![18
0
Asthma
Asthma is a heterogeneous disease, usually characterized by chronic airway
inflammation. It is defined by the history of respiratory symptoms such as wheeze,
shortness of breath, chest tightness and cough that vary over time and in intensity,
together with variable expiratory airflow limitation. [GINA 2014]
COPD
COPD is a common preventable and treatable disease, characterized by persistent
airflow limitation that is usually progressive and associated with enhanced chronic
inflammatory responses in the airways and the lungs to noxious particles or gases.
Exacerbations and comorbidities contribute to the overall severity in individual
patients. [GOLD 2015]
Asthma-COPD overlap syndrome (ACOS) [a description]
Asthma-COPD overlap syndrome (ACOS) is characterized by persistent airflow
limitation with several features usually associated with asthma and several features
usually associated with COPD. ACOS is therefore identified by the features that it
shares with both asthma and COPD.
Definitions](https://image.slidesharecdn.com/slsqasthmamanagementpptv050811piccomp-copy-160406221639/85/COPD-back-to-basis-180-320.jpg)
Uploaded byAshraf ElAdawy
COPD back to basis
COPD is a progressive lung disease characterized by breathlessness. Smoking is the primary risk factor. The disease involves inflammation in the lungs over many years leading to damage of lung tissue and airflow limitation. Symptoms worsen over time and include cough, sputum production, and shortness of breath. Lung function progressively declines and hyperinflation develops due to air trapping. Underdiagnosis is common and spirometry is required for diagnosis. COPD has systemic effects and frequent exacerbations increase mortality rates.
More Related Content
Similar to COPD back to basis
More from Ashraf ElAdawy
COPD back to basis
- 2.
- 3.
- 4.
- 5. Smoking Is theSingle Most Important Risk Factor for COPD Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease, Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2008. Available from: http://www.goldcopd.org.
- 7. COPD is theonly chronic disease that is rapidly increasing in prevalence on a worldwide basis
- 8.
- 9.
- 10. Mortality : Global burdenof Disease study • Almost 90% of COPD deaths occur in low- and middle-income countries.
- 11.
- 12. COPD is aCinderella Condition Limited recognition from patients Limited recognition from physicians QuickT ime™ and a T IF F (Uncompressed) decompressor are needed to see this picture. COPD is Underestimated Underdiagnosed Undertreated
- 13. Physician Specialty SeenMost Often Respiratory Specialist, 22% Internal Medicine, 15% General/Family Medicine, 52% Cardiologist, 3% Other, 2% Not Sure, 5% Allergist, 1%
- 14. Under diagnosis ofCOPD in the United States Over 12 million people in the United States have been diagnosed with COPD; another 12 million are estimated to be undiagnosed1 Data from NHANES III indicate that approximately 24 million US adults have evidence of impaired lung function indicative of COPD2,3 Most (70%) of patients with undiagnosed COPD are <65 years 70% <Age 65 30% ≥Age 65 Percent With Undiagnosed COPD 1. NHLBI; available at http://www.nhlbi.nih.gov/health/public/lung/copd/index.html. 3. Mannino DM, et al. Proc Am Thorac Soc. 2007;4:502-306 2. Mannino DM, et al. MMWR Surveill Summ. 2002:1-16.
- 15. An estimated 210million people worldwide have COPD More than 3 million people died of COPD in 2005 , this represented 5% of all deaths worldwide COPD disproportionately affects the world's poorest WHO , 2009. COPD: Global Burden
- 16. COPD IsDeadly But Treatable -- And Preventable disease , responsible for a large human and economic burden around the world Encourage the health care community to take a more active role in developing programs for COPD prevention Stimulate effective management programs to treat those with the disease
- 17.
- 18. Common preventable &treatable disease Characterized by persistent airflow limitation that is usually progressive Associated with an enhanced chronic inflammatory response in the airways & the lung to noxious particles or gases Exacerbations & comorbidities contribute to the overall severity in individual patients Definition of COPD 2014
- 19. 19 COPD is usedto describe emphysema, chronic bronchitis or a combination of the two.
- 20. Burden of COPD COPDis a leading cause of morbidity & mortality worldwide The burden will increase in coming decades due to continued exposure to risk factors & the aging of the world’s population COPD is associated with significant economic burden
- 21. Prevalence Buist AS, McBurnieMA, Vollmer WM, et al. International variation in the prevalence of COPD (the BOLD Study): a population-based prevalence study. Lancet. 2007; 11.8% 8.5%10.1% overall
- 22. Chapman KR, etal. Chest. 2001. COPD Misdiagnosis Is Common in Women Hypothetical Male Patient With COPD Symptoms Hypothetical Female Patient With COPD Symptoms Diagnosed as COPD by 65% of physicians Diagnosed as COPD by 49% of physicians 65% 49% COPD symptoms in women were most commonly misdiagnosed as asthma
- 23. Risk Factors forCOPD Genes Infections Socio-economic status Aging Populations © 2015 Global Initiative for Chronic Obstructive Lung Disease
- 24.
- 25.
- 26.
- 27. Adapted from FletcherCM, Peto R. Brit Med J. 1977;1:1645-1648. Accelerated Lung-Function Decline in COPD 0 20 40 60 80 100 20 30 40 50 60 70 80 90 Age (years) Death Disability Symptoms Nonsmoker COPD
- 28. Average Decrease inFEV1 / year Males Females Former smokers 30 ml/year 22 ml/year Current smokers 66 ml/year 54 ml/year Anthonisen NR, et.al. Am J Respir Crit Care Med 166:675-9, 2002.
- 29. Fletcher & Peto,BMJ 1977;1:1645 Susceptibility Genes Protective Genes PULMONARY FUNCTION DECLINE OVER TIME MODEL: BETWEEN INDIVIDUAL VARIATION IN SUSCEPTIBILITY TO CIGARETTE SMOKE
- 30. Not only smokingbut smoke Air pollution resulting from the burning of wood and other biomass fuels is estimated to kill two million women and children each year.
- 31.
- 32.
- 33. LUNG INFLAMMATION COPD PATHOLOGY Oxidative stressProteinases Host factors Amplifying mechanisms Cigarette smoke Biomass particles Particulates Pathogenesis of COPD
- 34. LUNG INFLAMMATION COPD PATHOLOGY Oxidative stressProteinases Repair mechanisms Anti-proteinases Anti-oxidants Host factors Amplifying mechanisms Cigarette smoke Biomass particles Particulates Pathogenesis of COPD
- 36. Chronic Inflammation playsa central role in COPD Adapted from Barnes PJ, in Stockley, et al (editors), Chronic Obstructive Pulmonary Disease. Oxford, England: Blackwell Publishing; 2007 Smoke Pollutants Inflammation Chronic inflammation Structural changes Neutrophils CD8+ T-lymphocytes Macrophages Key inflammatory cells Systemic inflammation Airflow limitation Bronchoconstriction, oedema, mucus, emphysema Acute exacerbation
- 37.
- 38. Mast cell CD4+ cell (Th2) Eosinophil Allergens Epcells ASTHMA Bronchoconstriction AHR Alv macrophageEp cells CD8+ cell (Tc1) Neutrophil Cigarette smoke Small airway narrowing Alveolar destruction COPD Reversible Not fully reversibleAirflow Limitation
- 39. Pathology The site ofpathology in COPD
- 40. COPD comprisespathological changes in four different compartments of the lungs 1. Central airways 2. Peripheral airways 3. Lung parenchyma 4. Pulmonary vasculature 40
- 41. PATHOLOGY COPD comprisesmajor pathological changes in the following four different compartments of the lung, which are variably present in individuals with the disease: 1. Central airways (cartilaginous airways >2mm of internal diameter) 2. Peripheral airways (noncartilaginous airways <2mm internal diameter) 3. Lung parenchyma (respiratory bronchioles, alveoli and capillaries) 4. Pulmonary vasculature 41
- 42. 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 Patients Source: Peter J. Barnes, MD
- 43. 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
- 44. 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
- 45. 45 Lung parenchyma(respiratory bronchioles, alveoli and capillaries) Alveolar wall destruction, apoptosis of epithelial and endothelial cells. There are two major types : 1) Centrilobular emphysema: dilatation & destruction of respiratory bronchioles; most commonly seen in smokers 2) Panacinar emphysema: destruction of alveolar sacs as well as respiratory bronchioles; most commonly seen in alpha-1 antitrypsin deficiency
- 46.
- 47. Endothelial dysfunction Intimal hyperplasia Smoothmuscle hyperplasia ↑ Inflammatory cells (macrophages, CD8+ lymphocytes) Changes in Pulmonary Arteries in COPD Patients Source: Peter J. Barnes, MD
- 48. Chronic hypoxia Pulmonary vasoconstriction Muscularization Intimal hyperplasia Fibrosis Obliteration Pulmonaryhypertension Cor pulmonale Death Edema Pulmonary Hypertension in COPD Source: Peter J. Barnes, MD
- 49. Pathogenic mechanisms Pathological changesin COPD Physiological abnormalities: Mucous hypersecretion & ciliary dysfunction Airflow obstruction & hyperinflation Gas exchange abnormalities Pulmonary hypertension & systemic effects Pathophysiology
- 50.
- 51. -Chronic Bronchitis predominant -Airwayobstruction is the main problem Normal Elastic Recoil Chronic Bronchitis Elastic Recoil Increased airway resistance due to thickened wall and secretions Airway supported by connective tissue
- 52. -Emphysema Predominant -This resultsin a loss of the elastic recoil of the lungs on expiration -This also results in loss of tethering or support of the most distal portions of the airway leading to collapse on expiration Normal Elastic Recoil Airway supported by connective tissue Decreased Elastic Recoil = Lower Flow Loss of support = Airway collapses= Air gets trapped in lung
- 53.
- 55. Alveolar Emptying inCOPD In COPD, airflow is limited because small airways are narrowed, alveoli lose their elasticity, and supportive structures are lost.
- 56. COPD is aComplex Disease Progressive Loss of Lung Function Reduced Quality of Life Exacerbations Mortality Broncho- constriction Inflammation Structural Changes Airflow Limitation & Hyperinflation
- 57.
- 58.
- 59.
- 60.
- 61.
- 62. Clinical Course ofCOPD Air Trapping Expiratory Flow Limitation Breathlessness Inactivity Poor Health-Related Quality of Life Hyperinflation Deconditioning COPD EXACERBATIONS Disability Disease progression Death Reduced Exercise Capacity
- 63.
- 64. COPD is aprogressive disease The Downward Spiral in COPD
- 65. 65 Is it InevitablyAll Downhill ?
- 66.
- 67. What is Progressionof COPD? *GOLD Guidelines. Am J Respir Crit Care Med. 0 At Risk I Mild II Moderate III Severe IV Very Severe Health Prevalent Disease Progressive Disease Death ??? Incident Disease
- 68.
- 69. Natural History ofCOPDLungFunction Time (Years) Exacerbation Exacerbation Exacerbation Never smoked Smoker Fletcher C. Br Med J. 1977
- 70. Frequent exacerbations areassociated with increased mortality A = No exacerbations B = 1-2 exacerbations C = 3 or more exacerbations Soler-Cataluna JJ, et al. Thorax 2005;60:925-931. p < 0.0001 1.0 Probabilityofsurviving 0.8 0.6 0.4 0.2 0.0 0 10 20 30 40 50 60 Time (months) A B C p = 0.069 p < 0.0002
- 71. COPD is: a multi-component disease with systemic involvement & inflammation Respiratory system Systemic inflammation Target organs QuickTime™ and a TIFF (Uncompressed) decompressor are needed to see this picture. COPD is: More than just a lung disorder
- 72. Barnes PJ (2010)Chronic Obstructive Pulmonary Disease: Effects beyond the Lungs. Mechanism linking COPD to systemic manifestations
- 73. Declining lung function Symptoms Exacerbations Decreasedexercise tolerance Deteriorating health status and increasing morbidity Mortality Airflow limitation Systemic component Structural changes Mucociliary dysfunction Airway inflammation Agusti. Respir Med 2005 Agusti et al. Eur Respir J 2003 Bernard et al. Am J Respir Crit Care Med 1998 COPD is a multicomponent disease with inflammation at its core leading to mortality
- 76. Lung Volumes IRV TV ERV 4Volumes 4 Capacities – Sum of 2 or more lung volumes RV IC FRC VC TLC RV
- 77. Lung Volumes inObstructive DiseaseLung Volumes in Obstructive Disease VT VT NormalNormal COPDCOPD RVRV RVRV TLCTLC FRCFRC ICIC ICIC TLCTLC FRCFRC VolumeVolume
- 78. 78 Progressive Hyperinflation Reduces InspiratoryCapacity FRC/ EELV
- 79.
- 80. Effects of Exerciseon Hyperinflation VT IRVERV IC RV Normal Years - Decades Progression Rest Static Hyperinflation Air Trapping at Rest Seconds - Minutes Exercise Dynamic Hyperinflation Air Trapping During Exercise
- 81. 81 Dynamic hyperinflation inpatients with emphysema during exercise. Note that V T increases with exercise. Note also that the expiratory phase decreases progressively with continued exercise indicating progressive air trapping .
- 82. Despite itsheterogeneity, the pathophysiological hallmark of COPD is expiratory flow limitation and Lung hyperinflation Dyspnea (breathlessness) and exercise intolerance are the most common symptoms in COPD and progress relentlessly as the disease advances. 82
- 83. To the COPD patient,this is a breathtaking view Diagnosis
- 84. o Many patientswith COPD remain undiagnosed until the more advanced stages of the disease. o Delayed diagnosis results in patients suffering symptoms and limitations that could otherwise be alleviated by treatment. Diagnosis of COPD Early diagnosis of COPD can be challenging
- 85. The COPD patient Generally over 40 years A smoker or ex- smoker Presentation with: – cough – excessive sputum production – shortness of breath Dyspnea is the reason most patients seek medical attention. 1. BTS, 1997; 3. GOLD, 2003
- 87. SYMPTOMS Cough Sputum Shortness of breath EXPOSURETO RISK FACTORS Tobacco Occupation Indoor/outdoor pollution SPIROMETRY Diagnosis of COPD
- 88.
- 89.
- 90.
- 91. Normal Trace ShowingFEV1 and FVC 1 2 3 4 5 6 1 2 3 4 Volume,liters Time, seconds FVC5 1 FEV1 = 4L FVC = 5L FEV1/FVC = 0.8
- 92. Criteria for Normal Post-bronchodilatorSpirometry FEV1: % predicted > 80% FVC: % predicted > 80% FEV1/FVC: > 0.7 - 0.8, depending on age
- 93. 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
- 94. Obstructive Pattern FEV1:< 80% predicted ● FVC: can be normal or reduced – usually to a lesser degree than FEV1 FEV1/FVC: <70% predicted FEV1 used to grade the severity
- 95. Volume,liters Time, seconds FEV1 =1.9L FVC = 2.0L FEV1/FVC = 0.95 1 2 3 4 5 6 5 4 3 2 1 Spirometry: Restrictive Disease Normal Restrictive
- 96. FEV1: Normalor mildly reduced – usually to a lesser degree than FVC FVC: < 80% predicted FEV1/FVC: Normal or increased > 0.7 Restrictive Pattern
- 97. Mixed Obstructive andRestrictive Volume,liters Time, seconds Restrictive and mixed obstructive-restrictive are difficult to diagnose by spirometry alone; full pulmonary function tests are usually required FEV1 = 0.5L FVC = 1.5L FEV1/FVC = 0.30 Normal Obstructive - Restrictive
- 98. Mixed Obstructive/Restrictive FEV1:< 80% predicted FVC: < 80% predicted FEV1 /FVC: < 0.7
- 99.
- 100. Spirometric Diagnosis ofCOPD COPD is confirmed by post–bronchodilator FEV1/FVC < 0.7 ● Post-bronchodilator FEV1/FVC measured 15 minutes after : e – 4 puffs Salbutamol 100 MDI with AeroChamber OR – Salbutamol 2.5mg nebuliser.
- 101.
- 102.
- 103. Spirometry Definition forReversibility: – FEV1 and/or FVC >12% and >200 mL ATS/ERS,2005 – FEV1 >12% and >200 mL GOLD,2010
- 104.
- 105. Algorithm for InterpretingSpirometry Results 105 Petty TL. Spirometry made simple. National Lung Health Education Program website. http://www.nlhep.org/resources/SpirometryMadeSimple.htm. Published January 1999. Acceptable spirogram Restrictive defect Is FVC low? Yes Further testing Normal Yes Obstructive defect Is FVC low? Near-total reversal with use of beta agonist? Yes Mixed obstructive/ restrictive defect or hyperinflation No Pure obstruction No Is FEV1/FVC ratio low? No Yes No Asthma COPDFurther testing
- 106.
- 107.
- 108. Spirometry is requiredfor the diagnosis of COPD SPIROMETRY REQUIRED TO DIAGNOSE COPD Presence of a post-bronchodilator FEV1/FVC < 0.70 confirms the presence of persistent airflow limitation and thus of COPD. Key Indicators to Consider COPD Diagnosis: 1 • SYMPTOMS • Dyspnea-progressive (worsens over time and with exercise) • Chronic cough • Sputum 2 • HISTORY OF EXPOSURE TO RISK FACTORS • Tobacco smoke • Smoke from home cooking/heating fuels • Occupational dusts and chemical 3 • FAMILY HISTORY OF COPD Adapted from GOLD 2014
- 109.
- 110. The ATS/ERS guidelines(2005) suggest that other measures, in addition to the degree of airflow obstruction, can be useful in predicting treatment outcomes such as • Body mass index • Degree of airflow Obstruction • Dyspnea • Exercise capacity measured by the 6-minute walk test These parameters, when combined, have been shown to predict a higher risk of death than lung function alone. BODE Index
- 111.
- 112. Composite scores The cutoffvalues for the assignment of points are shown for each variable. The total possible values range from 0 to 10, with higher scores indicating a greater risk of death. Approximate 4 Year Survival Interpretation 0-2 Points: 80% 3-4 Points: 67 % 5-6 Points: 57% 7-10 Points: 18%
- 114. What can wedo ???COPD
- 115. Disease Management shouldnow be focusing on 2 key areas 1. Goal of COPD Management
- 116.
- 117. COPD: Management Clinical diagnosis Spirometry GoldSeverity stage Drugs a/t stages
- 118. 11 8 FEV1 used tograde the severity
- 119.
- 120.
- 121.
- 122. GOLD 2011 © 2013Global Initiative for Chronic Obstructive Lung Disease
- 123. Looks at3 things (combined assessment): 1) FEV1 2) Symptoms 3) History of exacerbations Revised GOLD classification
- 124.
- 126. In patients withFEV1/FVC <0.70 GOLD 1 Mild FEV1>80% GOLD 2 Moderate 50%<FEV1<80% GOLD 3 Severe 30%<FEV1<50% GOLD 4 Very severe FEV1<30% Grading severity of airflow Point out that FEV1/FVC ratio used to be the only factor in the old classification system. In a sense, we are using the same 1-4 ratios of FEV1 as the old system here, but it is now one of three factors in the new classification system Low risk Hig h Risk
- 127. Combined Assessment ofCOPD Assess symptoms Assess degree of airflow limitation using spirometry Assess risk of exacerbations Assess comorbidities COPD Assessment Test (CAT) or mMRC Breathlessness scale
- 128.
- 129. Grading symptoms 0-1 =less breathlessness >2 = more breathlessness
- 130. Patients readthe two statements for each item, and decide where on the scale they fit Scores for each of the 8 items are summed to give single, final score (minimum 0, maximum 40) This is a measure of the overall impact of a patient’s condition on their life 1 Jones P et al. Eur Respir J 2009; 34: 648-654 COPD Assessment Test (CAT)
- 131. 13 1 Cough Sputum Chest tightness Walking uphill ADLs Leaving the house Sleep Energy levels
- 132. COPD Assessment Test(CAT) Aim of the COPD Assessment Test(CAT) is to grade the impact of COPD on health status.
- 133. Assess risk ofexacerbations History of exacerbations (Two or more exacerbations in the preceding year). Spirometry (GOLD 3 or GOLD 4 categories). Combined Assessment of COPD Adapted from GOLD 2014
- 134. 1) Assess symptomsfirst 2) Assess risk of exacerbations next 3) When assessing risk, choose the highest risk according to GOLD grade or exacerbation history Patient is now in one of four categories Adapted from GOLD 2014 Combined Assessment of COPD
- 135. Combined Assessment ofCOPD (C) (D) (A) (B) mMRC 0-1 CAT < 10 mMRC > 2 CAT > 10 Symptoms (mMRC or CAT score)) If mMRC 0-1 or CAT < 10: Less Symptoms (A or C) If mMRC > 2 or CAT > 10: More Symptoms (B or D) Assess symptoms first www.goldcopd.org
- 136. Risk (GOLDClassificationofAirflowLimitation) Risk (Exacerbationhistory) > 2 1 0 (C) (D) (A)(B) mMRC 0-1 CAT < 10 4 3 2 1 mMRC > 2 CAT > 10 Symptoms (mMRC or CAT score)) If GOLD 1 or 2 and only 0 or 1 exacerbations per year: Low Risk (A or B) If GOLD 3 or 4 or two or more exacerbations per year: High Risk (C or D) Assess risk of exacerbations next www.goldcopd.org Combined Assessment of COPD
- 137.
- 138. Global Strategy forDiagnosis, Management and Prevention of COPD. Updated 2011 Risk (GOLDClassificationofAirflowLimitation) Risk (Exacerbationhistory) > 2 1 0 (C) (D) (A) (B) mMRC 0-1 CAT < 10 or CCQ<1 4 3 2 1 mMRC > 2 CAT > 10 or CCQ>1 Symptoms A: Les symptoms, low risk B: More symtoms, low risk C: Less symptoms, high risk D: More Symtoms, high risk
- 139. GOLD 2011 Combinedassessment of COPD Less symptoms High risk Less symptoms Low risk More symptoms low risk More symptoms high risk GOLD 1 GOLD 2 GOLD 3 GOLD 4 (GOLDClassificationofAirflowLimitation) Symptoms ≥2 or 1 (not leading to hospital admission) 0 RISK (EXACERBATIONHISTORY) Adapted from GOLD 2014 ≥1 leading to hospital admission Breathlessness mMRC 0–1 mMRC ≥ 2 CAT < 10 CAT≥10 Risk
- 140.
- 141. Manage Stable COPD:Pharmacologic Therapy Patient Recommended 1st choice Alternative choice Other Possible Treatments A SAMA prn or SABA prn LAMA or LABA or SABA & SAMA Theophylline B LAMA or LABA LAMA & LABA SABA and/or SAMA Theophylline C ICS + LABA or LAMA LAMA & LABA or LAMA & PDE4-inh. or LABA & PDE4-inh. SABA and/or SAMA Theophylline D ICS + LABA and/or LAMA ICS + LABA & LAMA or ICS+LABA & PDE4-inh. or LAMA & LABA or LAMA & PDE4-inh. Carbocysteine SABA and/or SAMA Theophylline From the Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease, Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2011. http://www.goldcopd.org.
- 142.
- 143.
- 144.
- 145.
- 146. Smoking cessationis the single most effective and cost-effective intervention to reduce the risk of developing COPD and stop its progression (Evidence A)
- 147. COPD progression Age (year) FEV1%ofvalueatage25yr 100 75 50 25 502575 Death Disability Adapted from:Fletcher C,et al.Br Med J.1977;1:1645-1648 Nonsmokers 20-30 ml/year COPD 60 mL/year symptoms
- 148. Age 40-50 50-5555-60 60-70 Age (years) Death Disability Symptoms Not SusceptibleSusceptible Smokers Stopped smoking at 45 (mild COPD) Stopped smoking at 65 (severe COPD) 30 40 50 60 70 80 90 0 20 40 60 80 20 100 Adapted from Fletcher CM, Peto R. BMJ 1977
- 149.
- 150.
- 151.
- 152. 15 2 Role ofBronchodilators in COPD
- 153. Expiratory flow-limitation andlung hyperinflation that are only partially reversible to bronchodilator therapy are pathophysiological hallmarks of COPD
- 154. V BD Air flowDeflation Improvement in flow – FEV1 Improvement in volumes – FVC and IC Bronchodilator therapy deflates the lung BD = bronchodilator; V = ventilation; FEV1= forced expiratory volume in 1 second; FVC= forced vital capacity; IC = inspiratory capacity
- 155. Bronchodilators work by: EurRespir Rev 2006; 15: 99, 37–41 Relieve dyspnea by deflating the lungs Allowing improved lung emptying with each breath Improvement in exercise tolerance Reduces the elastic load on the inspiratory muscles.
- 156.
- 157. Current Bronchodilator Optionsfor COPD Short-acting Long-acting -agonists: Albuterol Fenoterol Terbutaline Anticholinergic: Ipratropium -agonists: Salmeterol Formoterol Anticholinergic: Tiotropium Methylxanthine: Theophylline Fixed Combination Albuterol + ipratropium Fenoterol + ipratropium Budesonide + Formoterol Fluticasone + Salmeterol
- 158. The useof bronchodilators is now recommended as the cornerstone of maintenance treatment of COPD , since this disease is no longer regarded as one characterised by irreversible airflow limitation but rather as a disease with at least partial reversibility of airflow limitation. 15 8
- 159. Short-acting andlong-acting bronchodilators form the cornerstone of pharmacologic management. Unlike asthmatic patients who experience dyspnea when acute bronchospasm occurs, patients with COPD most commonly experience dyspnea due to increased respiratory demands, such as occurs with exertion. 15 9
- 160. Besides bronchodilatation, inhaled bronchodilators, probably by reducing hyperinflation both at rest and during exercise (a so-called pharmacological volume reduction effect), offer beneficial effects on real world outcomes important for the patient, such as symptoms (dyspnoea), exercise tolerance (endurance), exacerbation/hospitalisation rate and health-related quality of life. 16 0
- 161. Bronchodilator effect : Indacaterol> Formoterol or Salmeterol Indacaterol = Tiotropium (Evidence A) There is no evidence to recommend one class of long acting bronchodilators over the another for initial treatment. In the individual patient, the choice should be in the patient's perception of symptom relief. Manage Stable COPD: Pharmacologic Therapy
- 162. ● None ofthe existing medications for COPD has been shown conclusively to modify the long-term decline in lung function. ● Therefore, pharmacotherapy for COPD is used to decrease symptoms, complications, or both. © 2013 Global Initiative for Chronic Obstructive Lung Disease COPD treatment options
- 163. The overallapproach to the management of stable COPD is a stepwise increase in treatment, depending on disease severity. Bronchodilators (especially inhaled ) form the cornerstone of pharmacologic treatment for COPD 16 3 COPD treatment options
- 164.
- 166. Inhaled corticosteroids(ICS) are now very widely used in high doses in the management of COPD patients , in sharp contrast to the situation in asthma 16 6
- 167. ASTHMA AND COPD Macrophages Neutrophils Tc1cells Mast cells Eosinophils Th2 cells Airway Inflammation ASTHMA COPD Inflammatory gene expression NF-κB AP-1 Steroid sensitive Steroid resistant
- 168. Combination inhalers inCOPD Symbicort 320 Turbohaler and Seretide 500 Accuhaler
- 169.
- 170. ICS/LABA combination therapy Inhaled steroids not licensed for use in COPD except as combination – ICS must be used in combination with LABA for patients with COPD – ICS monotherapy only FDA approved for treatment of asthma, not COPD 17 0
- 171. Since COPDis usually progressive recommendations for the pharmacological treatment of COPD reflect the following general principles: 1. Treatment tends to be cumulative with more medications being required as the disease state worsens. 2. Regular treatment needs to be maintained at the same level for long periods of time unless significant side effects occur or the disease worsens.17 1
- 172.
- 173.
- 175. Treatment algorithm forpatients without frequent exacerbations
- 176. Pharmacological options forthe prevention of exacerbations in frequent exacerbators
- 177.
- 178.
- 180. 18 0 Asthma Asthma is aheterogeneous disease, usually characterized by chronic airway inflammation. It is defined by the history of respiratory symptoms such as wheeze, shortness of breath, chest tightness and cough that vary over time and in intensity, together with variable expiratory airflow limitation. [GINA 2014] COPD COPD is a common preventable and treatable disease, characterized by persistent airflow limitation that is usually progressive and associated with enhanced chronic inflammatory responses in the airways and the lungs to noxious particles or gases. Exacerbations and comorbidities contribute to the overall severity in individual patients. [GOLD 2015] Asthma-COPD overlap syndrome (ACOS) [a description] Asthma-COPD overlap syndrome (ACOS) is characterized by persistent airflow limitation with several features usually associated with asthma and several features usually associated with COPD. ACOS is therefore identified by the features that it shares with both asthma and COPD. Definitions
- 181.
- 182.
- 183.
- 184.
- 185.
- 186.
- 187.
- 188.
- 189.
- 190.