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COPD(PPO
K)1
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Differential Diagnosis
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Chronic
Bronchitis 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
Bronchitis
Chronic
Bronchitis
trachea
bronchi
alveoli
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ASTHMA v COPD
Inflammation ASTHMA COPD
CELLS Mast cells
EosinophilsCD4 T cellsMacrophages
NeutrophilsCD8 T cellsMacrophages++
MEDIAT!S LTD4"histamine IL#4"IL#5" !S $%!eacti&e
'i(ati&e Stress
LTB4’
IL-8, TNFa,RO+++
E))ECTS All air*a+s
Little fi,rosisEp she((ing
Periph air!a"s
Lu#g $estructio#Fi%rosis +& 'etaplasia
!esponse steroi(s $$$ (
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Frequent targets of ROS
O2-
H2O2
HOClOH
gut
heartvessel
s
airways
brain
nerves
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Antioxidant inhibits the ROS ChainReaction
Mengam,il e# (ari antio!si"an
/ehilangan e# (iam,il 3 Atom 2 sta,il (gn 0 e#
Atom 2 sta,il
Antio!si"an ele,ihan 1 e#
Example of Oxygen atom
Terpapar one
%mis 3
! S !eacti&e 'i(ati&e Stress.
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8/580!a,e /6 7 Engl 8 Me( 299.35-051#054
COPD is a preventable and treatable diseasewith some signifcant extra pulmonary eectsthat may contribute to the severity inindividual patients
!ts pulmonary component is characteri"ed byair#ow limitation that is not $ully reversible
%he air#ow limitation is usually progressiveand associated with an abnormalin#ammatory response o$ the lung to noxious
particles or gases
Defnition o$ COPDGOLD 2008
0
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Muscleweakness
Cancer
CVD
Cachexa
Depresson Cognt!e"eclne
Osteopoross
#nema
CO$D
Ther6 A(&ances in !esp 6Dis 299.14.
CO$D not %ust a "sease of the lungs
CO$CO$
DD
'ystemc'ystemc
conse(uencconse(uenc
eses
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The Vicios Cycle of COPD
Depression Depression
social isolationsocial isolation
hort#ess o)%reathhort#ess o)%reath
Re$uce$ acti*itiesRe$uce$ acti*ities
#iet" #iet"
#alnutrition#alnutrition
Re$uce$
acti*ities
Re$uce$
acti*ities
Muscle
!ea#ess
Muscle
!ea#ess
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12!a,e /6 7 Engl 8 Me( 299.35-051#054
Causes of Death in Patients with COPD
$ethal in many ways
Car"iovascular
Disease
2%&
;
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#anagement 'ssues of COPD
COPDE(acerbation
$ung
)unction
#ortality
*uality of $ife
Dyspnea
$ocal +tress O(i"ative
+ystemic O(i"ative +tress
+ystemic 'nflammation$ocal 'nflammation
Airway Clearance
A,#, +a"ows!a et, al'ntern, .ourn, of COPD 2//0 134 October 2//0, PulmPharm, 5her 2/ 2//%4 6-22, ,,
E(ercise Performance
O(i"ative +tressO(i"ative +tress
)n*ammat)n*ammat
onon
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7is! )actors for COPD
Host )actors
>enes %e6g6 alpha1#antitr+psin (eficienc (eficienc+
H+perresponsi&eness
L
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COPD
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!acts A"ot
COPD COPD is the &th leading cause o$ death in
the 'nited States (behind heart disease)
cancer) and cerebrovascular disease* !n +,,,) the -.O estimated +/& million
deaths worldwide $rom COPD
!n 011,) COPD was ran2ed 0+th as aburden o$ disease3 by +,+, it is pro4ectedto ran2 5th
1-
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1.
Cigarette
smo!e
l*eolar 'acrophage
Neutrophils
58)- an" '$-9 in COPD
58)-
'$-9
.pithelial cells
58)-
'$-9
8)- B
IL-8 ge#e
'$-9
1.
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+P
Mucus gla#$ h"perplasia
/o%let cell h"perplasia
Mucus
e#sor" #er*eCholi#ergic #er*e
ACh
8E
Neutrophils
.pitheliu'
'8)$A##A5'O8
C"toi#esRO
? Acetylcholine? 5achy!inins? Proteinases neutrophil elastase? Cyto!ines 0TNF- 1
? O(i"ants
? :rowth factors
? ↑ #;C genes #;C
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Chronic%ronchitis
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Presence of chronic
pro"uctive cough for@ months in each of
2 successive years in a
patient in whom other
causes of chronic coughhave been e(clu"e"
Air passagenarro*e( ,+pl
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2121
Bronchus
?all thic!ening
inflammation
-- mucus glan"
hypertrophy
+ecretions
Alveoli
?all thinning -inflammation -
elastolysis
Coalescence
Elasticity
Bronchiole
?all thic!ening
inflammation
repair-- remo"eling
$oss of alveolar
attachments
THM
PPO2
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COPD Pathology and Abnormal 6reathing 7echanics
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+ Airway resistance
8 9lastic recoil 9xpiratory #ow
limitation
+ -or2 o$breathing:purse lps
Dyspnea) cough andother respiratory 8 ;uality o$ li$e
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2323
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!ator resio yg lain
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Ris2 >actors $or COPD
8utrition8utrition
'nfections'nfections
+ocio-economic+ocio-economic
statusstatus
Aging PopulationsAging Populations Agingpop
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2-
Pero2o2 6aru
Setiap hari:
14,000 hingga 15,000 golongan
muda dari negara berpendapatantinggi menjadi perokok
68,000 hingga 84,000 golongan
muda dari negara berpendapatanrendah dan sederhana menjadiperokok
?orl" Ban! 7eport 1666
S o < r c e 3 A C o r l ( a n 1 ; < , l i c a t i o n
2-
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2.2.
In'onesia ( ) %esar *egarPengonsmsi +oo
NegaraNegara JumlahJumlahPerokokPerokok(Sumber:(Sumber:
WHO)WHO)
% Pria% PriaPerokokPerokok(Sumber:(Sumber:
WHO)WHO)
ChinaChina 350,000,00350,000,0000
53.%53.%
!n"ia!n"ia #$0,000,00#$0,000,0000
$.%$.%
!n"on!n"one&iae&ia '$,00,'$,00,000000 '.0%'.0%
+ource1,http>>bola,o!eone,com>in"e(,php>7ea"+tory>2//9>//2>1/>www,republi!a,co,i">!oranG"etail,aspFi"@16/1%!atGi"@ 9,
,http>>www,tempointera!tif,com>hg>nasional>2//%>/@/>br!2//%/tahun4
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2020
+esio meroo
Riwayat mero2o2 Pero2o2 pasi$
Pero2o2 a2ti$
6e2as pero2o2 Dera4at berat mero2o2 inde2s 6rin2man
(!6* yaitu per2alian 4umlah rata=rata batangro2o2 per hari di2ali2an lama ro2o2 dalam
tahun , ? +,, ringan
+,, ? @,, sedang
@,, berat
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2:
Tol
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Perbandingan 6ahan dalamAsap Aliran 'tama dan Asap AliranSisi
a"ah niko*in
+&e*on
ar
Hi"rogen &iani"
-arbon monok&i"a
oluen
en/en
+nilin
Nitrosamin (bahan karsinogen)
$ kali lia*1gan"a
$25 kali gan"a
3 kali gan"a
2' kali gan"a
5 kali gan"a
'2 kali gan"a
#0 kali gan"a
30 kali gan"a
50 kali gan"a
Asap Aliran 'tama vs Asap Aliran Sisi
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$ung
Cancer
12@///
Other
Cancers@@///
Chronic $ung
Diseasepeny,paru
!roni!4
%////
+tro!e
23///
'schemic
Heart
Disease69///
Other
Diagnoses
9@///
+ource CDC ##?7 302/4
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Dera1at Peny.Par O"strsi5roni ai"at asa$ roo
Stage , (at ris2* normal spirometry
chronic symptoms o$cough and sputum
production Bchronic non=
obstructive bronchitis
Stage ! (mild* >90:>C E /,F
>90 G,F o$
predicted
-ith or without chronicsymptoms (cough)sputum) dyspnea*
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Dera1at 'a
Stage !! (moderate* >90:>C E /,F
>90 H,F and E
G,F o$ predicted
!!AI >90 5,F and
E G,Fo$ predicted
!!6I >90 H,F and
E 5,Fo$ predicted
-ith or without chronicsymptoms (cough)sputum) dyspnea*
!mportant stage $orintervention
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Dera1at tiga
2men1 mat4 Stage !!! (severe* >90:>C E /,F
>90 E H,F o$
predicted) or
>90 E 5,F o$ predictedplus respiratory $ailureo$ clinical signs o$ rightheart $ailure
!dentifes a group o$
patients li2ely to reJuireoxygen) transplantation)lung volume reduction)or palliative:end=stagecare
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Patogenesis of COPD
Obstru2si yang ter4adi bersi$atireversibel
%er4adi 2arena perubahan stru2turalpada saluran na$as 2ecil
%er4asi in#amasi) fbrosis) metaplasisel goblet dan hipertropi otot polos
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#6$an'e' View of #tiology0 Pathogenesis an' Pathology in
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3-
$ gy g gyCOPD
3-
8o(ious stimulation
Chronic
inflammation
Destruction
repair an"remo"eling
Abnormal function
an" symptoms
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3.
%iomass !el an' COPD
3.'n"oor Air Pollution
)uture
COPD
case
)uture
asthmatic
)uture COPD
if smo!er
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3030
',M$-OM'CO.G/
'$.-.MD,'$E#
E1$O'.E -O)'3 4#C-O'-o5acco 'moke
Occupaton)n"oor 6 out"oor
polluton
7 2
!+NOS!SO4 COP
!+NOS!SO4 COP
+P'7O#E57=
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3:
Spirometr+ for C;D@ASTHMA Diagnosis an( Classification
of Se&erit+
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Diagnosis "an'ing
Asma
SOP%
Pneumothora2s
Kagal 4antung 2roni2
6ron2ie2tasis
Destroyed lung
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COPD ( S7MPTOMS
CO'K. ALD 7'CO!D SP'%'7
DMSPLO9A = SNO-NM PROKR9SS!9
-.999
O9D97A (!> COR P'N7OLAN9*
-!L%9R 9AC9R6A%!OLS
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COPD ( SI8*S
.MP9R!L>NA%!OL D9CR9AS9D 9PALS!OL C.9S%
PRONOLK9D 9P!RA%!OL:Q-.999:P'RS N!PS S!KLS P'N7OLARM .MP9R%9LS!OL
ALD:OR R. (Q CARD!AC >A!N'R9*
CMALOS!S .MP9RCAPL!A
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4343
#A8A:E +5AB$E COPD
ED;CA5'O8 PHA7#ACO$O:'C 8O8 PHA7#ACO$O:'C
# stop smo!ing# "isease course# me"ication# prevention of "isease
progression# trigger avoi"ance
7E:;$A7
Broncho"ilator
-Anticholinergic#Beta 2 agonist#Iantin#+ABAJ$ABA
-$ABAJ'C+
As ne"ee"- E(pectorant
- #ucolytic
- Antio(y"ant
- Kaccine
#7ehabilitation#Kaccination#8utrition##echanical vent#surgical 'ntervention
8OLD 8 i' li f COPD
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8OLD 8i'elines for COPD
Diagnosis
Chroniccough:sputum
P>%s within
normal limits Lo symptoms
%reatment
Avoid ris2$actors(smo2ing
cessation*
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+tage / At 7is!
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8OLD 8i'elines for COPD
Diagnosis
>90 G,Fpredicted
>90:>C E/,F
-ith:withoutsymptoms
%reatment
Avoid ris2$actors
Short=acting
bronchodilatorPRL
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+tage ' #il"
8OLD 8i'elines for COPD
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4-
8OLD 8i'elines for COPD
Diagnosis
? 5,F ≤≤ >90 EG,F predicted
? >90:>C E/,F
? -ith:withoutsymptoms
%reatment
Avoid ris2 $actors
Regular therapy with≥ 0 bronchodilators
!nhaled corticosteroidsi$ signifcant symptoms
and lung $unctionresponse
Rehabilitation
4-
+tage '' #o"erate
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4.
8OLD 8i'elines for COPD
Diagnosis
H,F ≤ >90 E5,F predicted
>90:>C E /,F
-ith:withoutsymptoms
%reatment
Avoid ris2 $actors
Regular therapy with≥ 0 bronchodilators
Rehabilitation
!nhaled corticosteroids
i$ signifcant symptomsand lung $unctionresponse or i$ repeatedexacerbations
4.
+tage '''+evere
8OLD 8i'elines for COPD
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8OLD 8i'elines for COPD
Diagnosis >90 E H,F
predicted
>90:>C E /,F
Respiratory $ailure
Right=side=o$=the=
heart $ailure
%reatment
Avoid ris2 $actors
Regular therapy with
≥0 bronchodilators
!nhaled corticosteroids i$signifcant symptoms and lung
$unction response or repeatedexacerbations
Rehabilitation
%reatment o$ complications
Nong=term O+ therapy $or hypoxic
respiratory $ailure 9valuate $or surgical treatment
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+tage 'K Kery +evere
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4:
Acte #6acer"ations of
COPD 2A#COPD4 Common during winter months Symptoms
6reathlessness -hee"e Cough !ncreased sputum production
Causes iral in$ection (eg) rhinovirus*
9nvironmental causes (including smo2ing* Allergy 6acterial in$ection
4:
9The Downwar' S$iral:
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The Downwar' S$iral
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COPD
Airway
obstruction
E(acerbation
#ucus
hypersecretion
Continue"
smo!ing
$ung
inflammation
Alveolar
"estruction
'mpaire"mucus clearance
+ubmucosal glan"
hypertrophy
E(acerbation
E(acerbation
Hypo(emia
DEA5H
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Com"ine' "roncho'ilator thera$y;
Nong=acting beta=+ agonists incombination with theophylline !mproved bronchodilation with combined
salmeterol and theophylline than eitheralone) as well as a reduction inexacerbations in 0),,, patients
Nong=acting beta=+ agonists in
combination with anticholinergics !mproved bronchodilation with
salmeterol or $ormoterol and ipratropium
51
ZuWallack et al . Chest 2001;119:1347-56 ZuWallack et al . Chest 2001;119:1347-56
van Noor et al. !ur "es#$r % 2000;1&:157 van Noor et al. !ur "es#$r % 2000;1&:157
'(ur)o et al. Chest 2001; 119:1247-56 '(ur)o et al. Chest 2001; 119:1247-56
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β
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MA*A8I*8 #=AC#+%ATIO*S
AL%!6!O%!CS COL%RONN9D OMK9L 6ROLC.OD!NA%OR = 69%A AKOL!S%
AL%!C.ON!L9RK!C) Q%.9OP.MNN!L9 S%9RO!DS !L%'6A%!OL:9L%!NA%!OL %R9A% .9AR% >A!N'R9 !> PR9S9L%
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Anti"iotics
Acute exacerbations o$ COPD arecommonly assumed to be due to
bacterial in$ection) since they may beassociated with increased volume andpurulence o$ the sputum
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Manage #6acer"ations5ey Points
!nhaled bronchodilators (beta+=
agonists and:or anticholinergics*)theophylline) and systemic)pre$erably oral) glucocortico=steroids are eective $or thetreatment o$ COPD exacerbations (9vidence A*
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5-
Manage #6acer"ations5ey Points
Patients experiencing COPDexacerbations with clinical signs
o$ airway in$ection (eg)increased volume and change o$color o$ sputum) and:or $ever*
may beneft $rom antibiotictreatment (9vidence 69:
5-
COPD M 8 lCOPD M t 8 l
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5.5.
COPD> Management 8oalCOPD> Management 8oal
Relieve symptoms !mprove exercise tolerance !mprove health status Prevent and treat exacerbations 7odi$y natural course Reduce mortality Prevent and treat complications 7inimi"e side eects $rom
treatment
7e"ucing7e"ucing
airflowairflowobstructionobstruction
THE E7D
-hank yo%anah Not = 6ali
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-hank yo %anah Not = 6ali