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Definitions of COPD

Chronic bronchitis = defined in the basis of history as:

q        Persisted cough with sputum, for at least 3 consecutive months, ≥ 2 successive yrs.

q        Providing other causes of productive cough (e.g. bronchiectasis & untreated chronic asthma) have been excluded.

 

Emphysema = defined pathologically as:

q        Permanent dilation & destruction of lung tissue distal to terminal bronchioles.

q        With destruction of their walls.

 

A mixed syndrome of chronic bronchitis & emphysema is much more commonly seen.

 

Pathophysiology

 

Chronic bronchitis

õ     Pathology: hypertrophy of mucus-secreting glands of bronchial tree, which is evenly distributed throughout lung, esp. in large bronchi.

q       Initially

¡       Small airways are affected initially without development of significant breathlessness.

¡       Reversible à accounts for improvement in airway function if smoking is stopped early.

q       Progression à Squamous cell metaplasia + bronchial wall fibrosis à airflow limitation.

 

Emphysema

 

Loss of lung elastic recoil          à ↑ TLC.

Loss of alveoli                          à ↓ Gas transfer.

à Expiratory airflow limitation & air trapping

q       Damage & mucus plugging of small airways from chronic bronchitis

Rapid expiratory closure of small airways owing to loss of elastic recoil 

à VA / Q mismatch.

 

õ     Pathology:

Major

Minor

Centri-acinar = Centri-lobar (90%)

Hyper-inflation

Pan-acinar = Pan-lobar

Senile

Para-septal                               à

Bullous à pneumothorax

Irregular

Interstitial

 

CO2 is normally the major stimulant of respiratory center.

Prolonged high PaCO2    à ↓ This sensitivity

à Hypoxia becomes chief drive to respiration.

Attempt to correct hypoxemia by administration of O2 à ↓ Respiratory drive à ↑ PaCO2.

 

Pathogenesis

 

Cigarette smoking

q       Inflammation à PMNs à Release enzymes (protease + elastase + oxidants).

q       Inactivates anti-protease (e.g. α1-anti-trypsin).

à Damaged lung tissue

q       > a/w Centri-acinar (in emphysema).

 

Infections

q       Aggravating factor (not a cause!) à Release enzymes from PMNs à tissue damage.

 

α1-anti-trypsin deficiency (2% of emphysema cases)

q       3 main phenotypes: MM (normal), MZ (heterozygous), ZZ (homozygous deficiency).

q       > a/w Panacinar (in emphysema).

 

 

Clinical Features

 

Cough with sputum + wheeze + breathlessness: follow many years of smoker’s cough.

 

Complications

 

Respiratory failure

Cor pulmonale


written by: Khalid Bin Yaroof. FMHS, UAE University.

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