by Scott Cerreta, BS, RRT Director of Education www.copdfoundation.org COPD Pathology with 3D Interactive COPD: Change in Definition • COPD used to include 5 disease processes 1 1 Chronic Bronchitis 2 Emphysema 3 Asthma 4 Bronchiectasis 5 Cystic fibrosis & fibrosis from Tb • Differential diagnosis separates 3 to 5 COPD: Definitions of 21st Century 1 • Preventable and treatable • Airflow limitation that is not fully reversible • Progressive disease • Abnormal inflammatory response of the lungs • Subsets of patients Chronic bronchitis Emphysema Asthma COPD COPD D C COPD Includes Chronic Bronchitis 2 • Productive cough for 3 months in 2 consecutive years with intermittent wheezing and variable degrees of recurring dyspnea on exertion • Inflammation of cells that line the bronchus resulting in excess sputum • Mucous glands enlarge and bronchial walls thicken, resulting in a deformed and narrow airway lumen
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by
Scott Cerreta, BS, RRT
Director of Education
www.copdfoundation.org
COPD Pathology with3D Interactive
COPD: Change in Definition
• COPD used to include 5 disease processes1
1 Chronic Bronchitis
2 Emphysema
3 Asthma
4 Bronchiectasis
5 Cystic fibrosis & fibrosis from Tb
• Differential diagnosis separates 3 to 5
COPD: Definitions of 21st Century1
• Preventable and treatable
• Airflow limitation that is not fully reversible
• Progressive disease
• Abnormal inflammatory response of the lungs
• Subsets of patients
Chronic bronchitis Emphysema
Asthma
COPDCOPDDC
COPD Includes Chronic Bronchitis2
• Productive cough for 3 months in 2 consecutive years with intermittent wheezing and variable degrees of recurring dyspnea on exertion
• Inflammation of cells that line the bronchus resulting in excess sputum
• Mucous glands enlarge and bronchial walls thicken, resulting in a deformed and narrow airway lumen
COPD Includes Emphysema2
• Abnormal permanent enlargement of the airspaces distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis.
• Destruction occurs in the alveoli and the orderly appearance of the acinus is disturbed.
• Normal elasticity is lost, air becomes trapped in over-inflated lungs.
COPD: Airway Effects7
Normal Emphysema
Structural changes of Emphysema10 Pathology, Pathogenesis, & Pathophysiology
• Pathology– Characteristics and effects of COPD
• Pathogenesis– Origin and cause of COPD
• Pathophysiology– Biologic and physical manifestations of COPD
• Processes within the body that result in signs and symptoms
COPD: Anatomy Review
Divisions of lower respiratory tract1. Trachea – cartilage; conducting airway
3. Lung parenchyma – respiratory bronchioles, alveoli, and
capillaries
• Emphysema – enlargement of air spaces distal to terminal
bronchioles, Two types
1. Centrolobular – dilation and destruction of respiratory bronchioles
2. Panlobular – destruction of entire acinus, Alpha1-antitrypisin
• Loss of alveolar attachments – airway collapse
• Inflammation similar to previous
• Development of bullae
Alveolar wall destruction
Loss of elasticity
Destruction of pulmonary
capillary bed
↑ Inflammatory cells
macrophages, CD8+ lymphocytes
Source: Peter J. Barnes, MD
Changes in the Lung Parenchyma in COPD Patients10
COPD: Pathology1
COPD Compromises Four Compartments of the Lung
4. Pulmonary vasculature
• Begins early in disease
• Vessel wall thickening and endothelial dysfunction
• Increased vascular smooth muscle tone
• Infiltration of vessel wall with CD8+ and T lymphocytes
• Advanced stages – develop collagen deposition and capillary
bed destruction leading to pulmonary hypertension and cor-
pulmonale
Endothelial dysfunction
Intimal hyperplasia
Smooth muscle hyperplasia
↑ Inflammatory cells
(macrophages, CD8+ lymphocytes)
Source: Peter J. Barnes, MD
Changes in Pulmonary Arteries in COPD Patients10
COPD: Key Concept
Not everyone that smokes gets
COPD
Age (years)25 35 45 55 65
4
3
2
1
0
Disability
Death
Nonsmoker
Average
smoker
“Susceptible”
smoker
FE
V1 (
lite
rs)
70 75
Susceptible Smokers & COPD14
10-15ml/yr
15-25ml/yr
40-80ml/yr
0 1 2 3 4 5 6 7 8 10 119
2.8
2.6
2.4
2.2
2.0
FE
V1, lit
ers
3 4 5 6 7 8
Years of followup
Sustained quitters
Continuous smokers
Anthonisen et al, AJRCCM, 2002
COPD: Benefits of Smoking Cessation Lung Health Study
Age (years)25 35 45 55 65
4
3
2
1
0
Disability
Death
Nonsmoker
Average
smoker
“Susceptible”
smoker
FE
V1 (
lite
rs)
70 75
Susceptible Smokers & COPD14
COPD: Pathogenesis1
• Tobacco smoking is the main risk factor for COPD
• Some smokers display an exaggerated protected inflammatory response, which causes tissue destruction, impairs defense and repair mechanisms, thus leading to characteristics of COPD
COPD: Pathogenesis1
Three processes important to Pathogenesis
1. Inflammation cascade
• Differs from bronchial asthma cascade
2. Proteinase and antiprotease imbalance
• Released by inflammatory cells
3. Oxidative Stress
• Oxidizing biological molecules leads to cell
dysfunction and/or death
LUNG INFLAMMATION
COPD PATHOLOGY
Oxidative
stressProteinases
Repair
mechanisms
Anti-proteinasesAnti-oxidants
Host factors
Amplifying mechanisms
Cigarette smokeBiomass particles
Particulates
Source: Peter J. Barnes, MD
COPD: Pathogenesis10
COPD
Macrophages
PMNs
CD8 T cells
proteases
LTB4
IL-8, TNF-a
Asthma
Eosinophils
Mast cells
CD4 T cells
mediators
LTD4
IL-4, IL-5, Il-13
Inflammation in Asthma & COPD1
COPD: Pathophysiology1
Pathogenic mechanisms produce pathological changes, giving rise to four physiological abnormalities in COPD
1. Mucous hypersecretion and ciliary dysfunction
• First physiologic abnormality developed in COPD
• Enlarged mucous glands and epithelial cell metaplasia
• An exacerbation of COPD is an event in the natural course of the disease characterized by a sudden change in the patients baseline symptoms: dyspnea, cough, and/or sputum that is beyond normal day-to-day variations
• May warrant a change in regular medication usage
COPD Exacerbations: Epidemiology
• Exacerbations play a role in decline of FEV1
– Decline in FEV1 of 46.1 ml/yr with frequent (>1.5) exacerbations per year
– Decline in FEV1 of 25.3 ml/yr with infrequent (<1.5) exacerbations per year
– Greater lung function decline value observed in COPD exacerbations amongst current smokers
Donaldson et al, Thorax 2002;57;847-52)
COPD Exacerbations: Epidemiology1
• Seasonality
– 50% more likely in the winter
• Recurrent Exacerbations
– 30% of those hospitalized have another
exacerbation within 8 weeks
COPD Exacerbations: Epidemiology8
• The most common causes are:– Infection of the tracheobronchial tree
– Air pollution
• Cause of 1/3 of severe exacerbations unknown
• Conditions that mimic exacerbations: pneumonia, CHF, PE, pneumothorax, pleural effusions, arrhythmia– Important to Differential Diagnosis
WORLD COPD DAYNovember 16, 2011
Raising COPD Awareness Worldwide
Interactive COPD Education System
Click to Launch the
COPD Active Learning Module
This interactive module is provided by Syandus, Inc.
References
1. American Thoracic Society – European Respiratory Society: Standards for the Diagnosis and Management of Patients with COPD, 2004. download manual:
http://www.thoracic.org/sections/copd
2. Arizona Department of Health Services: Arizona Comprehensive Lung Disease Control Plan, download manual: http://www.azdhs.gov/phs/tepp/pdf/lungdiseaseplan.pdf
3. National Heart Lung and Blood Institute, COPD Learn More Breathe Better: COPD: It has a Name, 2007. download provider edition:
7. National Lung Health Education Program: Prevent COPD Now! Information for Patients Who May Be Developing COPD, 2007. download Save Your Breath, America!:
http://www.nlhep.org/pdfs/saveyourbreath.pdf
8. Global Initiative for Chronic Lung Disease, Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease: Executive Summary, 2006. download manual: http://www.goldcopd.com/Guidelineitem.asp?l1=2&l2=1&intId=996
9. Global Initiative for Chronic Lung Disease, Pocket Guide to COPD Diagnosis, Management, and Prevention: A Guide for Health Care Professionals, 2006. download manual:
11. National Lung Health Education Program and AlphaMedia, Inc., Simple Office Spirometry, Thomas L. Petty, M.D., and Paul L. Enright, M.D., download manual:
12. American Thoracic Society – European Respiratory Society: Standards for the Diagnosis and Management of Individuals with Alpha-1 Antitrypsin Deficiency, 2006. download manual:
13. Rau JL: Respiratory Care Pharmacology, Mosby, 2002.
14. American Lung Association of Minnesota, COPD Educator Course, 2006. Cheryl Sasse; Jeff Rubins, MD; Kathy Schultz, RRT; Charles McArthur, RRT, RPFT; Janet Malkiewicz, RN, PHN; Lynn Sieben, RRT; Dick Stenholz LSW; Bob McVoy, RRT, FAARC; Charlene McEvoy, MD
15. Arizona Department of Health Services, Tobacco Education & Prevention Program, University of Arizona HealthCare Partnership, Basic Tobacco Intervention Skills Certification Guidebook, 2006.
Medical Reviewer: Dr. David R. Sanderson, M.D., Professor of Medicine: Emeritus Mayo Clinic College of Medicine