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Chronic Obstructive Pulmonary Disease & Chronic Bronchitis

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.HA

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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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Prevalence rates for airflow obstruction

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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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Gold Criteria for COPD Severity

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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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CXR . . .

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CXR . . .

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Emphysema

reduced parenchymal markings

mediastinal shift to the left (hyperinflation)

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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.