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
2. Harris Kristanto Aknowledgement for our supervisor :

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
8. Ahmad Rafiqi RSUP HAM/RS USU Medan

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 COPD –physical examination
Chronic bronchitis dominant:
+ 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 –physical examination
Chronic bronchitis dominant:
+ 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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MANAGEMENT –
STABLE COPD

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MANAGEMENT –
STABLE COPD
Group a
Group b
Group c
Group D

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MANAGEMENT –
STABLE COPD
Group a
Group b
Group c
Group D

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MANAGEMENT –
STABLE COPD
Group a
Group b
Group c
Group D

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MANAGEMENT –
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.

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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 prevention
Tertiary 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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