DR.S.H.HASHEMI
Chronic Obstructive Pulmonary Disease
&
Chronic Bronchitis
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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
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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%
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among non-smokers, and up to 60% among smokers .
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.
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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
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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 manifestation
History
 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:
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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.
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