Chronic Obstructive Pulmonary Disease


Figure 2: An Axial Image from a Chronic Obstructive Pulmonary Disease Global Initiative for Chronic Obstructive Lung Disease Stage 3 Subject


biochemistry and organ function.32 The mechanism of these effects is


not known, but is believed to be related to enhanced systemic inflammation and oxidative stress.33


Weight loss is considered to be a


poor prognostic factor in COPD. Up to ~50% of patients with COPD suffer from protein-calorie malnutrition. Loss of lean body mass also results in peripheral muscle dysfunction, reduction in tolerance to effort and decreased quality of life.34


Peripheral skeletal muscle dysfunction is


another systemic feature of COPD. The weakness is predominantly in the lower limbs owing to gait-related limitation from dyspnea. The cause might relate to an intrinsic reduction in the number of mitochondria in the muscles, and is contributed to by nutritional depletion, corticosteroid use, systemic inflammation, deconditioning, hypoxia, and decreased anabolic hormone levels.35


Osteoporosis is frequently found


in patients with COPD and could be related to the use of corticosteroids. Both inhaled and oral corticosteroids can cause bone loss in this patient population, although there are studies showing decreased bone density in patients not receiving corticotherapy.36


COPD is also The image displays signs of centrilobular emphysema in the lung apices.


resonance imaging (MRI). Chest X-ray features in COPD are shown in Figure 1. Although the chest X-ray is commonly available, it lacks sensitivity in detecting both airway disease and mild emphysema, and is not generally amenable to objective analysis. CT has become the standard modality to visualize lung disease objectively. It can provide useful measures of the presence and extent of emphysema, airway disease, and, more recently, pulmonary vascular disease for clinical correlation (see Figure 2). However, it does face limitations in standardization across brands and generations of scanners, and the ionizing radiation associated with image acquisition is of concern to both patients and healthcare providers. Newer techniques, such as OCT and MRI, offer exciting in vivo insights into lung structure and function that were previously available only in necropsy specimens and physiology laboratories.28


Laboratory


Arterial blood gases typically reveal mild to moderate hypoxemia without hypercapnia in mild COPD. As the disease progresses, the hypoxemia becomes more severe and hypercapnia develops.


Hypercapnia occurs with increasing frequency as the FEV1 falls below one liter or 40% of predicted value.29


during exacerbations, exercise and sleep.30


should be completed when emphysema is present in a young individual (e.g. ≤45 years of age), or in a non-smoker or minimal smoker. AAT deficiency should also be suspected when emphysema is characterized by predominant basilar changes on the chest radiograph and in patients with a family history of emphysema and/or liver disease or if a history of current or previous panniculitis is present.31


Systemic Manifestation of Chronic Obstructive Pulmonary Disease


The pathogenesis and clinical manifestations of COPD are not restricted to pulmonary inflammation and structural remodeling. Rather, this disease is associated with clinically significant systemic alterations in


10


Blood gas abnormalities worsen AAT deficiency testing


considered an independent risk factor for cardiovascular disease, including coronary artery and cerebrovascular disease. Endothelial dysfunction, owing to excessive systemic inflammation and hypoxia is believed to be the cause. Although COPD is traditionally associated with polycythemia, the systemic inflammatory components can interfere with erythropoietin and result in anemia of chronic disease,38 shown to be linked to an increased mortality risk in these patients.38


which was Treatment


COPD therapy should be approached in a stepwise manner based on a scale of severity. The most frequently used scale is based on the GOLD guidelines.7


Therapy Irrespective of Chronic Obstructive Pulmonary Disease Stage


Vaccination constitutes one of the preventive strategies of infective exacerbations in COPD. Pneumococcal vaccination is recommended for


patients older than 65 years or whose predicted FEV1 is <40%. Unlike in the general population, randomized trials failed to show benefit of the vaccine on either morbidity or mortality.39


Annual influenza vaccination is


also recommended and is associated with a significant reduction in the rate of COPD exacerbation.40


Smoking cessation is the one intervention


that is shown to reduce the accelerated decline in lung function associated with COPD. The US Public Health Service recommends a five-step program intervention to healthcare professionals to help their patients stop smoking. Medical therapy includes nicotine replacement therapy, bupropion and varenicline, whereas counseling programs include social support and behavior modification techniques. This approach is associated with an ~25% long-term abstinence rate.41–44


Therapy by Stage


For mild COPD (FEV1 ≥80%), bronchodilators are the mainstay of therapy, improving symptoms by reducing hyperinflation. They are delivered by various methods, including metered dose inhalers (MDI), a dry powder inhaler, or aerolized solution. In mild COPD, symptoms are usually intermittent and it is common to prescribe an as-needed short-acting bronchodilator. Inhaled β-agonists and an anticholinergic are frequently used together as their effect is additive. Both are equally effective in improving symptoms and lung function, but neither was


US RESPIRATORY DISEASE


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