Obstructive Lung Diseases
Pathology · Respiratory · lean revision notes
Obstructive Lung Diseases
Obstructive lung diseases are a group of disorders characterised by limitation of airflow, usually on expiration, due to increased resistance in the conducting airways. From a Pathology standpoint, the four classic entities are emphysema, chronic bronchitis, bronchial asthma and bronchiectasis — the high-yield "morphology + named structure" group that NEET PG loves to test as single-best-answer triggers (Reid index, Curschmann spirals, Charcot-Leyden crystals).
Definition & the obstructive vs restrictive divide
Obstructive disease = increased resistance to airflow because of partial/complete obstruction at any level (trachea → respiratory bronchioles). The hallmark on spirometry is a reduced FEV1/FVC ratio (< 0.7) with a relatively preserved or increased total lung capacity (air trapping).
| Feature | Obstructive | Restrictive |
|---|---|---|
| FEV1 | ↓↓ (markedly) | ↓ |
| FVC | ↓ or normal | ↓↓ |
| FEV1/FVC | ↓ (< 0.7) | Normal or ↑ |
| TLC | Normal/↑ (air trapping) | ↓ |
| Examples | COPD, asthma, bronchiectasis | Fibrosis, ARDS, kyphoscoliosis |
High-yield: The single discriminator between obstructive and restrictive disease is the FEV1/FVC ratio — it falls in obstruction and is preserved/raised in restriction.
The four COPD-spectrum diseases are often grouped as CABE: Chronic bronchitis, Asthma, Bronchiectasis, Emphysema.
1. Emphysema
Definition: Permanent, abnormal enlargement of airspaces distal to the terminal bronchiole, accompanied by destruction of alveolar walls without obvious fibrosis (the "without fibrosis" clause is examined). It is a disease of the acinus.
Pathogenesis — the protease–antiprotease & oxidant–antioxidant hypothesis
The acinar wall is destroyed when elastase (protease) activity exceeds antiprotease (α1-antitrypsin) activity.
Cigarette smoke → recruits neutrophils & macrophages → release elastase + reactive oxygen species → ROS inactivate α1-antitrypsin (a "functional α1-AT deficiency") → unopposed elastolysis → alveolar wall destruction.
- α1-antitrypsin (α1-AT) deficiency is the genetic cause; the PiZZ genotype (Pi = protease inhibitor) gives the lowest levels and severe panacinar emphysema, classically lower-lobe and in young non-smokers, plus liver cirrhosis (PAS-positive, diastase-resistant globules in hepatocytes).
- Matrix metalloproteinases (MMP-9, MMP-12 from macrophages) also contribute.
Morphological types (most-tested table)
| Type | Part of acinus | Location | Association |
|---|---|---|---|
| Centriacinar (centrilobular) | Central/proximal — respiratory bronchioles; distal alveoli spared | Upper lobes / apices | Smoking (most common type) |
| Panacinar (panlobular) | Entire acinus, uniformly | Lower lobes / bases | α1-AT deficiency |
| Paraseptal (distal acinar) | Distal acinus, near pleura/septa | Upper lobe, adjacent to fibrosis | Spontaneous pneumothorax in young adults; forms bullae |
| Irregular | Acinus irregularly involved | Around scars | Clinically silent; commonest overall (scar) |
High-yield: Centriacinar = smoking = upper lobe; Panacinar = α1-AT deficiency = lower lobe. Paraseptal emphysema causes spontaneous pneumothorax in tall young males and large apical bullae.
Clinical correlate — the "Pink Puffer"
- Emphysema-predominant patient: pink puffer — dyspnoeic, barrel chest, pursed-lip breathing, weight loss, mild hypoxia, often normal/low CO2 until late, uses accessory muscles.
- Gross: voluminous, pale lungs that do not collapse; bullae (> 1 cm) and blebs (subpleural).
- X-ray: hyperinflation, flat diaphragm, increased retrosternal air, decreased vascular markings.
High-yield: Emphysema chest X-ray = flattened diaphragm + increased retrosternal airspace + attenuated peripheral vessels. CT shows low-attenuation areas.
2. Chronic Bronchitis
Definition (clinical): Persistent productive cough for at least 3 months in 2 consecutive years, in the absence of other identifiable cause. This is one of the most quoted definitions in NEET PG.
Pathogenesis & morphology
The earliest and defining change is hypersecretion of mucus, beginning in the large airways.
- Hypertrophy of submucosal mucous glands in trachea & bronchi (large airways).
- Goblet cell hyperplasia/metaplasia in small airways (bronchioles) → mucus plugging, inflammation, fibrosis (chronic bronchiolitis / small airway disease), which is the main site causing airflow obstruction.
- Squamous metaplasia and dysplasia of bronchial epithelium (predisposes to carcinoma).
The Reid Index — the single most asked fact here
High-yield: Reid index = thickness of the submucosal mucous gland layer ÷ thickness of the bronchial wall (between epithelial basement membrane and perichondrium). Normal ≤ 0.4; in chronic bronchitis it is > 0.4 (often quoted > 0.5). A raised Reid index = mucous gland hypertrophy = chronic bronchitis.
Clinical correlate — the "Blue Bloater"
- Chronic-bronchitis-predominant patient: blue bloater — cyanosed, productive cough, hypoxia + hypercapnia, secondary polycythaemia, cor pulmonale (right heart failure with oedema), recurrent infections.
| Feature | Pink Puffer (emphysema) | Blue Bloater (chronic bronchitis) |
|---|---|---|
| Body habitus | Thin, wasted | Obese, oedematous |
| Cough | Late, scant | Early, copious sputum |
| Dyspnoea | Severe, early | Mild |
| Cyanosis | Late ("pink") | Early ("blue") |
| PaO2 | Mildly ↓ | Markedly ↓ |
| PaCO2 | Normal/low | ↑ (CO2 retainer) |
| Cor pulmonale | Late | Early & prominent |
| Elastic recoil | ↓↓ | Normal |
High-yield: Mnemonic — "Blue Bloater = Bronchitis" (both start with B). The blue bloater retains CO2 and develops early cor pulmonale and polycythaemia.
3. Bronchial Asthma
Definition: A chronic inflammatory disorder of the airways causing reversible bronchospasm, characterised by recurrent wheeze, cough, chest tightness and dyspnoea, with airway hyper-responsiveness.
Classification
| Type | Trigger / mechanism |
|---|---|
| Atopic (extrinsic, allergic) | Type I IgE-mediated hypersensitivity; positive family history, ↑ IgE, eosinophilia, skin-test positive; commonest type, begins in childhood |
| Non-atopic (intrinsic) | Viral infections, cold air, exercise, irritants; negative skin tests, often normal IgE |
| Drug-induced (aspirin/NSAID) | Samter triad: asthma + nasal polyps + aspirin sensitivity; via shunting of arachidonic acid to leukotrienes (cyclo-oxygenase inhibition) |
| Occupational | Fumes, dusts, gases |
Pathophysiology of atopic asthma
Allergen → dendritic cell presentation → TH2 cells → IL-4/IL-5/IL-13 → IgE class switching + eosinophil recruitment.
- Early (immediate) phase — allergen cross-links IgE on mast cells → degranulation → histamine, leukotrienes (LTC4/D4/E4), prostaglandin D2 → bronchoconstriction, increased vascular permeability, mucus.
- Late phase (4–24 h) — eosinophils (recruited by IL-5, eotaxin), neutrophils, more TH2 cells → sustained inflammation.
- Airway remodelling — sub-basement membrane fibrosis (thickening), smooth muscle hypertrophy & hyperplasia, mucous gland hypertrophy, angiogenesis.
High-yield: IL-5 = eosinophils, IL-4 = IgE class switching, IL-13 = mucus + IgE. Major basic protein from eosinophils damages epithelium.
Classic morphology & named structures (NEET PG gold)
- Curschmann spirals — whorls of shed epithelium forming spiral mucus plugs.
- Charcot-Leyden crystals — needle/bipyramidal crystals from eosinophil membrane protein galectin-10 (lysophospholipase).
- Creola bodies — clusters of sloughed epithelial cells.
- Mucus plugging of bronchi, goblet cell hyperplasia, thickened basement membrane, eosinophil-rich infiltrate.
High-yield: Curschmann spirals + Charcot-Leyden crystals + eosinophils in sputum = asthma. Charcot-Leyden crystals are made of galectin-10 / lysophospholipase.
Status asthmaticus & ABPA
- Status asthmaticus = severe, unrelenting attack unresponsive to therapy; can be fatal.
- Allergic bronchopulmonary aspergillosis (ABPA) — hypersensitivity to Aspergillus; very high IgE, central bronchiectasis, fleeting infiltrates.
4. Bronchiectasis
Definition: Permanent abnormal dilatation of bronchi and bronchioles caused by destruction of the muscle and elastic supporting tissue, resulting from or associated with chronic necrotising infection.
Note: Bronchiectasis is not a primary disease — it is the consequence of conditions causing obstruction + infection. The two key ingredients are obstruction and chronic infection.
Causes
- Obstruction — tumour, foreign body, mucus impaction.
- Congenital/hereditary — cystic fibrosis (commonest cause in children/young), Kartagener syndrome, intralobar sequestration, immunodeficiency.
- Necrotising infection — Staphylococcus, Klebsiella, TB (post-tubercular is a common cause in India), measles, pertussis, adenovirus.
- ABPA, rheumatic conditions.
Kartagener syndrome (primary ciliary dyskinesia)
High-yield: Kartagener triad = situs inversus + bronchiectasis + chronic sinusitis (± infertility). Caused by a defect in the dynein arms of cilia (immotile/primary ciliary dyskinesia) → defective mucociliary clearance + defective sperm motility + failed organ rotation in embryogenesis.
Morphology
- Usually affects lower lobes bilaterally, most severe in the distal/vertical air passages.
- Airways dilated up to 4× normal, visible almost to the pleural surface.
- Gross patterns: cylindrical, fusiform (varicose), and saccular/cystic.
- Histology: intense acute & chronic inflammation, desquamation of epithelium, ulceration, squamous metaplasia, fibrosis; in severe cases lung abscess.
Clinical features
- Severe, persistent cough with copious foul-smelling, purulent sputum, often worse in certain postures (postural drainage).
- Haemoptysis (can be massive), recurrent pneumonia, clubbing, exertional dyspnoea.
- Investigation of choice: High-resolution CT (HRCT) — shows "signet-ring sign" (dilated bronchus larger than its accompanying artery) and tram-track lines / lack of bronchial tapering.
High-yield: Investigation of choice for bronchiectasis = HRCT chest; the diagnostic radiological sign is the signet-ring sign.
Diagnosis & investigation of choice (overview)
- Spirometry — confirms obstruction: post-bronchodilator FEV1/FVC < 0.7 = COPD. In asthma, obstruction is reversible (≥ 12% and 200 mL improvement in FEV1 after bronchodilator).
- DLCO — reduced in emphysema (loss of alveolar surface), normal or raised in asthma/chronic bronchitis — a useful discriminator.
- HRCT — best for emphysema pattern, bullae, bronchiectasis.
- α1-AT level / phenotype — for young/non-smoker/lower-lobe emphysema.
| Disease | Site of obstruction | DLCO | Key test/feature |
|---|---|---|---|
| Emphysema | Acinus (alveolar wall loss) | ↓ | HRCT, ↓ recoil, α1-AT |
| Chronic bronchitis | Bronchi/bronchioles (mucus) | Normal | Clinical definition, Reid index |
| Asthma | Bronchi (reversible) | Normal/↑ | Reversibility, eosinophils |
| Bronchiectasis | Dilated bronchi + infection | Variable | HRCT signet-ring sign |
Management / drug of choice (concise)
- Asthma: Inhaled short-acting β2 agonist (salbutamol) for rescue; inhaled corticosteroid (ICS) is the cornerstone controller; add LABA, leukotriene receptor antagonists (montelukast — drug of choice in aspirin-sensitive/exercise asthma), and biologics (omalizumab = anti-IgE; mepolizumab = anti-IL-5) in severe disease.
- COPD: Smoking cessation (only intervention that alters natural history), long-acting bronchodilators (LAMA — tiotropium, LABA), ICS in frequent exacerbators, long-term oxygen therapy (improves survival when PaO2 ≤ 55 mmHg), vaccination.
- Bronchiectasis: Postural drainage/physiotherapy, antibiotics for exacerbations, treat underlying cause; surgery for localised disease.
- α1-AT deficiency: α1-antitrypsin augmentation therapy + smoking cessation.
Complications
- Cor pulmonale & right heart failure (especially chronic bronchitis — blue bloater).
- Secondary polycythaemia from chronic hypoxia.
- Spontaneous pneumothorax (paraseptal emphysema bullae rupture).
- Respiratory failure (type II — hypercapnic — in chronic bronchitis).
- Recurrent infection, lung abscess, amyloidosis (AA type) and massive haemoptysis in bronchiectasis.
- Increased risk of bronchogenic carcinoma in smokers (squamous metaplasia/dysplasia).
Key differentials
- Asthma vs COPD: asthma is reversible, younger onset, atopic history, eosinophilic, DLCO normal; COPD is largely irreversible, smoker, neutrophilic.
- Chronic bronchitis vs bronchiectasis: both produce sputum, but bronchiectasis sputum is copious, foul, purulent with clubbing and HRCT changes.
- Emphysema vs asthma on PFT: both obstruct, but emphysema has low DLCO and irreversible obstruction.
- Centriacinar vs panacinar: distribution (upper vs lower) and cause (smoking vs α1-AT).
Recently asked / exam angle
- "Reid index > 0.4 (or > 0.5)" → answer chronic bronchitis (mucous gland hypertrophy). Know the exact definition (gland layer ÷ wall thickness).
- "Curschmann spirals / Charcot-Leyden crystals" in sputum → bronchial asthma; Charcot-Leyden = galectin-10/eosinophil lysophospholipase.
- "Upper-lobe emphysema in a smoker" → centriacinar; "lower-lobe in young non-smoker + cirrhosis" → panacinar / α1-AT (PiZZ).
- "Spontaneous pneumothorax in a tall young male" → paraseptal emphysema / apical bullae.
- "Situs inversus + sinusitis + bronchiectasis" → Kartagener (dynein arm defect).
- "Pink puffer vs blue bloater" matching questions are recurrent.
- "Signet-ring sign on HRCT" → bronchiectasis.
- "Permanent enlargement of airspaces distal to terminal bronchiole without fibrosis" → verbatim definition of emphysema.
- "DLCO reduced" among obstructive diseases → emphysema.
- Samter/aspirin triad (asthma + nasal polyps + aspirin sensitivity) and the leukotriene mechanism.
Rapid revision
- Obstruction = ↓ FEV1/FVC (< 0.7); restriction = preserved/raised ratio with ↓ TLC.
- Emphysema = airspace enlargement distal to terminal bronchiole, alveolar wall destruction without fibrosis.
- Centriacinar = smoking, upper lobe; panacinar = α1-AT deficiency (PiZZ), lower lobe; paraseptal = pneumothorax/bullae.
- α1-AT deficiency also causes cirrhosis with PAS-positive, diastase-resistant hepatocyte globules.
- Chronic bronchitis = productive cough ≥ 3 months for 2 consecutive years; key lesion = mucous gland hypertrophy.
- Reid index > 0.4 (often quoted > 0.5) = chronic bronchitis = gland thickness ÷ wall thickness.
- Pink puffer = emphysema (thin, normal CO2); blue bloater = bronchitis (cyanosed, cor pulmonale, polycythaemia).
- Asthma = reversible, type I IgE / TH2 (IL-4, IL-5, IL-13) disease; sputum shows Curschmann spirals + Charcot-Leyden crystals (galectin-10).
- Montelukast is drug of choice in aspirin-sensitive & exercise-induced asthma; omalizumab = anti-IgE, mepolizumab = anti-IL-5.
- Bronchiectasis = permanent bronchial dilatation from obstruction + chronic infection; investigation of choice HRCT (signet-ring sign); commonest paediatric cause = cystic fibrosis.
- Kartagener syndrome = situs inversus + bronchiectasis + sinusitis, due to dynein arm defect (primary ciliary dyskinesia).
- DLCO is reduced only in emphysema among the obstructive diseases; smoking cessation is the only therapy altering COPD's natural history.