ASTHMA AND COPD.ppt

8/9/2019 ASTHMA AND COPD.ppt

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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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ASTHMA AND COPD.ppt

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