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SOURCE

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Source: Bourdet SV, Williams DM. Chronic obstructive pulmonary disease. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM, eds. Pharmacotherapy: A Pathophysiologic Approach. 10th ed. New York, NY: McGraw-Hill; 2017. http://accesspharmacy.mhmedical.com/content.aspx?bookid=1861&sectionid=146058280. Accessed April 13, 2017.

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CONDITION/DISORDER SYNONYMS

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  • Chronic Obstructive Pulmonary Disease (COPD)

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DEFINITION

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  • Lung disease characterized by air flow limitation that is not fully reversible and is both chronic and progressive.

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ETIOLOGY

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  • Cigarette smoking accounts for 85–90% of cases.

  • Other causes include environmental exposures and host factors.

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PATHOPHYSIOLOGY

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  • Inhalation of noxious particles and gases activates neutrophils, macrophages, and lymphocytes that release tumor necrosis factor-α and other inflammatory mediators, causing destructive lung changes.

  • Oxidants from cigarette smoke cause tissue damage, promote inflammation, and inhibit antiprotease activity.

  • Hereditary deficiency of α1-antitrypsin increases risk for premature emphysema.

  • Inflammatory exudate leads to increased number and size of goblet cells, increased mucus secretion, and impaired ciliary motility.

  • Airway smooth muscle and connective tissue thickens; chronic inflammation causes fibrosis and narrowing of small airways.

  • Late structural changes increase pulmonary pressures; in severe COPD, secondary pulmonary hypertension leads to right-sided heart failure (cor pulmonale).

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EPIDEMIOLOGY

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  • 24 million Americans have COPD.

  • COPD accounts for about 12,000 deaths in the United States annually, making it the 3rd leading cause of death.

  • Women are twice as likely to be diagnosed with COPD compared to men.

  • Mortality rate is six times higher in men, but death rate in women has doubled over last 25 years.

  • Mortality rate is higher in whites than blacks.

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PREVENTION AND SCREENING

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  • Abstention from cigarette smoking best means of preventing COPD.

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RISK FACTORS

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  • Environmental exposures: tobacco smoke, occupational dusts and chemicals, air pollution.

  • Host factors: genetic predisposition (eg, α1-antitrypsin deficiency [AAT]), airway hyperresponsiveness, impaired lung growth.

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CLINICAL PRESENTATION

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SIGNS AND SYMPTOMS
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  • Initially, chronic cough and sputum production; symptoms may be present for several years before dyspnea develops.

  • Physical examination often normal in mild disease. With more severe disease, patients may have cyanosis, “barrel chest,” resting tachypnea, shallow breathing, pursing of lips during expiration, and use of accessory respiratory muscles.

  • During COPD exacerbations, patients may have worsening dyspnea, increased sputum volume and purulence, chest tightness, increased need for bronchodilators, malaise, fatigue, and decreased exercise tolerance.

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DIAGNOSIS

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MEANS OF CONFIRMATION AND DIAGNOSIS
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  • Diagnosis based in part on symptoms and history of exposure to risk factors.

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LABORATORY TESTS
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  • Arterial blood gases (ABG) with low PaO2 (45–60 mm Hg) and elevated PaCO2 (50–60 mm Hg) in more severe disease.

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