Asthma Ilmu Penyakit Paru Compatibility Mode
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Transcript of Asthma Ilmu Penyakit Paru Compatibility Mode
5/18/2011
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Departemen Pulmonologi
Fakultas Kedokteran
Universitas Sumatera Utara
2008
Tamsil Syafiuddin-Bintang Sinaga
Asthma
Levels of competence
Standar Kompetensi Dokter , Konsil Kedokteran Indonesia, 2006
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Standar Kompetensi Dokter , Konsil Kedokteran Indonesia, 2006
Level of competence 4:
• Dokter mampu membuat diagnosis klinik
berdasarkan ‘pemeriksaan fisik’ dan
‘pemeriksaan tambahan’ yang diminta oleh
dokter (misalnya: pemeriksaan laboratorum
sederhana atau X-ray).
• Dokter dapat memutuskan dan mampu menangani
problem itu secara mandiri hingga tuntas.
Recent issuesRecent issues
in asthma managementin asthma management
••“The Unmet Needs of asthma ““The Unmet Needs of asthma “
Theme of World Asthma Day 2005/2006Theme of World Asthma Day 2005/2006
“You can control your asthma ““You can control your asthma “
Theme of World Asthma Day 2007/2008Theme of World Asthma Day 2007/2008
••“Adherence ““Adherence “
Self ManagementSelf Management
••“UUD No 29 / 2004” : Praktik Kedokteran“UUD No 29 / 2004” : Praktik Kedokteran
CompetencyCompetency
••“Pharmacoeconomic consideration”“Pharmacoeconomic consideration”
Quality of LifeQuality of Life
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Asthma is an inflammatory diseasesAsthma is an inflammatory diseases
Definition of asthma�� Chronic inflammatory disease of airways
(AW)�� ↑ responsiveness of tracheobronchial tree
�� Physiologic manifestation: AW narrowing relieved spontaneously or with
BD ± Cster�� Clinical manifestations:
a triad of paroxysms of cough, dyspnea and wheezing.
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Disease Pattern�� Episodic --- acute exacerbations
interspersed
with symptom-free periods
�� Chronic --- daily AW obstruction which
may be mild, moderate or severe ±
superimposed acute exacerbations
�� Life-threatening--- slow-onset or fast-onset
(fatal within 2 hours)
Classification :
• Level of asthma severity(by Clinical Features Before Treatment)
• Level of asthma control
(by Clinical Features After Treatment)
( GINA 2006 )
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Classification of Asthma Severity by
Clinical Features Before Treatment:
Intermittent:Symptoms less than once a week
Brief exacerbations
Nocturnal symptoms not more than twice a month
• FEV1 or PEF ≥ 80% predicted
• PEF or FEV1 variability < 20%
Mild Persistent:Symptoms more than once a week but less than once a day
Exacerbations may affect activity and sleep
Nocturnal symptoms more than twice a month
• FEV1 or PEF ≥ 80% predicted
• PEF or FEV1 variability < 20 – 30%
Moderate Persistent:Symptoms daily
Exacerbations may affect activity and sleep
Nocturnal symptoms more than once a week
Daily use of inhaled short-acting 2-agonist
• FEV1 or PEF 60-80% predicted
• PEF or FEV1 variability > 30%
Severe Persistent:Symptoms daily
Frequent exacerbations
Frequent nocturnal asthma symptoms
Limitation of physical activities
• FEV1 or PEF ≤ 60% predicted
• PEF or FEV1 variability > 30%
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Characteristic Controlled(All of the following)(All of the following)
Partly Controlled(Any measure present
in any week)
Uncontrolled
Daytime symptoms None (twice or
less/week)
More than twice/week Three or more features of partly controlled asthma present in any week
Limitations of
activities
None Any
Nocturnal
symptoms/awakening
None Any
Need for reliever/
rescue treatment
None (twice or
less/week)
More than twice/week
Lung function (PEF or
FEV1)
NormalNormal < 80% predicted or
personal best
(if known)
ExacerbationsExacerbations NoneNone One or more/yearOne or more/year One in any weekOne in any week
Levels of Asthma Control
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NormalNormal AsthmaAsthma
InflammationInflammation(+)(–)
Bronchial hyperreactivity ( + )Bronchial hyperreactivity ( - )
Symptoms (+)Symptoms (+)Symptoms (Symptoms (--))
• •
•
•
•••
•••
Bronchoconstriction ( - ) Bronchoconstriction ( + )
The pathogenesis of asthma
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Ig EIg E
AgAg
YY
Methyl Methyl
transferasetransferasePhospholipidPhospholipid
PhosphatidylPhosphatidyl
ethanolamineethanolamine
Phosphatidyl Phosphatidyl
cholinecholine
PhosphoPhospholipase Alipase A22
CaCa++++ HistaminHistamin
CaCa++++ HistaminHistamin
ECF, NCFECF, NCFArachidonic acidArachidonic acid
lypoxygenaselypoxygenase cyclooxygenasecyclooxygenase
55--HETEHETE LeucotrienesLeucotrienesLTBLTB44LTCLTC44LTDLTD44LTELTE44
ThromboxanesThromboxanes
TXATXA22
ProstaglandinsProstaglandinsPGDPGD
PGFPGF22αααααααα
Mediator release in asthma reactions
Inflammation
Bronchial hyperreactivity
Symptoms
ControllerController
RelieverReliever
Medicines and Pathogenesis of asthma
Bronchoconstriction
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Asthma Therapy EvolutionAsthma Therapy Evolution
1975
1980
1985
1990 19952000
“Large use” of
short-acting
ß2-agonists
“Fear” of
short-acting
ß2-agonists
Single
inhaler
therapy
ICS+LABA
ICS treatment
introduced
1972
Adding
LAßA to ICS therapyKips et al, AJRCCM 2000
Pauwels et al, NEJM 1997
Greening et al, Lancet 1992
Bronchospasm Inflammation Remodelling
DIAGNOSIS EXACERBATION : “CLINICAL”
�� Episodic asthma:Paroxysms of wheeze, dyspnoea and
cough, asymptomatic between attacks.
��Acute severe asthma:
• upright position, use accessory resp muscles, • can’t complete sentences in one breath,
• tachypnea > 25/min, tachycardia > 110/min, PEF 33-50% of pred or best, pulsus paradoxus,
chest hyperresonant, prolonged expiration, breath sounds decreased, inspiratory and
expiratory rhonchi, cough.
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�� Life-threatening features: PEF < 33% of pred or best,silent chest, cyanosis,
bradycardia, hypotension, feeble respiratory effort,
exhaustion, confusion, coma, PaO2 < 60,
PCO2 normal or increased,
acidosis (low pH or high [H+]).
��Chronic asthma:
Dyspnea on exertion, wheeze, chest tightness and cough
on daily basis, usually at night and early morning; intercurrent acute severe asthma (exacerbations)
and productive cough (mucoid sputum), recurrent respiratory infection, expiratory rhonchi throughout and accentuated on forced expiration.
�� Acute severe asthma:
MANAGEMENT 1
1.Immediate Rx:
O2 40-60% mask or cannula + SABA (salbutamol 5mg)/
nebulizer + ICS 200 mcg/ nebulizer or hydrocortisone
200mg IV. With lifethreatening features add 0.5mg
ipratropium to nebulized β2 agonist + Aminophyllin 250mg
iv over 20 min or salbutamol 250ug over 10 min.
2. Subsequent Rx:
Nebulized SABA 6 hourly + ICS 200mcg
or hydrocortisone 200mg 6 hourly IV + 40-60% O2.
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MANAGEMENT 2
�� No improvement after 15-30 min:Nebulized β2 agonist every 15-30 min + Ipratropium.
�� Still no improvement:Aminophyllin infusion 750mg/24H (small pt), 1 500mg/24H
(large pt), or alternatively salbutamol infusion.
�� Monitor Rx:
Aminophyllin blood levels + PEF after 15-30 min +
oxymetry (maintain SaO2 > 90) + repeat blood gases
after 2 hrs if initial PaO2 < 60, PaCO2 normal or raised andpatient deteriorates.
�� Deterioration:
ICU, intubate, ventilate + muscle relaxant.
ASTHMA MANAGEMENT: “CLINICAL”
• QUICK RELIEVE MEDICATION
• LONG TERM TREATMENT
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Guidelines on Asthma Management:
Past and Current Trends
LABA and ICSLABA and ICSLABA and ICSLABA and ICSICSICSICSICS
LABA+ICSLABA+ICSLABA+ICSLABA+ICS
GINA 1998 GINA 1998 GINA 1998 GINA 1998 (adapted)(adapted)(adapted)(adapted)GINA 2006GINA 2006GINA 2006GINA 2006Severe Severe Severe Severe persistentpersistentpersistentpersistentModerate Moderate Moderate Moderate persistentpersistentpersistentpersistentMild Mild Mild Mild persistentpersistentpersistentpersistentIntermittentIntermittentIntermittentIntermittent
SABA / Rapid onset of action LABA Rapid onset of action LABA Rapid onset of action LABA Rapid onset of action LABA ExacerbationExacerbation
Stable condition
Total control Partially control Uncontrol
Old classificationOld classificationOld classificationOld classificationNew classificationNew classificationNew classificationNew classification
Anti Inflammations is Anti Inflammations is
the mainstay therapythe mainstay therapy !
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Inhalation therapy is Inhalation therapy is
the mainstay therapythe mainstay therapy
Because minimally side effect
!
MBP, ECPMBP, ECP
Eosinophil
Epithelium
AIRWAY REMODELLING IN AIRWAY REMODELLING IN ASTHMAASTHMA
Desquamations of epitheliumDesquamations of epithelium
Thickening of basement membraneThickening of basement membrane
Increase in airway smooth muscleIncrease in airway smooth muscle
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Epithelial DamageEpithelial Damage
P Jeffery, in: Asthma, Academic Press 1998P Jeffery, in: Asthma, Academic Press 1998P Jeffery, in: Asthma, Academic Press 1998P Jeffery, in: Asthma, Academic Press 1998Basement Membrane Basement Membrane
ThickeningThickening
P Jeffery, in: Asthma, Academic Press 1998P Jeffery, in: Asthma, Academic Press 1998P Jeffery, in: Asthma, Academic Press 1998P Jeffery, in: Asthma, Academic Press 1998
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Smooth Muscle HyperplasiaSmooth Muscle Hyperplasia
P Jeffery, in: Asthma, Academic Press 1998P Jeffery, in: Asthma, Academic Press 1998P Jeffery, in: Asthma, Academic Press 1998P Jeffery, in: Asthma, Academic Press 1998Controller:Controller:
Anti inflammationAnti inflammation
• budesonide (Pulmicort®®)(Inflamid®®)
• beclomethasone dipropionate (Becotide®®)
• triamcinolone acetonide
• fluticasone(Flexotide®®)
• sodium chromoglicate
(Intal®®)
• ketotifen
• sodium nedocromil
Inhaled Cortico SteroidInhaled Cortico SteroidNon steroidNon steroid
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BronchodilatorBronchodilator
••ββββββββ2 2 -- agonistagonist
•• XanthinXanthin
••AnticholinergicAnticholinergic
RelieverReliever
BRONCHODILATORBRONCHODILATOR
Short Acting Short Acting ββββββββ22 AGONIST (SABA):AGONIST (SABA):
••salbutamol/albuterol (Ventolin salbutamol/albuterol (Ventolin ®®))
••terbutaline (Bricasmaterbutaline (Bricasma®®))
••procaterolprocaterol
••fenoterolfenoterol
••orciprenaline, etcorciprenaline, etc
ANTICHOLINERGIC:ANTICHOLINERGIC:
••atropine sulfate atropine sulfate
••ipratropium bromideipratropium bromide••tiotropium bromidetiotropium bromide
OTHER SYMPHATOMIMETIC: OTHER SYMPHATOMIMETIC:
••ephedrineephedrine••adrenaline, etcadrenaline, etc
XANTHINE:XANTHINE:
••theophyllinetheophylline
••aminophyllineaminophylline
Long Acting Long Acting ββββββββ22 AGONIST:AGONIST:
(LABA)(LABA)
••salmoterolsalmoterol
••formoterolformoterol
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Combination therapyCombination therapy
SymbicortSymbicort®®
Budesonide + FormoterolBudesonide + Formoterol
SeretideSeretide®®
Fluticasone + SalmoterolFluticasone + Salmoterol
The Beginning of The Beginning of
TreatmentTreatment
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ExacerbationExacerbation
The beginning of treatmentThe beginning of treatment?
Stable condition Stable condition √√√√
x
Asthma management
* Stable condition
* Long-term therapy
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Evaluations
Peak flow meterPeak flow meter
600-700
0
300
( normal )Objective Objective valuesvalues
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Peak Flow Meter /PEFR/APE
Must be avilable
PEFR Monitoring:PEFR Monitoring:PEFR Monitoring:PEFR Monitoring:PEFR Monitoring:PEFR Monitoring:PEFR Monitoring:PEFR Monitoring:A Major Tool in Asthma SelfA Major Tool in Asthma SelfA Major Tool in Asthma SelfA Major Tool in Asthma SelfA Major Tool in Asthma SelfA Major Tool in Asthma SelfA Major Tool in Asthma SelfA Major Tool in Asthma Self--------ManagementManagementManagementManagementManagementManagementManagementManagement
Chronic DiseasesChronic DiseasesChronic DiseasesChronic DiseasesChronic DiseasesChronic DiseasesChronic DiseasesChronic Diseases MonitorMonitorMonitorMonitorMonitorMonitorMonitorMonitor
HypertensionHypertensionHypertensionHypertensionHypertensionHypertensionHypertensionHypertension
DiabetesDiabetesDiabetesDiabetesDiabetesDiabetesDiabetesDiabetes
AsthmaAsthmaAsthmaAsthmaAsthmaAsthmaAsthmaAsthma
Blood pressureBlood pressureBlood pressureBlood pressureBlood pressureBlood pressureBlood pressureBlood pressure
Serum glucoseSerum glucoseSerum glucoseSerum glucoseSerum glucoseSerum glucoseSerum glucoseSerum glucose
PEFRPEFRPEFRPEFRPEFRPEFRPEFRPEFR
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DIFFERENTIAL DIAGNOSIS
1. Upper airway obstruction – glottic dysfunction.
2. Acute LV failure – pulmonary oedema.3. Pulmonary embolism.
4. Endobronchial disease.5. Chronic bronchitis.
6. Eosinophilic pneumonia.7. Carsinoid syndrome.
8. Vasculitis.
Life is not problem to be solved,Life is not problem to be solved,but a reality to be experienced but a reality to be experienced
( Soren Kierkegaard)( Soren Kierkegaard)
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