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Dept.Pulmonology, University of Szeged, Deszk, Hungary

Learn about Chronic Obstructive Pulmonary Disease (COPD), its causes, symptoms, and available treatment options. Gain insights into the impact of COPD on lung function, diagnosis, and management strategies.

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Dept.Pulmonology, University of Szeged, Deszk, Hungary

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  1. Attila Somfay Dept.Pulmonology, University of Szeged, Deszk, Hungary COPD

  2. Chronic obstructive bronchitis and emphysema chronic obstructive airway disease (COAD, COLD) (chronic obstructive pulmonary disease ) COPD

  3. COPD emphysema bronchitis „pink puffer” „blue bloater”

  4. CIBA Guest Symposium: Terminology, definitions and classifications ofchronic pulmonary emphysema and related conditions (1959) 1./ Obstructiveemphysema: abnormal permanent enlargement of the airspaces distal to the terminal bronchioles, accompanied by destruction of the alveolar walls and without obvious fibrosis. 2./ Chronic bronchitis: the presence of chronic productive cough for 3 months in each of 2 successive years in a patient in whom other causes (heart failure, tbc, bronchiectasis, tumor, lung abscess) of chronic cough have been excluded.

  5. 1. COPD, a common preventable and treatable disease, is characterized by persistent airflow limitation. 2. The airway obstruction is usually progessive and associated with an enhanced chronic ionflammatory response in the airways and the parenchyma to noxius particles and gases. 3. Exacerbations and comorbidities contribute to the overall severity in an individual patient. GOLD 2011

  6. Percent Change in Age-Adjusted Death Rates, U.S. Proportion of 1965 Rate 3.0 Coronary Heart Disease Stroke Other CVD COPD All Other Causes 2.5 2.0 1.5 1.0 0.5 –59% –64% –35% +163% –7% 0 1965 - 1998 1965 - 1998 1965 - 1998 1965 - 1998 1965 - 1998

  7. „Global burden of disease” (Science 1996; 274:740-743.)

  8. Mortality (Global Burden of Disease Study) Lozano, Lancet 2012 COPD death/ 100 000 77 44 inhabitant 1990 2010

  9. Epidemiology 4-7% of adult population, 9-10 % for those over 40 Prevalence expected to rise 3x in 10 years. By 2020, it becomes the 3rd most frequent cause of death

  10. COPD morbidity in Hungary PREVALENCE INCIDENCE 12 853 191 937 Korányi Bulletin, 2018

  11. Etiology: host factors

  12. Etiology: acquired risk

  13. Effect of smoking on annual decline in lung functionFletcher C, Peto R: BMJ 1977:i: 1645

  14. Pathology 1. chronic bronchitis– increased mucus production, chronic cough

  15. 2. obstructiv bronchiolitis– small airway obstruction with inflammation and fibrosis of bronchioles

  16. 3. Emphysema– alveolar destruction, hiperinflation, loss of elastic recoil, gázcserezavar, bronchiálisobstrukció

  17. Small airways in COPD Barnes, NEJM,2004

  18. Loss of alveolar attachmentsin smokers Normal Smoker Saetta et al. ARRD 1985

  19. Airway muscle thicknessincreases in COPD Non-smoker COPD Saetta. 1998

  20. Causes of Airflow Limitation • Irreversible • Fibrosis and narrowing of the airways • Loss of elastic recoil due to alveolar destruction • Destruction of alveolar support that maintains patency of small airways

  21. Causes of Airflow Limitation • Reversible • Accumulation of inflammatory cells, mucus, and plasma exudate in bronchi • Smooth muscle contraction in peripheral and central airways • Dynamic hyperinflation during exercise

  22. Driving pressure(parenchyma) Airflowlimitation = Resistance(small airways)

  23. Pathology and gas exchange in COPD Stockley,Rennard, Rabe, Celli, 2007

  24. Differential diagnosis of airway obstruction Chronicbronchitis Emphysema COPD Airflow obstruction Asthma Adapted from Snider 1995

  25. Differencial diagnostics • Asthma • CHF • Bronchiectasis • Bronchiolitis obliterans (young, non-smoker, RA, smoke exposition, HRCT:hypodens area) • Diffuse panbronchiolitis (non-smoker malei, sinusitis, HRCT:centrilobular foci and hyperinflation)

  26. Inflammation and lung function In asthma and COPD Barnes, 2009 Overlap ~ 10 - 40%

  27. asthma COPD neutrophils mildAHR* no(poor) bronchodilation no corticosteroid effect eosinophils AHR* good bronchodilator effect good corticosteroid effect 10 – 40 % “ Wheezy bronchitis ” reversibility threshold: 12 –15% (>200ml) FEV1- increase *AHR= airway hyperreactivity

  28. Characteristics of phenotypes bronchitis emphysema Dynamic lung volumesdecreased decreased ( FEV1 , FEV1/FVC) Static lung volumes TLCnormal or mild increase increased RV moderate increase increasd Diffusion capacitynormal or mild decreased decrease Blood gas hypoxaemia, hypercapnia hypoxaemia in end-stage exercisehypoxaemia: no change, improves hypoxaemia or deteriorates deteriorates Cor pulmonale frequent rare

  29. Diagnosis: postbronchodilator FEV1/FVC<70% Classification FEV1(ref %)symptoms cough, sputum mild 80 % morning sputum, minimal breathing dyscomfort moderate50 - 80 %dyspnea on moderate exertion with or without wheezing, discolored sputum severe 30 – 50 % acute worsening with infection, with significant erosion of QoL very severe < 30%n cough, wheezing, breathlessness on minimal exertion signs of RHF, significantly impaired QoL

  30. Pharm.spir. Beta-2 agonist Parasympatho- lytics Xantin derivate

  31. Systemic consequences/comorbiditiesin COPD COPD COPD Expiratory flow limitation Air trapping Exacerbation Hyperinflation Dyspnea Reduced exercise tolerance Inactivity Quality of life Deconditioning Systemic consequences e.g. Muscle atropgy/wasting, atherosclerosis, depression, osteoporosis, anaemia, diabetes

  32. Airway inflammation and systemic consequences in COPD (theory) Tüdő Inzulin resistance, II. type diabetes Muscle wasting/atrophy IL-6 TNFa ? Local inflammation Osteoporosis Cardiovascular events Liver CRP

  33. GOLD Workshop ReportFourcomponents of COPD Management • Asses and monitor disease • Reduce risk factors • Manage stabil COPD • Education • PharmacologicGyógyszeres • Non-pharmacologic • Manage exacerbations

  34. Smoking: early and late quit Doll, BMJ 2004 34 439 British male physicians, 1951-2001

  35. Combined assessment in COPD GOLD 2011 ≥ 2 or > 1 with hospital admission 1 (without hospitalization) 4 (C) (D) 3 Risk (Exacerbation history in the previous year) Risk GOLD stages by FEV1 2 (B) (A) 1 0 CAT < 10 CAT > 10 Symptoms mMRC > 2 mMRC 0–1 Dspnoe

  36. Dyspnea questionnaire (mMRC)

  37. CAT COPD Assessment Test

  38. Global Strategy for Diagnosis, Management and Prevention of COPDTreatment of stable COPD: Non-pharmacological

  39. Treatment of COPD SAMA – anticholinergics, ipratropium bromidspray, MDI, 4 x daily, Short , fast acting bronchodilator 1.. SABA - β2 agonist, salbutamolspray, MDI, 4 xdaily + LAMA - DPI(tiotropium, glycopyrronium, umeclidinium o.d., aclidinium b.i.d.) LABA - DPI (salmeterol, formoterol b.i.d.), (indacaterol, olodaterol napi 1x) 2.. Long acting bronchodilator +ICS/LABA (frequent AE, asthma in medical history) flutikazon/salmeterol, budezonid/formoterol, beklometazon/formoterol, b.i.d. 3.. Antiinflammatory drugs oral corticosteroid ± antibiotics 32 mg methylprednisolon for 5-10days Exacerbation =

  40. The new ABCD GOLD 2017

  41. Terápiás javaslat GOLD 2017

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