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Broncopneumopatia cronica ostruttiva (BPCO). COPD n Definition, Classification n Burden of COPD n Risk Factors n Pathogenesis, Pathology, Pathophysiology.

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Presentazione sul tema: "Broncopneumopatia cronica ostruttiva (BPCO). COPD n Definition, Classification n Burden of COPD n Risk Factors n Pathogenesis, Pathology, Pathophysiology."— Transcript della presentazione:

1 Broncopneumopatia cronica ostruttiva (BPCO)

2 COPD n Definition, Classification n Burden of COPD n Risk Factors n Pathogenesis, Pathology, Pathophysiology Practical Considerations n Definition, Classification n Burden of COPD n Risk Factors n Pathogenesis, Pathology, Pathophysiology Practical Considerations

3 COPD unremitting asthma chronic bronchitis emphysema

4 COPD: old definition.…airflow obstruction due to emphysema and chronic bronchitis

5 Definition of COPD n COPD is a preventable and treatable disease with some significant extrapulmonary effects that may contribute to the severity in individual patients. n Its pulmonary component is characterized by airflow limitation that is not fully reversible. n The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lung to noxious particles or gases.

6 Venn diagram illustrating the overlap between asthma and COPD Asthma ? Chronic bronchitis Emphysema Chronic bronchiolitis reversible irreversible COPD Jeffery, AJRCCM 2001

7 Tosse e catarro cronici possono precedere lo sviluppo di BPCO di molti anni Per converso, alcuni pazienti sviluppano una significativa ostruzione al flusso in assenza di sintomi respiratori cronici. Storia naturale della malattia

8 COPD is a multicomponent disease Inflammation Airway obstruction Structural changes Airflow limitation Muco-ciliary dysfunction Cazzola and Dahl, Chest 2004

9 Classification of COPD Severity by Spirometry Stage I: Mild FEV 1 /FVC < 0.70 FEV 1 > 80% predicted Stage II: Moderate FEV 1 /FVC < % < FEV 1 < 80% predicted Stage III: Severe FEV 1 /FVC < % < FEV 1 < 50% predicted Stage IV: Very Severe FEV 1 /FVC < 0.70 FEV 1 < 30% predicted or FEV 1 < 50% predicted plus chronic respiratory failure

10 Comparison of ATS 1995 and ATS/ERS 2004 disease staging systems

11 At Risk for COPD n COPD includes four stages of severity classified by spirometry. n A fifth category--Stage 0: At Risk--that appeared in the 2001 report is no longer included as a stage of COPD, as there is incomplete evidence that the individuals who meet the definition of At Risk (chronic cough and sputum production, normal spirometry) necessarily progress on to Stage I: Mild COPD. n The public health message is that chronic cough and sputum are not normal remains important - their presence should trigger a search for underlying cause(s).

12 Global Strategy for Diagnosis, Management and Prevention of COPD n Definition, Classification n Burden of COPD n Risk Factors n Pathogenesis, Pathology, Pathophysiology Practical Considerations n Definition, Classification n Burden of COPD n Risk Factors n Pathogenesis, Pathology, Pathophysiology Practical Considerations

13 Burden of COPD: Key Points COPD is a leading cause of morbidity and mortality worldwide and results in an economic and social burden that is both substantial and increasing COPD prevalence, morbidity, and mortality vary across countries and across different groups within countries The burden of COPD is projected to increase in the coming decades due to continued exposure to COPD risk factors and the changing age structure of the worlds population

14 Burden of COPD: Prevalence Many sources of variation can affect estimates of COPD prevalence, including e.g., sampling methods, response rates and quality of spirometry. Data are emerging to provide evidence that prevalence of Stage I: Mild COPD and higher is appreciably higher in: - smokers and ex-smokers - people over 40 years of age - males

15 COPD Prevalence Study in Latin America The prevalence of post- bronchodilator FEV 1 /FVC < 0.70 increases steeply with age in 5 Latin American Cities Source: Menezes AM et al. Lancet 2005

16 FEV 1 /FVC% in asymptomatic, elderly never- smokers Hardie J, ERJ 2002

17 Burden of COPD: Mortality COPD is a leading cause of mortality worldwide and projected to increase in the next several decades. COPD mortality trends generally track several decades behind smoking trends. In the US and Canada, COPD mortality for both men and women have been increasing. In the US in 2000, the number of COPD deaths was greater among women than men.

18 Percent Change in Age-Adjusted Death Rates, U.S., Proportion of 1965 Rate –59% –64% –35% +163% –7% Coronary Heart Disease Coronary Heart Disease Stroke Other CVD COPD All Other Causes All Other Causes Source: NHLBI/NIH/DHHS

19 Of the six leading causes of death in the United States, only COPD has been increasing steadily since 1970 Source: Jemal A. et al. JAMA 2005

20 COPD Mortality by Gender, U.S., Number Deaths x 1000 Source: US Centers for Disease Control and Prevention, 2002

21 Morbidità La morbidità è prevista in notevole aumento nel mondo con uno spostamento dal 12 ° al 6° posto. In termini di ricoveri ospedalieri in Italia i casi di BPCO risultano al 7° posto (fonte ISTAT 2003).

22 Bronchite cronica ostruttiva, con riacutizzazione icd9cm Ricoveri in Regime Ordinario (FONTE SDO – MINISTERO DELLA SALUTE) % sul totale dei ricoveri % % % % * Dati che, pur sottostimati a causa dei limiti di codifica, evidenziano un trend in netto aumento dei ricoveri

23 Prevalenza La BPCO è un problema non trascurabile fin dalletà giovanile. Studi epidemiologici hanno evidenziato che, nei soggetti tra 20 e 44 anni, il 10% presenta tosse ed espettorato senza segni di ostruzione bronchiale ed il 3.6% sintomi di ostruzione bronchiale (Stadi I - III). de Marco at al Thorax 2004; 59:

24 Global Strategy for Diagnosis, Management and Prevention of COPD n Definition, Classification n Burden of COPD n Risk Factors n Pathogenesis, Pathology, Pathophysiology Practical Considerations n Definition, Classification n Burden of COPD n Risk Factors n Pathogenesis, Pathology, Pathophysiology Practical Considerations

25 Risk Factors for COPD Lung growth and development Oxidative stress Gender Age Respiratory infections Socioeconomic status Nutrition Comorbidities Genes Exposure to particles Tobacco smoke Occupational dusts, organic and inorganic Indoor air pollution from heating and cooking with biomass in poorly ventilated dwellings Outdoor air pollution

26 Fletcher C & Peto R. BMJ 1977;1: FEV 1 (% predicted at age 25 years) Age (years) Never smoked or not susceptible to smoke Susceptible smoker Disability Death predicted decline if patient stops smoking COPD: Natural History

27 Totale Maschi Femmine FUMATORI12,2 milioni circa 6,9 milioni circa 5,3 milioni circa (24,3%) (28,6%) (20,3%) EX-FUMATORI 9 milioni circa 5,8 milioni circa 3,3 milioni circa (18,1%) (24%) = (11,2%) NON FUMATORI 29 milioni circa 11,4 milioni circa 17,5 milioni circa (57,6%) (47,4%) (67,1%) OSSFAD, Istituto Superiore di Sanità – Indagine DOXA 2006 Gli italiani secondo labitudine del fumo (stima su dati Doxa 2006)

28 Circa il 30% dei fumatori (> 10 pack-year) oltre i 40 anni presenta una limitazione al flusso aereo. Circa il 40-50% dei fumatori sviluppa BPCO. Fletcher C, Peto R. BMJ 1977; 1: 1645 Jyrki-Tapani K, et al.COPD 2005; 2:331 Lokke A, et al. Thorax 2006; 61:935 Shahab L, et al. Thorax 2006; 61:1043 Pelkonen M, et al. Chest 2006; 130:1129 Rennard SI, et al. Lancet 2006; 367:1216 Fumo di sigaretta

29 Fumo passivo Anche l`esposizione al fumo passivo può contribuire all`insorgenza di sintomi respiratori e della malattia, aumentando il carico globale di particelle e gas inalati. de Marco at al Thorax 2004; 59:

30 Association Studies for Assessment of Genetics in COPD ( ) alpha 1 -antitrypsinalpha 1 -antitrypsin alpha1-antichymotrypsinalpha1-antichymotrypsin MMPsMMPs TIMP-2TIMP-2 CFTRCFTR TNF /TNFRTNF /TNFR Vit D binding proteinVit D binding protein Microsomial epoxide hydrolaseMicrosomial epoxide hydrolase Heme-oxygenase-1Heme-oxygenase-1 GSH S-transferase (M1,T1,P)GSH S-transferase (M1,T1,P) IL-1 / IL-1RNIL-1 / IL-1RN beta2-adrenoceptorbeta2-adrenoceptor Cytochrome P450Cytochrome P450 Association in a given ethnic groupAssociation in a given ethnic group Incosistent results when repeated in different populations of the same ethnic group or tested in multiple ethnic groupsIncosistent results when repeated in different populations of the same ethnic group or tested in multiple ethnic groups Negative resultsNegative results

31 Why case-control association studies for the genetics of COPD have been so far poorly informative ? Silverman & Palmer AJRCMB 2000;22:645 IssueKey questionsPossible solutions Selection of geneBiologically ?Demonstration Positionally ?Linkage – Animal Group stratificationMatched ?Ethnicity Family-based ass. Unlinked markers Hardy-Weinberg e.Control in H-W e.?Calculation Multi.comparisonsHow many alleles?Bonferroni How many loci ?Empirical p value

32 Or is it a matter of a poor definition of the phenotype ? COPD

33 Extreme Phenotypes Can Be Determined in the Minority of COPD subjects

34 Emphysema and cigarette smoking

35 Inquinamento outdoor Ogni incremento di 10 µg/m 3 di particelle fini è associato a circa il 4% di aumento del rischio di mortalità per qualsiasi causa, il 6% per cause cardiopolmonari, l8% per cancro al polmone Pope CA 3 rd, Burnett RT, Thum MJ, Calle EE, et all. Lung cancer, cardiopulmonary mortality, and tong –term exposure to fine particulate air pollution. JAMA 2002;287:

36 Inquinamento indoor Nei Paesi a basso livello di sviluppo economico, lutilizzo di combustibili biologici in ambienti con scarsa ventilazione è un fattore causale di BPCO Warwick H, et al. ITDG Publishing, 2004: 103; Ezzati M. Lancet 2005; 336: 104; Oroczo-Levi M, et al. Eur Respir J 2006; 27: 542

37 Basso livello di stato socioeconomico E dimostrata una relazione significativa tra basso livello di istruzione ed aumento della mortalità per BPCO, indipendentemente dallabitudine al fumo Prescott E, Godtfredsen N, VestboJ, Osler M. Social position and mortality from respiratory diseases in males and females. Eur Respir j 2003;21:821-6

38 Risk Factors for COPD Nutrition Infections Socio-economic status Aging Populations

39 Probabilità di contrarre la malattia nei 10 anni successivi alletà del soggetto, in funzione dei fattori di rischio (ISS, 2004)

40 Global Strategy for Diagnosis, Management and Prevention of COPD n Definition, Classification n Burden of COPD n Risk Factors n Pathogenesis, Pathology, Pathophysiology Practical Considerations n Definition, Classification n Burden of COPD n Risk Factors n Pathogenesis, Pathology, Pathophysiology Practical Considerations

41

42 Global Strategy for Diagnosis, Management and Prevention of COPD n Definition, Classification n Burden of COPD n Risk Factors n Pathogenesis, Pathology, Pathophysiology Practical Considerations n Definition, Classification n Burden of COPD n Risk Factors n Pathogenesis, Pathology, Pathophysiology Practical Considerations

43 LUNG INFLAMMATION COPD PATHOLOGY Oxidativestress Proteinases Repairmechanisms Anti-proteinases Anti-oxidants Host factors Amplifying mechanisms Cigarette smoke Biomass particles Particulates Source: Peter J. Barnes, MD Pathogenesis of COPD

44 Anti-proteases SLPI 1 -AT Proteolysis O 2 -, H OH., ONOO - Mucus secretion Plasma leak Bronchoconstriction NF- B IL-8 Neutrophil recruitment TNF- TNF- Isoprostanes HDAC2 HDAC2InflammationSteroidresistance MacrophageNeutrophil Oxidative Stress in COPD Source: Peter J. Barnes, MD

45 Fixed effect meta-analysis results of selected biochemical variables Franciosi et al, Pulm Pharmacol Ther 2006;19:

46 Mucus gland hyperplasia Goblet cell 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

47 Ranked sputum neutrophil data demonstrating overlap of the ATS FEV 1 -based disease stages Franciosi et al, Pulm Pharmacol Ther 2006;19:

48 Disrupted alveolar attachments Inflammatory exudate 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

49 Alveolar wall destruction Loss of elasticity Destruction of pulmonary capillary bed Inflammatory cells macrophages, CD8 + lymphocytes Source: Peter J. Barnes, MD Changes in Lung Parenchyma in COPD

50 Normal Inspiration Expiration alveolar attachments Mild/moderate COPD loss of elasticity Severe COPD loss of alveolar attachments closure smallairway Dyspnea Exercise capacity Air trapping Hyperinflation Health Healthstatus Air Trapping in COPD Source: Peter J. Barnes, MD

51 COPD: Small Airway Abnormalities Normal COPD

52 COPD: Pulmonary Emphysema

53 Comparison of centrilobular and panacinar emphysema

54 Endothelial dysfunction Intimal hyperplasia Smooth muscle hyperplasia Inflammatory cells (macrophages, CD8 + lymphocytes) Changes in Pulmonary Arteries in COPD Patients Source: Peter J. Barnes, MD

55 COPD: Pulmonary Vascular Changes Normal COPD

56 COPD: Structure & Function Alveolar Wall Destruction Air Spaces Enlargement Alveolar Attachments Loss HIGH V A /Q RATIOS Capillary Network Reduction Small Airways Narrowing-Distortion Nonhomogeneous Inspired Air Distribution LOW V A /Q RATIOS Reduced Ventilation In Dependent Alveoli AIR TRAPPING- LUNG HYPERINFLATION Rodríguez-Roisin and MacNee. ERM 1998;7:103-6 AIRFLOW OBSTRUCTION AIR TRAPPING LUNG HYPERINFLATION AIRFLOW OBSTRUCTION

57 Chronic hypoxia Pulmonary vasoconstriction MuscularizationIntimalhyperplasiaFibrosisObliteration Pulmonary hypertension Cor pulmonale Death Edema Pulmonary Hypertension in COPD Source: Peter J. Barnes, MD

58 Assess for COPD: A Common Story Cough –intermittent or daily –present throughout day- seldom only nocturnal Sputum –Any pattern of chronic sputum production Dyspnea –Progressive and Persistent – "increased effort to breathe" "heaviness" "air hunger" or "gasping" –Worse on exercise –Worse during respiratory infections Exposure to risk factors –Tobacco smoke –Occupational dusts and chemicals –Smoke from home cooking and heating fuels

59 59 Assess and Monitor COPD: Key Points A clinical diagnosis of COPD should be considered in any patient who has dyspnea, chronic cough or sputum production, and/or a history of exposure to risk factors for the disease. The diagnosis should be confirmed by spirometry. A post-bronchodilator FEV 1 /FVC < 0.70 confirms the presence of airflow limitation that is not fully reversible. Comorbidities are common in COPD and should be actively identified.

60 60 Assess and Monitor COPD: Spirometry Spirometry should be performed after the administration of an adequate dose of a short- acting inhaled bronchodilator to minimize variability. A post-bronchodilator FEV 1 /FVC < 0.70 confirms the presence of airflow limitation that is not fully reversible. Where possible, values should be compared to age-related normal values to avoid overdiagnosis of COPD in the elderly.

61 SYMPTOMS cough sputum shortness of breath EXPOSURE TO RISK FACTORS tobacco occupation indoor/outdoor pollution SPIROMETRY Diagnosis of COPD è è è è è è

62 Spirometry: Normal and Patients with COPD

63 Age (years) COPD: Natural History Dyspnea Exercise Intolerance Exacerbations Hospitalizations FEV 1 (% predicted at age 25 years) Systemic Effects Respiratory Failure Pulm Hypertension

64 Assess: Physical Examination Rarely diagnostic in COPD Physical signs of airflow limitation –rarely present until significant impairment of lung function –low sensitivity and specificity

65 Assess: Additional Investigations > Stage II: Moderate COPD Bronchodilator reversibility testing –rule out asthma –establish best attainable lung function –gauge a patient's prognosis –guide treatment decisions Chest x-ray –seldom diagnostic unless obvious bullous disease –valuable in excluding alternative diagnoses –CT not routinely recommended

66 Hyperinflated Lungs : COPD

67 Apical bronchus of upper lobe Luminal areaWall thickness Computed Tomographic Measurements of Airways Dimensions and Emphysema in Smokers

68 Assess: Additional Investigations > Stage II: Moderate COPD Arterial blood gas measurement –In advanced COPD: FEV1 <40% predicted or with clinical signs suggestive of respiratory failure or right heart failure –central cyanosis, ankle swelling, JVD –Respiratory failure PaO2 50 mm Hg at sea level Alpha-1 antitrypsin deficiency screening –COPD at a young age –strong family history of the disease

69 Relationship between lung function and symptoms Patients with poor lung function tend to have worse dyspnoea than those with less severe disease

70 Relationship between symptoms and health status Health status encompasses respiratory symptoms as well as their impact on ability to function and on mood.

71 Relationship between lung function and health status Patients with severely impaired lung function show worse health status than those with more mild disease.

72 Relationship between lung function and mortality The risk of dying from COPD is higher in patients with poor lung function than in those with more mild disease.

73 Relationship between health status and mortality Poor health status is associated with increased risk of death from COPD and small improvements may be associated with important differences in prognosis.

74 AIRFLOW LIMITATION Airway Obstruction Structural Changes Mucociliary Dysfunction Polivalent Nature of COPD J COPD 2005;2: Systemic Effects

75 COPD and Co-Morbidities COPD patients are at increased risk for: Myocardial infarction, angina Osteoporosis Respiratory infection Depression Diabetes Lung cancer COPD patients are at increased risk for: Myocardial infarction, angina Osteoporosis Respiratory infection Depression Diabetes Lung cancer

76 Liver IL-6, TNF-α, IL-1β IL-6 CRP Cardiovascular disease Muscle wasting Skeletalmuscle OtherInflammatorydiseases Circulation SYSTEMIC EFFECTS OF COPD

77 COPD and Co-Morbidities COPD has significant extrapulmonary (systemic) effects including: Weight loss Nutritional abnormalities Skeletal muscle dysfunction COPD has significant extrapulmonary (systemic) effects including: Weight loss Nutritional abnormalities Skeletal muscle dysfunction

78 Respiratory system Target organs Systemic inflammation ?

79 Insufficienza cardiaca cronica Coronaropatia e Infarto miocardico Vasculopatia periferica Embolia polmonare Aritmie Neoplasia polmonare Sindrome metabolica Diabete mellito Osteoporosi Depressione Principali comorbidità

80 Effetti sistemici della BPCO Infiammazione sistemica (aumento di PCR, IL-6, IL-8, TNF-α; cellule infiammatorie circolanti; stress ossidativo sistemico) Alterazioni nutrizionali e cachessia (aumento del dispendio energetico e del catabolismo, alterata composizione del corpo) Alterazioni muscolo-scheletriche (perdita di massa muscolare; alterazioni della struttura e funzione, ridotta tolleranza allo sforzo) Aspetti cardiovascolari (malattia aterosclerotica) Alterazioni del metabolismo osseo (osteopenia, osteoporosi) Alterazioni ematologiche (anemia normocitica, normocromica)

81 Relazione fra prognosi e comorbidità (BPCO - Malattie cardiovascolari) Le comorbidità hanno un importante effetto sulla prognosi del paziente con BPCO. La coesistenza delle due malattie è condizione di peggioramento della prognosi. L'insufficienza respiratoria progressiva spiega solo un terzo circa della mortalità legata alla BPCO; quindi fattori diversi dalla progressione della malattia polmonare devono avere un ruolo di rilievo. I decessi dei pazienti con BPCO avvengono prevalentemente a causa delle comorbidità piuttosto che per la BPCO. Nei pazienti affetti da BPCO il 40-50% dei casi di morte è imputabile a cause cardiovascolari. Circa 1/3 dei pazienti affetti da cardiopatie è affetto anche da BPCO che ne aumenta il rischio di morte. La riduzione del VEMS è un fattore di rischio di mortalità per tutte le cause.

82 Comorbidità: prospettive future Nel programmare la gestione del paziente è indispensabile tener conto di possibili condizioni morbose concomitanti, molto comuni nei pazienti di età >65 anni. Non è noto se lapplicazione contemporanea di linee guida rivolte a differenti patologie interferisca con il raggiungimento degli obiettivi terapeutici di ciascuna condizione. In futuro la formulazione e limplementazione di specifiche linee guida dovrà avvalersi di un contributo multidisciplinare comprendente in particolare il medico di medicina generale.

83 Translating COPD Guidelines into Primary Care KEY POINTS n Spirometric confirmation is a key component of the diagnosis of COPD and primary care practitioners should have access to high quality spirometry. n Older patients frequently have multiple chronic health conditions. Comorbidities can magnify the impact of COPD on a patients health status, and can complicate the management of COPD. n Spirometric confirmation is a key component of the diagnosis of COPD and primary care practitioners should have access to high quality spirometry. n Older patients frequently have multiple chronic health conditions. Comorbidities can magnify the impact of COPD on a patients health status, and can complicate the management of COPD.

84 Consider: Lung Disease – (other than airways disorders) Pulmonary embolism Pleural effusions Lobar collapse Diaphragm weakness (Guillain Barre) Heart Disease – Myocardial infarction Cardiac rhythm disturbance Dissecting aneurysm Left ventricular failure Systemic Disease – Blood loss/anaemia Foreign Body Aspiration Patient presents with cough, wheeze, chest tightness or breathlessness SUDDEN / RECENT Consider: Lung Disease - (other than airways disorders) Infiltration (Malignancy, Sarcoidosis) Fibrosing/allergic alveolitis Eosinophilic pneumonia Diaphragm Weakness (Motor Neurone Disease) Chest wall deformity Asbestosis Heart Disease - Chronic heart failure, valve disease, cardiomyopathy Systemic Disorders - Anaemia, obesity, hyperthyroidism CHRONIC Consider: Blood Tests or Chest X-Ray or ECG

85 ERS Sep 2006www.consultmarklevy.com COPD: Making a diagnosis - Spirometry

86 Y Y Y Mast cell CD4+ cell (Th2)Eosinophil Allergens Ep cells ASTHMA BronchoconstrictionAHR Alv macrophage Ep cells CD8+ cell (Tc1) Neutrophil Cigarette smoke Small airway narrowing Alveolar destruction COPD Reversible Irreversible Airflow Limitation Source: Peter J. Barnes, MD

87 Overlap between COPD and asthma COPDASTHMA –Neutrophils –No airway hyperreactivity –No bronchodilator response –No corticosteroid response –Eosinophils –Airway hyperreactivity –Bronchodilator response –Corticosteroid response Wheezy bronchitis ~10% Barnes, Chest 2000

88 Modifiche patologiche nelle vie aeree di pazienti con BPCO e asma eosinofili membrana basale Fabbri et al, AJRCCM 2003

89 Bronchite eosinofilica Una percentuale di pazienti con BPCO mostra un certo grado di eosinofilia nellespettorato. E possibile che la presenza di eosinofili nelle vie aeree sia correlata allintensità del processo infiammatorio nella BPCO, che porta ad un reclutamento non specifico di queste cellule e alla loro attivazione. Il maggiore impatto sul FEV 1 avviene nei casi in cui sia la neutrofilia sia leosinofilia nellespettorato sono più intense, con una relazione diretta fra i numeri di neutrofili ed eosinofili. Una percentuale di pazienti con BPCO mostra un certo grado di eosinofilia nellespettorato. E possibile che la presenza di eosinofili nelle vie aeree sia correlata allintensità del processo infiammatorio nella BPCO, che porta ad un reclutamento non specifico di queste cellule e alla loro attivazione. Il maggiore impatto sul FEV 1 avviene nei casi in cui sia la neutrofilia sia leosinofilia nellespettorato sono più intense, con una relazione diretta fra i numeri di neutrofili ed eosinofili. Maestrelli et al, Thorax 2001

90 Differenze nelle risposte infiammatorie fra asma e BPCO

91 Iperinflazione del polmone in asma Donna di 38 anni, morta per assunzione di barbiturici, con una lunga storia di ripetuti attacchi asmatici Il muco occlude i lumi bronchiolari Gli spazi aerei sono allargati, senza distruzione del tessuto

92 Enfisema panlobulare Uomo di 62 anni deceduto per occlusione coronarica ma che aveva sintomi di malattia polmonare ostruttiva da 10 anni prima di morire. Gli spazi aerei dellintero acino e del lobulo sono allargati con solo occasionali alveoli rimasti intatti I bronchioli appaiono attenuati e collassati e le strutture alveolari non sono presenti

93 Differential Diagnosis: COPD and Asthma COPD ASTHMA Onset in mid-life Symptoms slowly progressive Long smoking history Dyspnea during exercise Largely irreversible airflow limitation Onset early in life (often childhood) Symptoms vary from day to day Symptoms at night/early morning Allergy, rhinitis, and/or eczema also present Family history of asthma Largely reversible airflow limitation

94 Come distinguere lasma dalla BPCO in base alla funzione polmonare? Un valore post BD FEV 1 /FVC <70% suggerisce fortemente una BPCO Una risposta al BD >12% (post BD FEV 1 -pre BD FEV 1 /pre-BD FEV 1 x 100) suggerisce fortemente unasma Che cosa ci dice una risposta positiva alla metacolina? Un valore post BD FEV 1 /FVC <70% suggerisce fortemente una BPCO Una risposta al BD >12% (post BD FEV 1 -pre BD FEV 1 /pre-BD FEV 1 x 100) suggerisce fortemente unasma Che cosa ci dice una risposta positiva alla metacolina?

95 Prevalence of hyperresponsiveness to different stimuli in asthma and COPD /39* Acetylcholine Methacholine Histamine Propranolol SO 2 AMP Hyperventilation § Fog COPDAsthmaStimulus * 90% in smokers, 39% in non-smokers. § Hyperventilation of cold air. Postma and Kerstjens, AJCCRM 1998

96 Percentage of deaths with COPD as primary or secondary diagnosis according to the histamine threshold in light, heavy, and never smokers Hospers et al, Lancet 2000

97 Problemi con i criteri funzionali polmonari Il rimodellamento nellasma può causare unostruzione fissa. I CSI riducono linfiammazione, quindi riducono la risposta al BD, e ciò pone seri dubbi sul concetto di considerare solo una risposta post BD >12% come significativa.

98 Reversibilità e patologia sofferta Sitkauskiene et al, Respir Med 2003

99 Ostruzione bronchiale reversibile e irreversibile quale predittore della mortalità complessiva in asma e BPCO La massima funzione polmonare ottenibile è il miglior indice spirometrico nella predizione della sopravvivenza a prescindere dai farmaci necessari per ottenerlo. Ciò è vero tanto per lasma quanto per la BPCO. Hansen et al, AJRCCM 1999

100 Reversibility testing

101 Other Diff Dx to Consider n Bronchiectasis Large volumes of purulent sputum bacterial infection CXR/CT shows bronchial dilation, bronchial wall thickening n TB History with the usual suspects n BOO and BOOP nonsmokers environmental exposures CT on expiration shows hypodense areas n Bronchiectasis Large volumes of purulent sputum bacterial infection CXR/CT shows bronchial dilation, bronchial wall thickening n TB History with the usual suspects n BOO and BOOP nonsmokers environmental exposures CT on expiration shows hypodense areas

102 Congestive Heart Failure n Fine basilar crackles on auscultation n Chest x-ray shows dilated heart, pulmonary edema n PFTs indicate restriction- not obstruction n BNP can help n Fine basilar crackles on auscultation n Chest x-ray shows dilated heart, pulmonary edema n PFTs indicate restriction- not obstruction n BNP can help

103 Monitoring: This is a progressive disease Lung function worsens over time- even with best care Monitor symptoms and objective measures of airflow limitation for development of complications and to determine when to adjust therapy Spirometry should be performed if there is a substantial increase in symptoms or a complication ABG should be considered in all patients with an FEV1 <40% predicted or clinical signs of respiratory failure or right heart failure (JVD/edema)


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