Emphysema Exam Study Guide Complete

Emphysema Exam Study Guide Complete Overview Chronic airflow obstruction disease characterized by permanent enlargement of air spaces distal to the terminal bronchioles and destruction of alveolar walls (without fibrosis) with accompanying exertional dyspnea One of several diseases usually labeled collectively as chronic obstructive pulmonary disease or chronic obstructive lung disease Three morphologic types: centriacinar (also known as centrilobular)—the most common type of emphysema, begins in respiratory bronchioles and spreads peripherally pan acinar—destroys the entire alveolus uniformly, most commonly in the lower portion of the lungs paraseptal (also known as distal acinar)—involves the distal airway structures, alveolar ducts, and alveolar sacs Pathophysiology Exposure to a noxious stimulus leads to recurrent inflammation associated with the release of proteolytic enzymes from lung cells, which causes abnormal, irreversible enlargement of the air spaces distal to the terminal bronchioles. Amount of alveolar surface area available for gas exchange decreases. This enlargement leads to the destruction of alveolar walls in the distal or terminal airways, which results in a breakdown of elasticity. Elastic recoil is reduced, limiting airflow. (See What happens in emphysema.) Supporting alveolar structures are lost, leading to narrowing of the airway, which further limits airflow. The airways and lung parenchyma are involved. These changes result in impaired carbon dioxide and oxygen exchange. Causes • Cigarette smoking (the most common cause) • Cigar and pipe smoking • Marijuana smoke • Passive smoke • Air pollution • Genetic deficiency of alpha1-antitrypsin Risk Factors • Smoking • Exposure to secondhand smoke • Occupational or environmental exposure to fumes, dust, pollution, or chemicals • Recurrent or chronic respiratory infections Complications • Recurrent respiratory tract infections • Cor pulmonale • Respiratory failure • Peptic ulcer disease • Spontaneous pneumothorax • Pneumomediastinum • Death Assessment History • Long-term cigarette smoking • Gradual decline in exercise ability that becomes more pronounced as the patient ages and the disease progresses • Shortness of breath • Dyspnea that begins on mild exertion and progresses to minimal exertion over time (dyspnea is the predominant symptom) • Frequent respiratory infections • Minimal cough with scant sputum • Anorexia and significant weight loss • Malaise Physical Findings • Barrel chest • Pursed-lip breathing • Use of accessory muscles • Cyanosis • Clubbed fingers and toes • Tachypnea • Decreased tactile fremitus • Decreased chest expansion • Hyper resonance • Decreased breath sounds • Crackles • Inspiratory wheeze • Prolonged expiratory phase with grunting respirations • Distant heart sounds • Increased jugular venous pressure (with advanced disease) • Peripheral edema (with advanced disease) • Paradoxical chest/abdominal wall movements • Deceased mental status related to hypercapnia or hypoxia Diagnostic Test Results Laboratory • Arterial blood gas (ABG) analysis shows decreased partial pressure of oxygen, normal partial pressure of carbon dioxide until late in the disease, and chronic respiratory acidosis leading to compensatory metabolic acidosis with disease progression. • Hemoglobin level test result is increased late in the disease; hematocrit is increased because of chronic hypoxemia. • Sputum examination reveals mucoid sputum with macrophages (in chronic disease) and purulent sputum with increased neutrophils and organisms (with