Chronic Obstructive Pulmonary Disease & Chronic Bronchitis DR.S.H.HASHEMI 1.
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Transcript of Chronic Obstructive Pulmonary Disease & Chronic Bronchitis DR.S.H.HASHEMI 1.
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COPD ranked as the fourth leading cause of death in 2000.
COPD : airflow limitation that is not fully reversible, . . . progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases .
Chronic bronchitis : cough with phlegm at least 3 months of the year, for at least 2 years.
* Emphysema : destruction and enlargement of the lung alveoli .
Occupational COPD or chronic bronchitis is best defined as ‘COPD or chronic bronchitis in a patient with a history of chronic exposure to pro-inflammatory agents in workplace air’.
Prevalence in occupational exposure M = W
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Risk factors
Major risk factors : tobacco smoke, occupational dust and chemicals, indoor/outdoor air pollution .
Mineral particulate and fibers Mining ( silica, gold, asbestos ) Tunneling ( dust, diesel exhaust ) Mineral processing Excavating Building Road construction Cement work Stone carving Farming Quarrying and carbon black manufacturing
Prevalence rates for COPD among miners range from 6 to 20% among non-smokers, and up to 60% among smokers .
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Risk factors . . .
Prevalence increases as exposure duration or intensity increases.
Among miners exposed to higher silica content dust even higher COPD rates are seen.
Welder & smelter ( metal fume, irritant gases ) Rubber manufacturing, tunnel workers and fire fighters ( irritant
gases , combustion products ). Organic dusts – wood, textiles, grain, food processing Organic dust exposure is associated with asthma,
hypersensitivity pneumonitis, chronic bronchitis, COPD.
Cedar sawmill workers and furniture workers ( wood dusts ) Food processing workers ( bakers ) Textile workers ( cotton dust → chronic bronchitis, byssinosis )
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Risk factors . . .
Agriculture Cereal grains dust Animal feed dust Manure gases and fumes Endotoxin and fungal components
Smoking Tobacco smoker Passive smoker
* Although pack-years of cigarette smoking is the most highly significant predictor of FEV1 only 15% of the variability in FEV1 is explained by pack-years.
* This finding suggests that additional environmental and/or genetic factors contribute to the impact of smoking on the development of airflow obstruction.
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Risk factors . . .
* Airway hyperresponsiveness is a risk factor for COPD .
* Although respiratory infections are important causes of exacerbations of COPD, the association of both adult and childhood respiratory infections to the development and progression of COPD remains to be proven.
* Severe α1 antitrypsin (α1AT) deficiency (Pi ZZ) is a proven genetic risk factor for COPD .
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Assessment of exposure
Most research indicates that the relevant exposure duration is measured in years (or even decades) .
Many patients will have held more than one job, and exposure duration should be summed over all jobs with relevant exposures.
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Clinical manifestationHistory Couph Productive sputum Exertional dyspnea
* Often described as increased effort to breathe, heaviness, air hunger, or gasping, can be insidious .
* Activities involving significant arm work, particularly at or above shoulder level, are particularly difficult for patients with COPD.
* Activities that allow the patient to brace the arms and use accessory muscles of respiration are better tolerated (pushing a shopping cart, walking on a treadmill, or pushing a wheelchair).
* Patients may also develop resting hypoxemia and require institution of supplemental oxygen.
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Clinical manifestation . . .
* Physical Findings* Early stages → usually have an entirely normal P/E* Severe disease →
* Prolonged expiratory phase and expiratory wheezing
* Signs of hyperinflation (barrel chest, enlarged lung volumes with poor diaphragmatic excursion )
* Use of accessory muscles of respiration, sitting in the characteristic "tripod" position to facilitate the actions of the sternocleidomastoid, scalene, and intercostal muscles.
* Cyanosis ( lips and nail beds )
* Systemic wasting, weight loss, bitemporal wasting, diffuse loss of subcutaneous adipose tissue
* Paradoxical inward movement of the rib cage with inspiration (Hoover's sign)
* Clubbing not a sign of COPD, and its presence should alert the clinician to initiate an investigation for causes of clubbing (lung cancer )
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Laboratory Findings
PFT The hallmark of COPD is airflow obstruction:
↓ FEV1 , ↓ FEV1/FVC ↑ TLC , ↑FRC , ↑ RV Emphysema : ↓ diffusing capacity
* In contrast to asthma, the reduced FEV1 in COPD seldom shows large responses to inhaled bronchodilators, although improvements up to 15% are common.
* Air trapping (↑ RV, ↑ RV/TLC )
* Body mass index is a better predictor of mortality than pulmonary function alone.
* The degree of airflow obstruction is an important prognostic factor in COPD and is the basis for the GOLD disease classification .
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Laboratory Findings
* ABG and oximetry → resting or exertional hypoxemia
* Echo → right ventricular hypertrophy
* CXR :* Emphysema: Obvious bullae, paucity of parenchymal markings,
hyperlucency* Hyperinflation: flattening of the diaphragm
* CT- scan is the current definitive test for establishing the presence or absence of emphysema
* Recent guidelines have suggested testing for α1AT deficiency in all subjects with COPD or asthma with chronic airflow obstruction.
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Treatment
* Smoking Cessation:* Middle-aged smokers who were able to successfully stop smoking
experienced a significant improvement in the rate of decline in pulmonary function.
* Bupropion
* Nicotine replacement therapy (gum, transdermal patches, inhaler, nasal spray )
* Bronchodilators* Inhaled route is preferred (the incidence of side effects is lower )
* Anticholinergic Agents:* Ipratopium bromide does not appear to influence the rate of decline of
lung function, it improves symptoms , produces acute improvement in FEV1 and ↓ sputum .
* Tiotropium bromide, a long- acting anticholinergic, improve symptoms and reduce exacerbations.
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Treatment . . .
* Beta Agonists:* Long-acting inhaled agonists, such as salmeterol, have
benefits comparable to ipratopium bromide.* Their use is more convenient than short-acting agents.
* The addition of a β agonist to inhaled anticholinergic therapy has been demonstrated to provide incremental benefit.
* Side effects : tremor, tachycardia
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Treatment . . .
* Inhaled Glucocorticoids:* Reduce exacerbation frequency by ~25% * Reduce mortality by ~25%
* Inhaled glucocorticoids should be considered in patients with:* Frequent exacerbations, defined as two or more per
year* Significant amount of acute reversibility in response to
inhaled bronchodilators (asthmatic component )
* Side effets : oropharyngeal candidiasis , loss of bone density
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Treatment . . .
* Oral Glucocorticoids:* Chronic use of oral glucocorticoids for treatment of COPD is not
recommended .
* Side effects: osteoporosis, weight gain, cataracts, glucose intolerance, increased risk of infection .
* Patients tapered off chronic low-dose prednisone(~10 mg/d) did not experience any adverse effect .
* Theophylline:* Moderate to severe COPD* Improvements in expiratory flow rates and vital capacity * Slight improvement in arterial oxygen and carbon dioxide
levels
* Side effect : Nausea, tachycardia , tremor
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Treatment . . .
* Oxygen:* Supplemental O2 is the only pharmacologic therapy demonstrated to
decrease mortality in patients with COPD.* Exertional hypoxemia * Nocturnal hypoxemia
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Treatment . . .
* N-acetyl cysteine:* Mucolytic * Antioxidant
* Intravenous α1AT augmentation therapy
* Influenza vaccine : annually
* Polyvalent pneumococcal vaccine
* Pulmonary Rehabilitation
* Lung Volume Reduction Surgery (LVRS):* Reduce the volume of lung in patients with emphysema
* Lung Transplantation :* COPD is the single leading indication for lung transplantation
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Exacerbations of COPD
* Episodes of increased dyspnea and cough and change in the amount and character of sputum.
* Fever, myalgias, and sore throat
* The frequency of exacerbations increases as airflow obstruction increases .
* Risk factors:* Bacterial respiratory infections* Viral respiratory infections
* Prevention: * Inhaled glucocorticoids did reduce the frequency of exacerbations by
25–30%* Chronic oral glucocorticoids are not recommended for this purpose.