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:: BPCOE FISIOPATOLOGIA ::
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Management of severe COPD
Wouters EF
- Department of Respiratory Medicine, UniversityHospitalMaastricht, 6229 HX Maastricht, Netherlands. e.wouters@lung.azm.nl
Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality worldwide, and the burden of the disorder will continue to increase over the next 20 years despite medical intervention. Apart from smoking cessation, no approach or agent affects the rate of decline in lung function and progression of the disease. Especially in the later phase, COPD is a multicomponent disorder, and various integrated intervention strategies are needed as part of the optimum management programme. This seminar describes largely non-pharmacological interventions aimed at improving health status and function of disabled patients. Exacerbations become progressively more troublesome as baseline lung function declines, commonly necessitating hospital admission and associated with the development of acute respiratory failure.
Publication Types:
• Review
• Review, Tutorial
PMID: 15351196 [PubMed - indexed for MEDLINE]
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Respiratory muscle fibres: specialisation and plasticity
Polla B, D'Antona G, Bottinelli R, Reggiani C
- Hospital S Biagio, Department of Pneumology, Alessandria, Italy. bpolla@ospedale.al.it
Skeletal muscles are composed of fibres of different types, each type being identified by the isoform of myosin heavy chain which is expressed as slow 1, fast 2A, fast 2X, and fast 2B. Slow fibres are resistant to fatigue due to their highly oxidative metabolism whereas 2X and 2B fibres are easily fatiguable and fast 2A fibres exhibit intermediate fatigue resistance. Slow fibres and fast fibres are present in equal proportions in the adult human diaphragm while intercostal muscles contain a higher proportion of fast fibres. A small fibre size, abundance of capillaries, and a high aerobic oxidative enzyme activity are typical features of diaphragm fibres and give them the resistance to fatigue required by their continuous activity. Because of their fibre composition, intercostal muscles are less resistant to fatigue. The structural and functional characteristics of respiratory muscle fibres are not fixed, however, and can be modified in response to several physiological and pathological conditions such as training (adaptation to changes in respiratory load), adaptation to hypoxia, age related changes, and changes associated with respiratory diseases. The properties of respiratory muscle fibres can also be modified by pharmacological agents such as beta2 agonists and corticosteroids used for the treatment of respiratory diseases.
Publication Types:
• Review
• Review, Tutorial
PMID: 15333861 [PubMed - indexed for MEDLINE]
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Pathophysiology of airflow limitation in chronic obstructive pulmonary disease
Hogg JC
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James Hogg iCAPTURE Centre for Cardiovascular and Pulmonary Research, University of British Columbia and St Paul's Hospital, Room 166-1081, Burrard Street, Vancouver, BCV6Z 1Y6, Canada. j.bekhof@isala.nl
The airflow limitation that defines chronic obstructive pulmonary disease (COPD) is the result of a prolonged time constant for lung emptying, caused by increased resistance of the small conducting airways and increased compliance of the lung as a result of emphysematous destruction. These lesions are associated with a chronic innate and adaptive inflammatory immune response of the host to a lifetime exposure to inhaled toxic gases and particles. Processes contributing to obstruction in the small conducting airways include disruption of the epithelial barrier, interference with mucociliary clearance apparatus that results in accumulation of inflammatory mucous exudates in the small airway lumen, infiltration of the airway walls by inflammatory cells, and deposition of connective tissue in the airway wall. This remodelling and repair thickens the airway walls, reduces lumen calibre, and restricts the normal increase in calibre produced by lung inflation. Emphysematous lung destruction is associated with an infiltration of the same type of inflammatory cells found in the airways. The centrilobular pattern of emphysematous destruction is most closely associated with cigarette smoking, and although it is initially focused on respiratory bronchioles, separate lesions coalesce to destroy large volumes of lung tissue. The panacinar pattern of emphysema is characterised by a more even involvement of the acinus and is associated with alpha1 antitrypsin deficiency. The technology needed to diagnose and quantitate the individual small airway and emphysema phenotypes present in people with COPD is being developed, and should prove helpful in the assessment of therapeutic interventions designed to modify the progress of either phenotype.
Publication Types:
• Review
• Review, Tutorial
PMID: 15325838 [PubMed - indexed for MEDLINE]
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Small airways in COPD
Barnes PJ
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National Heart and Lung Institute, ImperialCollege, London.
Publication Types:
• Comment
PMID: 15215476 [PubMed - indexed for MEDLINE]
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Chronic obstructive pulmonary disease
Calverley PM, Walker P
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Department of Medicine, University of Liverpool, Liverpool, UK. pmacal@liv.ac.uk
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Chronic obstructive pulmonary disease (COPD) is a major cause of death and disability worldwide. Recognition that the burden of this disorder will continue to increase over the next 20 years despite medical intervention has stimulated new research into the underlying mechanisms, leading to a rational basis for evaluation of existing therapies, and has suggested novel treatment approaches. Tobacco exposure remains the main but not exclusive cause of COPD. Whether the lung is injured by changes in the balance of proteases and antiproteases, tissue damage by oxidative stress, or a combination of the two is still not known. The genetic basis of susceptibility to COPD is now being studied as is the role of computed tomography in the identification of structural damage in individuals with less symptomatic disease. Clinical diagnosis still relies heavily on an appropriate history confirmed by abnormal spirometry. Smoking cessation is possible in a substantial proportion of individuals with symptoms but is most effective if withdrawal is supported by pharmacological treatment. Treatment with long-acting inhaled bronchodilators and, in more severe disease, inhaled corticosteroids reduces symptoms and exacerbation frequency and improves health status. Rehabilitation can be even more effective, at least for a year after the treatment. Recent guidelines have made practical suggestions about how to optimise these treatments and when to consider addition of oxygen, surgery, and non-invasive ventilation. Regular review of this guidance is important if future management advances are to be implemented effectively.
Publication Types:
• Review
• Review, Academic
PMID: 14522537 [PubMed - indexed for MEDLINE]
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