CHRONIC OBSTRUCTIVE PULMONARY DISEASE

(COPD)

MUHAMMAD ILYAS

DEPARTEMEN PULMONOLOGY AND RESPIRATORY MEDICINE

FACULTY OF MEDICINE UNIVERSITY OF HASANUDDIN
DR. WAHIDIN SUDIROHUSODO HOSPILTAL
 INTRODUCTION

COPD is one of the

INTRODUCTION
major causes of
Preventable and treatable
disease, airway and/or alveolar
morbidity and mortality abnormalities, caused by
throughout the world significant exposure to noxious
particles or gases
COPD
Characterized by persistent Prevalence of COPD
airflow limitation that is appreciably higher in smoker
usually progressive and ex-smoker than in non
smoker, in those over 40 yo
and in men

GOLD 2017 Wang L, et al. Chin Med J

2017;130:2107-11
 COPD

Genes Tobacco smoke

Airway - Occupational dust /
hyperresponsiveness chemicals
Lung growth Air pollution
Infection
Socioeconomic status

Host Exposures
Factor
 Chronic Obstructive Pulmonary Disease
(COPD)

► COPD is currently the fourth leading cause of death

in the world.1

► COPD is projected to be the 3rd leading cause of

death by 2020.2

► More than 3 million people died of COPD in 2012

accounting for 6% of all deaths globally.

► Globally, the COPD burden is projected to increase in

coming decades because of continued exposure to
COPD risk factors and aging of the population.

1. Lozano R, Naghavi M, Foreman K, et al. Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: a
systematic analysis for the Global Burden of Disease Study 2010. Lancet 2012; 380(9859): 2095-128.
2. Mathers CD, Loncar D. Projections of global mortality and burden of disease from 2002 to 2030. PLoS Med 2006; 3(11): e442.

© 2017 Global Initiative for Chronic Obstructive Lung Disease

 PREVALENS PPOK

RISKESDA 2013,
Indonesia 3.7 % per mile, higher in male.
East Nusa Tenggara (10.0%), Sulawesi Tengah
(8.0%), Sulbar dan Sulsel 6.7 %
RISKESDA KEMENKES RI 2013
 Cigarette smoke
and other irritants

IL-1β

IL-6

TGF-β
TGF-β
FGF
CXCL9
CXCL10
CXCL11
Neurtofil-
elastase
Proteases Cathepsins
CTGF IFN-γ MMPs
CXCR3

Perforin

Fibrosis (small airways)

NE, MMP9
Alveolar wall destruction Mucus hypersecretion

Barnes JP. Imnonology. 2008; 8:183-192

Pathology, pathogenesis & pathophysiology

► Pathology
 Chronic inflammation
 Structural changes

► Pathogenesis
 Oxidative stress
 Protease-antiprotease imbalance
 Inflammatory cells
 Inflammatory mediators
 Peribronchiolar and interstitial fibrosis

► Pathophysiology
 Airflow limitation and gas trapping
 Gas exchange abnormalities
 Mucus hypersecretion
 Pulmonary hypertension

© 2017 Global Initiative for Chronic Obstructive Lung Disease

 PPOK

Hipersekresi mukus,
Disfungsi cilia, hambatan aliran
udara, hiperinflasi paru,
PATOFISIOLOGI gangguan pertukaran gas,
hipertensi pulmonal & Cor
pulmonal
 COPD has pulmonary and systemic
components
Inhaled substances +
Genetic susceptibility

Airway Mucociliary Structural

inflammation dysfunction changes Systemic
inflammation
Airway limitation

Breathlessness
Bronchitis: coughing, sputum production Weight changes Co-morbidities
Emphysema: hyperinflation, wheezing (e.g. diabetes, cardiovascular disease)
Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease, Global Initiative for Chronic Obstructive Lung Disease
(GOLD) 2016 Available from www.goldcopd.org
Diagnosis PPOK

Diagnosis :
Sesak, batuk, produksi sputum
Atau riwayat paparan faktor risiko

Spirometri :
↓ VEF1, ↓ KVP and rasio VEP1/KVP < 70%
Diagnosis and Initial Assessment

© 2017 Global Initiative for Chronic Obstructive Lung Disease

 Spirometry

© 2017 Global Initiative for Chronic Obstructive Lung Disease

Classification of severity of airflow
limitation

© 2017 Global Initiative for Chronic Obstructive Lung Disease

 ROLE OF SPIROMETRY

© 2017 Global Initiative for Chronic Obstructive Lung Disease

 Assessment of COPD
1. Assess symptoms

GOLD recommends:
Use the COPD Assessment Test (CAT),
or the mMRC Breathlessness scale,
Or CCQ (Clinical COPD questionnaire)

•The characteristic symptoms of COPD are chronic and progressive

dyspnea, cough and sputum production that can be variable from
day-to-day
 mMRC Dyspnoe scale
(modified Medical Research Council)

Tingkat Tidak terganggu oleh sesak napas

1 kecuali saat olah-raga berat.

Terganggu dengan sesak napas ketika

Tingkat
terburu-buru berjalan di tanah yang datar
2
atau mendaki tanjakan.

Berjalan lebih lambat pada permukaan

yang datar dibandingkan orang seusia
Tingkat karena sesak napas atau harus berhenti
3 untuk bernapas ketika berjalan pada
kecepatan sendiri di permukaan yang
datar.

Berhenti untuk bernapas setelah berjalan

Tingkat
90 meter atau setelah beberapa menit di
4
permukaan yang datar

Terlalu sesak untuk meninggalkan rumah

Tingkat
atau sesak saat berpakaian atau berganti
5
pakaian.
1. Assess symptoms
2. Assess degree of airflow limitation using spirometry
3. Assess risk of exacerbations
4. Assess comorbidities

• Use history of exacerbations & spirometry. Two exacerbations

or more within the last year or an FEV1 < 50% of predicted
value are indicators of high risk.

• One or more hospitalizations for COPD exacerbations should

be considered high risk
Source: GOLD guideline 2015
 ABCD Assessment Tool

© 2017 Global Initiative for Chronic Obstructive Lung Disease

 Combined COPD Assesment

4 ≥ 2 or ≥ 1
(C) (D)

(Exacerbation history)
Dleading to
of Airflow Limitation) hospital
high risk
(Gold Classification

high risk
3 less symptoms high symptoms admission

Risk
Risk

2 (A) (B) 1 (not leading

low risk low risk to hospital
less symptoms high symptoms admission)
1

CAT < 10 CAT ≥ 10

mMRC 0–1 mMRC ≥ 2

CAT : COPD assessment test Symptoms

mMRC : modified medical research council Breathlessness
FEV1 : forced expiratory volume in 1
second
Global Strategy for The Diagnosis, Management, And Prevention of Chronic Obstructive
Pulmonary Disease (updated 2015)..
 Differential Diagnosis

© 2017 Global Initiative for Chronic Obstructive Lung Disease

 Goals of treatment for stable COPD

• Relieve symptoms
Goals
• Improve of treatment
exercise tolerance REDUCE
for stable SYMPTOMS
COPD
• Improve health status

and

• Prevent disease progression

• Prevent and treat exacerbations REDUCE RISK
• Reduce mortality

GOLD 2017
 Management of Stable COPD

Identify and reduce exposure to known risk factors

► Identification and reduction of exposure to risk factors is important in

the treatment and prevention of COPD.

► Cigarette smoking is the most commonly encountered and easily

identifiable risk factor for COPD, and smoking cessation should be
continually encouraged for all individuals who smoke.

► Reduction of total personal exposure to occupational dusts, fumes,

and gases, and to indoor and outdoor air pollutants, should also be
addressed.

© 2017 Global Initiative for Chronic Obstructive Lung Disease

Correct diagnosis and early treatment are important
for patients with COPD

Prevent or delay progression to

Early detection of
symptomatic COPD
asymptomatic COPD
through smoking cessation

Early detection of Smoking cessation and other

symptomatic COPD interventions to reduce progression

Improve current health status and

disease impact using proven healthcare
interventions

Reduce risk of exacerbations and

potentially deaths through proven
healthcare interventions

Soriano JB, et al. Lancet 2009

 Treatment of Stable COPD

Pharmacologic treatment

© 2017 Global Initiative for Chronic Obstructive Lung Disease

 Treatment of Stable COPD

© 2017 Global Initiative for Chronic Obstructive Lung Disease

 Management of stable COPD:
non-pharmacologic
Treatment Who
Essential
Smoking cessation All patients who smoke
(can include pharmacologic treatment)
Pulmonary rehabilitation GOLD B,C,D patients
Recommended
Daily physical activity All patients
Depending on local guidelines
Flu vaccination Depending on local guidelines
Pneumococcal vaccination
Other treatments
Oxygen To patients with PaO2 ≤7.3 kPa (55 mmHg)/
SaO2 ≤88%* or PaO2 7.3–8.0 kPa
(55–60 mmHg)/SaO2 88%†
*Withor without hypercapnia confirmed twice over a 3-week period; †if there is evidence of pulmonary hypertension, peripheral
edema suggesting congestive cardiac failure, or polycythemia (hematocrit >55%) GOLD = Global initiative for chronic Obstructive
Lung Disease; PaO2 = partial pressure of oxygen in arterial blood; SaO2 = saturation of oxygen in arterial blood
GOLD 2017
 Smoking cessation has
the greatest capacity to
influence the natural
history of COPD.

If effective resources and time

are dedicated to smoking
cessation, long-term quit
success rates of up to 25% can
be achieved
GOLD 2017
 Smoking cessation strategies

Brief advice can be summarised as 5 As :

ASK : Enquire about smoking habits with every contact.

ADVISE : Strongly advise all smokers to quit.
ASSESS : Determine willingness to make an attempt to quit.
ASSIST : Aid the patient in quitting by referring for further
counselling and providing pharmacotherapy
ARRANGE: Schedule follow-up contact.

Non-pharmacological management of COPD. CME 2009: 27(4);162-164

 Smoking Cessation Therapies

Smoking Cessation Therapies

Safka KA, et al / Ulster Med J 2014;83(1):13-21

 Exacerbations of COPD

COPD exacerbations are defined as an acute worsening of

respiratory symptoms that result in additional therapy.

► They are classified as:

 Mild (treated with short acting bronchodilators only, SABDs)

 Moderate (treated with SABDs plus antibiotics and/or oral
corticosteroids) or
 Severe (patient requires hospitalization or visits the emergency
room). Severe exacerbations may also be associated with acute
respiratory failure.

© 2017 Global Initiative for Chronic Obstructive Lung Disease

Management of Exacerbations

© 2017 Global Initiative for Chronic Obstructive Lung Disease