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Copd seminar
Chronic obstructive pulmonary disease (COPD) represents a major global health challenge. It is currently the fourth leading cause of death worldwide but is projected to become the third leading cause by 2020. The document defines COPD and discusses its types, risk factors, pathogenesis, clinical features, diagnosis, and management. The two main types are chronic bronchitis and emphysema. Smoking is the most important risk factor but other factors like indoor and outdoor air pollution also contribute to the disease burden. Symptoms include dyspnea, chronic cough, and sputum production. Spirometry is required to diagnose COPD by demonstrating airflow limitation.
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Copd seminar
- 1. COPD Chronic obstructive pulmonarydisease BY HEMIN KHALID SABER
- 2. Outline n INTRODUCTION n TYPES nPATHOLOGY n RISK FACTORS n CLINICAL FEATURES n DIAGNOSIS n MANAGEMENT n COMPLICATION n COPD AND ASTHMA
- 3. INTRODUCTION n (COPD) representsan important public health challenge and is a major cause of chronic morbidity and mortality throughout the world. n COPD is currently the fourth leading cause of death in the world but is projected to be the 3rd leading cause of death by 2020. n More than 3 million people died of COPD in 2012 accounting for 6% of all deaths globally. n Globally, the COPD burden is projected to increase in coming decades because of continued exposure to COPD risk factors and aging of the population.
- 4. Burden of COPD Theburden of COPD is projected to increase in coming decades due to continued exposure to COPD risk factors and the aging of the world’s population. COPD is associated with significant economic burden. © 2017Global Initiative for Chronic Obstructive Lung Disease
- 5. Definition of COPD COPD,a common preventable and treatable disease, is characterized by persistent airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases. © Global Initiative for Chronic Obstructive Lung Disease
- 6. COPD includes 1) ChronicBronchitis 2) Emphysema PRIOR TO 2004 Asthma was also included under the same umbrella.
- 7. Chronic bronchitis Defined asa chronic productive cough for three months in each of two successive years in a patient in whom other causes of chronic cough have been excluded
- 8. Emphysema Abnormal and permanentenlargement of the airspaces distal to the terminal bronchioles that is accompanied by destruction of the airspace walls, without obvious fibrosis
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- 11. Airways Chronic inflammation Increased numbers of goblet cells Mucus gland hyperplasia Fibrosis Narrowing and reduction in the number of small airways Airway collapse due to the loss of tethering caused by alveolar wall destruction in emphysema
- 13. Global Strategy forDiagnosis, Management and Prevention of COPD Mechanisms Underlying Airflow Limitation in COPD Small Airways Disease • Airway inflammation • Airway fibrosis • luminal plugs • Increased airway resistance Parenchymal Destruction • Loss of alveolar attachments • Decrease of elastic recoil
- 14. Lung Parenchyma Emphysema affectsthe structures distal to the terminal bronchiole, consisting of the respiratory bronchiole, alveolar ducts, alveolar sacs, and alveoli, known collectively as the acinus.
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- 16. Subtype of emphysema. Centrilobularemphysema (Proximal acinar) Abnormal dilation or destruction of the respiratory bronchiole, the central portion of the acinus. It is commonly associated with cigarette smoking,
- 17. Panacinar emphysema Refers toenlargement or destruction of all parts of the acinus. Seen in alpha-1 antitrypsin deficiency and in smokers
- 18. Paraseptal emphysema Distal acinar- the alveolar ducts are predominantly affected.
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- 20. Risk Factors forCOPD Genes Infections Socio-economic status Aging Populations© 2017 Global Initiative for Chronic Obstructive Lung Disease
- 21. The risk ofdeveloping COPD is related to the following factors: Tobacco smoke – including cigarette,pipe, cigar, water-pipe and other types of tobacco smoking popular in many countries, as well as environmental tobacco smoke(ETS)
- 22. Indoor air pollution- from biomass fuel used for cooking and heating in poorly vented dwellings, a risk factor that particularly affects women in developing countries • Genetic factors - such as severe hereditary deficiency of alpha-1 antitrypsin (AATD). • Age and gender - aging and female gender increase COPD risk.
- 23. Occupational exposures -including organic and inorganic dusts, chemical agents and fumes, are under-appreciated risk factors for COPD
- 24. The risk ofdeveloping COPD is related to the following factors: • Outdoor air pollution - also contributes to the lungs’ total burden of inhaled particles,although it appears to have a relatively small effect in causing COPD. Lung growth and development – any factor that affects lung growth durin gestation and childhood (low birth weight, respiratory infections, etc.) has the potential to increase an individual’s risk of developing COPD.
- 25. Socioeconomic status -there is strong evidence that the risk of developing COPD is inversely related to socioeconomic status. It is not clear, however, whether this pattern reflects exposures to indoor and outdoor air pollutants, crowding, poor nutrition, infections, or other factors related to low socioeconomic status. • Asthma and airway hyper-reactivity - asthma may be a risk factor for the development of airflow limitation and COPD. • Chronic bronchitis - may increase the frequency of total and severe exacerbations. • Infections - a history of severe childhood respiratory infection has been associated with reduced lung function and increased respiratory symptoms in adulthood.
- 26. Genetics Alpha 1-antitrypsin deficiencyis a genetic condition that is responsible for about 2% of cases of COPD. In this condition, the body does not make enough of a protein, alpha 1-antitrypsin. Alpha 1-antitrypsin protects the lungs from damage caused by protease enzymes, such as elastase and trypsin, that can be released as a result of an inflammatory response to tobacco smoke.
- 27. Smoking is byfar recognized to be most important risk factor for development of COPD
- 28. But smoking isnot the only risk factor! Biomass smoke Occupational exposure Outdoor pollution 3 billion people exposed to biomass fuel worldwide Long-term exposure to ambient air pollutants increased the risk of COPD by 2-fold Eur J Epidemiol 2003; 18: 45-53 , JAPI 2012; 60 (Suppl):5-7
- 29. Non smokers reportedgreater lifetime burdens of respiratory disease 10-12% of individuals with COPD have never smoked Indian Edition /Vol.4,No.1,2014
- 30. Mosquito coil One mosquitocoil emmits particulate matter equivalent to those with around 100 cigarettes Pulmonary tuberculosis Prevalence of airflow obstruction varies from 28 to 68%. Asthma 10-fold increased risk of chronic bronchitis and 17-fold increased risk of emphysema Alpha-1 antitrypsin deficiency and other genetic factors COPD in non smokers: Other causes
- 31. Global Strategy forDiagnosis, Management and Prevention of COPD Differential aspect: COPD and Asthma COPD •Onset in mid-life • Symptoms slowly progressive • Long smoking history ASTHMA • Onset early in life (often childhood) • Symptoms vary from day to day • Symptoms worse at night/early morning • Allergy, rhinitis, and/or eczema also present • Family history of asthma © 2017 Global Initiative for Chronic Obstructive Lung Disease Asthma patients frequently have symptom free periods but COPD patient can never be asymptomatic
- 32. Professor Peter J.Barnes, MD National Heart and Lung Institute, London UK
- 33. The characteristic symptomsof COPD are chronic and progressive dyspnea, cough, and sputum production that can be variable from day- to-day. Dyspnea: Progressive, persistent and characteristically worse with exercise. Chronic cough: May be intermittent and may be unproductive. Chronic sputum production: COPD patients commonly cough up sputum. Symptoms of COPD © 2017 Global Initiative for Chronic Obstructive Lung Disease
- 34. Other Clinical features Wheezing Chest tightness Wt.loss Respiratory infections
- 35. Physical signs: *Inspection: Barrel-shaped chest, Accessory respiratory muscle participate , Prolonged expiration during quiet breathing. Expiration through pursed lips Paradoxical retraction of the lower interspaces during inspiration (ie, hoover's sign) Tripod Position
- 37. Tripod Position Patients withend-stage COPD may adopt positions that relieve dyspnea, such as leaning forward with arms outstretched and weight supported on the palms or elbows.
- 38. *Palpation: Decreased fremitus vocalis *Percussion: Hyperresonant Depressed diaphragm, Dimination of the area of absolute cardiac dullness. *Auscultation: Prolonged expiration ； Reduced breath sounds; The presence of wheezing during quiet breathing Crackle can be heard if infection exist. Clinical sign
- 40. Key indicator forconsidering the diagnosis of COPD
- 42. SYMPTOMS chronic cough shortness ofbreath EXPOSURE TO RISK FACTORS tobacco occupation indoor/outdoor pollution SPIROMETRY: Required to establish diagnosis Diagnosis of COPD è sputum © 2017 Global Initiative for Chronic Obstructive Lung Disease
- 43. Diagnosis The presence ofa post-bronchodilator FEV1/FVC < 0.70 confirms the presence of persistent airflow limitation and thus of COPD. © 2017 Global Initiative for Chronic Obstructive Lung Disease
- 44. Spirometry: 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 © 2017 Global Initiative for Chronic Obstructive Lung Disease
- 45. 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 © 2017 Global Initiative for Chronic Obstructive Lung Disease
- 46. Classification of Severityof Airflow Limitation in COPD* In patients with FEV1/FVC < 0.70: GOLD 1: Mild FEV1 > 80% predicted GOLD 2: Moderate 50% < FEV1 < 80% predicted GOLD 3: Severe 30% < FEV1 < 50% predicted GOLD 4: Very Severe FEV1 < 30% predicted *Based on Post-Bronchodilator FEV1 © 2017 Global Initiative for Chronic Obstructive Lung Disease
- 47. Chest x-ray-Chronic bronchitis Noapparent abnormality Or thickened and increased lung markings are noted.
- 48. Chest X-Ray --emphysema Markedover inflation is noted with flattend and low diaphragm Intercostal space becomes widen A horizontal pattern of ribs A long thin heart shadow Decreased markings of lung peripheral vessels
- 50. CT(Computed tomography) Greater sensitivityand specificity for emphysema For evaluation of bullous disease
- 51. Global Strategy forDiagnosis, Management and Prevention of COPD Additional Investigations Lung Volumes and Diffusing Capacity: Help to characterize severity, but not essential to patient management. Oximetry and Arterial Blood Gases: evaluate oxygen saturation and need for supplemental oxygen therapy. Alpha-1 Antitrypsin Deficiency Screening: when COPD develops in patients of Caucasian descent under 45 years or with a strong family history of COPD.
- 52. Labortory Examination Blood examination Inexcerbation or acute infection in airway, leucocytosis may be detected. Sputum examination Streptococcus pneumonia haemophilus influenzae moraxella catarrhalis klebsiella pneumonia
- 53. Severity of COPD ©2017 Global Initiative for Chronic Obstructive Lung Disease
- 61. The goals ofCOPD assessment are to determine the severity of airflow limitation, its impact on the patient’s health status and the risk of future events (such as exacerbations, hospital admissions or death), in order to, eventually, guide therapy. To achieve these goals, COPD assessment must consider the following aspects of the disease separately 1- The presence and severity of the spirometric abnormality 2- Current nature and magnitude of the patient’s symptoms 3- Exacerbation history and future risk 4- Presence of comorbidities
- 62. severity of airflowobstruction
- 63. Global Strategy forDiagnosis, Management and Prevention of COPD Assessment of COPD symptoms © 2017 Global Initiative for Chronic Obstructive Lung Disease COPD Assessment Test (CAT) or Clinical COPD Questionnaire (CCQ) or mMRC Breathlessness scale
- 64. COPD Assessment Test(CAT): An 8-item measure of health status impairment in COPD Clinical COPD Questionnaire (CCQ): Self-administered questionnaire developed to measure clinical control in patients with COPD Modified British Medical Research Council (mMRC) Questionnaire: Breathlessness Measurement, relates well to other measures of health status and predicts future mortality risk. Global Strategy for Diagnosis, Management and Prevention of COPD Assessment of Symptoms © 2017Global Initiative for Chronic Obstructive Lung Disease
- 69. Global Strategy forDiagnosis, Management and Prevention of COPD Combined Assessment of COPD • The “ABCD” assessment tool of the 2011 GOLD update was a major advancement from the simple spirometric grading system of the earlier versions of GOLD because it incorporated patient-reported outcomes and highlighted the importance of exacerbation prevention in the management of COPD. • there were some important limitations. Firstly, the ABCD assessment tool performed no better than the spirometric grades for mortality prediction or other important health outcomes in COPD. • Moreover, group “D” outcomes were modified by two parameters: lung function and/or exacerbation history, which caused confusion. • To address these and other concerns (while at the same time maintaining consistency and simplicity for the practicing clinician), a refinement of the ABCD assessment tool is proposed that separates spirometric grades from the “ABCD” groups.
- 73. Example: Consider twopatients - both patients with FEV1 < 30% of predicted, CAT scores of 18 and one with no exacerbations in the past year and the other with three exacerbations in the past year. Both would have been labelled GOLD D in the prior classification scheme. However, with the new proposed scheme, the subject with 3 exacerbations in the past year would be labelled GOLD grade 4,group D; the other subject with no exacerbations would be labelled GOLD Grade 4, group B.
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- 75.
- 80. Management Based on theprinciples of Prevention of further progress of disease Preservation and enhancement of pulmonary functional capacity Avoidance of exacerbations in order to improve the quality of life.
- 84. 1.Bronchodilators Bronchodilators are centralto the symptomatic management of COPD. Improve emptying of the lungs,reduce dynamic hyperinflation and improve exercise performance .
- 85. Bronchodilators Three major classesof bronchodilators: β2 - agonists: Short acting: salbutamol & terbutaline Long acting :Salmeterol & formoterol Anticholinergic agents: Ipratropium,tiotropium Theophylline (a weak bronchodilator, which may have some anti-inflammatory properties)
- 122. 2.Glucocorticoids Regular treatment withinhaled glucocorticoids is appropriate for symptomatic patients with an FEV1<50%pred and repeated exacerbations. Chronic treatment with systemic glucocorticoids should be avoided because of an unfavorable benefit-to-risk ratio.
- 161. Influenza vaccines canreduce serious illness. 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. Other Pharmacologic Treatments
- 162. Alpha-1 antitrypsin augmentationtherapy: not recommended for patients with COPD that is unrelated to the genetic deficiency. Mucolytics:Patients with viscous sputum may benefit from mucolytics; overall benefits are very small. Antitussives: Not recommended. Global Strategy for Diagnosis, Management and Prevention of COPD Therapeutic Options: Other Pharmacologic Treatments
- 163. Oxygen Therapy Oxygen -->15 h /d Long-term oxygen therapy (LTOT) improves survival,exercise,sleep and cognitive performance in patients with respiratory failure. The therapeutic goal is to maintain SaO2 ≥ 90% and PaO2 ≥ 60mmHg at sea level and rest .
- 164. Pulmonary rehabilitation Nutrition Surgery: Bullectomy Lung volumereduction surgery Lung transplantation Other Treatments
- 165.
- 166. The mostcommon causes of COPD exacerbations are viral upper respiratory tract infections and infection of the tracheobronchial tree. The goal of treatment is to minimize the impact of the current exacerbation and to prevent the development of subsequent Global Strategy for Diagnosis, Management and Prevention of COPD Manage Exacerbations: Key Points
- 169. Smoking cessation hasthe greatest capacity to influence the natural history of COPD Pharmacotherapy and nicotine replacement reliably increase long-term smoking abstinence rates. Smoking cessation
- 171. Complications Pneumothorax Cor pulmonale Exacerbations ofcopd Respiratory failure
- 172. COPD Comorbidities COPD patientsare at increased risk for: Cardiovascular diseases Osteoporosis Respiratory infections Anxiety and Depression Diabetes Lung cancer Bronchiectasis These comorbid conditions may influence mortality and hospitalizations and should be looked for routinely, and treated appropriately.
- 173.
- 174. World No TobaccoDay - 31 May 2016
- 176.
- 177. Introduction L.Ca is themost common cause of cancer-related death in men and women worldwide, responsible for over 1 million deaths annually. Each year, more people die of L.Ca than of the next three leading causes of cancer death combined: breast, colon, and prostate cancer. Despite advances in surgical techniques and combined therapies, L.Ca remains a disease with a dismal prognosis. Although 1-year survival has improved over the past few decades, overall 5-year survival has remained relatively unchanged at 12% to 16% over the past 30 years
- 178. Genetic and Molecular Changesin Lung driver mutations & passenger mutations lung cancers harbor specific mutations that are essential for malignant growth (i.e., “driver mutations”), which lead to gain of function of oncogenes or loss of function of tumor suppressor genes (TSGs) harbor mutations that are functionally insignificant (i.e., “passenger mutations”).