Download RES-ML2-COPD_FINAL

TOBACCO AND CHRONIC OBSTRUCTIVE
PULMONARY DISEASE (COPD)
Mini Lecture 2
Module: Effects of Tobacco on the
Respiratory System
Objectives of the Mini Lecture
GOAL OF MINI LECTURE: Provide students with
knowledge about the harmful effects of tobacco on chronic
obstructive pulmonary disease (COPD), and the importance
of smoking cessation counseling for COPD patients.
LEARNING OBJECTIVES
Students will be able to:
• Describe the burden of smoking among COPD patients.
• Describe the association between smoking and COPD
and the impact of smoking on COPD.
• Understand the importance of cessation counseling for
COPD patients.
Contents
Core Slides
Optional Slides
1. Global Burden of COPD
2. Smoking: A Risk Factor for
COPD
3. Smoking and Respiratory
Infection: Mechanisms
4. Secondhand Smoke and
COPD
5. Indoor Air Pollution and
COPD
6. Smoking Cessation: COPD
Patients
7. Cessation Messages:
COPD Patients
1. COPD Prevalence in India
2. Pathophysiology of COPD
3. Immunological Aspect of
COPD
4. Smoking, Chronic
Bronchitis, and COPD
Mortality
CORE SLIDES
Tobacco and Chronic Obstructive
Pulmonary Disease (COPD)
Mini Lecture 2
Module: Effects of Tobacco on the
Respiratory System
Global Burden of COPD
• COPD is an inflammatory lung disease that is
characterised by almost irreversible airflow limitation.1
• In 2002, COPD was the 5th leading cause of death in the
world, and it is predicted to cause 7.8% of global deaths in
2030.2
1. Calverley and Walker 2003; 2. Mathers and Loncar 2006
Smoking: A Risk Factor for COPD
• Smoking leads to airway inflammation, and hence
induces hyper-production of mucus.1
• Chronic mucus production can lead to COPD, with
contributions from other factors: genetic, life-style,
infections, etc.1
• Chronic bronchitis is a strong predictor of COPD leading
to higher COPD hospitalisation and death rates.1
1. Pelkonen 2008
Smoking and Respiratory
Infection: Mechanisms
Structural changes:
• Peribronchiolar inflammation and fibrosis
• Mucosal permeability increase and changes in
pathogen adherence
• Impairment of the mucociliary clearance
• Disruption of the respiratory epithelium1
Immunologic mechanisms:
• Decreased immune response & circulating
immunoglobulins
• Impaired cellular immunity1
1. Arcavi and Benowitz 2004
Secondhand Smoke and COPD
• Exposure to SHS at home or at work, particularly high
levels of exposure, increases the chances of COPD by
as much as 50%.1
• In China, about 11.6% of deaths among never smokers
are attributable to COPD.1
1. Yin et al 2007
Indoor Air Pollution and COPD
• Indoor air pollution is cumulative: combustion of solid
fuels+ indoor smoking
• Increases risk of COPD, particularly in women and
children
• To reduce indoor air pollution:
• Substitute solid fuels with LPG or electricity
• Locate kitchen outside living/sleeping areas
• Adequately ventilate kitchens
• Minimize exposure (e.g., smokeless chullahs)
• Stop/minimize indoor smoking
Jindal 2004
Smoking Cessation: COPD Patients
• Smoking accelerates progression of COPD.1
• Smoking cessation programs can help COPD patients
quit for the long term.
• Even in severe COPD cases, cessation slows the loss of
lung function and improves survival.2
1. Sundblad et al. 2008; 2. Godtfredsen et al. 2008
Cessation Messages:
COPD Patients
• Smoking cessation is of critical importance for patients
with COPD.
• Doctors should ask all COPD patients about smoking
and second hand smoke exposure.
• Doctors should advise all COPD patients to quit smoking
and avoid second hand smoke.
OPTIONAL SLIDES
Tobacco and Chronic Obstructive
Pulmonary Disease (COPD)
Mini Lecture 2
Module: Effects of Tobacco on the
Respiratory System
COPD Prevalence in India
• Prevalence of COPD from India (from different
population-based studies): highly variable
• Male subjects: 2.12% to 9.4% (North India), 1.4% to
4.08% (South India)
• Female subjects: 1.33% to 4.9% (North India), 2.55% to
2.7% (South India)
• Median prevalence rates (>30 years): Male – 5%,
Female – 2.7%
• More common in males
• Median male to female ratio: 1.6:1
Jindal et al. 2004
Pathophysiology of COPD
• Basic mechanism: innate and adaptive inflammatory
immune response.1
• Airway limitation in COPD patients can occur through:
• Infiltration of inflammatory cells and occlusion of
airway by inflammatory exudates.
• Thickening of airway walls due to repair and
remodeling process—hyperactivity of epithelial cells.
• Decrease of elastic recoil pressure at respiratory
bronchioles.2
1. Calverley and Walker 2003; 2. Hogg and Timens 2009
Immunological Aspect of COPD
• “Danger hypothesis” by Matzinger: immune system is
triggered not by the infective material, but by the cellular
stress or tissue damage.1
• Three-step mechanisms leading to COPD:
• Step 1: Activation of macrophages and neutrophils as
initial response to cigarette smoke (a healthy smoker)
• Step 2: T-cell activation and proliferation (Global
Initiative for Chronic Obstructive Lung Disease
(GOLD) stage 1 or stage 2, with progression to GOLD
3 or 4 with severe failure)
• Step 3: Adaptive immune response (GOLD 3 or 4)1
1. Cosio et al. 2009
Smoking, Chronic Bronchitis,
and COPD Mortality
• Smoking is a risk factor for chronic bronchitis, COPD,
deteriorating lung function, and mortality as end point.1
• 40% of smoker will develop chronic bronchitis, 25% of
smoker will develop COPD.1
• Deterioration of lung function and obstruction of airways
among patient with chronic bronchitis will lead to COPD.1
• Patients with rapid decline of FEV1 have 40% higher
probability of hospitalization and COPD-related death.1
1. Pelkonen 2008
The most important health message a doctor
can give to patients is to quit smoking.