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Chronic obstructive lung disease(COPD)

 Is an obstructive lung diseases in which


irreversible lung damage has occured
types
1. Chronic bronchitis
2. Emphysema

although most of the time interrelated


PATHOGENESIS OF COPD
A. Chronic bronchitis

 Excess mucus production narrows the


airways; patients often have a productive
cough.
Inflammation and scarring in airways,
enlargement in mucous glands, and smooth
muscle hyperplasia lead to obstruction.
B. EMPHYSEMA

 Destruction of alveolar walls is due to relative excess in


protease (elastase) activity, or
 relative deficiency of antiprotease (α1-antitrypsin) activity in
the lung.
Elastase is released from PMNs and macrophages and digests
human lung. This is inhibited by α1-antitrypsin.
 Tobacco smoke increases the number of activated PMNs and
macrophages
This inhibits α1-antitrypsin, and increases oxidative stress on
the lung by free radical production.
causes
1. Smokers, 2nd hand smokers
2. Air polution
3. Occupational exposured e.g cool mining
4. a1-antitrypsin deficiency
5. Respiratory infections
Clinical features
 cough
Sputum production
Exertional dyspnea
 dyspnea may be severe in sever cases
Physical findings
Nicotine staining finger nails(smokers)
clubbing
Prolonged expiratory phase
Barrel chest
Use of accessory muscles for severe cases
Cachexia for advanced cases
Sings of right hear failure
Pink puffers and blue bloaters
 this term is not now widely used
 the clinical features are mostly overlapped
DIAGNOSIS
History and physical examination
Pulmonary function test( GOLD STANDARD)
Chest x-ray
ABG
ECG
PFTs
 Increased TLC, resudal volume and and
functional reserve capacity indicate air
trapping
Reduced DLC0 in emphysema
2. CHEST XRAY
Hyper inflation
Flat hemi diaphrams
Decreased peripheral vascular markings
Bulla some times
Some times diagnose pnemonia as a cause for
acute excacerbations
3. ABG
 Respiratory acidosis
Compensated metabolic alkalosis
4. ECG
 Signs of cor pormunale
1. right atrial enlargement
2. right ventricular enlargement
Complication of COPD
1. Acute exacerbation of copd
2. Respiratory failure
3. Pneumothorax
4. Cor pormunale
5. Polycythemia
6. Lung cancer
Acute exacerbation of copd
• as an acute change in a patient's baseline
dyspnea, cough, or sputum that is beyond
normal variability, and that is sufficient to
warrant a change in therapy.5 
• SEVERITY OF EXACERBATION
• DESCRIPTION
• Mild
• Can be controlled with an increase in dosage of regular
medications
• Moderate
• Requires treatment with systemic corticosteroids or antibiotics
• Severe
• Requires hospitalization or evaluation in the emergency
department
Management of exacerpation of copd
• Oxygenation and Ventilation
• Oxygen supplementation should be titrated to an oxygen
saturation level of at least 90 percent.
• High-flow oxygen devices deliver oxygen more reliably than
nasal prongs, but nasal prongs may be better tolerated.
• Noninvasive positive pressure ventilation (NIPPV) is indicated
if adequate oxygenation or ventilation cannot be achieved
using a high-flow mask.
• Patients requiring NIPPV should be monitored continuously
for decompensation.
• .
• If the patient cannot be adequately
oxygenated, complications, such as pulmonary
embolism or edema, should be considered.6
 Carbon dioxide retention is possible in
moderately and severely ill patients;
therefore, ABG should be measured 30 to 60
minutes after initiating oxygen
supplementation
• Therapeutic Options
• SHORT-ACTING BRONCHODILATORS
• Inhaled short-acting bronchodilators include beta
agonists and anti-cholinergics (e.g., ipratropium.
• 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.
•  If the patient is not already taking ipratropium, it can be
added to the treatment regimen.5
• 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).
• ANTIBIOTICS
• One half of patients with COPD exacerbations
have high concentrations of bacteria in their
lower airways.
•  Cultures often show multiple infectious agents
• 2nd and third generation
cephasporins,respirotory quinolones,
• Others doxycycline, augmentin etc
• Preventing Future Exacerbations
• Smoking cessation, immunization against influenza and
pneumonia, and pulmonary rehabilitation have been
shown to improve function and reduce subsequent COPD
exacerbations.
• Long-term oxygen therapy decreases the risk of
hospitalization and shortens hospital stays in severely ill
patients with COPD.
• indications for long-acting inhaled bronchodilators and
inhaled corticosteroids to improve symptoms and reduce
the risk of exacerbation is also needed

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