copd (basic) 2014
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Reference: GOLD 20131
COPDBasic
Reference for Year 3 and Final Year Students
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Module Year 3 / Final Year
Title COPD
Lecturer Dr. Hla MyintAims and Objectives Aims
Getting the correct diagnosis of COPD is the crucial step in the management of COPD ObjectivesExpected to know:(1) Definition (2) Risk Factors (3) Mechanisms underlying airflow limitation(4) Diagnosis (5) Differential diagnosis(6) Commonly Used Drugs (7) Assess and monitoring disease(8) Management of stable and acute exacerbationSpecial emphasis on no 8 for Year 4 (MBS 362)
Assumed Knowledge The concept of physiology and pathology in accordance with the knowledge obtained from BCS module in Phase I B/2nd
yearLecture Contents 1. Definition
2. Pathophysiology3. Diagnosis4. Assessment of disease5. Medications6. Management of Stable COPD and COPD exacerbations
Clinical Relevance Diagnosis and management based on the knowledge learned from this seminar
References The Global Initiative for Chronic Obstructive Lung Disease (GOLD)". 2014.
Seminar Outline
Global Initiative for Chronic Obstructive Lung Disease (GOLD)
♗ COPD is a common preventable and treatable disease
♗ Characterized by persistent airflow limitation that is
usually progressive and associated with an enhanced
chronic inflammatory response in the airways and the
lung to noxious particles and gases.
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COPD
♗ Exacerbations and comorbidities contribute to the
overall severity in individual patients.
This definition does not use the terms chronic bronchitis and emphysema and
excludes asthma (reversible airflow limitation).
♗ The chronic airflow limitation characteristic of COPD
is caused by a mixture of small airway disease
(obstructive bronchiolitis) and parenchymal destruction
(emphysema), the relative contributions of which vary
from person to person.
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EMPHYSEMA
A - Centriacinar emphysema
It usually involves upper lobes and superior segments of
lower lobes and is the most common type of emphysema.
Associated with smoking and coal dust.
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EMPHYSEMA
B - Panacinar emphysema
In panacinar (panlobular) emphysema, there is
involvement of the complete respiratory lobule .
Typically involves the lower zones.
Associated with alpha 1-antitrypsin deficiency
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α1 ANTITRYPSIN DEFICIENCY
Protease inhibitor (PI or SERPINA1) locus that encodes α1AT
1. M allele: normal α1AT levels
2. S allele: slightly reduced α1AT levels
3. Z allele: markedly reduced α1AT levels (>1% in most Caucasian
populations)
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α 1 ANTITRYPSIN DEFICIENCY
4. Rare individuals inherit null alleles absence of any
α1AT production
The most common form of severe α1AT deficiency:
Individuals with two Z alleles or one Z and one null allele
are referred to as PiZ
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Airflow Limitation in COPD
A mixture of small airway disease (obstructive bronchiolitis) and parenchymal destruction
(emphysema)
1. Chronic inflammation structural changes and narrowing of
the small airways
2. Destruction of the lung parenchyma loss of alveolar
attachments to the small airways decreases lung elastic recoil
diminished ability of the airways to remain open during expiration
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Small airway disease Parenchymal destruction
Airway inflammation Loss of alveolar attachments
Airway fibrosis; luminal plugs Decrease of elastic recall
Increased airway resistance
AIRFLOW LIMITATION
Mechanisms Underlying Airflow Limitation in COPD
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Disease development and progression
1. Genes (alpha-1 antitrypsin, rare recessive trait disorder,
leading cause of panlobular emphysema); suspect age
< 45
2. Age (cumulative exposure) and Gender (now F=M)
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Risk Factors for COPD
3. Lung Growth and Development
Any factor that affects lung growth during gestation
and childhood has the potential for increasing an
individuals risk of developing COPD.
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Risk Factors for COPD
4. Exposure to particles
• Tobacco smoke
• Occupational organic and inorganic dusts and chemical
agents and fumes
• Wood, animal dung, crop residues and coal burned in open
fires or poorly functioning stoves
• Outdoor air pollution (Mechanism unknown)
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Risk Factors for COPD
5. Respiratory infections
A history of severe childhood respiratory infection has
been associated with reduced lung function and
increased respiratory symptoms in adulthood.
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Risk Factors for COPD
6. Socioeconomic status
7. Asthma may be risk factor for the development of
COPD, although the evidence is not conclusive.
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Pathological changes characteristic of COPD
• Airways
• Lung parenchyma
• Pulmonary vasculature
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Physiological changes characteristic of the disease
• Airflow limitation and air trapping
• Gas exchange abnormalities
• Mucus hypersecretion
• Pulmonary hypertension
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Systemic features of COPD
Skeletal muscle wasting and cachexia
IHD & HF
Anemia
Osteoporosis
Diabetes and metabolic syndrome
Depression
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Differences in Pulmonary Inflammation Between Asthma and COPD
COPD Asthma Severe asthma
Cells Neutrophils ++Macrophages +++CD8+ T cells (Tc1)
Eosinophils ++Macrophages +CD4+ T cells (Th2)
Neutrophils +MacrophagesCD4+ T cells (Th2), CD8+ T cells (Tc1)
Key mediators IL-8TNF-⍺, IL-1β, IL-6NO +
EotaxinIL-4, IL-5, IL-13NO +++
IL-8IL-5, IL-13NO ++
Oxidative stress Peripheral airwaysLung parenchymaPulmonary vessels
Proximal airways Proximal airwaysPeripheral airways
Site of disease +++ + +++
Consequences Squamous metaplasiaMucous metaplasiaSmall airway fibrosisParenchymal destructionPulmonary vascularremodeling
Fragile epitheliumMucous metaplasia↑Basement membraneBronchoconstriction
Response to therapy Small b/d responsePoor response to steroids
Large b/d responseGood response to steroids
Smaller b/d responseReduced response to steroids
NO = nitric oxide, b/d = bronchodilator