes?

A

Worldwide, the most important cause of COPD is tobacco smoking. Approximately 12.5% of current smokers and 9% of former smokers have COPD.4 Smoking also accounts for 85% to 90% of COPD- related deaths in both men and women. The risk for development of COPD is dose-related and increases with the number of cigarettes smoked per day and dura- tion of smoking.5,6 The risk of death from COPD is 13 times higher in female smokers and 12 times higher in male smokers than in nonsmokers of the same gender.5 Despite the increased risk, only about one in five chronic smokers develop COPD. This observation suggests that genetic susceptibility to the production of inflammatory mediators (i.e., cytokines) in response to smoke expo- sure plays an important role. In addition to cigarette smoking, long-term exposure to occupational and envi- ronmental pollutants and the absence or deficiency of α1-antitrypsin are other factors that contribute to COPD. α1-antitrypsin is made in the liver and neutral- izes neutrophil elastase.

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3
Q

what is the pathophysiology?

A

Chronic exposure to cigarette smoke induces pathophys- iologic responses of the airways and lung tissue. Chronic bronchitis involves the large and small airways. In the large airways, tobacco smoke and irritants induce thick- ened bronchial walls with in ammatory cell in ltrate, increased size of the mucous glands, and goblet cell hyperplasia. Obstruction is exacerbated in the small airways by narrowing, scarring, increased sputum pro- duction, mucous plugging, and collapse of peripheral airways resulting from the loss of surfactant7 (Figure 7-1). Obstruction is present on both inspiration and expiration
Emphysematous changes occur as chronic smoke inhalation injures lung parenchyma. The alveolar epithe- lium is damaged, causing a release of inflammatory mediators that attract activated macrophages and neu- trophils. These in ammatory cells release enzymes (elastase) that destroy the alveolar walls, resulting in enlarged air spaces distal to the terminal bronchioles and loss of elastic recoil of the lungs (Figure 7-2). Obstruc- tion is caused by the collapse of these unsupported and enlarged air spaces and is evident on expiration—not inspiration.7
COPD usually is progressive, and the course is one of deterioration and periodic exacerbations, unless inter- vention is provided early in its onset.6 The types of complications that develop vary depending on the site of damage. With continued exposure to primary etiologic factors (cigarette smoking, environmental pollutants), COPD usually results in progressive dyspnea and hyper- capnia to the point of severe debilitation (clinically significant disability will develop in 15% to 20% of the patients).8 Recurrent pulmonary infections with Haemophilus influenzae, Moraxella catarrhalis, and Streptococcus pneumoniae are especially common with bronchitis. These acute exacerbations are managed with antibiotics. Pulmonary hypertension can develop and, in the absence of supplemental oxygen therapy, lead to cor pulmonale (right-sided heart failure). Patients with emphysema more frequently are found to have enlarged air spaces, with a higher incidence of thoracic bullae and pneumothorax. Poor quality of sleep secondary to noc- turnal hypoxemia is common with COPD. Although COPD is an irreversible process for which no cure exists, avoidance of pulmonary irritants can be of signi cant bene t in decreasing the morbidity and mortality rates for both diseases.

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4
Q

what does COPD have to do with nitrous?

A

• Contraindication of nitrous oxide – COPD is one of them. If they have emphysema, and these emphysema bullae then you can get a gas coming in very quickly, more quickly than leaving so you could get that “balloon” popping and you could have a pneumothorax.

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