PENYAKIT PARU

OBSTRUKSI
KRONIK (PPOK)
SUB-BAGIAN PULMONOLOGI
BAG.PENY. DALAM FK UNHAS
 Definisi COPD

Suatu kondisi penyakit yang dapat dicegah

dan ditangani, dikarakteristikkan dengan
keterbatasan aliran udara persisten yang
biasanya bersifat progresif dan
berhubungan dengan peningktan respon
inflamasi kronik jalan napas dan paru-paru
terhadap partikel atau gas yang berbahaya.
Eksaserbasi dan adanya penyakit komorbid
berkontribusi terhadap beratnya penyakit
pada setiap individu.
GOLD Update
2011
FAKTOR-FAKTOR RESIKO
Rokok
Pollusi udara
Riwayat infeksi saluran napas berulang
Defisiensi alfa1 antitripsin (AAT)
Lain-lain
Faktor Risiko COPD
Nutrition

Infections

Socio-economic
status

Aging Populations
GOLD Update
2011
 PATOGENESIS PPOK
Pajanan terhadap partikel atau gas
berbahaya dapat menyebabkan:
inflamasi paru,
kerusakan jaringan, mekanisme pertahanan,
dan perbaikan tubuh
sehingga menyebabkan hipersekresi
mukus, penyempitan, dan fibrosis saluran
napas, kerusakan parenkim, dan
perubahan vaskular menimbulkan
PPOK.

5
 PATHOGENESIS OF COPD
PARTICLE
NOXIOUS GASES

HOST FACTORS
ANTI OXIDANTS
[ environmental ]

LUNG INFLAMMATION

ANTI OXIDANTS ANTI PROTEINASES

[ genetic ]

OXIDATIVE STRESS PROTEINASE IMBALANCE

REPAIR REPAIR
MECHANISM MECHANISM

COPD
COPD ANTI PROTEASE ENZYME
1-Antitrypsin
 Mechanisms Underlying
Airflow Limitation in COPD

Small Airways Disease Parenchymal

Airway inflammation Destruction
Airway fibrosis, luminal Loss of alveolar
plugs attachments
Increased airway resistance Decrease of elastic recoil

AIRFLOW LIMITATION
GOLD Revision 2011
 PERBEDAAN PATOGENESIS
ASMA DAN PPOK

Perbedaan nyata baik dalam

hal mekanisme selular, jenis
mediator yang berperan, efek
inflamasi yang terjadi,
maupun dalam hal respons
terhadap cortikosteroid
8
PERBEDAAN INFLAMASI ASMA DAN PPOK

9 Eur Respir J 2003

OVERLAP
TUMPANGBETWEEN
TINDIH ANTARA
COPD AND
ASMA
ASTHMA
DAN PPOK

COPD ASTHMA
PPOK ASMA
Neutrophils
Neutrofil Eosinophils
Eosinofil

No AHR ~10%
HBr Jarang ~10% AHR HBr

No steroid response Steroid respon

Respons steroid Respons steroid
kurang

Wheezy bronchitis
10
Chest 2000; 117: S10-4.
Bronkitis Kronik
Gangguan saluran napas yang ditandai oleh batuk
kronik berdahak, minimal tiga bulan dalam setahun,
paling sedikit dua tahun berturut-turut. Tidak
disebabkan penyakit yang lain.

Emfisema
Suatu kelainan paru anatomis yang luas, ditandai
oleh pelebaran saluaran napas distal bronkiolus
terminalis, disertai kerusakan dinding alveoli.
 Penyakit Paru
Obstruktif Kronik
ATS
suatu penyakit yang dapat dicegah dan
diobati ditandai dengan keterbatasan aliran
udara yang tidak sepenuhnya reversibel.
Keterbatasan aliran udara ini bersifat
progresif dan berhubungan dengan
respons inflamasi paru abnormal
terhadap partikel atau gas beracun
terutama disebabkan oleh rokok.
PPOK mempengaruhi paru, tetapi juga
menimbulkan konsekuensi sistemik yang
bermakna
 Merokok
Merokok dan
dan Penurunan
Penurunan Faal
Faal Paru
Paru
(% Nilai pada umur 25 th)

10 Tidak pernah merokok

0 atau tidak sensitif
terhadap rokok
75
Merokok reguler dan
VEP1

sensitif terhadap Stop pada umur 45

50 th
rokok
Cacat
25 Stop pada umur 65 th
Meninggal
0
25 50 75
Umur (th)

Adapted with permission from Fletcher C, Peto R. BMJ. 1977;1:1645

 Emphysema. Graphic depiction of
centrilobular versus panlobular emphysema
PENYEBAB OBSTRUKSI SAL.NAPAS.
Reversibel :
1. Akumulasi sel inflamasi,mukus,eksudat
plasma di SP
2. Kontraksi otot polos pada SP perifer dan
sentral.
3. Hiperinflasi dinamik selama latihan fisik.

Ireversibel:
1. Fibrosis dan penyempitan SP
2. Hilangnya rekoil elastis disebabkan oleh
destruksi alv.
 Assessment of COPD

Assess symptoms
Assess degree of airflow limitation using
spirometry
Assess risk of exacerbations

Assess comorbidities

GOLD Revision 2011

 Symptoms of COPD

The characteristic symptoms of COPD are

chronic and progressive dyspnea, cough, and
sputum production.

Dyspnea: Progressive, persistent and

characteristically worse with exercise.

bChronic cough: May be intermittent and may

be unproductive.

Chronic sputum production: COPD patients

commonly cough up sputum.
GOLD Revision 2011
 COPD is a Multicomponent disease
Mucus-hypersecretion Goblet cell hyperplasia/
Reduced muco-ciliary metaplasia
transport Mucous gland
Mucosal damage hypertrophy
Muco-ciliary Structural Increased smooth
dysfunction changes muscle mass
Airway fibrosis
Alveolar destruction
Airway
inflammation Systemic
Airflow
limitation component
Poor nutritional
status
Reduced BMI
Loss of alveolar
Increased numbers of inflammatory
attachments Impaired skeletal
cells/ activation:
Loss of elastic muscle:
- CD8+ lymphocytes
recoil - weakness
- monocytes/macrophages
- neutrophils - wasting
Increased smooth
muscle contraction Elevated inflammatory mediators:
IL-8, TNF, LTB4 and oxidants
Protease/anti-protease imbalance
 Assessment of COPD
Assess symptoms
Assess degree of airflow limitation using
spirometry
Use the COPD Assessment
Assess risk ofTest(CAT)
exacerbations
Assess comorbidities
or
mMRC Breathlessness scale

GOLD Revision 2011

 CAT

COPD Assessment
Test (CAT): An 8-
item measure of
health status
impairment in COPD
(http://catestonline.or
g).
 Assessment of COPD
Assess symptoms
Assess degree of airflow limitation using
spirometry
Assess risk of exacerbations
Use spirometry for grading severity
Assess comorbidities
according to spirometry, using four
grades split at 80%, 50% and 30% of
predicted value

GOLD Revision 2011

 Classification of Severity of
Airflow Limitation in COPD*
In patients with FEV1/FVC < 0.70:

GOLD 1: Mild FEV1 > 80%

predicted

GOLD 2: Moderate 50% < FEV1 < 80%

predicted

GOLD 3: Severe 30% < FEV1 < 50%

predicted
GOLD Revision 2011
 Assessment of COPD
Assess symptoms
Assess degree of airflow limitation using
spirometry
Assess
Userisk of exacerbations
history of exacerbations and
Assess comorbidities
spirometry.
Two exacerbations or more within the last
year
or an FEV1 < 50 % of predicted value are
indicators of high risk

GOLD Revision 2011

Combined Assessment
of COPD
(GOLD Classification of Airflow Limitation)
4

(C) (D) >2

(Exacerbation history)
3

Risk
Risk

2
1
(A) (B)
1 0

mMRC 0-1 mMRC > 2

CAT < 10 CAT > 10
Symptoms
(mMRC or CAT score) GOLD Revision 2011
 Combined
Assessment of
COPD
When assessing risk, choose the highest
risk according to GOLD grade or
exacerbation history

Patie Characteristic Spirometric Exacerbatio mMR CAT

nt Classificatio ns per year C
n
Low Risk
A GOLD 1-2 1 0-1 < 10
Less Symptoms
Low Risk
B GOLD 1-2 1 >2 10
More Symptoms
High Risk
C GOLD 3-4 >2 0-1 < 10
Less Symptoms
High Risk 10
D GOLD 3-4 >2 >2
More Symptoms
GOLD Revision 2011
 Assess COPD
Comorbidities
COPD patients are at increased risk for:
Cardiovascular diseases
Osteoporosis
Respiratory infections
Anxiety and Depression
Diabetes
Lung cancer
These comorbid conditions may influence
mortality and hospitalizations and should be
looked for routinely, and treated
appropriately.
GOLD Revision 2011
 DIAGNOSIS
DIAGNOSIS
OF
OF COPD
COPD

1 2

EXPOSURE TO
SYMPTOMS RISK FACTORS
COUGH Tobacco Smoke
SPUTUM Occupation
DYSPNEA Indoor / outdoor
pollution

SPIROMETRY
 COPD
COPD
Complications
Complications
NUTRITIONAL
NUTRITIONAL CARDIO
CARDIO
DISORDER
DISORDER VASCULAR
VASCULAR
DISORDER
DISORDER
SYSTEMIC
SYSTEMIC
EFFECT
EFFECT
OF RESPIRATORY
SYSTEMIC
SYSTEMIC OF COPD
COPD RESPIRATORY
INFLAMMATOR MUSCLE
MUSCLE
INFLAMMATOR
YY DISFUNCTION
DISFUNCTION
RESPONS
RESPONS
PSYCHOLOGICAL
PSYCHOLOGICAL
FACTOR
FACTOR
ANXIETY
ANXIETY--
DEPRESSION
DEPRESSION

HANDICAP
HANDICAP//DISABILITY
DISABILITY
PENATALAKSANAAN PPOK
 Manage Stable
COPD:
Goals of Therapy
Relieve symptoms
Reduce
Improve exercise tolerance symptoms
Improve health status

Prevent disease progression

Reduce
Prevent and treat exacerbationsrisk
Reduce mortality

GOLD Revision 2011

 Manage Stable COPD:
All COPD Patients
Avoidance of risk factors
- smoking cessation
- reduction of indoor pollution
- reduction of occupational exposure
Influenza vaccination

GOLD Revision 2011

 Manage Stable COPD :

Patien Pharmacologic
First choice
Second choice Therapy
Alternative Choices
t
LAMA
SAMA prn or
A or LABA Theophylline
SABA prn or
SABA and SAMA
LAMA
SABA and/or SAMA
B or LAMA and LABA
Theophylline
LABA
ICS + LABA
PDE4-inh.
or
C LAMA and LABA SABA and/or SAMA
LAMA
Theophylline

ICS and LAMA or

ICS + LABA
ICS + LABA and LAMA or Carbocysteine
or
D ICS+LABA and PDE4-inh. or SABA and/or SAMA
LAMA
LAMA and LABA or Theophylline
LAMA and PDE4-inh.
 GOALS OF
2
COPD TREATMENT
SHORT
GLOBAL GOLD TERM
1 GOALS
SMOKING IMMEDIATE BENEFITS
CESSATION 3 RELIEF OF SYMPTOMS
[ BREATHLESSNESS ]
LONG TERM
GOALS

PREVENT DISEASE PROGRESSIVE

REDUCE EXACERBATIONS

IMPROVE QUALITY OF LIFE

IMPROVE EXERCISE TOLERANCE

REDUCE MORTALITY
The Vicious Cycle of
COPD
Shortness of
breath

Reduced
Anxiety
activities

Reduced Muscle
activities weakness

Depression &
Malnutrition
social isolation
DIFFERENTIAL DIAGNOSIS
Asthma : Onset early in life ( >>
childhood)
- Symptom vary from day
to day.
- Symptom at night/early
morning.
- Allergy,rhinitis,and/or
eczema.
DD cont.
Bronchiectasis :
- Large volumes of purulent
sputum.
- Commonly associated w/
b.infection
- Coarse crackles/clubbing
on auscult
-Chest X ray/CT sho ws
DD cont.
Tuberculosis :
- Onset all ages.
- Chest X-ray shows lung
infiltrate or
nodul lesions.
- Microbialogical
conformation.
DD cont.
Congestive Heart Failure :
- Fine basilar crackles on
auscultation.
-Chest X-ray delated heart,
pulmonary edema
-Pulmonary function tests indicate
volume
retriction, not airflow limitation
 COPD
Prevention is always better
than cure

you !
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