Eneutron, profile picture
Uploaded byEneutron
PPT, PDF1,805 views

Chronic Obstructive Pulmonary Disease - COPD

COPD is characterized by airflow limitation caused by chronic inflammation in the lungs in response to noxious particles. The document discusses the pathogenesis and pathology of COPD, including oxidative stress and protease-antiprotease imbalance leading to lung destruction and inflammation. Cigarette smoke and other irritants are major risk factors that induce inflammation through recruitment of cells like macrophages and neutrophils. This causes emphysema of the lung parenchyma and obstruction of small airways.

Embed presentation

Downloaded 48 times
CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)
lobal Initiative for Chronic bstructive ung isease G O L D © Global Initiative for Chronic Obstructive Lung Disease
Global Strategy for Diagnosis, Management and Prevention of COPD Definition, Classification Burden of COPD Risk Factors Pathogenesis, Pathology, Pathophysiology Management of COPD Primary Care Recommendations
Definition of COPD COPD is a preventable and treatable disease with some significant extrapulmonary effects that may contribute to the severity in individual patients. Its pulmonary component is characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lung to noxious particles or gases.
Sponsored Medical Lecture Notes – All Subjects USMLE Exam (America) – Practice
History COPD has probably always existed but has been called by different names in the past. Bonet described a condition of “voluminous lungs” in 1679. In 1769, Giovanni Morgagni described 19 cases where the lungs were “turgid” particularly from air. The first description and illustration of the enlarged airspaces in emphysema was provided by Ruysh in 1721."History of pathologic descriptions of COPD" (PDF). Matthew Baillie illustrated an emphysematous lung in 1789 and described the destructive character of the condition. Badham used the word "catarrh" to describe the cough and mucus hypersecretion of chronic bronchitis in 1814. He recognised that chronic bronchitis was a disabling disorder. René Laennec, the physician who invented the stethoscope, used the term "emphysema" in his book A Treatise on the Diseases of the Chest and of Mediate Auscultation (1837) to describe lungs that did not collapse when he opened the chest during an autopsy. He noted that they did not collapse as usual because they were full of air and the airways were filled with mucus. In 1842, John Hutchinson invented the spirometer, which allowed the measurement of vital capacity of the lungs. However, his spirometer could only measure volume, not airflow. Tiffeneau in 1947 and Gaensler in 1950 and 1951 described the principles of measuring airflow. The terms chronic bronchitis and emphysema were formally defined at the CIBA guest symposium of physicians in 1959. The term COPD was first used by William Briscoe in 1965 and has gradually overtaken other terms to become established today as the preferred name for this disease.
Classification of COPD Severity by SpirometryStage I: Mild FEV1/FVC < 0.70 FEV1 > 80% predicted Stage II: Moderate FEV1/FVC < 0.70 50% < FEV1 < 80% predicted Stage III: Severe FEV1/FVC < 0.70 30% < FEV1 < 50% predicted Stage IV: Very Severe FEV1/FVC < 0.70 FEV1 < 30% predicted or FEV1 < 50% predicted plus
“At Risk” for COPD COPD includes four stages of severity classified by spirometry. A fifth category--Stage 0: At Risk--that appeared in the 2001 report is no longer included as a stage of COPD, as there is incomplete evidence that the individuals who meet the definition of “At Risk” (chronic cough and sputum production, normal spirometry) necessarily progress on to Stage I: Mild COPD. The public health message is that chronic cough and sputum are not normal remains important - their presence should trigger a search for underlying cause(s).
Global Strategy for Diagnosis, Management and Prevention of COPD Definition, Classification Burden of COPD Risk Factors Pathogenesis, Pathology, Pathophysiology Management Primary Care Recommendations
Burden of COPD: Key Points  COPD is a leading cause of morbidity and mortality worldwide and results in an economic and social burden that is both substantial and increasing.  COPD prevalence, morbidity, and mortality vary across countries and across different groups within countries.  The burden of COPD is projected to increase in the coming decades due to continued exposure to COPD risk factors and the changing age structure of the world’s population.
Burden of COPD: Prevalence  Many sources of variation can affect estimates of COPD prevalence, including e.g., sampling methods, response rates and quality of spirometry.  Data are emerging to provide evidence that prevalence of Stage I: Mild COPD and higher is appreciably higher in: - smokers and ex-smokers - people over 40 years of age - males
COPD Prevalence Study in Latin America (Platino) The prevalence of post- bronchodilator FEV1/FVC < 0.70 increases steeply with age in 5 Latin American Cities Source: Menezes AM et al. Lancet 2005
Burden of COPD: Mortality  COPD is a leading cause of mortality worldwide and projected to increase in the next several decades.  COPD mortality trends generally track several decades behind smoking trends.  Between 1999 and 2006, death rates for COPD have declined among U.S. men; there has been no significant change among death rates among U.S. women.
Of the six leading causes of death in the United States, only COPD has been increasing steadily since 1970 Source: Jemal A. et al. JAMA 2005
Global Strategy for Diagnosis, Management and Prevention of COPD Definition, Classification Burden of COPD Risk Factors Pathogenesis, Pathology, Pathophysiology Management Primary Care Recommendations
Risk Factors for COPD Lung growth and development Oxidative stress Gender Age Respiratory infections Socioeconomic status Nutrition Comorbidities Genes Exposure to particles ● Tobacco smoke ● Occupational dusts, organic and inorganic ● Indoor air pollution from heating and cooking with biomass in poorly ventilated dwellings ● Outdoor air pollution
Risk Factors for COPD NutritionNutrition InfectionsInfections Socio-economicSocio-economic statusstatus Aging PopulationsAging Populations
Global Strategy for Diagnosis, Management and Prevention of COPD Definition, Classification Burden of COPD Risk Factors Pathogenesis, Pathology, Pathophysiology Management Primary Care Recommendations
LUNG INFLAMMATIONLUNG INFLAMMATION COPD PATHOLOGYCOPD PATHOLOGY OxidativeOxidative stressstress ProteinasesProteinases RepairRepair mechanismsmechanisms Anti-proteinasesAnti-proteinasesAnti-oxidantsAnti-oxidants Host factors Amplifying mechanisms Cigarette smokeCigarette smoke Biomass particlesBiomass particles ParticulatesParticulates Source: Peter J. Barnes, Pathogenesis of COPD
Mucus gland hyperplasia Goblet cell hyperplasia Mucus hypersecretion Neutrophils in sputum Squamous metaplasia of epithelium ↑ Macrophages No basement membrane thickening Little increase in airway smooth muscle ↑ CD8+ lymphocytes Changes in Large Airways of COPD PatientsChanges in Large Airways of COPD Patients Source: Peter J. Barnes, MD
Disrupted alveolar attachments Inflammatory exudate in lumen Peribronchial fibrosis Lymphoid follicle Thickened wall with inflammatory cells - macrophages, CD8+ cells, fibroblasts Changes in Small Airways in COPD Patients Source: Peter J. Barnes, MD
LUNG INFLAMMATIONLUNG INFLAMMATION COPD PATHOLOGYCOPD PATHOLOGY OxidativeOxidative stressstress ProteinasesProteinases RepairRepair mechanismsmechanisms Anti-proteinasesAnti-proteinasesAnti-oxidantsAnti-oxidants Host factors Amplifying mechanisms Cigarette smokeCigarette smoke Biomass particlesBiomass particles ParticulatesParticulates Pathogenesis of COPD Source: Peter J. Barnes,
Cigarette smokeCigarette smoke (and other irritants)(and other irritants) PROTEASESPROTEASES Neutrophil elastaseNeutrophil elastase CathepsinsCathepsins MMPsMMPs Alveolar wall destructionAlveolar wall destruction (Emphysema)(Emphysema) Mucus hypersecretionMucus hypersecretion CD8CD8++ lymphocytelymphocyte Alveolar macrophageAlveolar macrophageEpithelialEpithelial cellscells FibrosisFibrosis (Obstructive(Obstructive bronchiolitis)bronchiolitis) FibroblastFibroblast MonocyteMonocyteNeutrophilNeutrophil Chemotactic factorsChemotactic factors Inflammatory Cells Involved in COPD Source: Peter J. Barnes, MD
Anti-proteases SLPI α1-AT Proteolysis OO22 -- , H, H220022 OHOH.. , ONOO, ONOO-- ↑ Mucus secretion Plasma leak Bronchoconstriction NF-NF-κκBB IL-8IL-8 NeutrophilNeutrophil recruitmentrecruitment TNF-TNF-αα IsoprostanesIsoprostanes ↓↓ HDAC2HDAC2 ↑↑InflammationInflammation SteroidSteroid resistanceresistance Macrophage Neutrophil Oxidative Stress in COPD Source: Peter J. Barnes, MD
NormalNormal Inspiration Expiration alveolar attachments Mild/moderateMild/moderate COPDCOPD loss of elasticity SevereSevere COPDCOPD loss of alveolar attachments closure smallsmall airwayairway Dyspnea ↓ Exercise capacity Air trappingAir trapping HyperinflationHyperinflation ↓↓ HealthHealth statusstatus Air Trapping in COPD Source: Peter J. Barnes,
Chronic hypoxiaChronic hypoxia Pulmonary vasoconstrictionPulmonary vasoconstriction MuscularizationMuscularization IntimalIntimal hyperplasiahyperplasia FibrosisFibrosis ObliterationObliteration Pulmonary hypertensionPulmonary hypertension Cor pulmonaleCor pulmonale Death EdemaEdema Pulmonary Hypertension in COPD Source: Peter J. Barnes, MD
Macrophages TNF-α IL-8 IL-6 Bacteria Viruses Non-infective Pollutants Epithelial cells Oxidative stressOxidative stress Neutrophils Inflammation in COPD Exacerbations Source: Peter J. Barnes,
Alveolar wall destruction Loss of elasticity Destruction of pulmonary capillary bed ↑ Inflammatory cells macrophages, CD8+ lymphocytes Source: Peter J. Barnes, MD Changes in Lung Parenchyma in COPD
Chronic hypoxiaChronic hypoxia Pulmonary vasoconstrictionPulmonary vasoconstriction MuscularizationMuscularization IntimalIntimal hyperplasiahyperplasia FibrosisFibrosis ObliterationObliteration Pulmonary hypertensionPulmonary hypertension Cor pulmonaleCor pulmonale Death EdemaEdema Pulmonary Hypertension in COPD Source: Peter J. Barnes, MD
YYYY YY Mast cellMast cell CD4+ cellCD4+ cell (Th2)(Th2) EosinophilEosinophil AllergensAllergens Ep cellsEp cells ASTHMAASTHMA BronchoconstrictionBronchoconstriction AHRAHR Alv macrophageAlv macrophageEp cellsEp cells CD8+ cellCD8+ cell (Tc1)(Tc1) NeutrophilNeutrophil Cigarette smokeCigarette smoke Small airway narrowingSmall airway narrowing Alveolar destructionAlveolar destruction COPDCOPD Reversible Irreversible Airflow LimitationAirflow Limitation Source: Peter J. Barnes, MD
Symptoms of COPD One of the most common symptoms of COPD is shortness of breath (dyspnea). People with COPD commonly describe this as: "My breathing requires effort," "I feel out of breath," or "I can't get enough air in". People with COPD typically first notice dyspnea during vigorous exercise when the demands on the lungs are greatest. Over the years, dyspnea tends to get gradually worse so that it can occur during milder, everyday activities such as housework. In the advanced stages of COPD, dyspnea can become so bad that it occurs during rest and is constantly present.
Symptoms of COPD Other symptoms of COPD are a persistent cough, sputum or mucus production, wheezing, chest tightness, and tiredness. People with advanced (very severe) COPD sometimes develop respiratory failure. When this happens, cyanosis, a bluish discoloration of the lips caused by a lack of oxygen in the blood, can occur. An excess of carbon dioxide in the blood can cause headaches, drowsiness or twitching (asterixis). A complication of advanced COPD is cor pulmonale, a strain on the heart due to the extra work required by the heart to pump blood through the affected lungs. Symptoms of cor pulmonale are peripheral edema, seen as swelling of the ankles, and dyspnea.
Symptoms of COPD There are a few signs of COPD that a healthcare worker may detect although they can be seen in other diseases. Some people have COPD and have none of these signs. Common signs are: tachypnea, a rapid breathing rate wheezing sounds or crackles in the lungs heard through a stethoscope breathing out taking a longer time than breathing in enlargement of the chest, particularly the front-to-back distance (hyperaeration) active use of muscles in the neck to help with breathing breathing through pursed lips increased anteroposterior to lateral ratio of the chest (i.e. barrel chest).
Spirometry - Introduction Spirometry is the gold standard for COPD diagnosis Underuse leads to inaccurate COPD diagnosis Widespread uptake has been limited by: Concerns over technical performance of operators Difficulty with interpretation of results Lack of approved local training courses
What is Spirometry? Spirometry is a method of assessing lung function by measuring the total volume of air the patient can expel from the lungs after a maximal inhalation.
Why Perform Spirometry? Measure airflow obstruction to help make a definitive diagnosis of COPD Confirm presence of airway obstruction Assess severity of airflow obstruction in COPD Detect airflow obstruction in smokers who may have few or no symptoms Monitor disease progression in COPD Assess one aspect of response to therapy Assess prognosis (FEV1) in COPD Perform pre-operative assessment
Spirometry – Additional Uses Make a diagnosis and assess severity in a range of other respiratory conditions Distinguish between obstruction and restriction as causes of breathlessness Screen workforces in occupational environments Assess fitness to dive Perform pre-employment screening in certain professions
Types of Spirometers Bellows spirometers: Measure volume; mainly in lung function units Electronic desk top spirometers: Measure flow and volume with real time display Small hand-held spirometers: Inexpensive and quick to use but no print out
Volume Measuring Spirometer
Flow Measuring Spirometer
Desktop Electronic Spirometers
Small Hand-held Spirometers
Standard Spirometric Indicies FEV1 - Forced expiratory volume in one second: The volume of air expired in the first second of the blow FVC - Forced vital capacity: The total volume of air that can be forcibly exhaled in one breath FEV1/FVC ratio: The fraction of air exhaled in the first second relative to the total volume exhaled
Criteria for Normal Post-bronchodilator Spirometry FEV1: % predicted > 80% FVC: % predicted > 80% FEV1/FVC: > 0.7 - 0.8, depending on age
Normal Trace Showing FEV1 and FVC 1 2 3 4 5 6 1 2 3 4 Volume,liters Time, sec FVC5 1 FEV1 = 4L FVC = 5L FEV1/FVC = 0.8
SPIROMETRY OBSTRUCTIVE DISEASE
Spirometry: Obstructive Disease Volume,liters Time, seconds 5 4 3 2 1 1 2 3 4 5 6 FEV1 = 1.8L FVC = 3.2L FEV1/FVC = 0.56 Normal Obstructive
Spirometric Diagnosis of COPD COPD is confirmed by post– bronchodilator FEV1/FVC < 0.7 Post-bronchodilator FEV1/FVC measured 15 minutes after 400µg salbutamol or equivalent
Bronchodilator Reversibility Testing Provides the best achievable FEV1 (and FVC) Helps to differentiate COPD from asthma Must be interpreted with clinical history - neither asthma nor COPD are diagnosed on spirometry alone
Bronchodilator Reversibility Testing Can be done on first visit if no diagnosis has been made Best done as a planned procedure: pre- and post-bronchodilator tests require a minimum of 15 minutes Post-bronchodilator only saves time but does not help confirm if asthma is present Short-acting bronchodilators need to be withheld for at least 4 hours prior to test
Bronchodilator Reversibility Testing Bronchodilator* Dose FEV1 before and after Salbutamol 200 – 400 µg via large volume spacer 15 minutes Terbutaline 500 µg via Turbohaler® 15 minutes Ipratropium 160 µg** via spacer 45 minutes * Some guidelines suggest nebulised bronchodilators can be given but the doses are not standardised. “There is no consensus on the drug, dose or mode of administering a bronchodilator in the laboratory.” Ref: ATS/ERS Task Force : Interpretive strategies for Lung Function Tests ERJ 2005;26:948 ** Usually 8 puffs of 20 µg
Global Strategy for Diagnosis, Management and Prevention of COPD Definition, Classification Burden of COPD Risk Factors Pathogenesis, Pathology, Pathophysiology Management Primary Care Recommendations
Four Components of COPD Management 1. Assess and monitor disease 2. Reduce risk factors 3. Manage stable COPD Education Pharmacologic Non-pharmacologic 4. Manage exacerbations
• Relieve symptoms • Prevent disease progression • Improve exercise tolerance • Improve health status • Prevent and treat complications • Prevent and treat exacerbations • Reduce mortality GOALS of COPD MANAGEMENT VARYING EMPHASIS WITH DIFFERING SEVERITY
Four Components of COPD Management 1. Assess and monitor disease 2. Reduce risk factors 3. Manage stable COPD Education Pharmacologic Non-pharmacologic 4. Manage exacerbations
Management of Stable COPD Assess and Monitor COPD: Key Points A clinical diagnosis of COPD should be considered in any patient who has dyspnea, chronic cough or sputum production, and/or a history of exposure to risk factors for the disease. The diagnosis should be confirmed by spirometry. A post-bronchodilator FEV1/FVC < 0.70 confirms the presence of airflow limitation that is not fully reversible. Comorbidities are common in COPD and should be actively identified.
SYMPTOMS cough sputum shortness of breath EXPOSURE TO RISK FACTORS tobacco occupation indoor/outdoor pollution SPIROMETRY Diagnosis of COPD
Differential Diagnosis:Differential Diagnosis: COPD and AsthmaCOPD and Asthma COPD ASTHMA • Onset in mid-life • Symptoms slowly progressive • Long smoking history • Dyspnea during exercise • Largely irreversible airflow limitation • Onset early in life (often childhood) • Symptoms vary from day to day • Symptoms at night/early morning • Allergy, rhinitis, and/or eczema also present • Family history of asthma • Largely reversible airflow limitation
COPD and Co-Morbidities COPD patients are at increased risk for: • Myocardial infarction, angina • Osteoporosis • Respiratory infection • Depression • Diabetes • Lung cancer
Four Components of COPD Management 1. Assess and monitor disease 2. Reduce risk factors 3. Manage stable COPD Education Pharmacologic Non-pharmacologic 4. Manage exacerbations
Management of Stable COPD Reduce Risk Factors: Key Points Reduction of total personal exposure to tobacco smoke, occupational dusts and chemicals, and indoor and outdoor air pollutants are important goals to prevent the onset and progression of COPD. Smoking cessation is the single most effective — and cost effective — intervention in most people to reduce the risk of developing COPD and stop its progression (Evidence A).
Brief Strategies to Help the Patient Willing to Quit Smoking • ASK Systematically identify all tobacco users at every visit • ADVISE Strongly urge all tobacco users to quit • ASSESS Determine willingness to make a quit attempt • ASSIST Aid the patient in quitting • ARRANGE Schedule follow-up contact.
Management of Stable COPD Reduce Risk Factors: Smoking Cessation  Counseling delivered by physicians and other health professionals significantly increases quit rates over self-initiated strategies. Even a brief (3-minute) period of counseling to urge a smoker to quit results in smoking cessation rates of 5-10%.  Numerous effective pharmacotherapies for smoking cessation are available; pharmacotherapy is recommended when counseling is not sufficient to help patients quit smoking.
Management of Stable COPD Reduce Risk Factors: Indoor/Outdoor Air Pollution Reducing the risk from indoor and outdoor air pollution is feasible and requires a combination of public policy and protective steps taken by individual patients. Reduction of exposure to smoke from biomass fuel, particularly among women and children, is a crucial goal to reduce the prevalence of COPD worldwide.
Four Components of COPD Management 1. Assess and monitor disease 2. Reduce risk factors 3. Manage stable COPD Education Pharmacologic Non-pharmacologic 4. Manage exacerbations
Management of Stable COPD Pharmacotherapy: Bronchodilators  Bronchodilator medications are central to the symptomatic management of COPD (Evidence A).  Bronchodilators are prescribed on an as-needed or on a regular basis to prevent or reduce symptoms.  The principal bronchodilator treatments are ß2- agonists, anticholinergics, and methylxanthines used singly or in combination (Evidence A).  Long-acting bronchodilators are more effective and convenient than treatment with short-acting bronchodilators (Evidence A).
Management of Stable COPD Pharmacotherapy: Glucocorticosteroids  Regular treatment with inhaled glucocorticosteroids reduces frequency of exacerbations for symptomatic COPD patients with an FEV1 < 50% predicted (Stage III: Severe COPD and Stage IV: Very Severe COPD) and repeated exacerbations.  Treatment with inhaled glucocortciosteroids increases the likelihood of pneumonia and does not reduce overall mortality.
Management of Stable COPD Pharmacotherapy: Combination Therapy Glucocorticosteroids and Long-Acting ß2-agonist  An inhaled glucocorticosteroid combined with a long-acting ß2-agonist is more effective than the individual components in reducing exacerbations and improving lung function (Evidence A).  Combination therapy increases the likelihood of pneumonia and has no impact on mortality.  Addition of a long-acting ß2-agonist /inhaled gluco- Corticosteroid comgination to an anticholinergic (tiotropium) appears to provide additional benefits.
Management of Stable COPD Pharmacotherapy: Systemic Glucocorticosteroids  Chronic treatment with systemic glucocorticosteroids should be avoided because of an unfavorable benefit-to-risk ratio (Evidence A).
Management of Stable COPD Pharmacotherapy: Phosphodiesterase-4 Inhibitors  In patients with Stage III: Severe COPD or Stage IV: Very Severe COPD and a history of exacerbations and chronic bronchitis, the phospodiesterase-4 inhibitor, roflumilast, reduces exacerbations treated with oral glucocorticosteroids.
Management of Stable COPD Pharmacotherapy: Vaccines  In COPD patients influenza vaccines can reduce serious illness (Evidence A).  Pneumococcal polysaccharide vaccine is recommended for COPD patients 65 years and older and for COPD patients younger than age 65 with an FEV1 < 40% predicted (Evidence B).  Influenza, not pneumococcal vaccination is associated with reduced risk of all-cause mortality in COPD (Evidence B).
Management of Stable COPD All Stages of Disease Severity Avoidance of risk factors - smoking cessation - reduction of indoor pollution - reduction of occupational exposure Influenza vaccination
IV: Very SevereIII: SevereII: ModerateI: Mild Therapy at Each Stage of COPD*  FEV1 /FVC < 70%  FEV1 > 80% predicted  FEV1 /FVC < 70%  50% < FEV1 < 80% predicted  FEV1 /FVC < 70%  30% < FEV1 < 50% predicted  FEV1 /FVC < 70%  FEV1 < 30% predicted or FEV1 < 50% predicted plus chronic respiratory failure Add regular treatment with one or more long-acting bronchodilators (when needed); Add rehabilitation Add inhaled glucocorticosteroids if repeated exacerbations Active reduction of risk factor(s); influenza vaccination Add short-acting bronchodilator (when needed) Add long term oxygen if chronic respiratory failure. Consider surgical treatments *Postbronchodilator FEV1 is recommended for the diagnosis and assessment of severity of COPD
Management of Stable COPD Other Pharmacologic Treatments  Antibiotics: Only used to treat infectious exacerbations of COPD  Antioxidant agents: No effect of n-acetyl- cysteine on frequency of exacerbations, except in patients not treated with inhaled glucocorticosteroids  Mucolytic agents, Antitussives, Vasodilators: Not recommended in stable COPD
Management of Stable COPD Non-Pharmacologic Treatments  Rehabilitation: All COPD patients benefit from exercise training programs, improving with respect to both exercise tolerance and symptoms of dyspnea and fatigue (Evidence A).  Oxygen Therapy: The long-term administration of oxygen (> 15 hours per day) to patients with chronic respiratory failure has been shown to increase survival (Evidence A).
Four Components of COPD Management 1. Assess and monitor disease 2. Reduce risk factors 3. Manage stable COPD Education Pharmacologic Non-pharmacologic 4. Manage exacerbations
Management COPD Exacerbations Key Points An exacerbation of COPD is defined as: “An event in the natural course of the disease characterized by a change in the patient’s baseline dyspnea, cough, and/or sputum that is beyond normal day-to-day variations, is acute in onset, and may warrant a change in regular medication in a patient with underlying COPD.”
Management COPD Exacerbations Key Points The most common causes of an exacerbation are infection of the tracheobronchial tree and air pollution, but the cause of about one-third of severe exacerbations cannot be identified (Evidence B). Patients experiencing COPD exacerbations with clinical signs of airway infection (e.g., increased sputum purulence) may benefit from antibiotic treatment (Evidence B).
Manage COPD Exacerbations Key Points  Inhaled bronchodilators (particularly inhaled ß2-agonists with or without anticholinergics) and oral glucocortico- steroids are effective treatments for exacerbations of COPD (Evidence A).
Management COPD Exacerbations Key Points  Noninvasive mechanical ventilation in exacerbations improves respiratory acidosis, increases pH, decreases the need for endotracheal intubation, and reduces PaCO2, respiratory rate, severity of breathlessness, the length of hospital stay, and mortality (Evidence A).  Medications and education to help prevent future exacerbations should be considered as part of follow-up, as exacerbations affect the quality of life and prognosis of patients with COPD.
Global Strategy for Diagnosis, Management and Prevention of COPD Definition, Classification Burden of COPD Risk Factors Pathogenesis, Pathology, Pathophysiology Management Primary Care Recommendations
Translating COPD Guidelines into Primary Care KEY POINTS Better dissemination of COPD guidelines and their effective implementation in a variety of health care settings is urgently required. In many countries, primary care practitioners treat the vast majority of patients with COPD and may be actively involved in public health campaigns and in bringing messages about reducing exposure to risk factors to both patients and the public.
Translating COPD Guidelines into Primary Care KEY POINTS Spirometric confirmation is a key component of the diagnosis of COPD and primary care practitioners should have access to high quality spirometry. Older patients frequently have multiple chronic health conditions. Comorbidities can magnify the impact of COPD on a patient’s health status, and can complicate the management of COPD.
Global Strategy for Diagnosis, Management and Prevention of COPD SUMMARY Definition, Classification Burden of COPD Risk Factors Pathogenesis, Pathology, Pathophysiology Management Primary Care
Global Strategy for Diagnosis, Management and Prevention of COPD: Summary  COPD is increasing in prevalence in many countries of the world.  COPD is treatable and preventable.  The GOLD program offers a strategy to identify patients and to treat them according to the best medications available.
 COPD can be prevented by avoidance of risk factors, the most notable being tobacco smoke.  Patients with COPD have multiple other conditions (comorbidities) that must be taken into consideration.  GOLD has developed a global network to raise awareness of COPD and disseminate information on diagnosis and treatment. Global Strategy for Diagnosis, Management and Prevention of COPD: Summary
WORLD COPD DAY November 16, 2011 Raising COPD Awareness Worldwide

More Related Content

PPTX
COPD - Chronic obstructive pulmonary disease - Aby
byAby Thankachan
 
PPTX
Bronchitis
byZuzyrie Garrovillas
 
DOCX
Respiratory acidosis
byAbdul Fatah Abro
 
PPT
Pneumonia
byDjlab Alcatraz
 
PPTX
Pulmonary hypertension
byZulcaif Ahmad
 
PPTX
COPD
byShima Ghavimi, MD
 
PPT
Chronic obstructive pulmonary disease
byimangalal
 
PPT
Bronchial Asthma
byEneutron
 
COPD - Chronic obstructive pulmonary disease - Aby
byAby Thankachan
 
Bronchitis
byZuzyrie Garrovillas
 
Respiratory acidosis
byAbdul Fatah Abro
 
Pneumonia
byDjlab Alcatraz
 
Pulmonary hypertension
byZulcaif Ahmad
 
COPD
byShima Ghavimi, MD
 
Chronic obstructive pulmonary disease
byimangalal
 
Bronchial Asthma
byEneutron
 

What's hot

PPT
Pneumonia
byHariomSuman
 
PPT
Introduction to Respiratory Peds.ppt
byMahdi Hemmat
 
PPTX
Emphysema
byLayla Aziz
 
PPTX
Copd
bySandra McClain
 
PPTX
CHRONIC BRONCHITIS
byThulasithiruPriya
 
PPTX
Pneumothorax
byWaqas Ahmed Khan
 
PDF
Coal workers pneumoconiosis
byPhelix Owenga
 
PPTX
Copd
byOM VERMA
 
PPTX
Cystic fibrosis
bySanil Varghese
 
PPTX
Silicosis disease
byJayesh Rajput
 
PPTX
Asthma
byeducation4227
 
PPTX
Copd seminar
byhemin sab
 
PPTX
Complication of long term ventilation
bysaman priyantha
 
PPTX
Interstitial Lung Diseases [ILD] Approach to Management
byArun Vasireddy
 
PPTX
Pneumonia
byAbhishek Achar
 
PDF
Chronic bronchitis
byPrasad CSBR
 
PPTX
pneumonia ppt
bysaif ali khan
 
PPTX
Pickwickian syndrome
byFeba
 
PPTX
Asthma Attack – Causes And Prevention
byErin Bell
 
PPT
Asthma
bySanil Varghese
 
Pneumonia
byHariomSuman
 
Introduction to Respiratory Peds.ppt
byMahdi Hemmat
 
Emphysema
byLayla Aziz
 
Copd
bySandra McClain
 
CHRONIC BRONCHITIS
byThulasithiruPriya
 
Pneumothorax
byWaqas Ahmed Khan
 
Coal workers pneumoconiosis
byPhelix Owenga
 
Copd
byOM VERMA
 
Cystic fibrosis
bySanil Varghese
 
Silicosis disease
byJayesh Rajput
 
Asthma
byeducation4227
 
Copd seminar
byhemin sab
 
Complication of long term ventilation
bysaman priyantha
 
Interstitial Lung Diseases [ILD] Approach to Management
byArun Vasireddy
 
Pneumonia
byAbhishek Achar
 
Chronic bronchitis
byPrasad CSBR
 
pneumonia ppt
bysaif ali khan
 
Pickwickian syndrome
byFeba
 
Asthma Attack – Causes And Prevention
byErin Bell
 
Asthma
bySanil Varghese
 

Similar to Chronic Obstructive Pulmonary Disease - COPD

PPT
Gold - global initiative against COPD
byadithya2115
 
PPT
C O P D By Dr Sarma
bygoolappa
 
PPT
Copd update 2015
byVeerendra Singh
 
PPTX
COPD back to basis
byAshraf ElAdawy
 
PPTX
Chronic Obstructive Pulmonary Disease. ppt
bysarahahmed321934
 
PDF
COPD-Slides.pdf copd copd copd copd copd
bysaifalkayid
 
PDF
COPD
byHamdi Turkey
 
PPT
Copd
byrahulverma1194
 
PPT
Non Communicable Diseases: COPD
byRalph Bawalan
 
PPTX
Chronic Obstructive Lung Disease
byVitrag Shah
 
PDF
300007-World COPD (Chronic Obstructive Pulmonary Disease) Day-4-3.pdf
bybutcherofblaviken001
 
PDF
COPD First Session
byGamal Agmy
 
PPTX
COPD.pptx
byyilkalmossie1
 
PPTX
Chronic obstructive pulmonary disease.pptx
byMohammedSElreishi
 
PDF
Vogelmeier et al-2017-american_journal_of_respiratory_and_critical_care_medicine
bydefrichandra85
 
PDF
Chronic obstructive pulmonary diseases presentation at Hackensack Meridian he...
byRaghunath Ramanarasimhaiah MS, MD
 
PDF
2018 GOLD POCKET GUIDE
byUtai Sukviwatsirikul
 
PPTX
COPD AND ICU MANAGEMENT : DR DEVAWRAT BUCHE
byDevawrat Buche
 
PPTX
COPD TALK CIPLA.pptx
bylokeshlalwani8
 
PPTX
Gold guideline ppt 2019 final shivaom
byShivaom Chaurasia
 
Gold - global initiative against COPD
byadithya2115
 
C O P D By Dr Sarma
bygoolappa
 
Copd update 2015
byVeerendra Singh
 
COPD back to basis
byAshraf ElAdawy
 
Chronic Obstructive Pulmonary Disease. ppt
bysarahahmed321934
 
COPD-Slides.pdf copd copd copd copd copd
bysaifalkayid
 
COPD
byHamdi Turkey
 
Copd
byrahulverma1194
 
Non Communicable Diseases: COPD
byRalph Bawalan
 
Chronic Obstructive Lung Disease
byVitrag Shah
 
300007-World COPD (Chronic Obstructive Pulmonary Disease) Day-4-3.pdf
bybutcherofblaviken001
 
COPD First Session
byGamal Agmy
 
COPD.pptx
byyilkalmossie1
 
Chronic obstructive pulmonary disease.pptx
byMohammedSElreishi
 
Vogelmeier et al-2017-american_journal_of_respiratory_and_critical_care_medicine
bydefrichandra85
 
Chronic obstructive pulmonary diseases presentation at Hackensack Meridian he...
byRaghunath Ramanarasimhaiah MS, MD
 
2018 GOLD POCKET GUIDE
byUtai Sukviwatsirikul
 
COPD AND ICU MANAGEMENT : DR DEVAWRAT BUCHE
byDevawrat Buche
 
COPD TALK CIPLA.pptx
bylokeshlalwani8
 
Gold guideline ppt 2019 final shivaom
byShivaom Chaurasia
 

More from Eneutron

PDF
PGCET Textile 2018 question paper
byEneutron
 
PDF
PGCET Polymer science 2018 question paper
byEneutron
 
PDF
PGCET Mechanical 2018 question paper
byEneutron
 
PDF
PGCET Environmental 2018 question paper
byEneutron
 
PDF
PGCET Electrical sciences 2018 question paper
byEneutron
 
PDF
PGCET Computer science 2018 question paper
byEneutron
 
PDF
PGCET Civil 2018 question paper
byEneutron
 
PDF
PGCET Chemical 2018 question paper
byEneutron
 
PDF
PGCET Biotechnology 2018 question paper
byEneutron
 
PDF
Pgcet Architecture 2018 question paper
byEneutron
 
PDF
Pgcet Architecture 2017 question paper
byEneutron
 
PDF
PGCET MBA 2018 question paper
byEneutron
 
PDF
Civil Service 2019 Prelims Previous Question Paper - 2
byEneutron
 
PDF
Civil Service 2019 Prelims Previous Question Paper - 1
byEneutron
 
PDF
Civil Service 2018 Prelims Previous Question Paper - 2
byEneutron
 
PDF
Civil Service 2018 Prelims Previous Question Paper - 1
byEneutron
 
PDF
Civil Service 2017 Prelims Previous Question Paper - 2
byEneutron
 
PDF
Civil Service 2017 Prelims Previous Question Paper - 1
byEneutron
 
PDF
SNAP 2013 Answer Key
byEneutron
 
PDF
SNAP 2014 Answer Key
byEneutron
 
PGCET Textile 2018 question paper
byEneutron
 
PGCET Polymer science 2018 question paper
byEneutron
 
PGCET Mechanical 2018 question paper
byEneutron
 
PGCET Environmental 2018 question paper
byEneutron
 
PGCET Electrical sciences 2018 question paper
byEneutron
 
PGCET Computer science 2018 question paper
byEneutron
 
PGCET Civil 2018 question paper
byEneutron
 
PGCET Chemical 2018 question paper
byEneutron
 
PGCET Biotechnology 2018 question paper
byEneutron
 
Pgcet Architecture 2018 question paper
byEneutron
 
Pgcet Architecture 2017 question paper
byEneutron
 
PGCET MBA 2018 question paper
byEneutron
 
Civil Service 2019 Prelims Previous Question Paper - 2
byEneutron
 
Civil Service 2019 Prelims Previous Question Paper - 1
byEneutron
 
Civil Service 2018 Prelims Previous Question Paper - 2
byEneutron
 
Civil Service 2018 Prelims Previous Question Paper - 1
byEneutron
 
Civil Service 2017 Prelims Previous Question Paper - 2
byEneutron
 
Civil Service 2017 Prelims Previous Question Paper - 1
byEneutron
 
SNAP 2013 Answer Key
byEneutron
 
SNAP 2014 Answer Key
byEneutron
 

Recently uploaded

PPTX
Sample Acceptance-Rejection-Criteria in lab
byKISMAT ALI
 
PDF
Dr. David Ford Wilson - Provides Holistic Mental Health Care
byDr. David Ford Wilson
 
PPTX
ANTIMICROBIAL STEWARDSHIP PROGRAME Vijay.pptx
byVIJAYARengan1
 
PPTX
ONFH[AVN HIP] -TRIPLE REGIME -A NOVAL SURGICAL CONCEPT .pptx
bydrashraf369
 
PPTX
DNS deviated nasal septum ent ward s.pptx
bysyedahiba121
 
PPTX
BENIGN BREAST DISEASES BBD/ Fibroadenoma, Fibrocystic Diseases/ ANDI.pptx
byDr Sushil Gyawali
 
PPT
Rethinking Pulmonary Fibrosis: From Fine-Tuning Diagnosis to Illuminating Nov...
byPVI, PeerView Institute for Medical Education
 
PPTX
HYPERTENSION III SEMESTER ADULT HEALTH NURSING-I
bykeerthi samuel
 
PDF
Preparing Medicare Cost Reports Seems Easy Until It's Not
byNMP Professional Services, Inc
 
PPT
Treating With Precision in CRSwNP: Defining the Role of Targeted Biologic The...
byPVI, PeerView Institute for Medical Education
 
PPTX
INTERCEPTIVE ORTHODONTICS in DENTISTRY.pptx
byChukwuebukaJoshuaOra
 
PPTX
TRIGEMINAL NERVE trigeminal nuclei .pptx
byTanushKumar13
 
PDF
Antitubercular agents medicinal chemistry.pdf
byPrerana Jadhav
 
PDF
Seminario biología molecula - EBV-miR-BART5-3p
bysalvarez1862004
 
PPTX
CTEV [ clubfoot] DR ARUN LAL ,DR MOHAMED ASHRAF travancore medical college k...
bydrashraf369
 
PDF
SEMINARIO BIOMOL.pdf (Samuel Cantillo y Karen Bohorquez)
bySamuelCantillo7
 
PDF
A beginner-friendly introduction to gym training
bydarrennickerson2
 
PPTX
Dental plaque dental plaque periodontology.pptx
bymohdx8884
 
PPTX
“Autoimmune Hemolytic Anemia (AIHA) with Pleural Effusion – Clinical Case Pre...
byPriyankapadvalkar
 
PPTX
WHEN NOT TO DO TENDOACHILLES TENOTOMY.pptx
byUmeshPrasadChoudhary
 
Sample Acceptance-Rejection-Criteria in lab
byKISMAT ALI
 
Dr. David Ford Wilson - Provides Holistic Mental Health Care
byDr. David Ford Wilson
 
ANTIMICROBIAL STEWARDSHIP PROGRAME Vijay.pptx
byVIJAYARengan1
 
ONFH[AVN HIP] -TRIPLE REGIME -A NOVAL SURGICAL CONCEPT .pptx
bydrashraf369
 
DNS deviated nasal septum ent ward s.pptx
bysyedahiba121
 
BENIGN BREAST DISEASES BBD/ Fibroadenoma, Fibrocystic Diseases/ ANDI.pptx
byDr Sushil Gyawali
 
Rethinking Pulmonary Fibrosis: From Fine-Tuning Diagnosis to Illuminating Nov...
byPVI, PeerView Institute for Medical Education
 
HYPERTENSION III SEMESTER ADULT HEALTH NURSING-I
bykeerthi samuel
 
Preparing Medicare Cost Reports Seems Easy Until It's Not
byNMP Professional Services, Inc
 
Treating With Precision in CRSwNP: Defining the Role of Targeted Biologic The...
byPVI, PeerView Institute for Medical Education
 
INTERCEPTIVE ORTHODONTICS in DENTISTRY.pptx
byChukwuebukaJoshuaOra
 
TRIGEMINAL NERVE trigeminal nuclei .pptx
byTanushKumar13
 
Antitubercular agents medicinal chemistry.pdf
byPrerana Jadhav
 
Seminario biología molecula - EBV-miR-BART5-3p
bysalvarez1862004
 
CTEV [ clubfoot] DR ARUN LAL ,DR MOHAMED ASHRAF travancore medical college k...
bydrashraf369
 
SEMINARIO BIOMOL.pdf (Samuel Cantillo y Karen Bohorquez)
bySamuelCantillo7
 
A beginner-friendly introduction to gym training
bydarrennickerson2
 
Dental plaque dental plaque periodontology.pptx
bymohdx8884
 
“Autoimmune Hemolytic Anemia (AIHA) with Pleural Effusion – Clinical Case Pre...
byPriyankapadvalkar
 
WHEN NOT TO DO TENDOACHILLES TENOTOMY.pptx
byUmeshPrasadChoudhary
 

Chronic Obstructive Pulmonary Disease - COPD

  • 1.
  • 2.
    lobal Initiative forChronic bstructive ung isease G O L D © Global Initiative for Chronic Obstructive Lung Disease
  • 3.
    Global Strategy forDiagnosis, Management and Prevention of COPD Definition, Classification Burden of COPD Risk Factors Pathogenesis, Pathology, Pathophysiology Management of COPD Primary Care Recommendations
  • 4.
    Definition of COPD COPDis a preventable and treatable disease with some significant extrapulmonary effects that may contribute to the severity in individual patients. Its pulmonary component is characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lung to noxious particles or gases.
  • 5.
    Sponsored Medical Lecture Notes– All Subjects USMLE Exam (America) – Practice
  • 6.
    History COPD has probablyalways existed but has been called by different names in the past. Bonet described a condition of “voluminous lungs” in 1679. In 1769, Giovanni Morgagni described 19 cases where the lungs were “turgid” particularly from air. The first description and illustration of the enlarged airspaces in emphysema was provided by Ruysh in 1721."History of pathologic descriptions of COPD" (PDF). Matthew Baillie illustrated an emphysematous lung in 1789 and described the destructive character of the condition. Badham used the word "catarrh" to describe the cough and mucus hypersecretion of chronic bronchitis in 1814. He recognised that chronic bronchitis was a disabling disorder. René Laennec, the physician who invented the stethoscope, used the term "emphysema" in his book A Treatise on the Diseases of the Chest and of Mediate Auscultation (1837) to describe lungs that did not collapse when he opened the chest during an autopsy. He noted that they did not collapse as usual because they were full of air and the airways were filled with mucus. In 1842, John Hutchinson invented the spirometer, which allowed the measurement of vital capacity of the lungs. However, his spirometer could only measure volume, not airflow. Tiffeneau in 1947 and Gaensler in 1950 and 1951 described the principles of measuring airflow. The terms chronic bronchitis and emphysema were formally defined at the CIBA guest symposium of physicians in 1959. The term COPD was first used by William Briscoe in 1965 and has gradually overtaken other terms to become established today as the preferred name for this disease.
  • 7.
    Classification of COPD Severity bySpirometryStage I: Mild FEV1/FVC < 0.70 FEV1 > 80% predicted Stage II: Moderate FEV1/FVC < 0.70 50% < FEV1 < 80% predicted Stage III: Severe FEV1/FVC < 0.70 30% < FEV1 < 50% predicted Stage IV: Very Severe FEV1/FVC < 0.70 FEV1 < 30% predicted or FEV1 < 50% predicted plus
  • 8.
    “At Risk” forCOPD COPD includes four stages of severity classified by spirometry. A fifth category--Stage 0: At Risk--that appeared in the 2001 report is no longer included as a stage of COPD, as there is incomplete evidence that the individuals who meet the definition of “At Risk” (chronic cough and sputum production, normal spirometry) necessarily progress on to Stage I: Mild COPD. The public health message is that chronic cough and sputum are not normal remains important - their presence should trigger a search for underlying cause(s).
  • 9.
    Global Strategy forDiagnosis, Management and Prevention of COPD Definition, Classification Burden of COPD Risk Factors Pathogenesis, Pathology, Pathophysiology Management Primary Care Recommendations
  • 10.
    Burden of COPD:Key Points  COPD is a leading cause of morbidity and mortality worldwide and results in an economic and social burden that is both substantial and increasing.  COPD prevalence, morbidity, and mortality vary across countries and across different groups within countries.  The burden of COPD is projected to increase in the coming decades due to continued exposure to COPD risk factors and the changing age structure of the world’s population.
  • 11.
    Burden of COPD:Prevalence  Many sources of variation can affect estimates of COPD prevalence, including e.g., sampling methods, response rates and quality of spirometry.  Data are emerging to provide evidence that prevalence of Stage I: Mild COPD and higher is appreciably higher in: - smokers and ex-smokers - people over 40 years of age - males
  • 12.
    COPD Prevalence Study inLatin America (Platino) The prevalence of post- bronchodilator FEV1/FVC < 0.70 increases steeply with age in 5 Latin American Cities Source: Menezes AM et al. Lancet 2005
  • 13.
    Burden of COPD:Mortality  COPD is a leading cause of mortality worldwide and projected to increase in the next several decades.  COPD mortality trends generally track several decades behind smoking trends.  Between 1999 and 2006, death rates for COPD have declined among U.S. men; there has been no significant change among death rates among U.S. women.
  • 14.
    Of the six leadingcauses of death in the United States, only COPD has been increasing steadily since 1970 Source: Jemal A. et al. JAMA 2005
  • 15.
    Global Strategy forDiagnosis, Management and Prevention of COPD Definition, Classification Burden of COPD Risk Factors Pathogenesis, Pathology, Pathophysiology Management Primary Care Recommendations
  • 16.
    Risk Factors forCOPD Lung growth and development Oxidative stress Gender Age Respiratory infections Socioeconomic status Nutrition Comorbidities Genes Exposure to particles ● Tobacco smoke ● Occupational dusts, organic and inorganic ● Indoor air pollution from heating and cooking with biomass in poorly ventilated dwellings ● Outdoor air pollution
  • 17.
    Risk Factors forCOPD NutritionNutrition InfectionsInfections Socio-economicSocio-economic statusstatus Aging PopulationsAging Populations
  • 18.
    Global Strategy forDiagnosis, Management and Prevention of COPD Definition, Classification Burden of COPD Risk Factors Pathogenesis, Pathology, Pathophysiology Management Primary Care Recommendations
  • 20.
    LUNG INFLAMMATIONLUNG INFLAMMATION COPDPATHOLOGYCOPD PATHOLOGY OxidativeOxidative stressstress ProteinasesProteinases RepairRepair mechanismsmechanisms Anti-proteinasesAnti-proteinasesAnti-oxidantsAnti-oxidants Host factors Amplifying mechanisms Cigarette smokeCigarette smoke Biomass particlesBiomass particles ParticulatesParticulates Source: Peter J. Barnes, Pathogenesis of COPD
  • 21.
    Mucus gland hyperplasia Gobletcell hyperplasia Mucus hypersecretion Neutrophils in sputum Squamous metaplasia of epithelium ↑ Macrophages No basement membrane thickening Little increase in airway smooth muscle ↑ CD8+ lymphocytes Changes in Large Airways of COPD PatientsChanges in Large Airways of COPD Patients Source: Peter J. Barnes, MD
  • 22.
    Disrupted alveolar attachments Inflammatoryexudate in lumen Peribronchial fibrosis Lymphoid follicle Thickened wall with inflammatory cells - macrophages, CD8+ cells, fibroblasts Changes in Small Airways in COPD Patients Source: Peter J. Barnes, MD
  • 23.
    LUNG INFLAMMATIONLUNG INFLAMMATION COPDPATHOLOGYCOPD PATHOLOGY OxidativeOxidative stressstress ProteinasesProteinases RepairRepair mechanismsmechanisms Anti-proteinasesAnti-proteinasesAnti-oxidantsAnti-oxidants Host factors Amplifying mechanisms Cigarette smokeCigarette smoke Biomass particlesBiomass particles ParticulatesParticulates Pathogenesis of COPD Source: Peter J. Barnes,
  • 24.
    Cigarette smokeCigarette smoke (andother irritants)(and other irritants) PROTEASESPROTEASES Neutrophil elastaseNeutrophil elastase CathepsinsCathepsins MMPsMMPs Alveolar wall destructionAlveolar wall destruction (Emphysema)(Emphysema) Mucus hypersecretionMucus hypersecretion CD8CD8++ lymphocytelymphocyte Alveolar macrophageAlveolar macrophageEpithelialEpithelial cellscells FibrosisFibrosis (Obstructive(Obstructive bronchiolitis)bronchiolitis) FibroblastFibroblast MonocyteMonocyteNeutrophilNeutrophil Chemotactic factorsChemotactic factors Inflammatory Cells Involved in COPD Source: Peter J. Barnes, MD
  • 25.
    Anti-proteases SLPI α1-AT Proteolysis OO22 -- , H,H220022 OHOH.. , ONOO, ONOO-- ↑ Mucus secretion Plasma leak Bronchoconstriction NF-NF-κκBB IL-8IL-8 NeutrophilNeutrophil recruitmentrecruitment TNF-TNF-αα IsoprostanesIsoprostanes ↓↓ HDAC2HDAC2 ↑↑InflammationInflammation SteroidSteroid resistanceresistance Macrophage Neutrophil Oxidative Stress in COPD Source: Peter J. Barnes, MD
  • 26.
    NormalNormal Inspiration Expiration alveolar attachments Mild/moderateMild/moderate COPDCOPD loss ofelasticity SevereSevere COPDCOPD loss of alveolar attachments closure smallsmall airwayairway Dyspnea ↓ Exercise capacity Air trappingAir trapping HyperinflationHyperinflation ↓↓ HealthHealth statusstatus Air Trapping in COPD Source: Peter J. Barnes,
  • 27.
    Chronic hypoxiaChronic hypoxia PulmonaryvasoconstrictionPulmonary vasoconstriction MuscularizationMuscularization IntimalIntimal hyperplasiahyperplasia FibrosisFibrosis ObliterationObliteration Pulmonary hypertensionPulmonary hypertension Cor pulmonaleCor pulmonale Death EdemaEdema Pulmonary Hypertension in COPD Source: Peter J. Barnes, MD
  • 28.
    Macrophages TNF-α IL-8 IL-6 BacteriaViruses Non-infective Pollutants Epithelial cells Oxidative stressOxidative stress Neutrophils Inflammation in COPD Exacerbations Source: Peter J. Barnes,
  • 29.
    Alveolar wall destruction Lossof elasticity Destruction of pulmonary capillary bed ↑ Inflammatory cells macrophages, CD8+ lymphocytes Source: Peter J. Barnes, MD Changes in Lung Parenchyma in COPD
  • 30.
    Chronic hypoxiaChronic hypoxia PulmonaryvasoconstrictionPulmonary vasoconstriction MuscularizationMuscularization IntimalIntimal hyperplasiahyperplasia FibrosisFibrosis ObliterationObliteration Pulmonary hypertensionPulmonary hypertension Cor pulmonaleCor pulmonale Death EdemaEdema Pulmonary Hypertension in COPD Source: Peter J. Barnes, MD
  • 31.
    YYYY YY Mast cellMast cell CD4+cellCD4+ cell (Th2)(Th2) EosinophilEosinophil AllergensAllergens Ep cellsEp cells ASTHMAASTHMA BronchoconstrictionBronchoconstriction AHRAHR Alv macrophageAlv macrophageEp cellsEp cells CD8+ cellCD8+ cell (Tc1)(Tc1) NeutrophilNeutrophil Cigarette smokeCigarette smoke Small airway narrowingSmall airway narrowing Alveolar destructionAlveolar destruction COPDCOPD Reversible Irreversible Airflow LimitationAirflow Limitation Source: Peter J. Barnes, MD
  • 32.
    Symptoms of COPD Oneof the most common symptoms of COPD is shortness of breath (dyspnea). People with COPD commonly describe this as: "My breathing requires effort," "I feel out of breath," or "I can't get enough air in". People with COPD typically first notice dyspnea during vigorous exercise when the demands on the lungs are greatest. Over the years, dyspnea tends to get gradually worse so that it can occur during milder, everyday activities such as housework. In the advanced stages of COPD, dyspnea can become so bad that it occurs during rest and is constantly present.
  • 33.
    Symptoms of COPD Othersymptoms of COPD are a persistent cough, sputum or mucus production, wheezing, chest tightness, and tiredness. People with advanced (very severe) COPD sometimes develop respiratory failure. When this happens, cyanosis, a bluish discoloration of the lips caused by a lack of oxygen in the blood, can occur. An excess of carbon dioxide in the blood can cause headaches, drowsiness or twitching (asterixis). A complication of advanced COPD is cor pulmonale, a strain on the heart due to the extra work required by the heart to pump blood through the affected lungs. Symptoms of cor pulmonale are peripheral edema, seen as swelling of the ankles, and dyspnea.
  • 34.
    Symptoms of COPD Thereare a few signs of COPD that a healthcare worker may detect although they can be seen in other diseases. Some people have COPD and have none of these signs. Common signs are: tachypnea, a rapid breathing rate wheezing sounds or crackles in the lungs heard through a stethoscope breathing out taking a longer time than breathing in enlargement of the chest, particularly the front-to-back distance (hyperaeration) active use of muscles in the neck to help with breathing breathing through pursed lips increased anteroposterior to lateral ratio of the chest (i.e. barrel chest).
  • 35.
    Spirometry - Introduction Spirometryis the gold standard for COPD diagnosis Underuse leads to inaccurate COPD diagnosis Widespread uptake has been limited by: Concerns over technical performance of operators Difficulty with interpretation of results Lack of approved local training courses
  • 36.
    What is Spirometry? Spirometryis a method of assessing lung function by measuring the total volume of air the patient can expel from the lungs after a maximal inhalation.
  • 37.
    Why Perform Spirometry? Measureairflow obstruction to help make a definitive diagnosis of COPD Confirm presence of airway obstruction Assess severity of airflow obstruction in COPD Detect airflow obstruction in smokers who may have few or no symptoms Monitor disease progression in COPD Assess one aspect of response to therapy Assess prognosis (FEV1) in COPD Perform pre-operative assessment
  • 38.
    Spirometry – Additional Uses Makea diagnosis and assess severity in a range of other respiratory conditions Distinguish between obstruction and restriction as causes of breathlessness Screen workforces in occupational environments Assess fitness to dive Perform pre-employment screening in certain professions
  • 39.
    Types of Spirometers Bellowsspirometers: Measure volume; mainly in lung function units Electronic desk top spirometers: Measure flow and volume with real time display Small hand-held spirometers: Inexpensive and quick to use but no print out
  • 40.
  • 41.
  • 42.
  • 43.
  • 44.
    Standard Spirometric Indicies FEV1- Forced expiratory volume in one second: The volume of air expired in the first second of the blow FVC - Forced vital capacity: The total volume of air that can be forcibly exhaled in one breath FEV1/FVC ratio: The fraction of air exhaled in the first second relative to the total volume exhaled
  • 45.
    Criteria for Normal Post-bronchodilatorSpirometry FEV1: % predicted > 80% FVC: % predicted > 80% FEV1/FVC: > 0.7 - 0.8, depending on age
  • 46.
    Normal Trace ShowingFEV1 and FVC 1 2 3 4 5 6 1 2 3 4 Volume,liters Time, sec FVC5 1 FEV1 = 4L FVC = 5L FEV1/FVC = 0.8
  • 47.
  • 48.
    Spirometry: Obstructive Disease Volume,liters Time, seconds 5 4 3 2 1 12 3 4 5 6 FEV1 = 1.8L FVC = 3.2L FEV1/FVC = 0.56 Normal Obstructive
  • 49.
    Spirometric Diagnosis ofCOPD COPD is confirmed by post– bronchodilator FEV1/FVC < 0.7 Post-bronchodilator FEV1/FVC measured 15 minutes after 400µg salbutamol or equivalent
  • 50.
    Bronchodilator Reversibility Testing Provides thebest achievable FEV1 (and FVC) Helps to differentiate COPD from asthma Must be interpreted with clinical history - neither asthma nor COPD are diagnosed on spirometry alone
  • 51.
    Bronchodilator Reversibility Testing Can bedone on first visit if no diagnosis has been made Best done as a planned procedure: pre- and post-bronchodilator tests require a minimum of 15 minutes Post-bronchodilator only saves time but does not help confirm if asthma is present Short-acting bronchodilators need to be withheld for at least 4 hours prior to test
  • 52.
    Bronchodilator Reversibility Testing Bronchodilator*Dose FEV1 before and after Salbutamol 200 – 400 µg via large volume spacer 15 minutes Terbutaline 500 µg via Turbohaler® 15 minutes Ipratropium 160 µg** via spacer 45 minutes * Some guidelines suggest nebulised bronchodilators can be given but the doses are not standardised. “There is no consensus on the drug, dose or mode of administering a bronchodilator in the laboratory.” Ref: ATS/ERS Task Force : Interpretive strategies for Lung Function Tests ERJ 2005;26:948 ** Usually 8 puffs of 20 µg
  • 53.
    Global Strategy forDiagnosis, Management and Prevention of COPD Definition, Classification Burden of COPD Risk Factors Pathogenesis, Pathology, Pathophysiology Management Primary Care Recommendations
  • 54.
    Four Components ofCOPD Management 1. Assess and monitor disease 2. Reduce risk factors 3. Manage stable COPD Education Pharmacologic Non-pharmacologic 4. Manage exacerbations
  • 55.
    • Relieve symptoms •Prevent disease progression • Improve exercise tolerance • Improve health status • Prevent and treat complications • Prevent and treat exacerbations • Reduce mortality GOALS of COPD MANAGEMENT VARYING EMPHASIS WITH DIFFERING SEVERITY
  • 56.
    Four Components ofCOPD Management 1. Assess and monitor disease 2. Reduce risk factors 3. Manage stable COPD Education Pharmacologic Non-pharmacologic 4. Manage exacerbations
  • 57.
    Management of StableCOPD Assess and Monitor COPD: Key Points A clinical diagnosis of COPD should be considered in any patient who has dyspnea, chronic cough or sputum production, and/or a history of exposure to risk factors for the disease. The diagnosis should be confirmed by spirometry. A post-bronchodilator FEV1/FVC < 0.70 confirms the presence of airflow limitation that is not fully reversible. Comorbidities are common in COPD and should be actively identified.
  • 58.
    SYMPTOMS cough sputum shortness of breath EXPOSURETO RISK FACTORS tobacco occupation indoor/outdoor pollution SPIROMETRY Diagnosis of COPD
  • 59.
    Differential Diagnosis:Differential Diagnosis: COPDand AsthmaCOPD and Asthma COPD ASTHMA • Onset in mid-life • Symptoms slowly progressive • Long smoking history • Dyspnea during exercise • Largely irreversible airflow limitation • Onset early in life (often childhood) • Symptoms vary from day to day • Symptoms at night/early morning • Allergy, rhinitis, and/or eczema also present • Family history of asthma • Largely reversible airflow limitation
  • 60.
    COPD and Co-Morbidities COPDpatients are at increased risk for: • Myocardial infarction, angina • Osteoporosis • Respiratory infection • Depression • Diabetes • Lung cancer
  • 61.
    Four Components ofCOPD Management 1. Assess and monitor disease 2. Reduce risk factors 3. Manage stable COPD Education Pharmacologic Non-pharmacologic 4. Manage exacerbations
  • 62.
    Management of StableCOPD Reduce Risk Factors: Key Points Reduction of total personal exposure to tobacco smoke, occupational dusts and chemicals, and indoor and outdoor air pollutants are important goals to prevent the onset and progression of COPD. Smoking cessation is the single most effective — and cost effective — intervention in most people to reduce the risk of developing COPD and stop its progression (Evidence A).
  • 63.
    Brief Strategies toHelp the Patient Willing to Quit Smoking • ASK Systematically identify all tobacco users at every visit • ADVISE Strongly urge all tobacco users to quit • ASSESS Determine willingness to make a quit attempt • ASSIST Aid the patient in quitting • ARRANGE Schedule follow-up contact.
  • 64.
    Management of StableCOPD Reduce Risk Factors: Smoking Cessation  Counseling delivered by physicians and other health professionals significantly increases quit rates over self-initiated strategies. Even a brief (3-minute) period of counseling to urge a smoker to quit results in smoking cessation rates of 5-10%.  Numerous effective pharmacotherapies for smoking cessation are available; pharmacotherapy is recommended when counseling is not sufficient to help patients quit smoking.
  • 65.
    Management of StableCOPD Reduce Risk Factors: Indoor/Outdoor Air Pollution Reducing the risk from indoor and outdoor air pollution is feasible and requires a combination of public policy and protective steps taken by individual patients. Reduction of exposure to smoke from biomass fuel, particularly among women and children, is a crucial goal to reduce the prevalence of COPD worldwide.
  • 66.
    Four Components ofCOPD Management 1. Assess and monitor disease 2. Reduce risk factors 3. Manage stable COPD Education Pharmacologic Non-pharmacologic 4. Manage exacerbations
  • 67.
    Management of StableCOPD Pharmacotherapy: Bronchodilators  Bronchodilator medications are central to the symptomatic management of COPD (Evidence A).  Bronchodilators are prescribed on an as-needed or on a regular basis to prevent or reduce symptoms.  The principal bronchodilator treatments are ß2- agonists, anticholinergics, and methylxanthines used singly or in combination (Evidence A).  Long-acting bronchodilators are more effective and convenient than treatment with short-acting bronchodilators (Evidence A).
  • 68.
    Management of StableCOPD Pharmacotherapy: Glucocorticosteroids  Regular treatment with inhaled glucocorticosteroids reduces frequency of exacerbations for symptomatic COPD patients with an FEV1 < 50% predicted (Stage III: Severe COPD and Stage IV: Very Severe COPD) and repeated exacerbations.  Treatment with inhaled glucocortciosteroids increases the likelihood of pneumonia and does not reduce overall mortality.
  • 69.
    Management of StableCOPD Pharmacotherapy: Combination Therapy Glucocorticosteroids and Long-Acting ß2-agonist  An inhaled glucocorticosteroid combined with a long-acting ß2-agonist is more effective than the individual components in reducing exacerbations and improving lung function (Evidence A).  Combination therapy increases the likelihood of pneumonia and has no impact on mortality.  Addition of a long-acting ß2-agonist /inhaled gluco- Corticosteroid comgination to an anticholinergic (tiotropium) appears to provide additional benefits.
  • 70.
    Management of StableCOPD Pharmacotherapy: Systemic Glucocorticosteroids  Chronic treatment with systemic glucocorticosteroids should be avoided because of an unfavorable benefit-to-risk ratio (Evidence A).
  • 71.
    Management of StableCOPD Pharmacotherapy: Phosphodiesterase-4 Inhibitors  In patients with Stage III: Severe COPD or Stage IV: Very Severe COPD and a history of exacerbations and chronic bronchitis, the phospodiesterase-4 inhibitor, roflumilast, reduces exacerbations treated with oral glucocorticosteroids.
  • 72.
    Management of StableCOPD Pharmacotherapy: Vaccines  In COPD patients influenza vaccines can reduce serious illness (Evidence A).  Pneumococcal polysaccharide vaccine is recommended for COPD patients 65 years and older and for COPD patients younger than age 65 with an FEV1 < 40% predicted (Evidence B).  Influenza, not pneumococcal vaccination is associated with reduced risk of all-cause mortality in COPD (Evidence B).
  • 73.
    Management of StableCOPD All Stages of Disease Severity Avoidance of risk factors - smoking cessation - reduction of indoor pollution - reduction of occupational exposure Influenza vaccination
  • 74.
    IV: Very SevereIII:SevereII: ModerateI: Mild Therapy at Each Stage of COPD*  FEV1 /FVC < 70%  FEV1 > 80% predicted  FEV1 /FVC < 70%  50% < FEV1 < 80% predicted  FEV1 /FVC < 70%  30% < FEV1 < 50% predicted  FEV1 /FVC < 70%  FEV1 < 30% predicted or FEV1 < 50% predicted plus chronic respiratory failure Add regular treatment with one or more long-acting bronchodilators (when needed); Add rehabilitation Add inhaled glucocorticosteroids if repeated exacerbations Active reduction of risk factor(s); influenza vaccination Add short-acting bronchodilator (when needed) Add long term oxygen if chronic respiratory failure. Consider surgical treatments *Postbronchodilator FEV1 is recommended for the diagnosis and assessment of severity of COPD
  • 75.
    Management of StableCOPD Other Pharmacologic Treatments  Antibiotics: Only used to treat infectious exacerbations of COPD  Antioxidant agents: No effect of n-acetyl- cysteine on frequency of exacerbations, except in patients not treated with inhaled glucocorticosteroids  Mucolytic agents, Antitussives, Vasodilators: Not recommended in stable COPD
  • 76.
    Management of StableCOPD Non-Pharmacologic Treatments  Rehabilitation: All COPD patients benefit from exercise training programs, improving with respect to both exercise tolerance and symptoms of dyspnea and fatigue (Evidence A).  Oxygen Therapy: The long-term administration of oxygen (> 15 hours per day) to patients with chronic respiratory failure has been shown to increase survival (Evidence A).
  • 77.
    Four Components ofCOPD Management 1. Assess and monitor disease 2. Reduce risk factors 3. Manage stable COPD Education Pharmacologic Non-pharmacologic 4. Manage exacerbations
  • 78.
    Management COPD Exacerbations KeyPoints An exacerbation of COPD is defined as: “An event in the natural course of the disease characterized by a change in the patient’s baseline dyspnea, cough, and/or sputum that is beyond normal day-to-day variations, is acute in onset, and may warrant a change in regular medication in a patient with underlying COPD.”
  • 79.
    Management COPD Exacerbations KeyPoints The most common causes of an exacerbation are infection of the tracheobronchial tree and air pollution, but the cause of about one-third of severe exacerbations cannot be identified (Evidence B). Patients experiencing COPD exacerbations with clinical signs of airway infection (e.g., increased sputum purulence) may benefit from antibiotic treatment (Evidence B).
  • 80.
    Manage COPD Exacerbations KeyPoints  Inhaled bronchodilators (particularly inhaled ß2-agonists with or without anticholinergics) and oral glucocortico- steroids are effective treatments for exacerbations of COPD (Evidence A).
  • 81.
    Management COPD Exacerbations KeyPoints  Noninvasive mechanical ventilation in exacerbations improves respiratory acidosis, increases pH, decreases the need for endotracheal intubation, and reduces PaCO2, respiratory rate, severity of breathlessness, the length of hospital stay, and mortality (Evidence A).  Medications and education to help prevent future exacerbations should be considered as part of follow-up, as exacerbations affect the quality of life and prognosis of patients with COPD.
  • 82.
    Global Strategy forDiagnosis, Management and Prevention of COPD Definition, Classification Burden of COPD Risk Factors Pathogenesis, Pathology, Pathophysiology Management Primary Care Recommendations
  • 83.
    Translating COPD Guidelinesinto Primary Care KEY POINTS Better dissemination of COPD guidelines and their effective implementation in a variety of health care settings is urgently required. In many countries, primary care practitioners treat the vast majority of patients with COPD and may be actively involved in public health campaigns and in bringing messages about reducing exposure to risk factors to both patients and the public.
  • 84.
    Translating COPD Guidelinesinto Primary Care KEY POINTS Spirometric confirmation is a key component of the diagnosis of COPD and primary care practitioners should have access to high quality spirometry. Older patients frequently have multiple chronic health conditions. Comorbidities can magnify the impact of COPD on a patient’s health status, and can complicate the management of COPD.
  • 85.
    Global Strategy forDiagnosis, Management and Prevention of COPD SUMMARY Definition, Classification Burden of COPD Risk Factors Pathogenesis, Pathology, Pathophysiology Management Primary Care
  • 86.
    Global Strategy forDiagnosis, Management and Prevention of COPD: Summary  COPD is increasing in prevalence in many countries of the world.  COPD is treatable and preventable.  The GOLD program offers a strategy to identify patients and to treat them according to the best medications available.
  • 87.
     COPD canbe prevented by avoidance of risk factors, the most notable being tobacco smoke.  Patients with COPD have multiple other conditions (comorbidities) that must be taken into consideration.  GOLD has developed a global network to raise awareness of COPD and disseminate information on diagnosis and treatment. Global Strategy for Diagnosis, Management and Prevention of COPD: Summary
  • 88.
    WORLD COPD DAY November16, 2011 Raising COPD Awareness Worldwide

Editor's Notes

  • #22 Changes in large airways of COPD patients. The epithelium often shows squamous metaplasia and there is goblet cell and submucosal gland hyperplasia, resulting in mucus hypersecretion. The airway wall is infiltrated with macrophages and CD8+ lymphocytes, whereas neutrophils predominate in the airway lumen and around submucosal glands. Airway smooth muscle and basement membrane are minimally increased compared to the findings in asthma.
  • #23 Changes in small airways in COPD patients. The airway wall is thickened and infiltrated with inflammatory cells, predominately macrophages and CD8+ lymphocytes, with increased numbers of fibroblasts. In severe COPD there are also lymphoid follicles. The lumen is often filled with an inflammatory exudate and mucus. There is peribronchial fibrosis and airway smooth muscle may be increased, resulting in narrowing of the airway.
  • #24 Pathogenesis of COPD, illustrating the central role of inflammation
  • #25 Inflammatory cells involved in COPD. Cigarette smoke activates macrophages and epithelial cells to release chemotactic factors that recruit neutrophils, monocytes and CD8+ T-lymphocytes from the circulation. They also release factors that activate fibroblasts leading to small airway obstruction (obstructive bronchiolitis). Proteases released from neutrophils and macrophages may cause mucus hypersecretion and emphysema.
  • #26 Oxidative stress in COPD has several detrimental consequences, including activation of the transcription factor nuclear factor-κB (NF-κB), reduction in antiproteases, plasma leakage and mucus hypersecretion. In addition it reduces histone deacetylase-2, resulting in amplified inflammation and reduced anti-inflammatory response to corticosteroids.
  • #27 Air trapping in COPD. During expiration small airways narrow but closure is prevented by the elasticity of alveolar attachments. In COPD patients there is a loss of elasticity with greater narrowing in small airways, which may close completely when there is loss of alveolar attachments as a result of emphysema. This results in air trapping and hyperinflation, leading to dyspnea and reduced exercise capacity.
  • #29 Inflammation in COPD exacerbations induced by several causal mechanisms. Increased numbers of inflammatory cells, particularly neutrophils, are seen with increased concentrations of inflammatory mediators and oxidative stress.
  • #31 New
  • #60 A diagnosis of COPD should be considered in any patient who has cough, sputum production, or dyspnea and/or a history of exposure to risk factors. The diagnosis is confirmed by spirometry. To help identify individuals earlier in the course of disease, spirometry should be performed for patients who have chronic cough and sputum production even if they do not have dyspnea. Spirometry is the best way to diagnose COPD and to monitor its progression and health care workers to care for COPD patients should have assess to spirometry.
  • #65 Reduction of total personal exposure to tobacco smoke, occupational dusts and chemicals, and indoor and outdoor air pollutants are important goals to prevent the onset and progression of COPD. Smoking cessation is the single most effective - and cost effective - intervention to reduce the risk of developing COPD and stop its progression. Brief tobacco dependence treatment is effective, and every tobacco user should be offered at least this treatment at every visit to a health care provider. Three types of counseling are especially effective: practical counseling, social support as part of treatment, and social support arranged outside of treatment.