COPD_bahan Kuliah Blok 16

8/15/2019 COPD_bahan Kuliah Blok 16

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Disease of COPD

Zulkarnain Arsyad

Pulmonology Subdivison

of Internal Medicine Medical FacultyAndalas University M D amil !os"ital

Padang


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INTRODUCTION

COPD is t#e $ t# leading cause of deat# in t#e UnitedStates %be#ind #eart disease& cancer& andcerebrovascular disease'(

In )***& t#e +!O estimated )(,$ million deat#s-orld-ide from COPD(

In .//*& COPD -as ranked .) t# as a burden ofdisease0 by )*)* it is "ro ected to rank 1 t#(

In Indonesia COPD in t#e no 2 t# of leading cause of

deat#

COPD is t#e $ t# leading cause of deat# in t#e UnitedStates %be#ind #eart disease& cancer& andcerebrovascular disease'(

In )***& t#e +!O estimated )(,$ million deat#s-orld-ide from COPD(

In .//*& COPD -as ranked .) t# as a burden ofdisease0 by )*)* it is "ro ected to rank 1 t#(

In Indonesia COPD in t#e no 2 t# of leading cause of

deat#


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Definition

Airflo- limitation t#at is 3O4 fully

reversibleProgressiveAssociated -it# an abnormal inflammatoryres"onse of t#e lungs to no5ious "articles orgases


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Pathogenesis

4#ree "rocesses6

O5idative stressImbalance of "roteinases and anti7"roteinasesC#ronic inflammation


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LUNG INFLAMMATIONLUNG INFLAMMATION

COPD PATHOLOGYCOPD PATHOLOGY

OxidativeOxidativestressstress ProteinasesProteinases

Re airRe air!e"hanis!s!e"hanis!s

Anti# roteinasesAnti# roteinasesAnti#oxidantsAnti#oxidants

Host fa"torsA! $if%ing !e"hanis!s

Cigarette s!o&e'io!ass arti"$es

Parti"($ates

Source : Peter J. Barnes,

Pathogenesis ofCOPD


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C#ronic Inflammation

C#ronic inflammation in air-ays&

"arenc#yma& "ulmonary vasculatureInflammatory cells involved are6

Macro"#ages leukotriene 8$

47lym"#ocytes %CD9' interleukin 9 3eutro"#ils 43F7:


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Cigarette s!o&eCigarette s!o&e)and other irritants*)and other irritants*

PROTEASESPROTEASESNeutrophil elastaseNeutrophil elastaseCathepsinsCathepsinsMMPsMMPs

Al eolar !all "estru#tionAl eolar !all "estru#tion$E%ph&se%a'$E%ph&se%a'

Mu#us h&perse#retiMu#us h&perse#retio

CD8CD8 ++lymphocytelymphocyte

Alveolar Alveolarmacrophagemacrophage

Epithelial Epithelial cellscells

(i)rosis(i)rosis$O)stru#ti e$O)stru#ti e

)ron#hiolitis')ron#hiolitis'

Fibroblast Fibroblast

Monocyte Monocyte Neutrophil Neutrophil

Che%ota#ti# *a#torsChe%ota#ti# *a#tors

In ammatory Cells Involved inCOPD

Source : Peter J. Barnes,MD


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;isk Factors

4obacco SmokeCigarettes&Pi"es& cigars < lo-er rates t#ancigarette smokers but #ig#ert#an non7smokers

Occu"ational dusts andc#emicals

=a"ors& irritants& fumes 3eed sufficiently intense or

"rolonged e5"osureIndoor air "ollution8iomass fuel used for cookingand #eating in "oorly ventedd-ellings

Outdoor air "ollutionMinor risk factor Passivecigarette smoke e5"osure

;es"iratory infections in earlyc#ild#ood>o-er socioeconomic status

association -it# COPDMay be secondary to cro-ding&

"oor nutrition& etc(


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Risk Factors for

COPDN(tritionN(trition

Infe"tionsInfe"tions

+o"io#e"ono!i"+o"io#e"ono!i"stat(sstat(s

Aging Po ($ationsAging Po ($ations


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Pat#ology

Central Air-ays6?nlarged mucus secretingglandsIncrease in goblet cells

Mucus #y"ersecretionPeri"#eral Air-ays

;e"eated cycles of in uryand re"air

Increased collagen@scarringin air-ay -all


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Pat#ology

Pulmonary vascular c#anges

4#ickening of vessel -all %intima'

Increase in smoot# muscle

Infiltration of vessel -all by inflammatory cellsAs COPD -orsens& more smoot# muscle& "roteoglycans andcollagen furt#er t#icken t#e vessel -all


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A$veo$ar ,a$$ destr("tion

Loss of e$asti"it%

Destr("tion of ($!onar%"a i$$ar% -ed

. Inf$a!!ator% "e$$s !a"ro hages/ CD0 1 $%! ho"%tes

Source : Peter J. Barnes, MD

Changes in Lung Parenchyma inCOPD


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Pat#o"#ysiology

Mucus #y"ersecretion

Ciliary dysfunction

Airflo- limitation

Pulmonary #y"erinflation

as e5c#ange abnormalities

Pulmonary #y"ertension

Cor "ulmonale

Mucus #y"erserection B ciliary dysfunction coug#& s"utum "roduction


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Medical !istory

?5"osure to ris& fa"tors & incl(intensity@duration!istory of e5acerbations or "revious

#os"itali ations for res"iratorydisorder Past medical #istory

Ast#ma& allergies& sinusitis@nasal "oly"s& res"iratory infections inc#ild#oodPresence of co7morbid conditions

!eart disease;#eumatic disease

Family !istoryCOPDOt#er c#ronic res"iratory diseases

Social !istoryIm"act of disease on "atientEs life&inc( activity& missed -ork andeconomic im"act?ffect on family routinesDe"ression@an5ietySocial and family su""ort availableto t#e "atient

Ot#er6A""ro"riateness of current medicaltreatmentsPossibilities for reducing riskfactors& es"( smoking cessation


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!istory of Present Illness

C#ronic Coug#Intermittently or every dayPresent t#roug#out t#e day0seldom only nocturnal

C#ronic s"utum "roductionAny "attern

;e"eated e"isodes of acute bronc#itis

C#ronic coug# and s"utum "roduction often "recede develo"mentof airflo- limitation by many years

3ot all "atients -it# t#ese sym"toms develo"COPD

Dys"nea on e5ertionProgressivePersistent+orse -it# e5ercise+orse during res"iratoryinfections

!istory of e5"osure to riskfactors

4obacco smokeOccu"ational dusts andc#emicalsSmoke from #ome cooking and#eating fuels


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P#ysical ?5amination

4#ora568arrel c#est

>ungsDecreased breat# sounds+#ee ing

Cardiac;ig#t7sided #eart failure

?dema& tender liver&distended abdomen

P#ysical signs are rarely a""arentuntil significant im"airment of lung

function #as occurred


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Diagnostic 4ests

C#est 7rayFlattened dia"#ragmsUse to e5clude ot#er diagnoses

!ig# resolution C4 3ot routinely recommendedIf in doubt about diagnosis ofCOPDIf considering bullectomy or lungvolume reduction surgery

C8CMay see increased#emoglobin@#ematocrit secondary to#emoconcentration

A8S"irometry


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S"irometry

Measure of F=C and F?= .F=C G forced vital ca"acity

Ma5imum volume of air forcibly e5#aled from t#e "oint of ma5imalin#alationF?= . G forced e5"iratory volume in . second

=olume of air e5#aled in t#e . st second of t#e F=C maneuver

Calculate t#e F=C@F?= . ratio

3ormal ratio G ,*@9*HCOPD ratio G ,*H "re7bronc#odilator F=C B F?= areCOPD ratio G 9*H "ost7bronc#odilator bot# decreased

?ssential to making t#e diagnosis of COPD


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Classi cation of COPDSeverity

y S!irometryStage I" #ild F$% &'F%C ( )*+)F$%& , -). !redicted

Stage II" #oderate F$% &'F%C ( )*+) /). ( F$% & ( -). !redicted

Stage III" Severe F$% &'F%C ( )*+)

0). ( F$% & ( /). !redicted

Stage I%" %ery Severe F$% &'F%C ( )*+) F$% & ( 0). !redicted or

F$%& ( /). !redicted plus


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Differential Diagnosis of

COPDAst#ma

;eversible airflo- limitation?arly onset %c#ild#ood'

Sym"toms vary day to dayCongestive #eart failure=olume restriction& 3O4 airflo-limitationC ; -it# dilated #eart& "ulmonaryedema

8ronc#iectasis>arge volumes of "urulent s"utumCommonly associated -it# bacterialinfection8ronc#ial dilation and bronc#ial-all t#ickening on C ; or C4

4uberculosisOnset at all agesC#est 57ray -it# infiltrate ornodular lesions

Obliterative bronc#iolitisJounger "atients@non7smokersMay #ave a #5 of r#eumatoidart#ritis or fume e5"osureC4 s#o-s #y"odense areas -it#e5"iration

Diffuse "anbronc#iolitisMale@non7smokersC#ronic sinusitisC ; and #ig# resolution C4 s#o-diffuse small centrilobular nodularo"acities and #y"erinflation


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COPD Management Program

O>D % lobal Initiative for C#ronicObstructive >ung Disease'

uidelines


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oals

Prevent disease "rogression;elieve sym"toms

Im"rove e5ercise toleranceIm"rove #ealt# statusPrevent and treat com"licationsPrevent and treat e5acerbations;educe mortalityPrevent or minimi e side effects from treatmentCessation of cigarette smoking


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eneral Princi"les

Determine disease severityIm"lement ste"7-ise

treatment "lan?ducate t#e "atient

Im"rove skillsIm"rove ability to co"e -it#illnessIm"rove #ealt# status

Prescribe 4reatmentP#armacologic

3on7"#armacologic;e#abilitation

?5ercise training 3utrition counseling

educationO5ygen t#era"y

Surgical interventions

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COPD_bahan Kuliah Blok 16