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Pulmonology Essentials for Junior Residents (Year 1)

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1. COPD (Chronic Obstructive Pulmonary Disease)

• Emphysema - destruction of alveolar walls distal to terminal bronchioles, caused by proteases (especially from neutrophils) released in response to cigarette smoke. Results in loss of elastic recoil, air trapping, and hyperinflation.
• Chronic Bronchitis - persistent productive cough for at least 3 months/year in 2 consecutive years, caused by mucus gland hyperplasia and small airway inflammation.

• Centriacinar (most common) - smoking-related; upper lobe predominant
• Panacinar - seen in alpha-1 antitrypsin (A1AT) deficiency; lower lobe predominant

• Smoking causes goblet cell metaplasia, ciliary dysfunction, reduced CFTR function, and increased MUC5AC/MUC5B mucin production (10- and 3-fold respectively in severe COPD)
• Mucus hyperconcentration leads to small airway occlusion and promotes colonization with H. influenzae
• Net result: airflow obstruction, air trapping, V/Q mismatch

• FEV1/FVC < 0.70 (post-bronchodilator) - confirms obstruction
• Reduced FEV1
• Increased TLC, RV (air trapping)
• Reduced DLCO (emphysema)

• All patients: smoking cessation (most important), influenza + pneumococcal vaccines
• Mild (GOLD 1-2): short-acting bronchodilators (SABA/SAMA) PRN
• Moderate-severe: long-acting bronchodilators (LABA + LAMA), e.g., tiotropium + salmeterol
• Frequent exacerbations: add ICS (e.g., fluticasone)
• Very severe (FEV1 <30%, hypoxemia): long-term oxygen therapy (LTOT) if PaO2 <55 mmHg or SpO2 <88%
• A1AT deficiency: augmentation therapy

• Most common triggers: respiratory infections (viral > bacterial), air pollution
• Management: controlled O2 (target SpO2 88-92%), short-acting bronchodilators, systemic steroids (prednisone 40 mg x 5 days), antibiotics if purulent sputum (amoxicillin, doxycycline, or azithromycin), NIV (BIPAP) if pH <7.35

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2. Asthma

• Atopic asthma (most common): Th2/IgE-mediated reaction to allergens
  • Early phase (minutes): mast cell degranulation - histamine, leukotrienes, prostaglandins
  • Late phase (hours): eosinophil/T-cell infiltration - IL-4, IL-5, IL-13
• Non-atopic triggers: infections, cold air, exercise, NSAIDs, beta-blockers, occupational exposures
• Airway remodeling (subbasement membrane thickening, smooth muscle hypertrophy) adds irreversible obstruction over time
• Eosinophil major basic protein damages airway epithelium

• FEV1/FVC reduced (obstruction)
• >12% and 200 mL improvement in FEV1 after bronchodilator = reversibility
• Methacholine challenge: positive if PC20 <8 mg/mL (confirms hyperreactivity)

• Step 1: SABA PRN (albuterol)
• Step 2: Low-dose ICS (preferred), or LTRA (montelukast)
• Step 3: Low-dose ICS + LABA (e.g., fluticasone/salmeterol)
• Step 4: Medium-dose ICS + LABA
• Step 5: High-dose ICS + LABA + biologics (anti-IL-5: mepolizumab; anti-IgE: omalizumab; anti-IL-4/13: dupilumab)

• Continuous SABA nebs, ipratropium, IV/oral steroids, IV magnesium sulfate (2g IV)
• Heliox for refractory bronchospasm
• Intubation if altered consciousness, silent chest, PaCO2 rising (permissive hypercapnia with low tidal volumes)

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3. Pneumonia

• Streptococcus pneumoniae - most common overall
• Mycoplasma pneumoniae, Chlamydophila pneumoniae - atypical (younger, milder)
• Haemophilus influenzae - COPD patients
• Klebsiella pneumoniae - alcoholics
• Staphylococcus aureus (including MRSA) - post-influenza
• Legionella pneumophila - water exposure, hyponatremia, diarrhea
• Respiratory viruses (influenza, SARS-CoV-2, RSV)

• Score 0-1: Outpatient treatment
• Score 2: Consider hospitalization
• Score 3+: Hospitalize; Score 4-5: consider ICU

• Outpatient, no comorbidities: Amoxicillin OR doxycycline OR azithromycin (low resistance)
• Outpatient with comorbidities: Respiratory fluoroquinolone (levofloxacin) OR amoxicillin-clavulanate + macrolide
• Inpatient, non-ICU: Beta-lactam + macrolide OR fluoroquinolone monotherapy
• ICU: Beta-lactam + azithromycin OR beta-lactam + fluoroquinolone; add anti-MRSA (vancomycin/linezolid) if risk factors

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4. Pulmonary Embolism (PE)

• Most PEs originate from deep vein thrombosis (DVT) of lower extremities (Virchow's triad: stasis, hypercoagulability, endothelial injury)
• Obstruction of pulmonary vasculature causes increased RV afterload - RV dilation and failure
• V/Q mismatch and dead space ventilation cause hypoxemia

• Classic triad: pleuritic chest pain + dyspnea + hemoptysis (uncommon; only ~20%)
• Tachycardia (most common sign), tachypnea, hypoxia, low-grade fever
• Massive PE: syncope, hypotension, cardiac arrest

• ECG: Sinus tachycardia (most common); S1Q3T3 pattern (right heart strain); new RBBB
• CXR: Usually normal; Hampton's hump (wedge-shaped infarct), Westermark sign (oligemia)
• D-dimer: High sensitivity; negative D-dimer rules out PE in low pre-test probability (Wells score)
• CT Pulmonary Angiography (CTPA): Gold standard imaging
• V/Q scan: For patients with contrast allergy or renal failure
• Troponin/BNP: Elevated = high short-term mortality risk

• DVT signs/symptoms: 3 pts
• PE more likely than alternative: 3 pts
• Heart rate >100: 1.5 pts
• Immobilization >3 days or surgery within 4 weeks: 1.5 pts
• Prior DVT/PE: 1.5 pts
• Hemoptysis: 1 pt
• Malignancy: 1 pt
• Score <2 = low probability; 2-6 = intermediate; >6 = high

• Anticoagulation (mainstay): Start immediately if clinical suspicion high
  • Unfractionated heparin (UFH) IV - preferred if thrombolysis possible or unstable
  • LMWH (enoxaparin) - outpatient/stable patients
  • DOACs (rivaroxaban, apixaban) - preferred for most patients; start directly
• Massive PE: Systemic thrombolysis (tPA 100 mg over 2h) if no contraindications; surgical embolectomy or catheter-directed therapy if thrombolysis fails/contraindicated
• Duration of anticoagulation: 3 months for provoked (transient risk factor); 3-6 months minimum for unprovoked (consider indefinite); indefinite for cancer-related PE
• IVC filter: Only for absolute contraindication to anticoagulation

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5. Interstitial Lung Disease (ILD)

• Idiopathic Pulmonary Fibrosis (IPF)
• Connective tissue disease-associated (RA, scleroderma, myositis)
• Hypersensitivity pneumonitis (HP)
• Sarcoidosis
• Drug-induced (amiodarone, methotrexate, bleomycin, nitrofurantoin)
• Occupational/environmental (pneumoconioses)

• Most common and most severe idiopathic ILD
• Age >60, male, smoker; insidious onset dyspnea + dry cough
• Pathology: Usual Interstitial Pneumonia (UIP) pattern - patchy fibrosis, fibroblastic foci, honeycombing
• Genetic risk: MUC5B promoter variant (increases risk 7-21x), telomerase mutations
• HRCT: Basilar, subpleural honeycombing with traction bronchiectasis
• PFTs: Restrictive pattern + reduced DLCO
• Anti-fibrotic treatment: Nintedanib or Pirfenidone (slow progression, do not reverse)
• Lung transplant for eligible patients

• Granulomatous disease (non-caseating granulomas), most common in young Black women
• Bilateral hilar lymphadenopathy (BHL) on CXR is classic
• Multi-system: skin (erythema nodosum, lupus pernio), eyes (uveitis), heart (heart block), hypercalcemia (activated macrophages produce 1,25-OH Vit D)
• Lofgren syndrome (acute): BHL + erythema nodosum + arthralgia - good prognosis
• ACE levels elevated (not specific); tissue biopsy confirms
• Treatment: Steroids when symptomatic or organ-threatening

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6. Pleural Disease

1. Pleural protein / serum protein > 0.5
2. Pleural LDH / serum LDH > 0.6
3. Pleural LDH > 2/3 upper limit of normal serum LDH

• Transudate: CHF (#1), cirrhosis, nephrotic syndrome, hypothyroidism
• Exudate: Pneumonia (parapneumonic), malignancy, PE, TB, lupus

• Primary spontaneous: Tall, thin, young men; subpleural bleb rupture
• Secondary: Underlying lung disease (COPD, asthma, CF, PCP)
• Tension pneumothorax: Tracheal deviation away, absent breath sounds, hypotension, JVD - do not wait for CXR; needle decompression at 2nd ICS MCL, then chest tube
• Treatment: Small, stable primary: observation/O2; larger/symptomatic: needle aspiration or chest tube

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7. Respiratory Failure & Mechanical Ventilation

• Onset: Within 1 week of insult
• Bilateral opacities on CXR/CT
• Not fully explained by cardiac failure
• PaO2/FiO2 ratio:
  • Mild: 200-300 (PEEP ≥5)
  • Moderate: 100-200 (PEEP ≥5)
  • Severe: <100 (PEEP ≥5)
• Key management: Lung-protective ventilation - low tidal volume (6 mL/kg ideal body weight), plateau pressure <30 cmH2O, PEEP titration, prone positioning for severe ARDS

• CPAP: ARDS, OSA, acute pulmonary edema
• BiPAP: COPD exacerbation with acidosis (pH <7.35), hypercapnia, immunocompromised patients with pneumonia

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8. Obstructive Sleep Apnea (OSA)

• Episodic upper airway collapse during sleep causing apnea/hypopnea
• Risk factors: Obesity, large neck circumference, retrognathia, male sex
• Symptoms: Snoring, witnessed apneas, excessive daytime somnolence, morning headache
• Diagnosis: Polysomnography (gold standard); AHI ≥5 = OSA; ≥30 = severe
• Treatment: Weight loss, CPAP (first-line), mandibular advancement device, surgery (uvulopalatopharyngoplasty)
• Complications: Systemic HTN, pulmonary HTN, arrhythmias, stroke, T2DM worsening

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9. Pulmonary Hypertension (PH)

• Group 1: Pulmonary arterial hypertension (PAH) - idiopathic, heritable, connective tissue disease, HIV, drugs
• Group 2: Left heart disease (most common cause of PH overall)
• Group 3: Lung disease/hypoxia (COPD, ILD)
• Group 4: Chronic thromboembolic PH (CTEPH)
• Group 5: Multifactorial/unclear

• Vasoreactivity testing: positive responders use CCBs (amlodipine, diltiazem)
• Endothelin receptor antagonists: bosentan, ambrisentan, macitentan
• PDE-5 inhibitors: sildenafil, tadalafil
• Prostacyclin analogs: epoprostenol (IV), treprostinil, iloprost
• Group 4 CTEPH: surgical pulmonary endarterectomy (potentially curative)

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10. Lung Cancer - Key Facts for Jr1

• Staging: NSCLC - I to IV (TNM); SCLC - Limited vs. Extensive
• NSCLC treatment: Surgery (Stage I-II), chemo-radiation (Stage III), targeted therapy (EGFR inhibitors if mutated), immunotherapy (pembrolizumab if PD-L1 ≥50%), palliative (Stage IV)
• SCLC: Very chemosensitive; cisplatin/etoposide + immunotherapy (atezolizumab); prophylactic cranial irradiation for limited stage

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Quick-Reference Pulmonology ABG Patterns

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Top "Don't Miss" Conditions on Call

1. Tension pneumothorax - needle decompression before CXR
2. Massive PE with hemodynamic compromise - systemic thrombolysis
3. Status asthmaticus / silent chest - escalate quickly to BiPAP or intubation
4. COPD exacerbation with acidosis - BiPAP, avoid high-flow O2 (suppress hypoxic drive)
5. ARDS - lung-protective ventilation, prone if PF ratio <150

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