Chronic obstructive pulmonary disease (COPD) is characterized by irreversible airway obstruction and lung impairment. The two most common conditions are chronic bronchitis and emphysema. Chronic bronchitis involves excessive mucus production due to smoking-induced airway inflammation. Emphysema is the abnormal enlargement of airspaces due to an imbalance between the protease elastase and its inhibitor. Symptoms include a productive cough, shortness of breath, and signs of pulmonary hypertension. Treatment involves smoking cessation, oxygen therapy, bronchodilators, steroids, and antibiotics for infections.

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CHRONIC OBSTRUCTIVE PULMONARY DISEASE
• Group of diseases characterized by airway obstruction, lung does not empty & air is trapped.
• Lung functions impaired (FEV1 , TLC)
• Obstruction is irreversible.
• Two most common conditions of COPD are
1. Chronic Bronchitis: Clinical entity & is defined as “Productive cough on most of the days for at
least 3 consequent months for more than 2 successive years.”
2. Emphysema: Pathological term & is defined as “abnormal & permanent dilatation of alveoli.”
➢ Etiology:
1. Smoking
2. Air pollution & biomass pollution
3. 1 antitrypsin deficiency
➢ Patho-physiology:
Chronic bronchitis:
• Smoking causes irritation of airways resulting in inflammatory changes with loss of respiratory
cillia & increase mucous secretion due to hypertrophy of mucinous glands.
• As excessive mucous is secreted & is not cleared due to loss of cillia, so mucous gets
accumulated in the respiratory passages hence body initiates cough reflex in order to clear
respiratory passages, But ongoing mucous accumulation not only increases incidence of
infections but also interfere with gases exchange (mucous plug obstructs gases exchange)
resulting in Cyanosis (PaO2< Hypoxia> & PaCO2 <Hypercapnia>). Hypoxia leads to
1. hematopoisis leading to Polycythemia(Increase RBCs production & hence Hb) &
2. vasoconstriction of pulmonary arteries leading to Corpulmonale via following mechanism:
• Vasoconstriction→Pulmonary HTN→Right ventricular failure→Corpulmonale
• Corpulmonale is characterised by Peripheral edema, Tender hepatomegally & JVP.
• Persons having these features (Cough,Cyanosis, Corpulmonale) are called Blue-Bloaters (Blue-
Cyanosis, Bloater-Edematous)
Emphysema:
• Alveoli normally expand during inspiration & squeeze (recoils) during expiration due to presence
of elastic tissues in alveolar wall.
• Elastase is produced from inflammatory cells (Neutrophils & Macrophages) & has capability of
destroying alveolar elastic tissues.
• Anti-elastase is an enzyme which prevents elastic tissue destruction by inhabiting enzyme
Elastase.
• In normal persons Elastase & Anti-elastase are balanced.
• When this balance is disturbed this causes elastase mediated alveolar damage:
o Elastase due to Smoking or Infections OR
o Anti-elastase as seen in 1 antitrypsin deficiency

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Elastase/Anti-elastase imbalance→Alveolar elastic tissue damaged→Alveoli unable to recoil (Alveoli
dilated, Lungs inflated & thus TLC increased)→Air trapping (Dyspnea predominant feature rather than
cough because no mucous secretion)→Slight variation in PaO2 & PaCO2→ No any significant hypoxia &
its further consequences.
• As these persons have no any significant hypoxia so they do not develop cyanosis & edema hence
are called Pink Puffers.
➢ Clinical features: Most of the patients have features of both Emphysema & Chronic Bronchitis.
1. Productive cough with chest tightness: Chest tightness is more pronounced during morning
because excessive mucous is collected during sleep, as patient clears mucous the chest tightness
is relieved.
2. Dyspnoea: Progressive
On examination:
Inspection:
o Barrel-shaped chest
o Patient is despnic
o Use of accessory muscles
o Pursing of lips
o Signs of Corpulmonale should also be noted
Palpation:
o Chest expansion decreased
o Apex beat not palpable
Auscultation:
o Bronchial breathing
o Crepitations at lung bases can be heard which disappears as person coughs
o Ronchi at expiration
Percussion: Hyper-resonance note
Blue Bloaters (Chronic Bronchitis) Pink Puffers (emphysema)
Major complaint is Productive cough Major complaint is dypnea
Patients usually of 30-40y age Patients are usually over 50y
Cyanosis common Cyanosis uncommon
Features of corpulmonale present like edema Features of corpulmonale absent
Hb usually elevated (15-18g/dl) Hb normal (15-15g/dl)
Significant variation in PaO2 & PaCO2 Slight variation in PaO2 & PaCO2
CXR shows prominent vascular markings CXR shows hyperinflation with flattened
diaphragm
PFTs (FEV1 & TLC usually normal) PFTs (FEV1 & TLC)

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➢ Investigations:
1. CXR: Shows vascular markings & Hyperinflation of lungs
2. ABGs: PaO2 & PaCO2
3. PFTs: FEV1 & TLC specially in Emphysema
4. Sputum C/S
5. ECG & Echo-cardiography: To rule out corpulmonale
6. 1 antitrypsin : Normal range is 2-4g/l
➢ Differential diagnosis:
1. Bronchial asthma
2. Bronchiectasis
3. Cystic fibrosis
4. Pneumonia
➢ Complications:
1. Respiratory failure
2. Secondary polycythemia (Chronic bronchitis)
3. Spontaneous pneumothorax due to rupture of Bullae
4. Pulmonary infections
5. Corpulmonale
➢ Management:
General:
1. Absolute cessation of smoking & change of occupation if exposed to smoke
2. Oxygen therapy
3. Steam inhalation to liquefy the sputum & to make it easier to cough out.
4. Chest physiotherapy to aid expectoration
5. Influenza & Pneumococcal vaccines to prevent infections.
Specific: Bronchodilators & steroids show good response.
Bronchodilators:
• Ipratropium bromide (Atem inhaler) 2-4 puffs x BD
• Albuterol (Ventoline) 2-4 puffs x BD
• Tab.Theograd 350mg x BD
Steroids:
• Becotide 2 puffs x BD
• Tab. Deltacortil 20-30 mg in divided doses (Only during acute exacerbations)
Antibiotics: In case of infections.
Surgery: Bullectomy→ removal of giant bullae in order to improve ventilation.