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Materi kuliah asma dan PPOK
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Dr. Syamsudin, M. BiomedFakultas 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 COPDIt 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 resikoKebiasaan merokok merupakan satu - satunya penyebab kausal yang terpenting, jauh
lebih pentingdari 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
PathogenesisThree processes:
Chronic inflammationImbalance of proteinases and anti-proteinasesOxidative stress
Chronic InflammationChronic inflammation in airways,
parenchyma, pulmonary vasculatureInflammatory cells involved are:
Macrophages leukotriene B4
T-lymphocytes (CD8) interleukin 8Neutrophils TNF-α
PathologyCentral Airways:
Enlarged mucus secreting glands
Increase in goblet cells
Mucus hypersecretionPeripheral Airways
Repeated cycles of injury and repair
Increased collagen/scarring in airway wall
PathologyPulmonary vascular changes
Thickening of vessel wall (intima)
Increase in smooth muscle
Infiltration of vessel wall by inflammatory cellsAs 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 klinisa. Anamnesis• - Keluhan• - Riwayat penyakit• - Faktor predisposisib. Pemeriksaan fisis
B. Pemeriksaan penunjang a. Pemeriksaan rutin b. Pemeriksaan khusus
Physical ExaminationThorax:
Barrel chestLungs
Decreased breath soundsWheezing
CardiacRight-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
SpirometryMeasure of FVC and FEV1
FVC = forced vital capacity Maximum volume of air forcibly exhaled from the point of
maximal inhalationFEV1 = forced expiratory volume in 1 second
Volume of air exhaled in the 1st second of the FVC maneuverCalculate the FVC/FEV1 ratio
Normal ratio = 70/80%COPD ratio = <70% pre-bronchodilator FVC & FEV areCOPD ratio = <80% post-bronchodilator both decreased
Essential to making the diagnosis of COPD
SpirometryBronchodilator 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
failureCentral cyanosis, ankle swelling, increase in
jugular venous pressure (JVP) ORRespiratory Failure:
PaO2 < 60 mm Hg with or without PaCO2 > 45 mm Hg while breathing air at sea level
Technique:Obtain by arterial puncture; DO NOT USE
finger or ear oximeters
Other TestsAlpha-1 antitrypsin
Consider in patients with COPD < age 45Strong 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
MedicationsGoals
Prevent and control symptomsReduce 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
BronchodilatorsCentral to symptom management
Used in all stages of COPD severity Inhaled forms are preferredCan be prescribed as needed OR regularly to prevent or
reduce symptomsLong-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
BronchodilatorsBeta2-agonists
Short-acting: albuterolLong-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
GlucocorticosteroidsUse 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 FEV1 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 FEV1
increase of 200 mL and 15% above baseline post-bronchodilator
GOLD Pocket Guide to COPD Diagnosis, Management, and Prevention
Inhaled GlucocorticoidsBeclomethasone (Vanceril™)Budesonide (Pulmicort™)Fluticasone (Flovent™)Triamcinolone (Azmacort™)
GOLD Pocket Guide to COPD Diagnosis, Management, and Prevention
ImmunizationsVaccines
Influenza yearly Reduces serious illness and death in COPD patients
by approximately 50% Give once yearly: autumn OR twice yearly: autumn
and winterPneumovax
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
COPDMucolytic 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 COPDNarcotics
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