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PPOK, adalah penyakit yg bisa dicegah dan diobati,
ditandai dengan hambatan aliran udara menetap
biasanya bersifat progresif dan berkaitan dgn
respon inflamasi kronis pada jalan napas dan paru
terhadap paparan bahan bahan partikel atau gas
yang beracun.
Eksaserbasi dan penyakit komorbid berkontribusi
dalam tingkat keparahan pasien.
Global Initiative for Chronic Obstructive Lung Disease (GOLD) Gu
idelines, 2011 Available from http://www.goldcopd.com/
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COMMON PREVENTABLE & TREATABLE DISEASE
PERSISTENT AIRFLOW LIMITATION
chronic inflammatory response
EXACERBATIONS
COMORBIDITIES
noxious particles /gases
SEVERITY LEVEL
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SMALL AIRWAY DISEASE PARENCHYMAL DESTRUCTION
Airway inflammation Loss of alveolar attachments
Airway fibrosis, luminal plugs Decrease of elastic recoil
Increased airway resistance
Global Initiative for Chronic Obstructive Lung Disease (GOLD) Guide
lines, 2011. Available from http://www.goldcopd.com/
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PPOK merupakan penyebab utama morbiditas dan
mortalitas didunia.
Beban PPOK diperkirakan akan meningkat dalam
dekade yang akan datang karena peningkatan
bahan paparan penyebab PPOK dan meningkatnya
penduduk berusia lanjut.
PPOK juga terbukti meningkatkan beban ekonomi
keluarga dan masarakat.

Global Initiative for Chronic Obstructive Lung Disease (GOLD) Gu
idelines, 2006. Available from http://www.goldcopd.com/
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70

0
0 60
0
1
50 Men
x

s
h 40
t
a Women
e
D 30

r
e 20
b
m
u 10
N
0
1980 1985 1990 1995 2000
Source: US Centers for Disease Control and Preventi
on, 2002
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Genetika
Pertumbuhan paru
Paparan partikel
Gender
Asap tembakau
umur
Debu tempat kerja
Infeksi paru
Polusi dalam ruangan.
Status sosial ekonomi.
dari pemanasan dan masak
menggunakan kayu bakar. Asma & hipersensitif sal.
Polusi luar ruangan. napas
Bronchitis kronis


Global Initiative for Chronic Obstructive Lung Disease (GOLD) G
uidelines, 2011 Available from http://www.goldcopd.com/
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Global Initiative for Chronic Obstructive Lung Disease (GOLD) Guidelines, 2011,
Available from http://www.goldcopd.com/
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BAHAN INDUSTRI
KAYU BAKAR
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Lama sebagai perokok
Jumlah rokok sehari
Jenis rokok
Cara merokok
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Asap rokok
genetika Inflamasi paru
LUNG INFLAMMATION
Inflammatory cells
Inflammatory mediators

Oxidative stress
proteases
Perubahan anatomi
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Asap rokok
genetika Inflamas
i paru
LUNG INFLA
MMATION
Inflammato
ry cells
Menghambat Inflammato
ry mediators
Kerusakan paru Oxidative
stress
proteases

Perubahan anatomi Kerusakan paru
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Global Initiative for Chronic Obstructive Lung Disease (GOLD) Guidelines, 2006.
Available from http://www.goldcopd.com/
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Global Initiative for Chronic Obstructive Lung Disease (GOLD) Guidelines, 2006.
Available from http://www.goldcopd.com/
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Male (though, numbers of female patients
are increasing!)
Over 50 years old (mean 60)
Long and heavy smoking history
Middle to low socioeconomic status
Often associated with alcohol abuse
Disease already severe when first seek
medical help
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Typically smokers - mean 20 cigs/day for 20 years
Usually present in 5th decade of life with
productive cough or acute chest illness when the
disease is far advanced
DOE usual until 6th or 7th decade
Patients who are dyspnea give up activities
wheezing accompanying dyspnea may lead to
erroneous diagnosis of asthma

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Sputum production initially only in AM
daily volume rarely exceeds 60 ml
usually mucoid
Acute exacerbations characterized by
increased cough, purulent sputum, wheezing,
dyspnea, sometimes fever
Interval between exacerbations grows shorter
with disease progression
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THE BLUE BOATER THE PINK PUFFER
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A condition of the lung characterized by
abnormal, permanent enlargement of
airspaces distal to the terminal bronchiole,
accompanied by the destruction of their
walls, and without obvious fibrosis
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Cough productive of sputum
on most days during at least
three consecutive months for
more than two successive
years

More profound hypoxemia at
rest
Elevated PaCO with chronic
2
respiratory acidosis
Cor pulmonale with right heart
failure
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Sutherland, E. R. et al. N Engl J Med 2004;350:2689-2697
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The cycle of physical, social and psychososial consequenses of COPD



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COPD patients are at increased risk for:
Myocardial infarction.
Osteoporosis.
Respiratory infection.
Diabetes.
Lung cancer.
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COPD has significant extrapulmonary
(systemic) effects including:
Weight loss
Nutritional abnormalities
Skeletal muscle dysfunction
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A major differential diagnosis is asthma
In some patients with chronic asthma, a clear
distinction from COPD is not possible
In these cases, current management is
similar to that of asthma
Other potential diagnoses are usually easier
to distinguish from COPD
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Onset in mid-life
Symptoms slowly progressive
Long smoking history
Dyspnea during exercise
Largely irreversible airflow limitation

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Onset early in life (often childhood)
Symptoms vary from day to day
Symptoms at night/early morning
Allergy, rhinitis, and/or eczema also present
Family history of asthma
Largely reversible airflow limitation


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ACUTE
EXACERBATION
COPD
IN PATIENTS BASELINE
ACUTE CHANGE
DYSPNOEA-COUGH-
BEYOND DAY TO DAY
SUFFICIENT TO WARRANT
CHANGE IN THERAPY

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1
KEADAAN
MEMBURUK
DALAM WAKTU
SINGKAT
2
3 4
INFEKSI VIRUS
POLUSI UDARA
K

A
A
S
U HAEMOPHILUS INLUENZA U
S
A
A

K
STREPTOCOCCUS PNEUMONIA
MORAXELLA CATARRHALIS
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Symptoms
Exacerbations
Exacerbations
Deterioration
Exacerbations
End of Life
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1

2

3

4
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ACUTE
EXACERBATION
COPD
CAUSES OF EXACERBATION
CAN BE BOTH
INFECTIOUS AND
MEDICAL THERAPY
INCLUDES :
BROCHODILATOR
STEROID

ANTIBIOTICS
OXYGEN
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Assess and monitor
disease
Reduce risk factors
Manage stable COPD
Education
Pharmacologic
Non-pharmacologic
Manage exacerbations

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VARYING EMPHASIS WITH DIFFERING SEVERITY
Relieve symptoms
Prevent disease progression
Improve exercise tolerance
Improve health status
Prevent and treat complications
Prevent and treat exacerbations
Reduce mortality
Adapted from Global Initiative for Chronic Obstructive Lung Disease (GOLD)
Guidelines, 2006. Available from http://www.goldcopd.com/
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cough tobacco
sputum
occupation
shortness of breath
indoor/outdoor pollution
Required to establish diagnosis
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Spirometry should be performed after the
administration of an adequate dose of a short-
acting inhaled bronchodilator to minimize
variability.
A post-bronchodilator FEV /FVC < 0.70 confirms
1
the presence of airflow limitation that is not fully
reversible.
Where possible, values should be compared to
age-related normal values to avoid overdiagnosis
of COPD in the elderly.
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Diagnosis
Assessing severity
Assessing prognosis
Monitoring
progression
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FEV Forced expired volume in the first
1
second
FVC Total volume of air that can be
exhaled from maximal inhalation to
maximal exhalation
FEV /FVC% - The ratio of FEV to FVC,
1 1
expressed as a percentage.
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Determine the severity of the disease, its impact on
the patient's health status and the risk of future
events (for example exacerbations) to guide therapy.
Consider the following aspects of the disease
separately:
current level of patient's symptoms
severity of the spirometric abnormality
frequency of exacerbations
presence of comorbidities.
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Reduction of total personal exposure to tobacco
smoke, occupational dusts and chemicals, and
indoor and outdoor air pollutants are important
goals to prevent the onset and progression of
COPD.

Smoking cessation is the single most effective
and cost effective intervention in most
people to reduce the risk of developing COPD
and stop its progression (Evidence A).
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Bronchodilator medications are central to the
symptomatic management of COPD (Evidence A).
They are given on an as-needed basis or on a regular

basis to prevent or reduce symptoms & exacerbations.
The principal bronchodilator treatments are - agonists,
2
anticholinergics, and methylxanthines used singly or in
combination (Evidence A).
Regular treatment with long-acting bronchodilators is
more effective and convenient than treatment with
short-acting bronchodilators (Evidence A).
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The addition of regular treatment with inhaled

steroid to bronchodilator treatment is appropriate

for symptomatic severe COPD, very severe COPD

and repeated exacerbations (Evidence A).

An inhaled steroid combined with a long-acting -
2
agonist is more effective than the individual
components (Evidence A).
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A
B
C
D
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