Transcript
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COPD IS NOT ASTHMA !COPD IS NOT ASTHMA !
Different causes
Different inflammatory cells
Different mediators
Different inflammatory consequences
Different response to treatment
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A condition characterised by wide variationsover short periods of time in resistance toair ow in intrapulmonary airways
Variability usually assessed by measuringchange in air ow rates ( > 15% !V1"
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AirwayHyperresponsi!ene F L A M M AT O
F L A M M AT O
SymptomsSymptoms
#R$%%&RS#R$%%&RS
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NormalNormal During anDuring anattackattack
Epithelium Submucosa
Smoothmuscle
Lumen
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Normal airwayNormal airway InflamedInflamedairwayairwayNo thickening belowbasement membrane
Blood vessels
Eosinophil infiltrationShedding of
epithelial cells
ormation of!mucus" plugs
#ollagen thickening$asodilatation increasedvascular permeability
with oedema
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Asthma $nfammatory (rocessAllergen &)posure
%lucocorticoidsBloc* acti!ation o this pathway
Arachidonic acid Cycloo)ygenase
+ipo)ygenase Chemotactic (latelet acti!atingactors actor -(A./ Histamine (rostaglandins
+eu*otrienes
Broncho $ncreased 0ecreased Chemota)is
$ncreasedconstriction mucus mucus!ascular
secretion clearancepermea"ility
Symptoms o Asthma
Schleimer %&' Am Rev of Respir Dis. ())*+(,(-. pt ./0S1)
Inflammatory mediators released
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Smooth MuscleDysfunction
Air ayInflammation
Inflammatory cell infiltration2
activation
3ucosal edema
#ellular proliferation
Epithelial proliferation
Bronchoconstriction
Bronchial hyperreactivity
4ypertrophy2hyperplasia
Inflammatory mediator release
Symptoms "#acer$ations
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KOMPONEN ASMA
Epidemiology 2 pathology
Barnes &5
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AsthmaAsthmaNormalNormal
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#onstitutional andenvironmental factors whichinduce or incite
Allergens$ccupational
chemicalVirusesenetic factors
&rematurity'ac breast feeding) *mo ing
umes+ smo e+ sprays,iurnal variation
!-ercise+ cold airog!motionAllergens+anaphyla-isViruses,rugs . /*A0,+ eta
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A2$&3*4*#!&20 0'023 2$ ,!V!'$& 0 ! A/20 $,0!*$6 !7&$*4 ! 2$ #$66$/
!/V0 $/6!/2A' A''! !/*
0 ! . '3#$& $2!0/ 8 m9w9 1:;+;;; daltons
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AI%&A' H'P"%%"SPONSI("N"SS
Chemota#is"ota#in)%ANT"S) MCP*+
CC%,
Sur-i-alI.*,) I.*/)0M*CS1
(CAM*2(.A+
Adhesion
3onemarro
I.*+
I.*/
Air ay -essel
Acti-ation
Th4 cell
3asicproteinsMediators
"OSINOPHI. %"C%5ITM"NT IN ASTHMA
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Eosinophil
Mast cell
Aller6en
Th2 cell
MOD"%N (I"& O1 ASTHMAMOD"%N (I"& O1 ASTHMA
(asodilatationNe -essels
Plasma lea7 Oedema
Neutrophil
Mucushypersecretion
hyperplasia
Mucus plu6
Macrophage
3ronchoconstrictionHypertrophy hyperplasia
Choliner6irefle#
"pithelial sheddin6
Su$epitheli
fi$rosisSensory ner-acti-ation
Ner-e acti-ation
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A#2$ * 0/ 0/ 'A66A2$ 3& $#!**
6!,0A2$ *
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/!4 A' 6!#
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!7A60/A20$/1; 66< "&!A= '$ (C1;;'@60/ $ CD;%& !,0#2!,"#3A/$*0*+ *3/#$&!+
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#$/ 0 60/ A*2
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2 $4 '!*$6! A*2
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A9 9&9A9A*2
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Chronic o$structi-e pulmonary disease isChronic o$structi-e pulmonary disease isdefined asdefined as
88a disease state characterised $y thea disease state characterised $y thepresence of airflo o$struction due topresence of airflo o$struction due tochronic $ronchitis or emphysema9 thechronic $ronchitis or emphysema9 theairflo o$struction is 6enerallyairflo o$struction is 6enerallypro6ressi-e) may $e accompanied $ypro6ressi-e) may $e accompanied $yair ay hyper*reacti-ity) and may $eair ay hyper*reacti-ity) and may $epartially re-ersi$le:partially re-ersi$le:
American Thoracic Society 2;;/
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acts About #$&,#$&, is the D th leading cause of death in the4nited *tates (behind heart disease+ cancer+and cerebrovascular disease"9
0n H;;;+ the
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Ci6arette smo7e
Alveolar macrophage
Neutrophil
P%OT"AS"S
Al-eolar all destruction
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SP5T5M C'TO@IN"S IN COPD
COPD patients: 2!" #$!2y% &E' ( ) $*! #* pre,icte,
L
A T N 1 *
< n m o
l ! l = B
Controls
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COPD ASTHMA
Neutrophils
No AH%
No steroid response
"osinophils
AH%
Steroid response
E2FG
&hee y $ronchitisJ
O("%.AP 3"T&""N COPD AND ASTHMAO("%.AP 3"T&""N COPD AND ASTHMA
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Mucus secretion
N1* 3
I.*>
Neutrophilrecruitment
TN1* a
%"ACTI(" OK'0"N SP"CI"S INCOPD
Plasma lea7 3ronchoconstrictionIsoprostanes
ANTIOKIDANTS(itamins C and "
N *acetyl cysteine0lutathione analo6uesNitrones
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Neutrophil elastase
Cathepsins MMP*2) MMP*;)MMP24 0ran ymes)perforins Others LL
P%OT"AS"*ANTIP%OT"AS" IM3A.ANC" IN COPP%OT"AS"*ANTIP%OT"AS" IM3A.ANC" IN COP
2*Antitrypsin S.PI "lafin TIMPs
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Alpha1.Antitrypsin ,eLciency!nMyme prevents loss of lungsNelastic Lbers,eLciency O &an.lobularemphysema
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Alpha1.Antitrypsin,eLciency&rogressive *$ in young patients
Q;% emphysema under D; yrsH% of all cases of #$&,&neumothora-+ esp9 failure+ #irrhosis
2reatment*top smo ingAvoid pollution@dust
ecombinant AA2ene therapy
(long arm chr 1D"
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&igh resol%tion '( scan sho)ing the characteristic #asalpanlo#%lar emphysema rather than the apical centrilo#%lar
disease seen in smo$ers )ho ha*e normal le*els of 1+antitrypsin
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SP
Mucus glan, hyperplasia
0o1let cell hyperplasia
Mucus
ensory nerveCholinergic nerve
AChN"
Neutrophils
Epithelium
IN1.AMMATION
Cyto3ines4O
Acetylcholine Tachy7inins Proteinases neutrophil elastase Cyto7ines 5TN&/ 6 O#idants
0ro th factors
M5C 6enes M5C/a) M5C>
M5C5S H'P"%S"C%"TION IN COPDM5C5S H'P"%S"C%"TION IN COPD
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A*2
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,! 0/0*0
0n amasi saluran napasabungan obstru si saluran napas ecil danerusa an paren im
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=4A'02A*
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a tor risi o
Asap ro o (:;% asus pero o @ mantan"&olusi udara
. dalam ruangan . luar ruangan
*tress o sidatif eneti
2umbuh embang paru
*osial ! onomi
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E(-./. A R-SK 4A'(.RSE(-./. A R-SK 4A'(.RS
NOXIOUS AGENT (tobacco smoke, pollutants, occupational agent )
COP
enetic factors
Respiratoryinfection
.thers NutritionNutrition InfectionsInfections
Socio*economic statusSocio*economic status
A0IN0 POP5.ATIONA0IN0 POP5.ATION
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#$&, . *36&2$6*#$4 < A/, 64#$0, *&4246,3*&/$!A . *'$ '3 & $ !**0V!
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#$&, . *0 /*
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#$/ 0 60/ #$&,*&0 $6!2 3 . $', 40,!'0/!*(,'#$"
!V! *0 0'023 ( !2AH A/, 0/
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#$/ 0 60/ #$&,*&0 $6!2 3 . $', 40,!'0/!*(,'#$"
!V! *0 0'023 ( !2AH A/, 0/
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F
2FF
4FF
,FF
+FF
/FF
2 4 , + / > ; 2F 22 242, 2+
P e a
7 f l o
< . ! m i n =
2 4 , + / > ; 2F 22 242, 2+
P e a
7 f l o
< . ! m i n =
Days
Prednisolone ,F m6 oLmL # 2+ days
Prednisolone ,F m6 oLmL # 2+ days
COPD
ASTHMA
F
2FF
4FF
,FF
+FF
/FF
T%IA. O1 ST %OIDS
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!liminate the irritant
*2$& *6$=0/#ounselling improves li elihood*mo ing cessation program&harmacotherapy
/icotine eplacement 2herapyupropion (?yban"
educe e-posure to environmental pollutants
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*mo ing #essation
*tops accelerated decline in !V10mproves possibility of o-ygen therapy beneLtsP.Q months after Ruitting8 end of cough@phlegm production1 year8 lung function increased P;mls1 year8 ris of *mall #ell 'ung #ancer halved5 years8 ris of any lung cancer halved
/o progression of #$&,*porting performance enhanced
6ethods of smo ing cessation
#ounselingJ /icotine replacementJ ehavior modiLcation
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$/#
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#$&, 6A/A !6!/2&A20!/2 !,4#A20$/ 2 !A2 !7A#! A20$/* !A '3 .
A/20 0$20#*+ *2! $0,*VA##0/!*(64#$'320#*"
!1Q
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#$&, & $ /$*0*!V1 C 19;' 5 3* . Q:% 1; 3* . D;%
V 5 3* . H5%
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%is7 1actors for COPD
Host 1actors 6enes -e'g' alpha(7antitrypsindeficiency/
4yperresponsivenessLung growth
"#posure 8obacco smoke9ccupational dusts and chemicalsInfectionsSocioeconomic status
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6A/A 0/!7A#! A20$/*A/20 0$20#*
#$/2 $''!, $73 !/
$/#0/24 A20$/@V!/20'A20$/ 2 !A2
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