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Chronic obstructive bronchitis and emphysema
chronic obstructive airway disease(COAD, COLD)
( chronic obstructive pulmonary disease )
COPD
COPD
emphysema bronchitis „pink puffer” „blue bloater”
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
Percent Change in Age-Adjusted Death Rates, U.S., 1965-1998Percent Change in Age-Adjusted Death Rates, U.S., 1965-1998
00
0.50.5
1.01.0
1.51.5
2.02.0
2.52.5
3.03.0
Proportion of 1965 Rate Proportion of 1965 Rate
1965 - 19981965 - 1998 1965 - 19981965 - 1998 1965 - 19981965 - 1998 1965 - 19981965 - 1998 1965 - 19981965 - 1998
–59%–59% –64%–64% –35%–35% +163%+163% –7%–7%
CoronaryHeart
Disease
CoronaryHeart
Disease
StrokeStroke Other CVDOther CVD COPDCOPD All OtherCauses
All OtherCauses
„Global burden of disease”
(Science 1996; 274:740-743.)
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
Epidemiology
COPD morbidityin Hungary
OKTPI, 2014
0
100
200
300
2003
2004
2005
2006
2007
2008
2009
2010
2011
2012
2013
%00
0
0500100015002000
%00
0
Ú j be tegek
Ös s zesreg is ztrá lt
Prevalence: 175 000
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.
Differential diagnosis of airway obstruction
Chronicbronchitis
Emphysema
Asthma
Airflow obstruction
COPD
Adapted from Snider 1995
Etiology: host factors
Etiology: acquired risk
Effect of smoking on annual decline in lung
function Fletcher C, Peto R: BMJ 1977:i: 1645
Alveolar macrophage
neutrophil chemotactic factorscytokines ( IL-8 )mediators ( LTB4 )
neutrophil
proteázokproteases
neurophil elastasecathepsinesmatrix metalloproteinases
proteaseinhibitors
increased mucus production( chronic bronchitis )
alveolar destruction
( emphysema)
?CD8+lymphocyta
alfa1-antitrypsinSLPI
-
Pathology
1. chronic bronchitis – increased mucus production, chronic cough
2. obstructiv bronchiolitis – small airway obstruction with inflammation and fibrosis of bronchioles
3. Emphysema – alveolar destruction, hiperinflation, loss of elastic recoil, gázcserezavar, bronchiális obstrukció
Small airways in COPDBarnes, NEJM,2004
Loss of alveolar attachmentsin smokers
Saetta et al. ARRD 1985
Normal Smoker
Airway muscle thicknessIncrease in COPD
Non-smoker COPD
Saetta. 1998
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
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
Airflowlimitation
=Driving pressure (parenchyma)
Resistance (small airways)
Pathology and gas exchange in COPD
Stockley, Rennard, Rabe, Celli, 2007
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)
Overlap ~ 10 - 40%
Inflammation and lung functionIn asthma and COPD Barnes, 2009
COPD asthma neutrophils
mild AHR*
no(poor) bronchodilation
no corticosteroid effect
10 – 40 %
eosinophils AHR*
good bronchodilator effect
good corticosteroid effect
“ Wheezy bronchitis ”
*AHR= airway hyperreactivity
reversibility threshold: 12 –15% (>200ml) FEV1-increase
Characteristics of phenotypes bronchitis emphysema
Dynamic lung volumes decreased decreased ( FEV1 , FEV1/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
Classification FEV1 (ref %) symptoms
cough, sputum mild 80 % morning sputum,
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
Diagnosis: postbronchodilator (4 puff salbutamol) FEV1/FVC<70%
Pharm.spir.
Beta-2 agonist
Parasympatho-lytics
Xantin derivate
Systemic consequences/comorbiditiesin COPD
Systemic consequences
Quality of life
e.g. Muscle atropgy/wasting, atherosclerosis, depression, osteoporosis, anaemia, diabetes
Air trappingExpiratory flow limitation
Dyspnea
Inactivity
Hyperinflation
Reduced exercisetolerance
COPDCOPD
Deconditioning
COPD
Exacerbation
Airway inflammation and systemic consequences in COPD (theory)
Muscle wasting/atrophy
Inzulin resistance,II. type diabetes
Osteoporosis
CRPCardiovascularevents
TNF IL-6
Liver
?
Tüdő
Localinflammation
GOLD Workshop Report
Four components of COPD Management
GOLD Workshop Report
Four components of COPD Management
1. Asses and monitor disease
2. Reduce risk factors
3. Manage stabil COPD Education PharmacologicGyógyszeres Non-pharmacologic
4. Manage exacerbations
1. Asses and monitor disease
2. Reduce risk factors
3. Manage stabil COPD Education PharmacologicGyógyszeres Non-pharmacologic
4. Manage exacerbations
Effects of smoking intervention and the use of aninhaled anticholinergic bronchodilator on the rateof decline of FEFV1Anthonisen N.R. és mtsai. JAMA 1994: 272, 1497-1505.
Smoking cessation is the only intervention whichmay retard the steep loss in lung function inCOPD
1/3 of patients are able to do this(nicotin replacement, bupropion, vareniclin)
Smoking: early and late quit
34 439 Brittish male physicians, 1951-2001
Doll, BMJ 2004
ipratropium bromid, (SAMA) MDI, 4 x 3-6 ( 60-120 µg ) puff
+ β2 agonist (SABA) MDI
4 x 2-4 puff ( 200-400 µg )
+ retard theophyllin tabl.
300-900 mg ( Se- level 8-12 µg/ml )
antibiotics(5-10 days) + corticosteroid
(32 mg methylprednisolon, 10-14 days)
Treatment of COPD
exacerbation
+ LAMA (tiotropium) DPI, 1x1 or LABA (salmeterol, formoterol) 2x1
(indacaterol) 1x1 ICS/LABAfluticason/salmeterol
or
budesonid/formoterol
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 2006)
Longterm oxygen in COPD
NOTT: Ann Intern Med, 1980BMC: Lancet, 1981
Indication: resting• PaO2 < 55 mmHg or SAT < 88%• 55 Hgmm < PaO2 < 60 mmHg, and pulmonary hypertension, polyglobulia or heart failure
Target: PaO2 ≈ 60 mmHg or SAT ≈ 90 % Pa CO2 increase < 15-20 mmHg
Dose: > 15 h/day, 1-2 L/min through nasal prong
the only treatment which prolongs life in hypoxic COPD
Respiratory insufficiency in COPD
pink puffer blue bloater partial global (hypoxaemic/transfer failure) (pump-, ventilatory failure)
acute exacerbation
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 (CO2 retention)
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
Non-invasive mechanical ventilation in respiratory insufficiency