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Obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is characterized by airflow limitation that is not fuUy reversible. The airflow limitation is usually both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases. The most common conditions comprising COPD are chronic bronchitis and emphysema. [Pg.921]

Chronic bronchitis is associated with chronic or recurrent excess mucus secretion into the bronchial tree with cough that occurs on most days for at least 3 months of the year for at least 2 consecutive years when other causes of cough have been excluded. [Pg.921]

Emphysema is defined as abnormal, permanent enlargement of the airspaces distal to the terminal bronchioles, accompanied by destruction of their walls, but without obvious fibrosis. [Pg.921]

The most common etiology is exposure to environmental tobacco smoke, but other chronic inhalational exposures can also lead to COPD. Inhalation of noxious particles and gases stimulates the activation of neutrophils, macrophages, and CDS lymphocytes, which release a variety of chemical mediators, including tumor necrosis factor-o interleukin-8, and leukotriene B4. These inflammatory cells and mediators lead to widespread destructive changes in the airways, pulmonary vasculature, and lung parenchyma. [Pg.921]

The protective antiprotease ttj-antitrypsin (AAT) inhibits several protease enzymes, including neutrophil elastase. In the presence of unopposed AAT activity, elastase attacks elastin, which is a major component of alveolar walls. A hereditary deficiency of AAT results in an increased risk for prematiue development of emphysema. In the inherited disease, there is an absolute deficiency of AAT. In emphysema resulting from cigarettesmoking, the imbalance is associated with increased protease activity or reduced activity of antiproteases. Activated inflammatory cells release several other proteases, including cathepsins and metalloproteinases. In addition, oxidative stress reduces antiprotease (or protective) activity. [Pg.921]

The cells and processes that underlie COPD have not yet been elucidated. However, it is now recognized that, although COPD and asthma are characterized by airflow limitation and a chronic persistent inflammatory process, the nature of the inflammation differs markedly among these diseases, so that different drugs are likely to be effective in the treatment of these diseases (7). [Pg.101]

what is the evidence that chemokines are involved in COPD Several chemokines are involved in neutrophil chemotaxis and mainly belong to the CXCL family, of which CXCL8 (lL-8) is the most prominent member relevant to COPD. [Pg.101]

Marcel Dekker, Inc. 270 Madison Avenue. New York, New Yoik 10016 [Pg.101]

IL-8 levels are markedly elevated in the sputum and bronchoalveolar lavage (BAL) of patients with COPD and correlated with the extent of neutrophilic inflammation and disease severity (5,8,9). [Pg.102]

Recent reports demonstrate that T cells (Thl/Tcl) from the bronchial mucosa of patients with COPD predominantly express interferon-y (IFNy) and the [Pg.102]


Decrements in vigilance (i.e., ability to detect small changes in one s environment that occur at unpredictable times) decreased exercise performance in both healthy persons and those with chronic obstructive pulmonary disease... [Pg.368]

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. [Pg.362]

Chronic Obstructive Pulmonary Disease. Table 1 Pathological changes in chronic obstructive pulmonary... [Pg.363]

Chronic Obstructive Pulmonary Disease. Figure 1 Pharmacotherapy of chronic obstructive pulmonary disease (COPD). [Pg.364]

Sin DD, Man SEP (2006) Pharmacotherapy for mortality reduction in chronic obstructive pulmonary disease. Proc Am Thorac Soc 3 624-629... [Pg.366]

Cell BR, Cote CG, Marin JM et al (2004) The body-mass index, airflow obstruction, dyspnea, and exercise capacity index in chronic obstructive pulmonary disease. New Engl J Med 350 1005-1012... [Pg.366]

COPD, chronic obstructive pulmonary disease EAE, experimental autoimmune encephalomyelitis RSV, respiratory syncytial virus SLE, systemic lupus erythematosus. [Pg.1211]

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. [Pg.333]

Sympathomimetics (drugs that mimic the sympathetic nervous system) are used primarily to treat reversible airway obstruction caused by bronchospasm associated with acute and chronic bronchial asthma, exercise-induced bronchospasm, bronchitis, emphysema, bronchiectasis (abnormal condition of the bronchial tree), or other obstructive pulmonary diseases. [Pg.336]

Jubran A, Gross N, Ramsdell J, et al. Comparative cost-effectiveness analysis of theophylline and ipratropium bromide in chronic obstructive pulmonary disease. A three-center study. Chest 1993 103 678-84. [Pg.588]

Tabak, C. et al.. Chronic obstructive pulmonary disease and intake of catechins, flavonols, and flavones the MORGEN Study, Am. J. Respir. Crit. Care Med., 164, 61, 2001. [Pg.144]

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]

Mitral stenosis or regurgitation Mitral valve prolapse Chronic obstructive pulmonary disease Pulmonary embolism Idiopathic ("lone" atrial fibrillation) Thoracic surgery ... [Pg.115]

Monitor for adverse effects of 3-blockers—heart rate, blood pressure, fatigue, masking of symptoms of hypoglycemia and/or glucose intolerance (in patients with diabetes), wheezing or shortness of breath (in patients with asthma or chronic obstructive pulmonary disease), etc. [Pg.125]

Adapted from GOLD Science Committee. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. Updated 2005. Available at www.goldcopd.com. Used with permission. [Pg.234]


See other pages where Obstructive pulmonary disease is mentioned: [Pg.263]    [Pg.7]    [Pg.193]    [Pg.362]    [Pg.362]    [Pg.363]    [Pg.364]    [Pg.365]    [Pg.402]    [Pg.502]    [Pg.685]    [Pg.798]    [Pg.798]    [Pg.965]    [Pg.1047]    [Pg.1053]    [Pg.1489]    [Pg.124]    [Pg.336]    [Pg.564]    [Pg.628]    [Pg.647]    [Pg.149]    [Pg.221]    [Pg.95]    [Pg.231]    [Pg.233]   


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