Supervisor : Dr.dr.noni N Soeroso, M.Ked(Paru), Sp.

P (K)
Journal reading
Co assistant’s Assignment
Monday, 12 November 2018
Journal Reading
Name :
1. Gilbert
Aknowledgement for our supervisor :
2. Harris Kristanto
3. Hanika Asyyifa
4. Siti Hasnita
Dr.dr.Noni N Soeroso, M.Ked(Paru), Sp,P (K)

5. Debby Anggraini Pulmonology and Respiratory Medicine Department

6. Aulia Rahman Medical Faculty of Sumatera Utara
7. Aquila Febe RSUP HAM/RS USU Medan
8. Ahmad Rafiqi
9. Femmy Legie
10. Mubarak Nisa
11. Justika U Aulya
12. Kevin Girsang

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Headline!
 Abstract
 Introduction
 Definition of Early COPD
 Pathoogenesis &Pathophysiology
 Challenges of Identifying Early COPD
 Diagnosis, Assesment of Early COPD
 Differential Diagnosis
 Treatment
 Prevention of Early COPD

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ABSTRACT
+ Chronic obstructive pulmonary disease (COPD) is characterized by
persistent respiratory symptoms and airflow limitation that is due to
airway and/or alveolar abnormalities usually caused by significant
exposure to noxious particles or gases.
+ The most common respiratory symptoms include dyspnea, cough
and/or sputum production
+ The main risk factor for COPD is tobacco smoking but other
environmental exposures may contribute.
+ COPD is, at present, the third leading cause of mortality worldwide

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DEFINITION
+ Chronic obstructive pulmonary disease (COPD) is a common,
preventable and treatble disease that is characterized by persistent
respiratory symptoms and airflow limitation that is due to airway
and/or alveolar abnormalities usually caused by significant exposure
to noxious particles or gases.
+ The chronic airflow limitation of COPD is caused by a mixture of
small airway disease (e.g., Obstructive bronchiolitis) and
parenchymal destruction (emphysema). The relative contriubtions of
which vary from person to person.

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Globally, there are around three million deaths annually, by 2030
there may be over 4.5 million deaths anually from COPD

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EPIDEMIOLOGY
+ It is estimated that the number of COPD cases was 384 million in
2010, with a global prevalence of 11.7%.
+ Globally, there are around three million deaths annually.
+ The prevalence of COPD is expected to rise over the next 30 years,
by 2030 there may be over 4.5 million deaths anually from COPD
and related conditions.

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ETIOLOGY
• Several distinct causes and pathogenic processes might lead to
limitation of airflow. Cigarette smoking is the most important risk
factor and cause for COPD and some definitions of COPD have
included smoking in the definition. However, other exposures,
including indoor and outdoor air pollution, can cause COPD.
.

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RISK FACTOR
+ Cigarette smoking
+ Indoor and outdoor air pollution
+ Workplace exposure
+ Genetic
+ Poor lung development
+ Age and gender
+ Recurrent lung infection
+ Hiperresponsif of bronchus
.

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PATHOGENESIS
.
CD8 cells Parenchymal
destruction
Macrophages
Airway
Irritants Neutrophils
inflammation
+
Mucus
Protease Hypersecretiom

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Challenges of identifying early COPD
+ . Distinguishing early from mild disease
Early implies a time in the natural history of COPD, either before the disease is
present or a time when the disease has not progressed to full clinical effect
+ Lung health and COPD natural histories
Lung volume and airflow continue to increase as the thorax grows, reaching a peak
in young adulthood (about 20 years of age). In healthy individuals, lung function
then plateaus for about 10 years, after which lung function is gradually lost.
Whether this loss is so-called normal ageing or represents a pathological process
remains undefined

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 Challenges of identifying early COPD
+ Early life events and COPD
Birthweight, prematurity, maternal smoking, and maternal nutrition have all been suggested as risk
factors. A multifactorial pathogenesis is supported by the idea that reduced early life lung function
itself is associated with reduced lung function in early adulthood (aged about 20–25 years)
+ Childhood and adolescent lung growth
Active smoking during childhood and adolescence compromises lung growth. Passive smoking in
childhood, independent of maternal smoking during pregnancy, is associated with reduced
maximum attained lung function. The presence of airways reactivity and blood eosinophilia,
presumably linked to asthma or related processes, is associated with reduced maximum attained
lung function

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Challenges of identifying early COPD
+ Plateau phase
After lung growth ceases in young adulthood (aged about 20–25 years), lung function
remains close to constant for about 10 years. Lung function then slowly decreases.37,38
Cigarette smoking shortens the duration of the so-called plateau phase of lung function
+ Accelerated loss of lung function
The idea that smokers lose lung function at an accelerated rate (about twice that of
nonsmokers) was lent support by the landmark study by Fletcher and colleagues

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Challenges of identifying early COPD
+ Interactions among natural histories
Although much remains unknown about the mechanisms that lead to the reduced lung
function in COPD, several distinct processes can contribute and these probably
synergise
+ Natural history beyond FEV1
Airflow limitation is used to define COPD, but it only partly captures the clinical
features of COPD. Cough and sputum probably result from airways metaplasia,
inflammation, and glandular hyperplasia. Dyspnoea in COPD is mostly due to dynamic
hyperinflation

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DIAGNOSIS COPD –history taking
+ history of smoking or ex-smoker with/without respiratory symptoms
+ History of irritant substance exposure
+ Predisposing factor in baby/child: intrauterine low birth weight , recurrent resp.
Tract infection, smoke, air pollution
+ Recurrent cough with/without sputum
+ Dyspnea with/without wheezing
+ Family history
+ History of entering hospital because of respiratory disease
+ Comorbid disease, such as: HF, osteoporosis, malignancy

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DIAGNOSIS
Chronic bronchitis dominant:
COPD –physical
examination
+ Patients may be obese
+ Frequent cough and expectoration are typical
+ Use of accessory muscles of respiration is common
+ Coarse ronchi and wheezing may be heard on auscultation
+ Patients may have signs of right HF (ie. Cor pulmonale), such as edema and cyanosis.

Emphysema dominant:
+ patients may be very thin with barrel chest
+ Typically have little or no cough or expectoration.
+ Breathing may be assisted by pursed lips and use of accessory respiratory muscles,
+ The chest may be hyperresonant, and wheezing may be heard

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DIAGNOSIS
Chronic bronchitis dominant:
COPD –physical
examination
+ Patients may be obese
+ Frequent cough and expectoration are typical
+ Use of accessory muscles of respiration is common
+ Coarse ronchi and wheezing may be heard on auscultation
+ Patients may have signs of right HF (ie. Cor pulmonale), such as edema and cyanosis.

Emphysema dominant:
+ patients may be very thin with barrel chest
+ Typically have little or no cough or expectoration.
+ Breathing may be assisted by pursed lips and use of accessory respiratory muscles,
+ The chest may be hyperresonant, and wheezing may be heard

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DIAGNOSIS COPD –Spirometry
+ Spirometry
 It is the most common lung function test to diagnose COPD
 It is the most reproducible and objective measurement of air flow limitation.
 It should measure the volume of air forcibly exhaled from the point of maximal
inspiration (forced vital capacity, FVC) and the volume of air exhaled during the
first second of this maneuver (forced expiratory volume in one second, FEV1), and
the ratio of these two measurements (FEV1/FVC) should be calculated.
 The spirometric criterion for airflow limitation remains a post-bronchodilator fixed
ratio of FEV1/FVC < 0.70.

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DIAGNOSIS COPD –Spirometry

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DIAGNOSIS COPD - Imaging
+ Chest X-Ray
• Hyperinflation (flattened diaphragms)
• Hyperlucency of the lungs
• Use to exclude other diagnose
+ CT- Scan
• Not routinely recommended
• If in doubt about diagnosis of COPD, example for detection of
bronchiectasis and COPD patients that meet the criteria for lung
cancer risk assesment.

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 DIFFERENTIAL DIAGNOSIS
All of the patients who present dyspnea, cough, and sputum production, the differential diagnosis
is broad (eg, heart failure, COPD, asthma, interstitial lung disease, etc). Typically, the finding of
persistent airflow limitation on pulmonary function testing and the absence of radiographic features
of heart failure or interstitial lung disease direct the clinician to a narrower differential such as :
+ COPD
+ Asthma
+ Bronchiectasis
+ Tuberculosis
+ Constrictive bronchiolitis
+ Diffuse panbronchiolitis.
Importantly, these conditions can commonly occur together, for example, patients with asthma may
develop COPD and patients with COPD may have bronchiectasis.

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DIFFERENTIAL DIAGNOSIS

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DIFFERENTIAL DIAGNOSIS

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MANAGEMENT – STABLE COPD
+ Smoking cessation
+ Pharmacological intervention

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MANAGEM
ENT –
STABLE
COPD

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MANAGEME
NT –
STABLE
COPD
Group a
Group b
Group c
Group D

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MANAGEME
NT –
STABLE
COPD
Group a
Group b
Group c
Group D

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MANAGEME
NT –
STABLE
COPD
Group a
Group b
Group c
Group D

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MANAGEME
NT –
STABLE
COPD
Group a
Group b
Group c
Group D

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Pharmacological therapy
1. Bronchodilators (Beta2agonists)
The principal action of Beta2agonists is to relax airway smooth muscle by
stimulating beta2-adrenergic receptors, which increasis cyclic AMP and
produces functional antagonism to bronchoconstriction.
a. SABA
Regular and as needed use of SABA improve FEV1 and symptoms
b. LABA
Formoterol and salmeterol are twice daily, while indacaterol is a once
daily LABA.

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Pharmacological therapy
2. Antimuscarinic drugs
Antimuscarinic drugs block the bronchoconstrictor effect of acetylcholine
on M3 muscarinic receptor expressed in airway smooth muscle.
a. SAMA (Short Acting Muscarinic Antagonist)
e.g : ipratropium, oxitropium
b. LAMA (Long Acting Muscarinic Antagonist)
e.g : tiotropium

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Pharmacological therapy
3. Methylxanthines
e.g : Theophylline
4. Combination bronchodilator therapy
- Combination of SABA and SAMA are superior to either medication
alone in improving FEV1 and symptoms
- Combination of LABA and LAMA increases FEV1 and reduces
symptoms compared to monotherapy.

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Pharmacological therapy
5. Anti-inflammatory agents
Long term azithromycin and erithromycin therapy reduce exacerbations
over one year
6. Inhaled corticosteroids
- An ICS combined with a LABA is more effective than the individual
components in improving lung function and health status and reducing
exacerbations in patient with exacerbations and moderate to very severe
COPD.
- Regular treatment with ICS increases the risk of pneumonia especially in
those with severe disease.

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Pharmacological therapy
7. PDE4 inhibitor
PDE4 inhibitor improves lung function and reduce moderate and severe
exacerbations.
8. Mucolytic/Antioxidants
Regular use of NAC and carbocystein reduces the risk of exacerbations in
select population.

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Want big impact? Use big image.

38
Want big impact? Use big image.

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Management of COPD Exacerbations
A COPD exacerbation is defined as an acute worsening of dyspnea and other
symptoms (e.g., increased sputum and mucus production and/or purulence,
and/or coughing and wheezing) that require additional therapy. The three
cardinal symptoms of COPD exacerbation include increases in dyspnea,
sputum volume, and sputum purulence.
The standard treatment for COPD exacerbations include bronchodilators
(e.g., SABA, anticholinergics), corticosteroids, and antibiotics.

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Management of COPD Exacerbations
SUPPLEMENTAL OXYGEN should also be initiated and titrated to achieve
an oxygen saturation of 88% to 92%.3 As an alternative to oxygen therapy,
oxygen via high-flow nasal cannula or noninvasive positive pressure
ventilation can also be used to improve oxygenation and ventilation and
decrease hypercarbia in acute hypoxemic respiratory failure.

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Management of COPD Exacerbations
SHORT-ACTING BRONCHODILATORS Inhaled short-acting
bronchodilators include beta agonists (e.g., albuterol, levalbuterol [Xopenex])
and anti-cholinergics (e.g., ipratropium [Atrovent]). These agents improve
dyspnea and exercise tolerance. The first step in treating a COPD exacerbation
is increasing the dosage of albuterol delivered via metered dose inhaler or
nebulizer. Levalbuterol is more expensive than albuterol but has similar
benefits and adverse effects. If the patient is not already taking ipratropium, it
can be added to the treatment regimen. Fixed-dose albuterol/ipratropium
(Combivent) is available.

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Management of COPD Exacerbations
CORTICOSTEROIDS Short courses of systemic corticosteroids increase the
time to subsequent exacerbation, decrease the rate of treatment failure, shorten
hospital stays, and improve hypoxemia and forced expiratory volume in one
second (FEV1). Administration of oral corticosteroids early in an exacerbation
decreases the need for hospitalization. High-dosage corticosteroid regimens
(methylprednisolone [Solu-Medrol], 125 mg intravenously every six hours)
and low-dosage regimens (prednisolone, 30 mg orally daily) decrease the
length of hospitalization and improve FEV1 compared with placebo.

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Management of COPD Exacerbations
ANTIBIOTICS One half of patients with COPD exacerbations have high concentrations of bacteria
in their lower airways. Cultures often show multiple infectious agents, including Streptococcus
pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, Mycoplasma pneumoniae, and viruses.
The use of antibiotics in moderately or severely ill patients with COPD exacerbations reduces the risk
of treatment failure and death. Antibiotics may also benefit patients with mild exacerbations and
purulent sputum. The optimal choice of antibiotic and length of use are unclear. Increasing microbial
resistance has prompted some physicians to treat exacerbations with broad-spectrum agents, such as
second- or third-generation cephalosporins, macrolides, or quinolones. The decision to use antibiotics
and the choice of antibiotic should be guided by the patient's symptoms (e.g., when a patient presents
with all three of the cardinal symptoms, or with increased sputum purulence plus one of the other
cardinal symptoms, or if the patient is mechanically ventilated (either invasive or noninvasive),
recent antibiotic use, and local microbial resistance patterns and are only recommended for 5 to 7
days for the following indications.

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Management of COPD Exacerbations
OTHER TREATMENT OPTIONS Parenteral methylxanthines, such as theophylline, are not
routinely recommended for the treatment of COPD exacerbations. These agents are less effective and
have more potentially adverse effects than inhaled bronchodilators. Several therapies lack adequate
evidence for routine use in the treatment of COPD exacerbations, including mucolytics (e.g.,
acetylcysteine [formerly Mucomyst]), nitric oxide, chest physiotherapy, antitussives, morphine,
nedocromil, leukotriene modifiers, phosphodiesterase IV inhibitors (drug class not available in the
United States), and immunomodulators (e.g., OM-85 BV, AM3 [neither drug available in the United
States]). summarizes the treatment options for acute COPD exacerbations.

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Pharmacological therapy
7. PDE4 inhibitor
PDE4 inhibitor improves lung function and reduce moderate and severe
exacerbations.
8. Mucolytic/Antioxidants
Regular use of NAC and carbocystein reduces the risk of exacerbations in
select population.

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COPD = chronic obstructive pulmonary disease; FEV1 = forced expiratory volume
in one second; MDI = metered dose inhaler; NA = not applicable; NIPPV =
noninvasive positive pressure ventilation; PaO2 = arterial partial pressure of
oxygen. 47
 Primary, Secondary and Tertiary
prevention
Primary prevention
+ Identification of modifiable risk factors of COPD has suggested
strategies to mitigate the risk
Secondary prevention
+ Lung function test (Spirometry) can be successfully used to assess
smoking cessation as a preventive measure for COPD progression

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Primary, Secondary and Tertiary
Tertiary prevention
prevention
+ (TORCH study) spirometry with fluticasone proprionate (13 mL/year),
salmeterol (13 mL/year), and the combination (16mL/year) compared to
placebo
+ (UPLIFT study) no significant difference in lung function loss between
patient given tiotropium versus placebo
+ The identification of individual with emphysema (by CT scan), chronic
bronchitis (by history), airway reactivity (by methacholine challenge)
+ Quantitative measures of disease severity in COPD, including dynamic
hyperinflation, execrise performance, activity levels, health status and
comorbidities.

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CONCLUSION
COPD is a major worldwide public health issue. Efforts to control cigarette
smoking will have a major effect on COPD prevention. However, smoking is
not the only risk factor for COPD and additional preventive efforts are needed.
The ability to assess disease progression combined with an understanding of
the complex and heterogeneous natural histories of COPD throughout the
entire life cycle is creating novel opportunities for preventive interventions,

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Thanks!
Any questions?

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