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 rata-rata batang
rokok dihisap sehari dikalikan lama merokok dalam tahun :
- Ringan : 0-200
- Sedang : 200-600
- Berat : >600

2. Riwayat terpajan polusi udara di lingkungan dan tempat kerja
3. Hipereaktiviti bronkus
4. Riwayat infeksi saluran napas bawah berulang
5. 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 leukotriene B4
T-lymphocytes (CD8) interleukin 8
Neutrophils 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 FEV
1
FVC = forced vital capacity
Maximum volume of air forcibly exhaled from the point of maximal
inhalation
FEV
1
= forced expiratory volume in 1 second
Volume of air exhaled in the 1
st
second of the FVC maneuver
Calculate the FVC/FEV
1
ratio
Normal ratio = 70/80%
COPD ratio = <70% pre-bronchodilator FVC & FEV are
COPD ratio = <80% post-bronchodilator both decreased
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 FEV
1
< 40% predicted OR
Clinical signs of respiratory or right heart failure
Central cyanosis, ankle swelling, increase in jugular
venous pressure (JVP) OR
Respiratory Failure:
PaO
2
< 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 FEV
1

Bronchodilators
Beta
2
-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 Prevention
Glucocorticosteroids
Use if FEV
1
< 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 ventilation-perfusion
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