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COPD AND ASTHMA
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Differential Diagnosis
2
ChronicBronchitis Emphysema
Asthma
COPD
AirflowObstruction
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Asthma Is A Disease Of The Large& COPD The Small Airways
3
Asthma
Emphysema
Chronic
Bronchitis
ChronicBronchitis
trachea
bronchi
alveoli
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ASTHMASensitizing agent
COPDNoxious agent
Airway inflammation
CD4+ T-lymphocytesEosinophils
Airway inflammation
CD8+ T-lymphocytesMacrophagesNeutrophils
Airflow limitationCompletelyreversible
Completelyirreversible
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COPD ASTHMA
Neutrophils
No AHR
No steroid response
Eosinophils
AHR
Steroid response
~10%
Wheezy bronchitis
OVERLAP BETWEEN COPD AND ASTHMA
AHR,Airway Hyper Responsiveness
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ASTHMA v COPDInflammation ASTHMA COPD
CELLS Mast cells
Eosinophils
CD4 T cells
Macrophages
Neutrophils
CD8 T cells
Macrophages++
MEDIATORS LTD4,histamine IL-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
8
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SP
Mucus gland hyperplasia
Goblet cellhyperplasia
Mucus
Sensory nerveCholinergicnerve ACh
NE
Neutrophils
Epithelium
INFLAMMATION
CytokinesROS
Acetylcholine Tachykinins Proteinases
neutrophil elastase Cytokines
(TNF-)
Oxidants
Growth factors MUC genes
MUC5a, MUC8
MUCUS HYPERSECRETION IN COPD
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Emphysema
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Inelastic/kku
collapsiblebronchioles
Enlarged air sacsdue to destructionof alveolar walls(bullae)
Abnormal
permanentenlargement of theair spaces distal tothe terminalbronchioles
accompanied bydestruction of theirwalls and withoutobvious fibrosis
Destruction of thealveolar walldamages
pulmonarycapillaries bytearing/sobk,fibrosis, orthrombosis
Walls of individualsacs torn (repair
not possible)Acc/mnyrtai,obvinytagfy
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Chronic
Bronchitis
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Presence of chronic
productive cough for3 months in each of2 successive years in apatient in whom other
causes of chronic coughhave been excluded
Air passagenarrowed byplugged/smbat andswollen mucousmembrane
Bronchiole
Mucus andpusimpede/menggu action ofrespiratorycilia
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Bronchus
Wall thickening inflammation -- mucus glandhypertrophy
Secretions
Alveoli
Wall thinning -inflammation -elastolysis
Coalescencegbn
ganhgy Elasticity
Bronchiole
Wall thickening inflammation
repair-- remodeling
Loss of alveolarattachments
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COPD Pathology and Abnormal Breathing Mechanics
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Airway resistance
Elastic recoil
Expiratory flow limitation
Work ofbreathing/purse lips
Dyspnea, cough and
other respiratory Quality of life
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Faktor resiko yg lain
Kebiasaan merokok merupakan satu-satunya penyebab kausal yangterpenting
Riwayat terpajan polusi udara dilingkungan dan tempat kerja
Hipereaktiviti bronkus
Riwayat infeksi saluran nafas bawahberualang
Defisiensi antitripsin alfa-1 (jarang di
Indonesia) 16
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Patogenesis of COPD
Obstruksi yang terjadi bersifat ireversibel
Terjadi karena perubahan struktural padasaluran nafas kecil
Terjasi inflamasi, fibrosis, metaplasi selgoblet dan hipertropi otot polos
17
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Diagnosis banding
Asma
SOPT
Pneumothoraks Gagal jantung kronik
Bronkiektasis
Destroyed lung
18
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COPD - SYMPTOMS
COUGH AND MUCOID SPUTUM
DYSPNOEA - SLOWLY PROGRESSIVE
WHEEZE OEDEMA (IF COR PULMONALE)
WINTER EXACERBATIONS
19
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COPD - SIGNS
HYPERINFLATION
DECREASED EXPANSION CHEST
PROLONGED EXPIRATION/WHEEZE
SIGNS PULMONARY HYPERTENSIONAND/OR RVH ( CARDIAC FAILURE)
CYANOSIS
HYPERCAPNIA
20
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The Vicious Cycle of COPD
Depression &social isolation
Shortness ofbreath
ReducedactivitiesAnxiety
Malnutrition
Reduced
activities
Muscle
weakness
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MANAGE STABLE COPD
EDUCATION PHARMACOLOGIC NON PHARMACOLOGIC
- stop smoking
- disease course- medication- prevention of disease
progression- trigger avoidance
REGULAR :
Bronchodilator-Anticholinergic-Beta 2 agonist-Xantin-SABA+LABA-LABA+ICS
As nedeed:
ExpectorantMucolyticAntioxydant
-Rehabilitation
-Vaccination-Nutrition-Mechanical vent-surgical Intervention
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GOLD Guidelines for COPD
Diagnosis Chronic
cough/sputum
PFTs within normal
limits No symptoms
Treatment
Avoid risk factors(smokingcessation)
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Stage 0: At Risk
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GOLD Guidelines for COPD
Diagnosis
FEV1 >80%predicted
FEV1/FVC
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GOLD Guidelines for COPD
Diagnosis
50% FEV1
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GOLD Guidelines for COPD
Diagnosis
30% FEV1 < 50%predicted
FEV1/FVC < 70%
With/withoutsymptoms
Treatment
Avoid risk factors
Regular therapy with 1 bronchodilators
Rehabilitation
Inhaled corticosteroids if
significant symptoms andlung function responseorif repeated exacerbations
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Stage III:Severe
GOLD Guidelines for COPD
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GOLD Guidelines for COPD
Diagnosis FEV1 < 30%
predicted
FEV1/FVC < 70% Respiratory failure
Right-side-of-the-
heart failure
Treatment Avoid risk factors
Regular therapy with1 bronchodilators
Inhaled corticosteroids ifsignificant symptoms and lungfunction response or repeatedexacerbations
Rehabilitation
Treatment of complications Long-term O2 therapy for
hypoxic respiratory failure
Evaluate for surgical treatment
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Stage IV: Very Severe
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Acute Exacerbations of COPD(AECOPD)
Common during winter months
Symptoms Breathlessness Wheeze Cough Increased sputum production
CausesViral infection (e.g., rhinovirus) Environmental causes (including smoking)Allergy
Bacterial infection 28
The Downward Spiral
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The Downward Spiral
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COPD
Airwayobstruction
Exacerbation
Mucushypersecretion
Continuedsmoking
Lung
inflammation
Alveolar
destruction
Impairedmucus clearance
Submucosal glandhypertrophy
Exacerbation
Exacerbation
Hypoxemia
DEATH
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2Agonist Bronchodilator Response
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Asthma Response COPD Response
Anticholinergic
Panel A Panel B
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MANAGING EXACERBATIONS
ANTIBIOTICS CONTROLLED OXYGEN
BRONCHODILATOR - BETA AGONISTANTICHOLINERGIC, THEOPHYLLINE
STEROIDS
INTUBATION/VENTILATION
TREAT HEART FAILURE IF PRESENT
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T t t f ECOPD(1#)
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Treatment of ECOPD(1#)
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Treatment of ECOPD(2#)
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COPD: Management Goals Relieve symptoms Improve exercise
tolerance Improve health status Prevent and treat
exacerbations Modify natural course
Reduce mortality Prevent and treat
complications Minimize side effects from
treatment
Reducing
airflowobstruction
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Asthma Bronchiale
Asthma is a common disease with significantmorbidity, mortality and cost.
To be prop early treated asthma must be
characterized by lung function, symptoms andmedication use.
Asthma is a variable disease. Stability translates intofewer exacerbations and lower cost.
Stability is best achieved with controller therapy.
Prop.mnopangdtgy
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Asthma
Definition: Airways hyper-responsiveness,reversible airways obstruction
Pathophysiology: Inflammation
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Fakta / Problem
Tingkat asma terkontrol sangatrendah
PASIEN DOKTERGuideline
Tidak tahu
Tidak mengerti
Motivasi rendah
Biaya
Kurang tersebar
Sulit
aplikasi/penerapan
Misdiagnosis
Under-treatment
Over-treatmentt.u.cortsteroid inh
konsep & tujuan terapi asma: terapi asma bukan
hanya terapi simtomatik !!!
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Physical Examination
Wheeze -Usually heard without a stethoscope
Dyspnoea -Rhonchi heard with a stethoscope
Use of accessory muscles
Remember -
Absence of symptoms at the time of examination doesnot exclude the diagnosis of asthma
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Bronchoconstriction
Before 10 Minutes AfterAllergen Challenge
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Evolusi Terapi Asma
1975
1980
1985
1990 19952000
Large use of
short-acting
2-agonists
Fear of
short-acting
2-agonists
Fix
combination
ICS+LABA
ICS treatment
introduced
1972
AddingLAA to ICS therapy
Kips et al, AJRCCM 2000Pauwels et al, NEJM 1997
Greening et al, Lancet 1992
Bronchospasm Inflammation Remodelling
SYM/016/Dec08-D
MODERN VIEW OF ASTHMA
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Eosinophil
Mast cell
Allergen
Th2 cell
MODERN VIEW OF ASTHMA
VasodilatationNew vessels
Plasma leakOedema
Neutrophil
Mucushypersecretionhyperplasia
Mucus plug
Macrophage
BronchoconstrictionHypertrophy/hyperplasia
Cholinergireflex
Subepitheliafibrosis
Sensory nerveactivation
Nerve activation
Mucus plugEpithelial shedding
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Antigen
2-Agonists
Corticosteroids
Virus?
Virus?Adenosine
ExerciseFog
AIRWAYHYPERRESPONSIVENESS
BRONCHOCONSTRICTION
Mast cell Airway smooth muscle
Macrophage Eosinophil
-lymphocyte
Barnes PJ
Complementary actions of long-acting b2-agonist(LABA) and
corticosteroids on the pathophysiology of asthma.
Reduction in Asthma Attack
Improvement in the control
of Asthma symptoms
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Bronchodilators
Inhaled therapy is preferred.
Regular treatment with long-acting
bronchodilators is more effective andconvenient than treatment with short-acting bronchodilators .(Evidence A)
45GOLD. update. 2007
Inhaled Corticosteroids (ICS): The Most Effective
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Inhaled Corticosteroids (ICS): The Most Effective
Long-Term Controller Medications for Asthma
The daily use of ICS results in the following:
Asthma symptoms will diminish and improvement continues
gradually
Occurrence of severe exacerbations is greatly reduced
Use of quick-relief medication decreases
Lung function improves significantly, as measured by PEF,
FEV1, and airway hyperresponsiveness Problems due to asthma may return if patients stop
taking ICS
Guidelines for the Diagnosis and Management of Asthma. 1997. NIH Publication No. 97-4051.
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Bagaimana Kortikosteroid bekerja mempengaruhi On & Off inflamasi
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InflamasiON :
Sel inflamasi
Enzym- Phospholipase A2
Arachidonic Acid Cascade
Pelepasan mediator
Inflamasi saluran napas
InflamasiOFF:
Steroid berikatan denganreseptor Kortikosteroid
Masuk ke inti sel
Produksi Lipocortin
Lipocortin
menghambat enzim
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What are the Therapeutic Targets?
Adapted from Bousquet et al. Am J Respir Crit Care Med. 2000;161:1720-1745.
Smooth muscledysfunction
Airwayinflammation
Inflammatory cellinfiltration/activation
Mucosal edema Cellular proliferation
Epithelial damage Basement membrane
thickening
Bronchoconstriction Bronchial hyperreactivity Hyperplasia/Hypertrophy Inflammatory mediator release
Symptoms/Exacerbations
Terapi Masa Depan
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Terapi Masa Depan
Intermiten
49
Asma
Persisten
Tidak terkontrol
MaintainLABACS
Tujuanpenatalaksanaan
asma :
TOTAL KONTROL
Boushey H. Is Asthma Control Achieveable ?, European Respiratory Journal , Dec 2004
Terkontrol
Tidak terkontrol Terkontrol
Tingkatkandosis
Quality of live
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PRINSIP TERAPI ASMA
Traditonal view : ABC
Modern view :CBA
A:Aminofilin B:Beta 2 Agonist/Bronkodilator
C:Cortikosteroid
50
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Beberapa jenis bronkodilator yang sering digunakanReliever(Pelega)
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Nama umum Nama dagang
Simpatomimetik
Mirip kafein
Anti-vagus
Salbutamol
Terbutalin
RimiterolFenoteral
Reproterol
Aminofilin
TeofilinKolin teofilinat
Ipratropium bromida
Suntikan atropin
Ventolin
Bricanyl
PulmadilBerotec
Bronchodil
Phyllocontin
NuelinCholedyl
Atrovent
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Pencegah/Controller(Pengontrol) Kortikosteroid inhalasi dan sistemik Sodium kromoglikat
Nedokromil sodium Metilsantin
Agonis beta-2 kerja lama inhalasi dan oral
Leukotriens modifier
Antagonis H-1
52
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B T i A S I i
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PengontrolMaintenance
Pelega (Reliever)
Terapi harian multi obatSteroid inhalasi (ICS)
Long Acting 2 -agonist (LABA)Oral steroid
Menghindari faktor pencetus
Terapi harianSteroid inhalasi (ICS)
Long Acting 2 -agonist (LABA)
Terapi harianSteroid inhalasi (ICS) Inhalasi 2-agonis prn
Tingkat 2: PERSISTEN RINGAN
Tidak perlu Inhalasi 2-agonis prn
Menghindari faktor pencetus
Menghindari faktor pencetus
Menghindari faktor pencetus
Tingkat 1: INTERMITEN
Inhalasi 2-agonis prn
Tingkat 4: PERSISTEN BERAT
Inhalasi 2-agonis prn
Tingkat 3: PERSISTEN SEDANG
Bagan Terapi Asma Saat Ini
Naikkan dosis jikatidak terkontrol
Turunkan dosisketika terkontrol
Penyesuaian dosissetelah 3 bulan terkontrol
harus tetapdimonitor/evaluasi
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THE E
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Thanks for your attention!!