Prof. Dr. Syamsudin, M.

Biomed
Fakultas Farmasi
Universitas Pancasila Jakarta

Definitions:
Asthma: It's a chronic respiratory condition

that causes the airways to constrict become

inflamed and collect mucus. It can be
triggered by natural allergens, cigarette
smoke, pets, exercise or emotional stress.
COPD: is characterized by air flow
obstruction. The airflow obstruction is usually
progressive, not fully reversible and doesn't
change markedly over several months. The
disease is predominantly caused by smoking.

Diagnosis of COPD
It should be considered in patients over the

age of 35 who have a risk factor, generally

smoking, and who present with exertional
dyspnoea, chronic cough, regular sputum
production, frequent winter bronchitis or
wheeze. The presence of airflow obstruction
should be confirmed by performing spirometry.
All health professionals should be
competent in the interpretation of the
results

Faktor faktor resiko

Kebiasaan merokok merupakan satu - satunya penyebab kausal yang terpenting, jauh
lebih penting
dari faktor penyebab lainnya.

a. Riwayat merokok
- Perokok aktif
- Perokok pasif
- Bekas perokok

b. Derajat berat merokok dengan Indeks Brinkman (IB), yaitu perkalian jumlah ratarata batang rokok dihisap sehari dikalikan lama merokok dalam tahun :
- Ringan : 0-200
- Sedang : 200-600
- Berat : >600

2.
3.
4.
5.

Riwayat terpajan polusi udara di lingkungan dan tempat kerja

Hipereaktiviti bronkus
Riwayat infeksi saluran napas bawah berulang
Defisiensi antitripsin alfa - 1, umumnya jarang terdapat di Indonesia

Pathogenesis
Three processes:
Chronic inflammation
Imbalance of proteinases and anti-proteinases
Oxidative stress

Chronic Inflammation
Chronic inflammation in airways, parenchyma,

pulmonary vasculature
Inflammatory cells involved are:
Macrophages
T-lymphocytes (CD8)
Neutrophils

leukotriene B4
interleukin 8
TNF-

Pathology
Central Airways:
Enlarged mucus

secreting glands
Increase in goblet cells
Mucus hypersecretion

Peripheral Airways
Repeated cycles of

injury and repair

Increased

collagen/scarring in
airway wall

Pathology
Pulmonary vascular changes
Thickening of vessel wall (intima)
Increase in smooth muscle
Infiltration of vessel wall by inflammatory cells
As COPD worsens, more smooth muscle,

proteoglycans and collagen further thicken the

vessel wall

Pathophysiology
Mucus hypersecretion
Ciliary dysfunction
Airflow limitation
Pulmonary hyperinflation
Gas exchange abnormalities
Pulmonary hypertension
Cor pulmonale
Mucus hyperserection & ciliary dysfunction cough, sputum production

Diagnosis
A. Gambaran klinis

a. Anamnesis
- Keluhan
- Riwayat penyakit
- Faktor predisposisi
b. Pemeriksaan fisis
B. Pemeriksaan penunjang
a. Pemeriksaan rutin
b. Pemeriksaan khusus

Physical Examination
Thorax:
Barrel chest

Lungs
Decreased breath sounds
Wheezing

Cardiac
Right-sided heart failure

Edema, tender liver,

distended abdomen
Physical signs are rarely
apparent until significant
impairment of lung function has
occurred

Diagnostic Tests
Chest X-ray
Flattened diaphragms
Use to exclude other diagnoses

High resolution CT
Not routinely recommended
If in doubt about diagnosis of

COPD
If considering bullectomy or
lung volume reduction surgery

CBC
May see increased

hemoglobin/hematocrit
secondary to
hemoconcentration

ABG
Spirometry

Spirometry
Measure of FVC and FEV1
FVC = forced vital capacity

Maximum volume of air forcibly exhaled from the point of

maximal inhalation

FEV1 = forced expiratory volume in 1 second

Volume of air exhaled in the 1st second of the FVC maneuver

Calculate the FVC/FEV1 ratio

Normal ratio = 70/80%
COPD ratio = <70% pre-bronchodilator

are
COPD ratio = <80% post-bronchodilator
decreased

FVC & FEV

both

Essential to making the diagnosis of COPD

Spirometry
Bronchodilator Reversibility Testing
Perform in the initial assessment of COPD in
order to:
Exclude asthma
Establish best attainable lung function
Gauge patient prognosis
Guide treatment decisions

Arterial Blood Gas (ABG)

Obtain in patients with FEV1 < 40%

predicted OR
Clinical signs of respiratory or right heart
failure
Central cyanosis, ankle swelling, increase in

jugular venous pressure (JVP) OR

Respiratory Failure:
PaO2 < 60 mm Hg with or without PaCO 2 > 45

mm Hg while breathing air at sea level

Technique:
Obtain by arterial puncture; DO NOT USE finger

or ear oximeters

Other Tests
Alpha-1 antitrypsin
Consider in patients with COPD < age 45
Strong family hx of early COPD or with alpha-1
antitrypsin deficiency

Differential Diagnosis of
COPD
Asthma

Reversible airflow limitation

Early onset (childhood)
Symptoms vary day to day

Congestive heart failure

Volume restriction, NOT airflow

limitation
CXR with dilated heart,
pulmonary edema

Bronchiectasis
Large volumes of purulent

sputum
Commonly associated with
bacterial infection
Bronchial dilation and bronchial
wall thickening on CXR or CT

Tuberculosis

Onset at all ages

Chest x-ray with infiltrate or

nodular lesions

Obliterative bronchiolitis
Younger patients/non-smokers
May have a hx of rheumatoid

arthritis or fume exposure

CT shows hypodense areas
with expiration

Diffuse panbronchiolitis
Male/non-smokers
Chronic sinusitis
CXR and high resolution CT

show diffuse small

centrilobular nodular opacities
and hyperinflation

Medications
Goals
Prevent and control symptoms
Reduce frequency and severity of exacerbations
Improve health status
Improve exercise tolerance

No existing medications can modify the long-term

decline in lung function

Reduction of therapy once symptom control
occurs is not normally possible
COPD is progressive and over time will require
progressive introduction of more treatments to
attempt to limit the impact of these changes

Bronchodilators
Central to symptom management
Used in all stages of COPD severity

Inhaled forms are preferred

Can be prescribed as needed OR regularly to prevent or

reduce symptoms
Long-acting inhaled bronchodilators are more effective and
convenient (but are more expensive)
Combining drugs with different mechanisms and durations
of action may increase the degree of bronchodilation for
equivalent or lesser side effects
All categories of bronchodilators have been show to increase
exercise capacity without necessarily producing significant
changes in FEV1

Bronchodilators
Beta2-agonists
Short-acting: albuterol
Long-acting: salmeterol (Serevent), formoterol

(Foradil)

Anticholinergics
Short acting: ipratropium bromide (Atrovent)
Long acting: tiotropium bromide (Spiriva)

Methylxanthines (Theophylline)
Combination bronchodilators
Fenoterol/ipratropium (Duovent)
Salbutamol/ipratropium (Combivent)

GOLD Pocket Guide to COPD Diagnosis, Management, and Preve

Glucocorticosteroids
Use if FEV1 < 50% predicted and repeated exacerbations,

e.g. three in the last three years

Severe COPD and Very Severe COPD

Does not modify the long-term decline in FEV 1 BUT does

reduce the frequency of excacerbations and improves health

status
The combination of a long-acting beta2-agonist and an
inhaled glucocorticosteroid is more effective than the
individual components
Long-term treatment with oral glucocorticoids is NOT
recommended
Glucocorticosteroid (inhaled) reversibility testing
Treatment trial of inhaled glucocorticosteroids for 6 to 12 weeks

then repeat spirometry with and without bronchodilators

Patients most likely to respond to inhaled steroids have an FEV 1
increase of 200 mL and 15% above baseline post-bronchodilator
GOLD Pocket Guide to COPD Diagnosis, Management, and Prevention

Inhaled Glucocorticoids
Beclomethasone (Vanceril)
Budesonide (Pulmicort)
Fluticasone (Flovent)
Triamcinolone (Azmacort)

GOLD Pocket Guide to COPD Diagnosis, Management, and Prevention

Immunizations
Vaccines
Influenza yearly
Reduces serious illness and death in COPD patients
by approximately 50%
Give once yearly: autumn OR twice yearly: autumn
and winter

Pneumovax

Sufficient data to support its general use in COPD is

lacking, but it is commonly used

Other Medications?
Alpha-1 Antitrypsin Augmentation Therapy
Only if this deficiency is present in an individual should they

undergo treatment

Antibiotics
Prophylactic use is NOT recommended
Can be used in the treatment of infectious exacerbations of

COPD

Mucolytic agents
Overall benefits are small, so currently not recommended for

widespread use
Types:

Ambroxol
Erdosteine (Erdostin, Mucotec)
Carbocysteine (Mucodyne)
Iodinated gylerol (Expigen)

GOLD Pocket Guide to COPD Diagnosis, Management, and Prevention

Other Medications?
Antioxidant agents
N-acetylcysteine (Bronkyl, Fluimucil, Mucomyst)
Have been shown to reduce the frequency of exacerbations and could

have a role in the treatment of patients with recurrent exacerbations

More studies are needed

Immunoregulators
Not recommended at this time
No reproducible studies are available

Antitussives
Regular use is contraindicated in stable COPD since cough has a

significant protective role

Vasodilators
Inhaled nitric oxide
Can worsen gas exchange because of altered hypoxic regulation of ventilationperfusion balance and is contraindicated in stable COPD

GOLD Pocket Guide to COPD Diagnosis, Management, and Prevention

Other Medications?
Respiratory stimulants
Doxapram (IV)
Almitrine bismesylate
Not recommended in stable COPD

Narcotics
Oral and parenteral opioids are effective for treating dyspnea in

patients with advanced COPD

Use this with caution; benefits may be limited to a few sensitive

subjects

nebulized opioids: insufficient evidence re: efficacy

Miscellaenous:
Nedocromil
Leukotriene modifiers
Alternative healing methods
None have been adequately studied in COPD patients at this time

GOLD Pocket Guide to COPD Diagnosis, Management, and Prevention