che cos’ è l’ asma bronchiale?
TRANSCRIPT
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Che cos’ è l’ asma bronchiale?
Malattia polmonare infiammatoria cronica caratterizzata
da iperreattività delle vie aeree.
L’ asma è un malattia allergica?
Si, ma non solo!
Asma estrinseco: scatenato da antigeni inalatori, frequente nei bambini. Tipicamente associato
con atopia.
Asma intrinseco: scatenato da fattori diversi in assenza di pregressa sensibilizzazione
e di una pregressa diatesi allergica, frequente negli adulti.
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Prevalenza dell’asma in Italia
Circa 2.6 milioni di pazienti. 4.5% della popolazione
300 milioni di pazienti nel mondo
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Prevalenza dell’asma
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Quante forme di asma?
• Asma allergico: forma più comune, specialmente nei bambini, in risposta ai
pollini, peli, acari.
• Asma infettivo: nei bambini, come conseguenza di infezioni da virus
respiratori.
• Asma da sforzo: soprattutto in ambienti freddi e secchi.
• Asma professionale: assimilabile all’ asma allergico, ma in alcuni casi sembra
essere coinvolto un meccanismo da diretta neurotossicità (iperreattività del
sistema parasimpatico).
• Asma da farmaci: più comune in pazienti in cui è già presente una diatesi
asmatica. Tra gli agenti scatenanti più comuni l’ aspirina.
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Il polmone sano
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Bronco
Tappo mucoso
Infiltrato infiammatorio
Ipertrofia ghiandole mucose
Ipertrofia membrana basale
Ipertrofia tonaca muscolare
Il polmone asmatico
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Reazioni da ipersensibilità
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Patogenesi dell’ asma brochiale: fasi iniziali
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Patogenesi dell’ asma brochiale: fasi intermedie
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AIRWAY HYPERRESPONSIVENESS
Chemotaxis Eotaxin,
RANTES, MCP-4
CCR3
Survival IL-3, IL-5,
GM-CSF
VCAM-1 VLA4
Adhesion
Bone marrow
IL-4
IL-5
Airway vessel
Activation
Th2 cell
Basic proteins
Mediators
EOSINOPHIL RECRUITMENT IN ASTHMA
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L’eosinofilo: una fabbrica di mediatori
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Major Basic Protein-1
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Eosinophil Peroxidase
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Eosinophil-Derived Neurotoxin
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Eosinophil Cationic Protein
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Eosinophil
Mast cell
Allergen
Th2 cell
MODERN VIEW OF ASTHMA
Vasodilatation
New vessels
Plasma leak Oedema
Neutrophil
Mucus
hypersecretion
hyperplasia
Mucus plug
Macrophage
Bronchoconstriction
Hypertrophy/hyperplasia
Cholinergic reflex
Epithelial shedding
Subepithelial
fibrosis
Sensory nerve activation
Nerve activation
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Ricordatevi che l’ asma è una malattia infiammatoria
cronica……….!!!!!
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Bronco
Tappo mucoso
Infiltrato infiammatorio
Ipertrofia ghiandole mucose
Ipertrofia membrana basale
Ipertrofia tonaca muscolare
Il polmone asmatico
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ASTHMA PATHOLOGY
• GROSS: VISCOUS SPUTUM / MUCUS
PLUGGING / HYPERINFLATION
• MICROSCOPIC: THICK BASEMENT
MEMBRANE / SM MUSCLE + / MUCOUS
GLANDS + / SUBMUCOSA OEDEMA AND
INFLAMMATION / MUCOSAL
DESTRUCTION AND METAPLASIA /
MUCUS ABNORMAL
• LATE FIBROSIS OF BRONCHIAL WALL
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ASTHMA AND COPD
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COPD IS NOT ASTHMA !
• Different causes
• Different inflammatory cells
• Different mediators
• Different inflammatory consequences
• Different response to treatment
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Inflammation ASTHMA COPD
CELLS Mast cells Eosinophils CD4 T cells macrophages
Neutrophils CD4, CD8 T cells Macrophages++
MEDIATORS LTD4,histamineL-4, IL-5,
ROS +
LTB4’ IL-8, TNFa, ROS+++
EFFECTS All airways Little fibrosis Ep shedding
Periph airways Lung destruction Fibrosis + Sq metaplasia
Response steroids +++ ±
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COPD ASTHMA
Neutrophils
No AHR
No steroid response
Eosinophils
AHR
Steroid response
~10%
“Wheezy bronchitis”
OVERLAP BETWEEN COPD AND ASTHMA
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Asthma Definition
• A condition characterised by wide
variations over short periods of time in
resistance to air flow in intrapulmonary
airways
• Variability usually assessed by measuring
change in air flow rates ( ± > 15% FEV1)
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ASTHMA PREVALENCE
• CURRENT 2 - 6% (CUMULATIVE 10%)
• ONSET <10y.o. in 50%
• INCREASED WITH “DEVELOPMENT”
• CHILDHOOD PREVALENCE NEAR 20%
IN IRELAND
• MORTALITY IRELAND < 100 / YEAR
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Constitutional and environmental
factors which induce or incite
• Allergens
• Occupational chemical
• Viruses
• Genetic factors
• Prematurity
• Lack breast feeding
• ? Smoking
• Fumes, smoke, sprays
• Diurnal variation
• Exercise, cold air
• Fog
• Emotion
• Allergens, anaphylaxis
• Viruses
• Drugs - NSAID, Beta
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ATOPY
• SUSCEPTIBILITY TO DEVELOP IGE
ANTIBODIES FROM EXPOSURE TO
COMMON ENVIRONMENTAL
ALLERGENS
• IGE - GLYCOPROTEIN : m.w. 190,000
daltons
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FACTORS IN
INFLAMMATORY PROCESS
• MEDIATORS
• HISTAMINE
• LEUCOCYTE C F
• PROSTAGLANDINS
• LEUKOTRIENES
• PAF
• KININS
• CELL TYPES
• MAST CELLS
• MACROPHAGES
• EOSINOPHILS
• T LYMPHOCYTES
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NEURAL MECHANISMS
PARASYMPATHETIC
AFFERENT SENSORY
HISTAMINE
KININS
EFFERENT
BRONCHOCONSTRICTOR
MUCUS SECRETION
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ASTHMA
CLINICAL FEATURES
• SYMPTOMS: WHEEZE, COUGH, SPUTUM, DYSPNOEA,TIGHTNESS.
• PERIODICITY: DIURNAL, SEASONAL, PROVOKING FACTORS (COLD, EXERCISE, SMELLS.
• ASSOCIATED: NASAL/SINUS, “COLDS”, ALLERGIES.
• SMOKING AND OCCUPATION
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EXAMINATION
• WHEEZES AND HYPERINFLATION
• TACHYCARDIA (>100 BPM)
• PULSUS PARADOXUS (>10 MMHG)
• PEAK FLOW (<100L/MIN OR <40% PREDICTED)
• CYANOSIS, SYNCOPE, HYPOTENSION, SILENT CHEST
• HYPOXEMIA (<8.5 KPA)
• HYPERCAPNIA EVEN MILD
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CONFIRMING ASTHMA
• SPIROMETRY FEV1 & REVERSIBILITY
• TRIAL OF TREATMENT
• ?ALLERGY TESTS
• (CXR)
• CHALLENGE TEST: SPECIFIC/NON-S
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TROUBLESOME ASTHMA
• INHALER TECHNIQUE/COMPLIANCE
• ALLERGENS - HDM, PETS, FOOD, DRUGS, DAMP HOUSE, ABPA.
• INFECTIONS
• AIR POLLUTION - SMOG, PASSIVE SMOKE,HYDROCARBONS
• SMOKING
• REFLUX DISEASE
• EXERCISE
• OCCUPATION (UP TO 10% OF PATIENTS)
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A.B.P.A.
• ASTHMA PLUS
• FEVER
• CXR INFILTRATES
• SEVERE BLOOD EOSINOPHILIA
• POSITIVE SEROLOGY OR SKINPRICK
• ORGANISM IN SPUTUM
• COMPLICATIONS - APICAL FIBROSIS,
BRONCHIECTASIS
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Definition of COPD
Chronic obstructive pulmonary disease is
defined as
‘a disease state characterised by the
presence of airflow obstruction due to
chronic bronchitis or emphysema; the
airflow obstruction is generally
progressive, may be accompanied by
airway hyper-reactivity, and may be
partially reversible’
American Thoracic Society 1995
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Facts About COPD
• COPD is the 4th leading cause of death in the United States (behind heart disease, cancer, and cerebrovascular disease).
• In 2000, the WHO estimated 2.74 million deaths worldwide from COPD.
• In 1990, COPD was ranked 12th as a burden of disease; by 2020 it is projected to rank 5th.
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Percent Change in Age-Adjusted Death Rates, U.S., 1965-1998
0
0.5
1.0
1.5
2.0
2.5
3.0
Proportion of 1965 Rate
0.0
0.5
1.0
1.5
2.0
2.5
3.0
1965 - 1998 1965 - 1998 1965 - 1998 1965 - 1998 1965 - 1998
–59% –64% –35% +163% –7%
Coronary Heart
Disease
Stroke Other CVD COPD All Other Causes
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Cost of COPD in United States
in 2000 31.9
20.7
11.2
0
5
10
15
20
25
30
35
Total Direct Indirect
American Lung Association, 2001
Costs
$Billions
10% of people with COPD responsible for >70% of COPD-related
medical care costs. In-patient hospitalization and emergency department
care accounts for >73% of this cost
COPD costs $1,522 per person per year (3 times asthma costs)
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Risk Factors for COPD
Host Factors Genes (e.g. alpha1-antitrypsin deficiency)
Hyperresponsiveness
Lung growth
Exposure Tobacco smoke
Occupational dusts and chemicals
Infections
Socioeconomic status
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Smoking prevalence - Europe
0 5 10 15 20 25 30 35 40 45 50 55
United States
Luxembourg
United Kingdom
Ireland
Italy
Germany (W)
Denmark
Spain
Greece
Germany (E)
France
Netherlands
European Union
Women
Men
News. Journal of the National Cancer Institute 1996 Volume 88: (17); 1190
Percentage of smokers by sex and country
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Cigarette smoke
Alveolar macrophage
Neutrophil
PROTEASES
Alveolar wall destruction
(Emphysema)
Mucus hypersecretion
(Chronic bronchitis)
PROTEASE
INHIBITORS
Neutrophil chemotactic factors
CELLULAR MECHANISMS OF COPD
Neutrophil elastase Cathepsins
Matrix metalloproteinases
Cytokines (IL-8) Mediators (LTB4) 4 ) )
? CD8+
lymphocyte
-
MCP-1
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SPUTUM CYTOKINES IN
COPD
COPD patients: 62.5 ±3.2y; FEV1 = 34.6±4 % predicted
0
2
4
6
8
L
[ T
NF
- (
nm
ol/
l)]
Controls (n=16)
Smokers (n=12)
COPD (n=14)
Asthma (n=22)
0
1
2
3
4
L
[IL
-8 (n
mo
l/l)
]
Controls (n=16)
Smokers (n=12)
COPD (n=14)
Asthma (n=22)
*
*
**
*
**
TNF- IL-8
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Cigarette
smoke
Alveolar macrophage
Neutrophils
TNF- and IL-8 in COPD
4 ) ) TNF-
IL-8
Epithelial cells
TNF-
IL-8
NF-B
IL-8 gene
IL-8
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Mucus secretion
NF-B
IL-8
Neutrophil
recruitment
TNF- a
REACTIVE OXYGEN SPECIES IN
COPD
Plasma leak Bronchoconstriction Isoprostanes
ANTIOXIDANTS Vitamins C and E
N-acetyl cysteine
Glutathione analogues
Nitrones (spin trap)
O2-, H202
OH., ONOO-
Anti-proteases
SLPI 1-AT
Proteolysis
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Neutrophil elastase
Cathepsins
MMP-1, MMP-9,
MMP12
Granzymes,
perforins
Others……..
PROTEASE-ANTIPROTEASE IMBALANCE IN COPD
1-Antitrypsin
SLPI
Elafin
TIMPs
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Alpha1-Antitrypsin Deficiency
• Enzyme prevents loss of lungs’ elastic
fibers
• Deficiency – Pan-lobular emphysema
• Homozygous – PiZZ – 15-30% of
normal AAT levels (PiMM) Earlier
development of COPD
– Airflow obstruction in early 40s
– Accelerated by 10 to 15 years
– occurs in 1:5000
• Heterozygous – PiMZ – 50-80% -
smokers
• Z allele – 3-5% population
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Alpha1-Antitrypsin Deficiency
• Progressive SOB in young patients
• 60% emphysema under 40 yrs
• 2% of all cases of COPD
• Pneumothorax, Resp. failure, Cirrhosis
• Treatment – Stop smoking
– Avoid pollution/dust
– Recombinant AAT
– Gene therapy
– (long arm chr 14)
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High resolution CT scan showing the characteristic basal
panlobular emphysema rather than the apical centrilobular
disease seen in smokers who have normal levels of 1-
antitrypsin.
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SP
Mucus gland hyperplasia
Goblet cell hyperplasia
Mucus
Sensory nerve Cholinergic nerve ACh
N
E
Neutrophils
Epithelium
INFLAMMATION
Cytokines
ROS
• Acetylcholine
• Tachykinins
• Proteinases
neutrophil elastase
• Cytokines (TNF-)
• Oxidants
• Growth factors
• MUC genes
MUC5a, MUC8
MUCUS HYPERSECRETION IN COPD
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ASTHMA v COPD Inflammation ASTHMA COPD
CELLS Mast cells Eosinophils CD4 T cells macrophages
Neutrophils CD8 T cells Macrophages++
MEDIATORS LTD4,histamineIL-4,IL-5,
ROS +
LTB4’ IL-8, TNFa, ROS+++
EFFECTS All airways Little fibrosis Ep shedding
Periph airways Lung destruction Fibrosis + Sq metaplasia
Response steroids +++ ±
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COPD - SYMPTOMS
• COUGH AND MUCOID SPUTUM
• DYSPNOEA - SLOWLY PROGRESSIVE
• WHEEZE
• OEDEMA (IF COR PULMONALE)
• WINTER EXACERBATIONS
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COPD - SIGNS
• HYPERINFLATION
• DECREASED EXPANSION CHEST
• PROLONGED EXPIRATION/±WHEEZE
• SIGNS PULMONARY HYPERTENSION AND/OR RVH (± CARDIAC FAILURE)
• CYANOSIS
• HYPERCAPNIA - ASTERIXUS, (PRE)-COMA
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CONFIRMING COPD
• SPIROMETRY - GOLD GUIDELINES
• (DLCO)
• REVERSIBILITY (BETA2 AND INHALED
STEROID TRIAL)
• CXR - HYPERINFLATION/BULLAE
• ECG
• ABG - ACUTE V CHRONIC STABLE
• ALPHA-1 SCREEN (<45 YO OR F.H.)
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0
100
200
300
400
500
1 2 3 4 5 6 7 8 9 10 11 12
13 14
Peak f
low
(L
/min
)
1 2 3 4 5 6 7 8 9 10 11 12
13 14
Peak f
low
(L
/min
)
Days
Prednisolone 30 mg o.m. x 14 days
Prednisolone 30 mg o.m. x 14 days
COPD
ASTHMA
0
100
200
300
400
500
TRIAL OF STEROIDS
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Eliminate the irritant
• STOP SMOKING
• Counselling improves likelihood
• Smoking cessation program
• Pharmacotherapy
– Nicotine Replacement Therapy
– Bupropion (Zyban)
• Reduce exposure to environmental pollutants
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Smoking Cessation
• Stops accelerated decline in FEV1
• Improves possibility of oxygen therapy benefits
• 3-6 months after quitting: end of cough/phlegm production
• 1 year: lung function increased 30mls
• 1 year: risk of Small Cell Lung Cancer halved
• 5 years: risk of any lung cancer halved
– No progression of COPD
– Sporting performance enhanced
• Methods of smoking cessation
– Counseling; Nicotine replacement; Behavior modification
– Hypnosis
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BRONCHODILATORS IN
COPD • FEV/FVC <70% : 50%< FEV <80% LONG-
ACTING BRONCHODILATOR
• FEV/FVC <70% : 30%< FEV <50% AND EXACERBATION-INHALED STEROID
• FEV/FVC <70% ; FEV <30% ±RESP, FAILURE, ±CCF - LTOT ± SURGERY
• ANY SYMPTOMS AND FEV/FVC <70% SHOULD HAVE SHORT ACTING B/DILATOR
• SEE WWW.GOLDCOPD.COM
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COPD MANAGEMENT
• PATIENT EDUCATION
• TREAT EXACERBATIONS EARLY -
ANTIBIOTICS, ±STEROIDS
• VACCINES
• (MUCOLYTICS)
• REHABILITATION PROGRAMMES
• LTOT ( >16 HOURS PER DAY)
• SURGERY - LVRS
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COPD PROGNOSIS
• FEV1 < 1.0L 5 YSR - 69%
• 10 YSR - 40%
• RVF 5 YSR - 25%
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MANAGING
EXACERBATIONS • ANTIBIOTICS
• CONTROLLED OXYGEN
• BRONCHODILATOR - BETA AGONIST ANTICHOLINERGIC, ±THEOPHYLLINE
• STEROIDS
• NIV BIPAP
• INTUBATION/VENTILATION
• TREAT HEART FAILURE IF PRESENT
• (RESPIRATORY STIMULANTS?)