Pulmonary COPD

Mr. Green is a 60-year-old former smoker with severe chronic obstructive pulmonary (COPD) and cardiac disease associated with frequent episodes of bronchospasm. Which of the following is a bronchodilator useful in COPD and least likely to cause cardiac arrh5rthmia ... 

TABLE 18.5 Models of Chronic Obstructive Pulmonary (COPD) Disease"... 

Pulmonary COPD, skeletal disorders which may restrict respiratory function Endocrine Addison s disease, thyroid dysfunction Gastrointestinal hepatic impairment, biliary tract impairment... 

Chronic obstructive pulmonary disease (COPD) affects over 5% of the adult population, is the fourth leading cause of death worldwide and is the only major cause of mortality that is increasing worldwide. It is an inflammatory disorder of the lungs, caused mainly, but not exclusively, by cigarette smoking. 15-20% of smokers develop COPD. 

During COPD, the following symptoms occur, usually in the order mucus hypersecretion, ciliary dysfunction, airflow limitation, pulmonary hyperinflation, gas exchange abnormalities, pulmonary hypertension and cor pulmonale. Acute exacerbations appear to be mainly triggered by bacteria, viruses or environmental pollutants. They lead to a worsening of lung functions, wasting and increased mortality their psychosocial impacts include depression and anxiety that may be associated with the will to die. 

Chronic Obstructive Pulmonary Disease. Figure 1 Pharmacotherapy of chronic obstructive pulmonary disease (COPD). 

COPD, chronic obstructive pulmonary disease EAE, experimental autoimmune encephalomyelitis RSV, respiratory syncytial virus SLE, systemic lupus erythematosus. 

Other disorders of the lower respiratory tract include emphysema (lung disorder in which the terminal bronchioles or alveoli become enlarged and plugged with mucus) and chronic bronchitis (chronic inflammation and possibly infection of die bronchi). Chronic obstructive pulmonary disease (COPD) is die name given collectively to emphysema and chronic bronchitis because die obstruction to die airflow is present most of the time. Asdima diat is persistent and present for most of die time may also be referred to as COPD. 

Con A Concanavalin A COPD Chronic obstructive pulmonary disease COS Fibroblast-like kidney cell line established from simian cells CoVF Cobra venom CP Creatine phosphate Cp Caeruloplasmin c.p.m. Counts per minute CPJ Cartilage/pannus junction Cr The chemical symbol fir chromium CR Complement receptor CRl, CR2 CR4 Complement receptor types 1, 2 and 4 CR3-a Complement receptor type 3-[Pg.281]

Smoking cessation is the only intervention known to slow the rate of decline in pulmonary function in patients with COPD. 

In symptomatic patients with severe COPD and frequent exacerbations, regular treatment with inhaled corticosteroids decreases the number of exacerbations per year and improves health status however, corticosteroids do not slow the longterm decline in pulmonary function. 

In advanced COPD, airflow obstruction, damaged bronchioles and alveoli, and pulmonary vascular abnormalities lead to impaired gas exchange. This results in hypoxemia and eventually hypercapnia. Hypoxemia is initially present only during exercise but occurs at rest as the disease progresses. Inequality in the ventilation/perfusion ratio (VAQ) is the major mechanism behind hypoxemia in COPD. 

Pulmonary hypertension develops late in the course of COPD, usually after the development of severe hypoxemia. It is the most common cardiovascular complication of COPD and can result in cor pulmonale, or right-sided heart failure. Hypoxemia plays the primary role in the development of pulmonary hypertension by causing vasoconstriction of the pulmonary arteries and by promoting vessel wall remodeling. Destruction of the pulmonary capillary bed by emphysema further contributes by increasing the pressure required to perfuse the pulmonary vascular bed. Cor pulmonale is associated with venous stasis and thrombosis that may result in pulmonary embolism. Another important systemic effect is the progressive loss of skeletal muscle mass, which contributes to exercise limitations and declining health status. 

A suspected diagnosis of COPD should be based on the patient s symptoms and/or history of exposure to risk factors. Spirometry is required to confirm the diagnosis. The presence of a postbronchodilator FEV,/FVC ratio less than 70% [the ratio of FEV, to forced vital capacity (FVC)] confirms the presence of airflow limitation that is not fully reversible.1,2 Spirometry results can further be used to classify COPD severity (Table 12-1). Full pulmonary function tests (PFTs) with lung volumes and diffusion capacity and arterial blood gases are not necessary to establish the diagnosis or severity of COPD. 

An integrated approach of health maintenance (e.g., smoking cessation), drug therapy, and supplemental therapy (e.g., oxygen and pulmonary rehabilitation) should be used in a stepwise manner. Table 12-2 provides an overview of the management of stable COPD. 

Pulmonary rehabilitation results in significant and clinically meaningful improvements in dyspnea, exercise capacity, health status, and health care utilization.10 It should be considered for patients with COPD who have dyspnea or other respiratory symptoms, reduced exercise capacity, a restriction in activities because of their disease, or impaired health status.1... 

Leukotriene modifiers (e.g., zafirlukast and montelukast) have not been adequately evaluated in COPD patients and are not recommended for routine use. Small, short-term studies showed improvement in pulmonary function, dyspnea, and quality of life when leukotriene modifiers were added on to inhaled bronchodilator therapy.27,28 Additional long-term studies are needed to clarify their role. 

A 65-year-old man with a history of osteoarthritis and chronic obstructive pulmonary disease (COPD) comes to your clinic complaining of burning abdominal pain. The pain has worsened over the past 2 weeks it is worse at night and after meals. 

Asthma, COPD, pulmonary embolism, pneumonia, hyperventilation Other... 

COPD, chronic obstructive pulmonary disease CVA, cerebrovascular accident. 

Improvement in symptoms should occur within 48 to 72 hours after initiation of therapy for most patients with CAP. Response to therapy could be slowed in patients with underlying pulmonary disease such as moderate to severe asthma, COPD, or emphysema. In patients not responding to therapy with no underlying factors that would suggest a slowed response to therapy, then other infectious and noninfectious reasons must be considered. The infection could be caused by a pathogen not covered by the initial therapy, a drug-resistant isolate could be present, or more severe infection could be present (nonpulmonary), and the patient should be... 

COPD Chronic obstructive pulmonary disease EENT Eyes, ears, nose, throat... 

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