🫁 Pulmonary Diseases A Comprehensive Reference for Medical Students · Diagnosis & Management

1. Obstructive Lung Diseases

Definition Airflow limitation, especially during expiration. ↓ FEV₁/FVC ratio. TLC ↑ or normal.

Chronic Obstructive Pulmonary Disease (COPD)

• Chronic Bronchitis: Productive cough ≥3 months/year for ≥2 years. Hypertrophy of submucosal glands (Reid index >0.5).
• Emphysema: Permanent enlargement of airspaces distal to terminal bronchioles.
  • Centriacinar: Upper lobes, associated with smoking.
  • Panacinar: Lower lobes, α₁‑antitrypsin deficiency.
  • Paraseptal: Subpleural, risk of spontaneous pneumothorax.
• Clinical: Dyspnea, chronic cough, wheezing. "Pink puffer" (emphysema) vs. "Blue bloater" (chronic bronchitis).
• Diagnosis: Spirometry: FEV₁/FVC <0.70 post‑bronchodilator. CXR: hyperinflation, flattened diaphragms, increased retrosternal airspace.
• Management: Smoking cessation, bronchodilators (LAMA/LABA), inhaled corticosteroids (if frequent exacerbations), pulmonary rehabilitation, oxygen if resting PaO₂ ≤55 mmHg or SpO₂ ≤88%.
• α₁‑Antitrypsin Deficiency: Early‑onset panacinar emphysema + liver cirrhosis. PAS‑positive globules in hepatocytes. Treatment: augmentation therapy.

Asthma

• Chronic inflammatory disorder with reversible bronchoconstriction. Triggers: allergens, exercise, cold air, URI.
• Pathology: Airway remodeling, smooth muscle hypertrophy, mucus plugging (Curschmann spirals), eosinophils, Charcot‑Leyden crystals.
• Diagnosis: Spirometry: ↓ FEV₁/FVC, reversibility (≥12% and ≥200 mL increase post‑bronchodilator). Peak flow variability. Methacholine challenge.
• Classification (GINA): Intermittent, mild persistent, moderate persistent, severe persistent.
• Management: Stepwise therapy: SABA as needed, low‑dose ICS, LABA, leukotriene modifiers, biologics (omalizumab for allergic asthma).
• Status Asthmaticus: Severe attack unresponsive to initial therapy. Risk factors: normal/high PaCO₂, silent chest, pulsus paradoxus.

Bronchiectasis

• Permanent, irreversible dilation of bronchi due to chronic inflammation/infection.
• Etiology: Cystic fibrosis, post‑infectious (TB, pertussis), allergic bronchopulmonary aspergillosis (ABPA), primary ciliary dyskinesia.
• Clinical: Chronic productive cough, large‑volume purulent sputum, hemoptysis, clubbing.
• Diagnosis: High‑resolution CT (HRCT): "signet ring" sign, tram‑track opacities.
• Management: Airway clearance, bronchodilators, antibiotics for exacerbations, possible surgery for localized disease.

2. Restrictive Lung Diseases

Definition Reduced lung expansion → ↓ TLC, ↓ FVC, normal or ↑ FEV₁/FVC. Due to intrinsic lung disease (ILD) or extrinsic factors.

Idiopathic Pulmonary Fibrosis (IPF)

• Most common idiopathic interstitial pneumonia. Progressive fibrosis, usual interstitial pneumonia (UIP) pattern.
• Clinical: Older adults, insidious dyspnea, dry cough, fine inspiratory crackles ("Velcro"), clubbing.
• Diagnosis: HRCT: subpleural, basal predominance, honeycombing, traction bronchiectasis. Surgical lung biopsy if HRCT not definitive.
• Treatment: Antifibrotics (pirfenidone, nintedanib). Lung transplantation.

Sarcoidosis

• Multisystem granulomatous disease of unknown etiology. Non‑caseating granulomas.
• Pulmonary: Bilateral hilar lymphadenopathy, reticulonodular opacities. Often asymptomatic or Löfgren syndrome (erythema nodosum, arthralgia, BHL).
• Extrapulmonary: Uveitis, lupus pernio, hypercalcemia (↑ 1α‑hydroxylase in macrophages), cardiac involvement.
• Diagnosis: CXR staging (I: BHL only; II: BHL + infiltrates; III: infiltrates only; IV: fibrosis). Elevated ACE level. Tissue biopsy.
• Treatment: Corticosteroids if symptomatic/progressive. Methotrexate, anti‑TNF for refractory.

Hypersensitivity Pneumonitis (HP)

• Immune‑mediated reaction to inhaled organic antigens (e.g., bird proteins, moldy hay).
• Types: Acute (flu‑like 4‑6h post exposure), subacute, chronic fibrotic.
• Diagnosis: Exposure history, HRCT (centrilobular nodules, mosaic attenuation, air trapping), lymphocytosis on BAL.
• Treatment: Antigen avoidance, corticosteroids.

Pneumoconioses

Disease	Exposure	CXR/CT Findings	Notes
Silicosis	Sandblasting, mining, stone cutting	Upper lobe nodules, eggshell calcification of hilar nodes	↑ Risk of TB (silica impairs macrophage function)
Coal Worker's Pneumoconiosis	Coal dust	Small rounded opacities upper lobes; progressive massive fibrosis	May be asymptomatic; Caplan syndrome (RA + coal nodules)
Asbestosis	Shipbuilding, insulation, construction	Lower lobe fibrosis, pleural plaques, rounded atelectasis	↑ Mesothelioma, lung cancer (synergistic with smoking). Ferruginous bodies.
Berylliosis	Aerospace, electronics	Non‑caseating granulomas (sarcoid‑like)	Diagnosis: lymphocyte proliferation test to beryllium

Other Restrictive Causes

• Connective Tissue Disease‑ILD: RA (UIP pattern), Scleroderma (NSIP pattern, esophageal dilation), Polymyositis/Dermatomyositis.
• Drug‑induced ILD: Amiodarone, methotrexate, bleomycin, nitrofurantoin.
• Extrinsic Restriction: Obesity, kyphoscoliosis, neuromuscular disease (e.g., ALS, myasthenia gravis).

3. Pulmonary Infections

Pneumonia

• Typical (lobar): Streptococcus pneumoniae (rusty sputum), Haemophilus influenzae, Moraxella. Abrupt onset, fever, consolidation.
• Atypical (interstitial): Mycoplasma pneumoniae, Chlamydia pneumoniae, Legionella. Gradual onset, dry cough, extrapulmonary manifestations (bullous myringitis, hyponatremia with Legionella).
• Aspiration Pneumonia: Anaerobes (Bacteroides, Peptostreptococcus). Dependent lung segments (RLL superior segment, posterior upper lobes).
• Hospital‑Acquired / Ventilator‑Associated: Pseudomonas, MRSA, Acinetobacter.
• Immunocompromised: Pneumocystis jirovecii (ground‑glass opacities, ↑ LDH, treat with TMP‑SMX), CMV, fungal.
• Diagnosis: CXR, sputum culture, blood cultures, urinary antigen (Legionella, Pneumococcus).

Tuberculosis (TB)

• Mycobacterium tuberculosis. Airborne transmission.
• Primary TB: Ghon focus (lower lobe) + hilar node = Ghon complex. Usually asymptomatic.
• Reactivation TB: Upper lobe cavitary lesions (due to high O₂ tension). Symptoms: night sweats, weight loss, hemoptysis.
• Miliary TB: Hematogenous dissemination, "millet seed" nodules.
• Diagnosis: Interferon‑gamma release assay (IGRA) or PPD. Sputum AFB smear, culture, NAAT (GeneXpert).
• Treatment (RIPE): Rifampin, Isoniazid, Pyrazinamide, Ethambutol. Latent TB: Isoniazid or Rifampin.

4. Pulmonary Vascular Diseases

Pulmonary Embolism (PE)

• Thrombus (usually from DVT) obstructing pulmonary arteries.
• Risk factors: Virchow's triad (stasis, hypercoagulability, endothelial injury).
• Clinical: Sudden dyspnea, pleuritic chest pain, hemoptysis, tachycardia. Massive PE: hypotension, RV strain.
• Diagnosis: CT pulmonary angiography (gold standard). V/Q scan if renal insufficiency. Wells score, D‑dimer (high sensitivity, low specificity).
• ECG: Sinus tachycardia, S1Q3T3 pattern, right axis deviation.
• Management: Anticoagulation (heparin → warfarin or DOAC). Thrombolytics for massive PE with shock. IVC filter if anticoagulation contraindicated.

Pulmonary Hypertension (PH)

• Mean pulmonary artery pressure ≥20 mmHg at rest (right heart cath).
• WHO Groups:
  1. Pulmonary Arterial Hypertension (PAH): idiopathic, heritable, connective tissue disease.
  2. PH due to left heart disease.
  3. PH due to lung disease/hypoxia (COPD, ILD).
  4. Chronic Thromboembolic PH (CTEPH).
  5. Multifactorial.
• Clinical: Progressive dyspnea, loud P2, right ventricular heave, eventually cor pulmonale.
• Treatment: PAH‑specific: PDE5 inhibitors (sildenafil), endothelin antagonists (bosentan), prostacyclin analogs.

5. Lung Cancer

Type	Frequency	Location	Associations / Features
Adenocarcinoma	Most common (40%)	Peripheral	Non‑smokers, women. Often with driver mutations (EGFR, ALK, KRAS).
Squamous Cell Carcinoma	~25%	Central (cavitary)	Smoking. May cause hypercalcemia (PTHrP). Keratin pearls.
Small Cell Carcinoma	~15%	Central	Strong smoking association. Neuroendocrine. Paraneoplastic: SIADH, Lambert‑Eaton, Cushing's. Rapid growth, early mets.
Large Cell Carcinoma	~5%	Peripheral	Poor prognosis.
Carcinoid Tumor	<5%	Central/Peripheral	Neuroendocrine, low‑grade. May cause carcinoid syndrome if liver mets.

Paraneoplastic Syndromes

• SIADH: Small cell.
• Hypercalcemia: Squamous cell (PTHrP).
• Lambert‑Eaton Myasthenic Syndrome: Small cell (antibodies vs. presynaptic VGCC).
• Hypertrophic Osteoarthropathy: Non‑small cell (clubbing, periostitis).

Superior Vena Cava Syndrome & Pancoast Tumor

• SVC syndrome: Obstruction → facial swelling, distended neck veins. Emergency (usually small cell or lymphoma).
• Pancoast tumor: Superior sulcus tumor → Horner syndrome (ptosis, miosis, anhidrosis), C8‑T1 nerve root involvement (hand weakness).

6. Pleural Diseases

Pleural Effusion

• Transudate vs. Exudate (Light's Criteria):
  • Exudate if ≥1: Pleural protein/serum protein >0.5; Pleural LDH/serum LDH >0.6; Pleural LDH >⅔ upper limit normal.
• Transudate causes: Heart failure, cirrhosis, nephrotic syndrome.
• Exudate causes: Pneumonia (parapneumonic), malignancy, TB, pulmonary embolism, rheumatoid arthritis.

Pneumothorax

• Primary spontaneous: Tall, thin young males, ruptured apical bleb.
• Secondary spontaneous: COPD, cystic fibrosis, TB, Marfan syndrome.
• Tension pneumothorax: Medical emergency. Tracheal deviation away, hypotension, absent breath sounds. Immediate needle decompression (2nd ICS midclavicular) → chest tube.

Mesothelioma

• Malignant tumor of pleura, strongly associated with asbestos (latency 20‑40 years).
• Presents with chest wall pain, pleural effusion, pleural thickening.
• Diagnosis: Pleural biopsy (cytology often insufficient).

7. Respiratory Failure

Acute Respiratory Distress Syndrome (ARDS)

• Diffuse alveolar damage, non‑cardiogenic pulmonary edema.
• Berlin Definition: Acute onset, bilateral opacities, PaO₂/FiO₂ ≤300 mmHg on PEEP ≥5, not fully explained by cardiac failure.
• Pathophysiology: Injury to alveolar epithelium and endothelium → increased permeability → protein‑rich edema, hyaline membranes.
• Management: Treat underlying cause, lung‑protective ventilation (low tidal volume 6 mL/kg ideal body weight), conservative fluid strategy, prone positioning for severe cases.

Obstructive Sleep Apnea (OSA)

• Recurrent upper airway collapse during sleep → apneas/hypopneas.
• Risk factors: Obesity, retrognathia, large neck circumference.
• Diagnosis: Polysomnography (apnea‑hypopnea index, AHI).
• Complications: Hypertension, atrial fibrillation, pulmonary hypertension, daytime somnolence.
• Treatment: CPAP, weight loss, oral appliances.

8. High‑Yield Comparisons & Mnemonics

Condition	Key Differentiator
COPD vs. Asthma	COPD: irreversible obstruction, older age, smoking. Asthma: reversible, younger, atopy.
Transudate vs. Exudate	Light's criteria. Transudate = low protein/LDH (CHF, cirrhosis).
Silicosis vs. Asbestosis	Silicosis: upper lobe nodules, eggshell calcification. Asbestosis: lower lobe fibrosis, pleural plaques.
Small Cell vs. Non‑Small Cell	Small cell: central, neuroendocrine, early mets, paraneoplastic (SIADH, LEMS).
TB primary vs. reactivation	Primary: Ghon complex (lower lobe). Reactivation: upper lobe cavitation.

9. Essential Imaging Patterns

Finding	Likely Diagnosis
Upper lobe cavitary lesion	Reactivation TB, squamous cell carcinoma, fungal (aspergilloma)
Bilateral hilar lymphadenopathy	Sarcoidosis, TB, lymphoma, silicosis (eggshell)
Pleural plaques	Asbestos exposure
Honeycombing, basal predominance	IPF (UIP pattern)
Ground‑glass opacities, crazy paving	PJP, ARDS, pulmonary edema, hypersensitivity pneumonitis
Hyperinflation, flattened diaphragms	COPD / Emphysema
Miliary nodules	Miliary TB, metastatic cancer, fungal

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