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CHRONIC OBSTRUCTIVE PULMONARY DISEASE PowerPoint Presentation
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CHRONIC OBSTRUCTIVE PULMONARY DISEASE

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

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CHRONIC OBSTRUCTIVE PULMONARY DISEASE

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  1. CHRONIC OBSTRUCTIVEPULMONARY DISEASE Dr.Sarma RVSN, M.D., M.Sc (Canada) Consultant in Medicine and Chest, President IMA – Tiruvallur Branch JN Road, Jayanagar, Tiruvallur, TN +91 98940 60593, (4116) 260593 Dr.Sarma@works

  2. GOLD GLOBAL INITIATIVE FOR CHRONICOBSTRUCTIVELUNGDISEASE NHLBI AND WHO COLLABORATIVE INITIATIVE Dr.Sarma@works

  3. WORLD COPD DAY November 19, EVERY YEAR Raising COPD Awareness Worldwide Dr.Sarma@works

  4. PURPOSE OF THIS TALK RELEVANCE • COPD is very common • COPD is often covert • COPD is treatable • Culprit is smoking • Symptoms + DD Use spirometry • GP must know to Dx. Tests, Rx. and refer • New advances in Rx. Present the Global strategy for the Diagnosis, Management and Prevention of COPD (updated Nov 2004) BASED ON THE GOLD, NICE NAEPP, CDC, BTS, GUIDELINES Dr.Sarma@works

  5. DEFINITIONS Dr.Sarma@works

  6. DEFINITION OF COPD CONTENTS • Definition - Key points • Epidemiology • Risk factors • Pathogenesis –Pathol • Clinical features • Diagnosis, Spirometry • Antismoking strateg. • Management Guide • Drug delivery options • Rehabilitation, Exace. • It is chronic • It is progressive • Mostly fixed airway obstruction • Non reversible by bronchodilators • Exposure to noxious agent is a must • Chronic obstructive lung disease (COLD) • Chronic obstru. airways disease (COAD) • Two entities in COPD – namely • Chronic Bronchitis 2. Emphysema Dr.Sarma@works

  7. 1. CHRONIC BRONCHITIS 2. EMPHYSEMA • Alveolar wall destruction • Irreversible enlargement of the air spaces • Distal to the terminal bronchioles • Without evidence of fibrosis • Productive cough • For a period of 3 months • In each of 2 consecutive years • Absence of any other identifiable cause of excessive sputum production • Airflow limitation that is not fully reversible • Abnormal inflammatory response to noxious agent - like smoking Dr.Sarma@works

  8. DEFINITION OF COPD CONTENTS • Definition - Key points • Epidemiology • Risk factors • Pathogenesis –Pathol • Clinical features • Diagnosis, Spirometry • Stop smoking strateg. • Management Guide • Drug delivery options • Rehabilitation, Exace. • ROAD – Recurrent Obstructive Airways Disease • Bronchial Asthma • Seasonal, Recurrent • Sensitizing Agent, Other Atopic disorders • Reversible obstruction, Inflammation • COLD – Irreversible, Chronic, Noxious agent • Chronic Bronchitis • Emphysema • Combination of both Dr.Sarma@works

  9. OBSTRUCTIVE LUNG DISEASES ASTHMA REVERSIBILITY OF AIR WAY OBSTRUTION CHRONIC BRONCHITIS EMPHYSEMA FULL NONE COPD ASTHMA Dr.Sarma@works

  10. EPIDEMIOLGY OF COPD Dr.Sarma@works

  11. KEY POINTS CONTENTS • Definition - Key points • Epidemiology • Risk factors • Pathogenesis –Pathol • Clinical features • Diagnosis, Spirometry • Stop smoking strateg. • Management Guide • Drug delivery options • Rehabilitation, Exace. • Underestimated, often covert • It is not diagnosed until clinically overt • By that time it is moderately advanced. • The global burden of COPD will increase • Toll from ↑ tobacco use in alarming Dr.Sarma@works

  12. BURDEN OF ILLNESS MORTALITY • COPD is the 4th leading cause of death (next to IHD, Cancer, CVA). • In 2000, the WHO estimated 2.74 million COPD deaths worldwide. • In 1990, COPD was ranked 12th among the burden of diseases • By 2020 it is projected to rank 5th. • Often, COPD is covert Dr.Sarma@works

  13. COPD PREVALENCE 2000 MORTALITY TRENDS 1965 - 2000 • Established Market Economies 6.98 • Formerly Socialist Economies 7.35 • India 4.38 • China 26.20 • Other Asia and Islands 2.89 • Sub-Saharan Africa 4.41 • Latin America and Caribbean 3.36 • Middle Eastern Crescent 2.69 • World 9.34 *From Murray & Lopez, 2001 Dr.Sarma@works

  14. WHAT IS WRONG ? MORBIDITY • Cigarette smoking is the primary cause. • USA - 47.2 million smoke, ♂ 28%,♀ 23% • WHO estimates 1.1 B smokers in world. • This increases to 1.6 billion by 2025. • Many countries, rates are ↑ alarmingly. • In India, 4,00,000 premature deaths annually to use of biomass fuels, like cow dung cakes, open fires • Indoor air pollution, Industrial pollution are the major risk factors in our country. Dr.Sarma@works

  15. SMOKING - THE CULPRIT Dr.Sarma@works

  16. RISK FACTORS FOR COPD MOST IMP RISK • Host Factors • Genes (alpha1- anti-trypsin↓) • Hyper responsiveness • Lung growth, low BW, Age • Exposure • Tobacco smoke, • Bio mass fuel smoke, open fires • Occupational dusts and chemicals • Chronic uncontrolled asthma • Infections, overcrowding, damp • Low socioeconomic status • Low dietary vegetable and fruit intake Dr.Sarma@works

  17. WOMEN SMOKERS PASSIVE SMOKERS Dr.Sarma@works

  18. INTENSE CAUSE FOR CONCERN ? COLLEGE STUDENTS TENDER AGE GROUPS Dr.Sarma@works

  19. COPD NH – EFFECT OF SMOKING Mortality among women smokers is on the rise globally Dr.Sarma@works

  20. PATHOGENESIS AND PATOLOGY Dr.Sarma@works

  21. PATHOGENESIS CONTENTS • Definition - Key points • Epidemiology • Risk factors • Pathogenesis –Pathol • Clinical features • Diagnosis, Spirometry • Stop smoking strateg. • Management Guide • Drug delivery options • Rehabilitation, Exace. NOXIOUS AGENT(tobacco smoke, pollutants, occupational exposures COPD Genetic factors Respiratory infection Others Dr.Sarma@works

  22. PATHOGENESIS • Definition -key points • Burden of COPD • Classification • Risk factors • Pathogenesis, • Pathophysiology, • Management • Future research Dr.Sarma@works

  23. PATHOGENESIS • Definition -key points • Burden of COPD • Classification • Risk factors • Pathogenesis, • Pathophysiology, • Management • Future research ATOPY Dr.Sarma@works

  24. SHIFT IN THE DELICATE BALANCE Nutrophil elastase Cathepsisns MMP-1, MMP- 9, MMP – 12 Granzymes Perforins Alpha 1 Anti-trypsin SLP 1, Elastin, TIMPs PROTEASES ANTI PROTEASES COPD Dr.Sarma@works

  25. PATHOLOGY CONTENTS • Definition - Key points • Epidemiology • Risk factors • Pathogenesis –Pathol • Clinical features • Diagnosis, Spirometry • Stop smoking strateg. • Management Guide • Drug delivery options • Rehabilitation, Exace. • Irreversible – COPD – Why ? • Fibrosis and narrowing of the airways • Loss of elastic recoil due to alveolar destruction • Destruction of alveolar support that maintains patency of small airways • Reversible – Bronchial Asthma • Accumulation of inflammatory cells, mucus, and exudates in bronchi • Smooth muscle contraction in peripheral and central airways • Dynamic hyperinflation during exercise Dr.Sarma@works

  26. PATHOLOGY in COPD COPD • Mucus gland hypertrophy • Smooth muscle hypertrophy • Goblet cell hyperplasia • Inflammatory infiltrate • Excessive mucus • Squamous metaplasia Normal bronchial architecture Dr.Sarma@works

  27. DISSECTING MICROSCOPIC APPEARENCE Normal parenchymal architecture Emphysematous Lung architecture Dr.Sarma@works

  28. PATHOLOGY – COPD ASTHMA • Eosinophilic inflamm. • CD4, Th2 Lymphocyte • Mast cells • Tissue destruct. less • Mainly allergic inflam. • Inflam. Mediators • LT D4 • IL 4 • IL 5 • Neutrophilic inflammation • Macrophages and CD8 T cells ↑ • Altered protease/antiprotiase balance • Tissue destruction progressive • Alpha1 AT↓- Young age emphysema • Goblet cell size and number ↑ in CB • Inflammatory mediators LT B4 IL 8 TNF-α Dr.Sarma@works

  29. PULMONARY HYPERTENSION IN COPD • Duplication of elastic lamina • Medial hypertrophy - PH Normal Pulmonary Artery Dr.Sarma@works

  30. CLINICAL FEATURES Dr.Sarma@works

  31. CHRONIC BRONCHITIS EMPHYSEMA • Severe dyspnea • Cough after dyspnea • Scant sputum • Less frequent infections • Terminal RF • PaCO2 35-40 mmHg • PaO2 65-75 mmHg • Hematocrit 35-45% • DLCO is decreased • Cor pulmonale rare. • Mild dyspnea • Cough before dyspnea starts • Copious, purulent sputum • More frequent infections • Repeated resp. insufficiency • PaCO2 50-60 mmHg • PaO2 45-60 mmHg • Hematocrit 50-60% • DLCO is not that much ↓ • Cor pulmonale common Dr.Sarma@works

  32. CHRONIC BRONCHITIS EMPHYSEMA BLUE BLOTTER PINK PUFFER Dr.Sarma@works

  33. ALPHA1 ANTITRYPSIN ↓ EMPHYSEMA Specific circumstances of Alpha 1- AT↓include. • Emphysema in a young individual (< 35) • Without obvious risk factors (smoking etc) • Necrotizing panniculitis, Systemic vasculitis • Anti-neutrophil cytoplasmic antibody (ANCA) • Cirrhosis of liver, Hepatocellular carcinoma • Bronchiectasis of undetermined etiology • Otherwise unexplained liver disease, or a • Family history of any one of these conditions • Especially siblings of PI*ZZ individuals. • Only 2% of COPD is alpha 1- AT ↓ Dr.Sarma@works

  34. ALPHA1 ANTITRYPSIN ↓ A1AT LEVELS • MM – A1AT 100% • MS – A1AT 75% • SS – A1AT 55% • MZ – A1AT 55% • SZ – A1AT 40% • ZZ – A1AT 8% Dr.Sarma@works

  35. CLINICAL SIGNS SPIROMETRY • Decreased FEV1 • Decreased FVC • FEV1 < 80% • FEV1 ÷ FVC < 70% • Post bronchodilator – no change in FEV1 • PEF is decreased • FET – is prolonged • V Max - decreased • Physical exam may be negative • Hyper-inflated chest, Barrel chest • Wheeze or quite breathing • Pursed lip / accessory muscles resp. • Peripheral edema • Cyanosis, ↑ JVP • Cachexia • Cough, wheeze, dyspnea, sputum Dr.Sarma@works

  36. MRC DYSPNOEA SCALE ABOUT SMOKING • No of cigarettes / day • No of smoker years • Age at starting • Time of 1st cigarette • Desire to quit • Barriers to quit • Passive smoking • Occupational expo. • Domestic pollution Dr.Sarma@works

  37. Slow up hill walking Brisk walking on level Medium up hill walk Brisk up hill walk Medium walking Self washing Bed making Sleeping Sitting Heavy shopping Slow walking Light shopping 0 10 OXYGEN COST DIAGRAM OCCUPATIONAL • Coal mining • Cotton dust • Cement dust • Oil fumes • Cadmium fumes • Grain dust – • Rice millers • Grain handlers • Flour millers Dr.Sarma@works

  38. PROGNOSTIC FACTORS ‘SUPPORT’ STUDY • Hypercapnic RF pts. • 1029 patients studied • 89% survived acute hospitalization for RF • Only 51% are alive at 2 years of follow-up • Prognostic factors are • Severity of RF • Low BMI • Older age • Low PaO2/FIO2 Several factors affect survival in COPD. • Age • Smoking status • Pulmonary artery pressure • Resting heart rate • Airway responsiveness • Hypoxemia • Most importantly the level of FEV1 • Use of long term oxygen therapy Dr.Sarma@works

  39. DIFF. Dx. of COPD & ASTHMA WHY D.D WITH ASTHMA ? • Different etiology • Different prognosis • Different therapy • Different response to therapy • DD includes • Bronchial Asthma • Bronchiectasis- CSLD • Bronchogenic Ca. Dr.Sarma@works

  40. COPD IMAGES Dr.Sarma@works

  41. CHEST SKIAGRAMS OF EMPHYSEMA Dr.Sarma@works

  42. V- P MISMATCH NUCLEOTIDE IMAGING Dr.Sarma@works

  43. CHEST SKIAGRAM OF CHRONIC BRONCHITIS Dr.Sarma@works

  44. CHEST LATERAL VIEW CHRONIC BRONCHITIS Dr.Sarma@works

  45. HRCT – NORMAL CHEST Dr.Sarma@works

  46. HRCT – EMPHYSEMA Dr.Sarma@works

  47. HRCT – EMPHYSEMA Dr.Sarma@works

  48. ASSESSMENT OF STABLE COPD Dr.Sarma@works

  49. MANAGEMENT OF COPD Rx. OBJECTIVES • Prevent disease progression • Relieve symptoms • Improve exercise tolerance • Improve health status • Prevent and treat exacerbations • Prevent and treat complications • Reduce mortality • Minimize side effects from treatment • Assess and monitor disease • Reduce risk factors • Manage stable COPD • Education • Pharmacologic • Non-pharmacologic • Manage exacerbations Dr.Sarma@works

  50. ASSESSMENT OF COPD MANAGEMENT • Definition - Key points • Epidemiology • Risk factors • Pathogenesis –Pathol • Clinical features • Diagnosis, Spirometry • Stop smoking strateg. • Management Guide • Drug delivery options • Rehabilitation, Exace. Diagnosis of COPD is based on • H/o exposure to noxious agent • Presence of Air flow limitation • Non-reversibility of the limitation • Chronic productive cough • Copious sputum, Dyspnea +/- Dr.Sarma@works