The diagnosis is confirmed by spirometry. Patients with COPD may have multiple physical findings as follows:ĬOPD is often evaluated in patients with relevant symptoms and risk factors. Acute exacerbations of COPD usually present with increased dyspnea, productive cough, and wheezing. Those with liver disease, basilar emphysema, and a family history of emphysema should raise suspicion for alpha-1 antitrypsin deficiency. Patients should be questioned on their past medical history for other diseases such as asthma, allergies, and childhood respiratory infections. Those with a confirmed diagnosis of COPD should be asked about previous exacerbations, nighttime awakenings, inhaler usage, and the impact of the disease on activity level. They should be questioned on exposure to second-hand smoke, occupational and environmental exposures, and family history. While a smoking history is present in most cases, there are many without such history. Patients may also have wheezing and chest tightness. Patients usually present with complaints of chronic and progressive dyspnea, cough, and sputum production. ĬOPD will typically present in adulthood and often during the winter months. There is an increase in inflammation and air trapping often requiring corticosteroid and bronchodilator treatment. Īcute exacerbations of COPD are common and usually occur due to a trigger (e.g., bacterial or viral pneumonia, environmental irritants). Pulmonary hypertension may occur due to diffuse vasoconstriction from hypoxemia. The reduction in ventilation or increase in physiologic dead space leads to CO2 retention. As the disease progresses, impairment of gas exchange is often seen. The inability to fully exhale also causes elevations in carbon dioxide (CO2) levels. Hyperinflation of the lungs is often seen on imaging studies and occurs due to air trapping from airway collapse during exhalation. The inflammatory response and obstruction of the airways cause a decrease in the forced expiratory volume (FEV1) and tissue destruction leads to airflow limitation and impaired gas exchange. As opposed to smoking-related emphysema, AATD primarily involves the lower lobes. AATD should be suspected in COPD patients who present with liver damage. AATD is caused by misfolding of the mutated protein which can accumulate in the liver. Īlpha-1 antitrypsin deficiency is a rare cause of emphysema which involves a lack of antiproteases and the imbalance leaves the lung parenchyma at risk for protease-mediated damage. The protease-mediated destruction of elastin leads to a loss of elastic recoil and results in airway collapse during exhalation. Oxidants and excess proteases leading to the destruction of the air sacs. Neutrophils and macrophages are recruited and release multiple inflammatory mediators. In emphysema, an irritant (e.g., smoking) causes an inflammatory response. Emphysema describes one of the structural changes seen in COPD where there is destruction of the alveolar air sacs (gas-exchanging surfaces of the lungs) leading to obstructive physiology. The process is thought to involve oxidative stress and protease-antiprotease imbalances. COPD is an inflammatory condition involving the airways, lung parenchyma, and pulmonary vasculature.
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