STEPTRACKERRESPIRATORY | PATHOLOGY + PHYSIOLOGY | HIGH-YIELD REVIEW

Emphysema & Chronic Bronchitis

COPD: chronic, poorly reversible airflow obstruction — destroyed alveolar walls, mucus-choked bronchi, or both.

FOCUS ON
Emphysema is protease (elastase) outweighing antiprotease. Smoking gives centriacinar, upper-lobe disease; α1-antitrypsin deficiency gives panacinar, lower-lobe disease plus liver injury. Chronic bronchitis is a clinical definition (cough ≥ 3 months in 2 consecutive years) with Reid index > 0.4. Only smoking cessation and long-term O₂ prolong survival.
TOPIC
DETAIL
MECHANISM
CLUE
COPD physiology
FEV1/FVC < 0.7, not fully reversible; ↑ TLC, ↑ RV, ↑ FRC.
Loss of elastic recoil and narrowed airways → air trapping
Smoking is the main cause
Centriacinar emphysema
Respiratory bronchioles destroyed; upper lobes.
Smoke recruits neutrophils/macrophages (elastase) and oxidants inactivate α1-AT
Smokers
Panacinar emphysema
Whole acinus destroyed; lower lobes; young adults.
α1-antitrypsin deficiency (SERPINA1, PiZZ); misfolded protein stuck in hepatocyte ER
Cirrhosis; PAS⁺ diastase-resistant liver globules
Paraseptal emphysema
Distal acinus next to pleura; apical bullae.
Unknown; often with centriacinar disease
Spontaneous pneumothorax in tall, thin young men
Emphysema — clinical
Dyspnea, pursed-lip breathing, barrel chest, prolonged expiration, weight loss, hyperresonance, flat diaphragms.
Alveolar walls lost → ↓ DLCO; hyperventilation keeps O₂ near normal until late
"Pink puffer"
Chronic bronchitis — definition
Productive cough ≥ 3 months in each of ≥ 2 consecutive years.
Clinical diagnosis
Smokers
Chronic bronchitis — pathology
Mucous gland hyperplasia (Reid index > 0.4), goblet cell hyperplasia, mucus plugs, squamous metaplasia.
Chronic irritation → hypersecretion and inflammation
Reid index = gland thickness ÷ wall thickness
Chronic bronchitis — clinical
Cyanosis, edema, recurrent infections (H influenzae, S pneumoniae, Moraxella), wheezes and crackles.
Early hypoxemia and hypercapnia → hypoxic vasoconstriction → pulmonary HTN → cor pulmonale; DLCO normal
"Blue bloater"; polycythemia
Management
Smoking cessation, long-term O₂ if hypoxemic (both prolong survival); LAMA/LABA; ICS for frequent exacerbators; vaccines; rehab.
Exacerbation: bronchodilators, steroids, antibiotics, non-invasive ventilation
High-flow O₂ can raise PaCO₂ in CO₂ retainers

Mechanism — two injuries from smoke

Smoke
→
Neutrophils, macrophagesElastase + oxidants
→
α1-AT overwhelmedor deficient
→
Elastin destroyedRecoil lost
→
Airways collapse on expirationAir trapping
Smoke irritation
→
Mucous gland hyperplasia
→
Mucus + inflammationNarrow bronchi, infections

Emphysema vs chronic bronchitis

FEATURE
EMPHYSEMA
CHRONIC BRONCHITIS
Defined by
Pathology: enlarged air spaces
Clinical: chronic productive cough
Key lesion
Alveolar wall destruction
Mucous gland hyperplasia
DLCO
↓
Normal
Blood gases
Hypoxemia late
Hypoxemia + hypercapnia early
Look
Thin, barrel chest, pursed lips
Cyanotic, edematous
Cor pulmonale
Late
Common

How it's tested

COMMON CONFUSIONDLCO separates them. Destroyed alveolar membrane lowers it in emphysema; chronic bronchitis leaves the membrane intact.
THE TRAPA 38-year-old non-smoker with basal emphysema and abnormal liver tests has α1-antitrypsin deficiency. Check the level and genotype, and screen the family.
YOUR APPROACHObstructive PFTs → DLCO → distribution (apical vs basal) → age and smoking history → α1-AT if the picture doesn't fit smoking.

If you see… think…

Young non-smoker with basal panacinar emphysema and cirrhosis → α1-antitrypsin deficiency
PAS⁺ diastase-resistant hepatocyte globules → PiZZ α1-AT
Smoker with upper-lobe centriacinar emphysema → smoking-related emphysema
Tall, thin young man with spontaneous pneumothorax → ruptured apical bleb
Productive cough every winter for 3 years in a smoker → chronic bronchitis
Reid index 0.6 → chronic bronchitis
Barrel chest, pursed-lip breathing, low DLCO → emphysema
Cyanotic, edematous, polycythemic smoker → chronic bronchitis with cor pulmonale
FEV1/FVC 0.55 with ↑ TLC → obstructive lung disease
Survival-improving COPD measures → stop smoking; long-term O₂ if hypoxemic