kuliah 2 umy ,copd

8/16/2019 Kuliah 2 Umy ,Copd

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1

COPD(PPO

K)1


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2

Differential Diagnosis

2

Chronic

Bronchitis Emphysema

Asthma

COPD

AirflowObstruction


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3

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

3

Asthma

Emphysema

Bronchitis

Chronic

Bronchitis

trachea

bronchi

alveoli


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44


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55

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.


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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10/5819

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

19


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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

13


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1414

7is! )actors for COPD

Host )actors

>enes %e6g6 alpha1#antitr+psin (eficienc (eficienc+

H+perresponsi&eness

L


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15

COPD

15


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1-

!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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10

+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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29

Chronic%ronchitis

29

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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22

COPD Pathology and Abnormal 6reathing 7echanics

22

+ 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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24

!ator resio yg lain


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25

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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39

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

39


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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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35

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

35

#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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49

Diagnosis "an'ing

Asma

SOP%

Pneumothora2s

Kagal 4antung 2roni2

6ron2ie2tasis

Destroyed lung

49


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41

COPD ( S7MPTOMS

CO'K. ALD 7'CO!D SP'%'7

DMSPLO9A = SNO-NM PROKR9SS!9

-.999

O9D97A (!> COR P'N7OLAN9*

-!L%9R 9AC9R6A%!OLS

41


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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

42


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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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44

8OLD 8i'elines for COPD

Diagnosis

Chroniccough:sputum

P>%s within

normal limits Lo symptoms

%reatment

Avoid ris2$actors(smo2ing

cessation*

44

+tage / At 7is!


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45


Diagnosis

>90 G,Fpredicted

>90:>C E/,F

-ith:withoutsymptoms

%reatment

Avoid ris2$actors

Short=acting

bronchodilatorPRL

45

+tage ' #il"



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4-


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.


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



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40


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

40

+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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59

The Downwar' S$iral

59

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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52

β


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53

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%

53


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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

54


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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*

55


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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

kuliah 2 umy ,copd

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