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

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Presentation on theme: "Chronic obstructive bronchitis and emphysema chronic obstructive airway disease (COAD, COLD) ( chronic obstructive pulmonary disease ) COPD."— Presentation transcript:

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

2 emphysema bronchitis pink puffer blue bloater

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

4 Evidence-based medicine (The Global Burden of Disease study) (Science 1996; 274:740-743.)

5 4-7% of adult population ( 600 million patients worldwide) Prevalence expected to rise 3x in 10 years. By 2020, it becomes the 3 rd most frequent cause of death ( 4,7 million cases of death – WHO, 1999) Epidemiology

6 COPD morbidity in Hungary

7 COPD is a preventable and treatable disease state characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases, primarly caused by cigarette smoking. Although COPD affects the lungs, it also produces significant systemic consequences. ATS/ERS Task Force, 2004 Definition

8 CIBA Guest Symposium: Terminology, definitions and classifications of chronic pulmonary emphysema and related conditions (1959) 1./ Obstructive emphysema: 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.

9 Differential diagnosis of airway obstruction Chronic bronchitis Emphysema Asthma Airflow obstruction COPD Adapted from Snider 1995

10 Etiology: host factors


12 Etiology: acquired risk

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


15 * p<0.05 with healthy nonsmokers § p<0.05 with stable CB T lymphocytes in COPD Zhu J et al. AJRCCM 2001; 164: 109-16

16 Cells orchestrating the inflammation in COPD

17 Oxidativ stress epithel, macroph.


19 Pathology Large airways : goblet cell metaplasia, increased mucus production Medium and small airways ( 7-9. generation) : inflammation similar to asthma in certain patients Small airways ( 13 - 15. generation) : bronchial wall inflammation, degeneration, fibrosis Alveoli : elastin loss and alveolar surface loss


21 Loss of alveolar attachments in smokers Saetta et al. ARRD 1985 NormalSmoker

22 Airway muscle thickness Increase in COPD Non-smokerCOPD Saetta. 1998

23 Small airways in COPD Barnes, NEJM,2004

24 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

25 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

26 Airflow limitation = Driving pressure (parenchyma) Resistance (small airways)

27 27 Low V A /Q areas High V A /Q areas Alveolar attachments loss Small airways narrowing EMPHYSEMA Airway wall thickening SMALL AIRWAYS ABNORMALITIES Barberà et al. ARRD 1990 Alveolar wall destruction Air space enlargement Capillary network reduction Structure - function relationships in COPD....

28 COPD asthma neutrophils no AHR* no bronchodilation no corticosteroid effect 10 – 40 % eosinophils AHR* good bronchodilator effect good corticosteroid effect Wheezy bronchitis * AHR= airway hyperreactivity reversibility threshold: 12 –15% (>200ml) FEV 1 - increase

29 Characteristics of phenotypes bronchitis emphysema Dynamic lung volumes decreased decreased ( FEV 1, FEV 1 /FVC) Static lung volumes TLC normal or mild increase increased RV moderate increase increasd Diffusion capacity normal or mild decreased decrease Blood gas hypoxaemia, hypercapnia hypoxaemia in end-stage exercise hypoxaemia: no change, improves hypoxaemia or deteriorates deteriorates Cor pulmonale frequently seldom

30 Classification ( GOLD 2006 ) FEV 1 (ref%* ) symptoms cough, sputum mild 80 % morning sputum, ( FEV1/FVC 70% ) minimal breathing dyscomfort moderate 50 - 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

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

32 Systemic consequences/comorbidities in COPD Systemic consequences Életminőség e.g. Muscle atrophy/wasting, CHD depression, osteoporosis, anaemia Air trapping Expiratory flow limitation Dyspnea Inactivity Hyperinflation Reduced exercise tolerance COPD Deconditioning COPD Exacerbation

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


35 GOLD Workshop Report Four components of COPD Management 1.Asses and monitor disease 2.Reduce risk factors 3.Manage stabil COPD l Education l PharmacologicGyógyszeres l Non-pharmacologic 4. Manage exacerbations 1.Asses and monitor disease 2.Reduce risk factors 3.Manage stabil COPD l Education l PharmacologicGyógyszeres l Non-pharmacologic 4. Manage exacerbations


37 I. mild II. moderate III. severe IV. very severe airway obstruction (FEV1/FVC < 70%) FEV1 80% 50% FEV1 < 80% 30% FEV1 < 50% FEV1 < 30% or without or with symptoms chronic respiratory or right heart failure Avoidance of risk factors, influenza vaccination Short acting anticholinergic and/or 2 -agonist as needed One or more long acting bronchodilators, rehabilitation inhalative corticosteroids ( 3 exacerbation in the previous 3 years) longterm oxigen treatment (chronic respiratoryy failure) Surgical treatment ? Treatment of COPD (GOLD 2003)

38 Respiratory insufficiency in COPD pink puffer blue bloater partial global (hypoxaemic/transfer failure) (pump-, ventilatory failure) acute exacerbation

39 Non-invasive mechanical ventilation in respiratory insufficiency

40 Main symptomps in acute exacerbation of COPD increased dyspnea wheezing, chest tightness, increased cough and sputum purulence +/- reduced exercise tolerance, fever, change in chest x-ray, leukocytosis +/- malice, disturbed sleep, daytime sleepiness, depression, confusion (CO 2 retention)

41 AE COPD hospitalisation re-admission death 1 Eriksen, Ugeskr Laeger 2003 2 Groenewegen, Chest 2003 3 Almagro, Chest 2002 4 Connors, Am J Respir Crit Care Med 1996

42 Exacerbations of COPD Viral infections (Rhino,Infl, Parainfl,Adeno, RSV) Bacterial infections (H.i.,S.p.,M.c.,P.a.,S.a., Enterobact.), atypical( M.p., C.p.) Inhalation of environmental irritants (NO2, SO2, PM10, ozone) deviation from diet Predisposing factors (smoking, severe comorbidity, bacterial colonisation in the stable phase)

43 New strains of bacteria and AE COPD Sethi, NEJM 2002 H.influenzae with new antigen structure Immune and inflammatory response AE

44 Role of antibiotics - fall and rise hypothesis Miravitlles M, ERJ 2002




48 Are antibiotics needed? (Procalcitonin Guided Therapy) Christ Crain, Lancet 2004 0 20 40 60 80 100 CAPAECOPDBronchitisAsthma Antibiotic prescriptions (%) Others Standard group Procalcitonin group 45/45 38/42 27/31 11/29 16/31 4/28 2/3 0/10 9/9 2/15 P=0.03P<0.0001P=0.003 P<0.0001 PCT (ng/ml) - < 0,1 not recommanded - > 0,5 strongly recommanded

49 Antibacterial treatment of AECOPD pathogens treatment 1./ acute tracheobronchitis atipical agent ? macrolide ? 2./ Chronic bronchitis H. influenzae aminopenicillin/cv without comorbidity M. catarrhalis cefalo. II, III ( FEV1 > 50% ) res. S. pneumoniae ? makrolide II. 3./ Chronic bronchitis with comorbidity ( FEV1 < 50% ) res. Pneumococcus ! respiratory kinolon 4./ Chronic bronchial infection respiratory kinolon Gram-neg enterobact. Ps. eruginosa = ciprofloxacin

50 COPD Exacerbation - Steroids COPD, no steroids 30 pack-years FEV1 < 1,5 l Group A: Placebo Group B: Methylprednisolone 4x125 mg i.v. –tappering until day 14 Niewoehner DE. N Engl J Med 1999; 340: 1941-47

51 Antibiotic Consumption in 26 Countries Goossens.HA. Lancet 2005; 365:579-87

52 Penicillin resistent S.pneumoniae EARSS, 2006

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