Kuliah 3 Uii Copd,Asthma

7/30/2019 Kuliah 3 Uii Copd,Asthma

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COPD AND ASTHMA


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Differential Diagnosis

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ChronicBronchitis Emphysema

Asthma

COPD

AirflowObstruction


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Asthma Is A Disease Of The Large& COPD The Small Airways

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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

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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

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Diagnosis banding

Asma

SOPT

Pneumothoraks Gagal jantung kronik

Bronkiektasis

Destroyed lung

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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 HYPERTENSIONAND/OR RVH ( CARDIAC FAILURE)

CYANOSIS

HYPERCAPNIA

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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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Diagnosis

FEV1 >80%predicted

FEV1/FVC


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Diagnosis

50% FEV1


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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



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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

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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

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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

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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




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!!

Kuliah 3 Uii Copd,Asthma

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