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MEDICINE II
1.6E CHRONIC OBSTRUCTIVE PULMONARY DISEASE
COPD
Chronic obstructive pulmonary disease(COPD) is a
preventable and treatable disease with some significant extra
pulmonary effects that may contribute to the severity in
individual patients. Its pulmonary component is characterized
by airflow limitation that is not fully reversible. The airflow
limitation is usually progressive and associated with an
abnormal inflammatory response of the lungs to noxious
particles or gases.
Emphysema
Chronic Bronchitis
4.
Non-pharmacologic
Manage exacerbations
GENETIC CONSIDERATIONS
Alpha1-antitrypsin deficiency
Encoded by protease Inhibitor (PI) locus
S allele slightly reduced levels
Z allele markedly reduced levels
Caucasian populations
Piz individuals severe deficiency
AIRFLOW LIMITATION
1.
2.
3.
4.
1.
2.
3.
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Other complications are the fact that chest wall recoil remains
inward, which results in a threshold load at the start of
inspiration; and the flattened, shortened diaphragm muscle,
which leads to inefficiency in force generation.
Patients work harder to breathe.
The posteroanterior (PA) and lateral chest radiographs shown
here illustrate advanced findings of COPD and hyperinflation.
Chest radiograph changes occur late. The expanded chest,
retrosternal air space, low and flat diaphragm, and decrease in
peripheral vascularity highlight the major radiographic findings.
Hyperinflation is readily apparent.
LARGE AIRWAYS
Mucous gland enlargement
Goblet cell hyperplasia
Cough and mucus
Squamous metaplasia of bronchi
Smooth muscle hypertrophy
Bronchial hyperreactivity
SMALL AIRWAYS
Goblet cell metaplasia
Replacement of surfactant-secreting Clara cells
Luminal narrowing
Decreased alveolar attachments
LUNG PARENCHYMA
COPD: UNDERSTANDING THE DISEASE
PATHOGENESIS
Airflow limitation
Inflammation
Extracellular Matrix Proteolysis
Cell death
Ineffective repair
Cough
Dyspnea
Sputum
SYMPTOMS
DIAGNOSIS
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symptom
Low risk
More
symptoms
High risk
Less
symptoms
High risk
More
symptoms
GOLD 1-2
<=1
>=2
>=10
C
GOLD 3-4
1.5C END STAGE
RENAL DISEASE
>=2
0-1
<10
>=2
>=2
>=10
CLASSIFICATION BY SEVERITY
STAGE
CHARACTERISTICS
I: Mild
FEV1/FVC < 70%; FEV1 80%
predicted
With or without chronic symptoms
(cough, sputum)
II: Moderate
FEV1/FVC < 70%; 50% FEV1 <
80% predicted
With or without chronic symptoms
III: Severe
FEV1/FVC < 70%; 30% FEV1 <
50% predicted
With or without chronic symptoms
IV: Very Severe
FEV1/FVC < 70%; FEV1 < 30%
predicted or
FEV1< 50% predicted plus chronic
respiratory failure
LABORATORY FINDINGS
ABGs
Oximetry
Hypoxemia
PaCO2> 45mmHg
Elevated Hematocrit
Right ventricular hypertrophy
Bullae
CHEST RADIOGRAPHY
Patient
A
ASSESSMENT OF COPD
Symptoms (CAT or mMRC)
Degree of airflow limitation
Risk of exacerbation
Co-morbidities
COMBINED COPD ASSESSMENT
Characteristic Spirometry Exacerbations
Low risk
GOLD 1-2
<=1
Less
mMRC
0-1
CAT
<10
GOLD 3-4
TREATMENT
Smoking Cessation
Bronchodilators
Anticholinergic Agents
Beta Agonists
Inhaled Glucocorticoids
Parenteral Corticosteroids
Theophylline
Oxygen
Others
MANAGEMENT
REDUCE RISK FACTORS
Three types of counseling are especially effective: practical
counseling, social support as part of treatment, and social
support arranged outside of treatment (Evidence A).
Several effective pharmacotherapies for tobacco dependence
are available (Evidence A), and at least one of these
medications should be added to counseling if necessary and in
the absence of contraindications.
Middle-aged smokers who were able to successfully stop
smoking experienced a significant improvement in the rate of
decline in pulmonary function, returning to annual changes
similar to that of nonsmoking patients; all patients with COPD
should be strongly urged to quit and educated about the
benefits of quitting
Combining pharmacotherapy with traditional supportive
approaches considerably enhances the chances of successful
smoking cessation two principal pharmacologic approaches:
BUPROPION originally developed as an antidepressant
medication, and NICOTINE replacement therapy
BENEFITS OF SMOKING CESSATION
20 MINUTES
Circulation improves.
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1 YEAR
Only therapy
demonstrated to decrease mortality
Bupoprion
Nicotine Replacement
BRONCHODILATORS
Bronchodilators are prescribed on an as-needed or on a
regular basis to prevent or reduce symptoms.
Regular treatment with long-acting inhaled bronchodilators is
more effective and convenient than treatment with short-acting
bronchodilators, but more expensive. Evidence A new
Combining bronchodilators may improve efficacy and decrease
the risk of side effects compared to increasing the dose of a
single bronchodilator.
INHALED CORTICOSTEROIDS
Regular treatment with inhaled glucocorticosteroids is
appropriate for symptomatic COPD patients with an FEV 1 <
60% predicted (Stages III & IV) and repeated exacerbations
e.g. 3 in the last three years (Evidence A was B)
Mahler et al ARJRCCM 2002;166:1084-91
Jones et al ERJ 2003; 21: 66-73
Calverley et al Lancet 2003;361:449-56
Szafranski et al ERJ 2003;21: 74-81
This treatment has been shown to reduce the frequency of
exacerbations and improve health status (Evidence A new).
3 of these studies, glucocorticosteroid combined with a LABA
was more effective than the individual components
Mahler et al ARJRCCM 2002;166:1084-91
Calverley et al Lancet 2003;361:449-56
Szafranski et al ERJ 2003;21: 74-81
Resting hypoxemia
19 hrs > 12 hrs/day
NON-PHARMACOLOGIC THERAPY
General Medical Care
Influenza vaccine
Pneumococcal vaccine
Pulmonary Rehabilitation
Lung Volume Reduction Surgery
Lung Transplantation
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Long-acting bronchodilator
Regular Ipratropium + long acting beta2-agonist ?
plus high dose inhaled corticosteroid
A sustained
worsening of the condition, from the stable
Persistent/severe dyspnoea
Long acting bronchodilators
Recurrent exacerbations
INVASIVE VENTILATION
Endotracheal tube
Severe respiratory distress
Life-threatening hypoxemia
Severe hypercapnia and/or acidosis
Mortality
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