1. Chronic Obstructive Pulmonary Disease & Chronic Bronchitis
DR.S.H.HASHEMI

2. 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

3. 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 .

4. 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 )

5. Risk factors . . . Agriculture Smoking
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.

6. 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 .

7. Prevalence rates for airflow obstruction

8. 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.

9. 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.

10. 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 )

11. 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 .

12. Gold Criteria for COPD Severity

13. 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.

14. CXR . . .

15. CXR . . .

16. Emphysema reduced parenchymal markings
mediastinal shift to the left (hyperinflation)

17. Treatment Smoking Cessation: Bronchodilators Anticholinergic Agents:
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.

18. 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

19. 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

20. 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

21. Treatment . . .
Oxygen:
Supplemental O2 is the only pharmacologic therapy demonstrated to decrease mortality in patients with COPD.
Exertional hypoxemia
Nocturnal hypoxemia

22. 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

23. 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.