Asthma
Pathophysiology
Asthma is a chronic inflammatory airway disease characterized by episodic, reversible airway obstruction, bronchial hyperresponsiveness, and airway remodeling. Key mechanism: Th2-mediated inflammation → mast cell degranulation (histamine, leukotrienes, prostaglandins) → bronchospasm, mucosal edema, increased mucus secretion. Chronic inflammation → subepithelial fibrosis, smooth muscle hypertrophy, goblet cell hyperplasia (remodeling).
Classification & Step Therapy
| Step | Severity | Controller Therapy | Reliever |
|---|
| 1 | Intermittent (<2d/week symptoms, <2 nights/month) | None (PRN SABA) | SABA (albuterol) |
| 2 | Mild persistent | Low-dose ICS | SABA PRN |
| 3 | Moderate persistent | Low-dose ICS + LABA or medium ICS | SABA PRN |
| 4 | Severe persistent | Medium-high dose ICS + LABA | SABA PRN |
| 5 | Very severe | High-dose ICS + LABA + tiotropium or biologic (omalizumab, mepolizumab) | SABA PRN |
🎯 Boards PearlPFTs in asthma: obstructive pattern (FEV1/FVC <0.70); FEV1 improves >12% and 200 mL post-bronchodilator = reversible obstruction. Methacholine challenge if spirometry normal but asthma suspected. Status asthmaticus: severe exacerbation not responding to bronchodilators; treat with IV magnesium sulfate, systemic steroids, heliox; avoid intubation if possible (high risk); intubate with permissive hypercapnia.
COPD
Pathophysiology
COPD is a progressive, largely irreversible airflow limitation caused by airway and/or alveolar damage from noxious particles or gases (smoking #1, alpha-1 antitrypsin deficiency). Two main phenotypes: Chronic bronchitis (productive cough ≥3 months/year for ≥2 consecutive years; mucus hypersecretion, airway inflammation) and Emphysema (destruction of alveolar walls → loss of elastic recoil → air trapping → hyperinflation).
Emphysema vs. Chronic Bronchitis
| Feature | Emphysema ("Pink Puffer") | Chronic Bronchitis ("Blue Bloater") |
|---|
| Body type | Thin, barrel chest | Overweight, cyanotic |
| Cough | Minimal, non-productive | Chronic productive cough |
| SpO2 | Near normal (pursed-lip breathing compensates) | Low (chronic hypoxemia/hypercapnia) |
| PFTs | Low DLCO (alveolar destruction), TLC increased | Normal or slightly decreased DLCO |
| CXR | Hyperinflation, flat diaphragms, bullae | Increased bronchovascular markings ("dirty chest") |
GOLD Staging (Spirometry-Based)
| GOLD Grade | FEV1 (% predicted) | Severity |
|---|
| 1 | ≥80% | Mild |
| 2 | 50–79% | Moderate |
| 3 | 30–49% | Severe |
| 4 | <30% | Very severe |
🏥 COPD ManagementSmoking cessation (#1 intervention to slow progression). Bronchodilators: SABA (albuterol) PRN → LAMA (tiotropium) or LABA → LAMA + LABA → add ICS. Phosphodiesterase-4 inhibitor (roflumilast) for frequent exacerbators with chronic bronchitis. Supplemental O2 if SaO2 ≤88% at rest (only intervention improving mortality). Pulmonary rehab. Vaccinate (influenza, pneumococcal, COVID-19). COPD exacerbation: nebulized bronchodilators, systemic steroids (5-day prednisone), antibiotics if purulent sputum (azithromycin, doxycycline, amoxicillin-clavulanate). Avoid high-flow O2 (hypoxic drive).
Pneumonia
| Type | Common Pathogens | Clinical Features | Treatment |
|---|
| CAP (typical) | S. pneumoniae (#1), H. influenzae, Moraxella catarrhalis | Acute onset, productive cough, lobar consolidation, pleuritic chest pain, fever | Outpatient: amoxicillin or doxycycline; Inpatient: beta-lactam + macrolide or respiratory fluoroquinolone |
| CAP (atypical) | Mycoplasma pneumoniae (#1 in young adults), Chlamydophila pneumoniae, Legionella | Gradual onset, dry cough, headache, myalgias; "walking pneumonia" | Doxycycline or macrolide; respiratory FQ for Legionella |
| HAP/VAP | P. aeruginosa, MRSA, Klebsiella, Enterobacter, Acinetobacter | Onset ≥48h after hospitalization; fever, leukocytosis, purulent sputum, new infiltrate | Anti-pseudomonal beta-lactam ± MRSA coverage (vancomycin/linezolid) |
| Aspiration | Mixed oral flora (anaerobes); RLL or RML typically | Risk factors: altered consciousness, dysphagia, GERD; putrid sputum, lower lobe infiltrate | Amoxicillin-clavulanate or clindamycin; treat any abscess |
🎯 Boards Pearl — Pneumonia SeverityCURB-65 (outpatient vs. inpatient): Confusion, Urea >20mg/dL (BUN >19), RR ≥30, BP <90 systolic or ≤60 diastolic, Age ≥65. Score 0–1: outpatient; 2: inpatient; ≥3: ICU consideration. PSI/PORT score is more complex but more predictive. "Silver-staining organism" seen with Pneumocystis jirovecii (PCP) in immunocompromised patients (HIV, CD4 <200).
Pulmonary Embolism
Pathophysiology
PE occurs when a thrombus (usually from DVT in proximal leg veins) embolizes to the pulmonary vasculature. Virchow's Triad: venous stasis + hypercoagulability + endothelial injury. Massive PE → acute right ventricular failure (RV afterload overload → RV dilation, interventricular septal shift → reduced LV preload → hemodynamic collapse).
Clinical Presentation & Wells Score
| Wells Criteria | Points |
|---|
| Clinical signs of DVT | 3 |
| Alternative diagnosis less likely than PE | 3 |
| HR >100 bpm | 1.5 |
| Immobilization or surgery within 4 weeks | 1.5 |
| Prior DVT/PE | 1.5 |
| Hemoptysis | 1 |
| Malignancy | 1 |
Score <2: low probability. 2–6: moderate. >6: high. Low/moderate → D-dimer (if negative, PE excluded). High probability or positive D-dimer → CT pulmonary angiography (gold standard).
🧠 Mnemonic — ECG in PE: S1Q3T3S wave in lead I · Q wave in lead III · T-wave inversion in lead III. Most common ECG findings: sinus tachycardia, right heart strain (RAD, RBB, RBBB, T inversion V1–V4). Normal ECG in PE does not exclude the diagnosis.
🏥 TreatmentHemodynamically stable: anticoagulation (LMWH, UFH, or DOAC — rivaroxaban or apixaban preferred). Hemodynamically unstable (massive PE): systemic thrombolytics (tPA) or surgical/catheter-directed embolectomy. Long-term anticoagulation: 3 months if provoked; indefinite if unprovoked or hypercoagulable state. IVC filter only if anticoagulation absolutely contraindicated.
Pneumothorax
| Type | Mechanism | Patient | Treatment |
|---|
| Spontaneous (primary) | Rupture of apical blebs; no underlying lung disease | Tall, thin young males; smokers | Small (<2cm): observation; Large or symptomatic: needle aspiration or chest tube |
| Spontaneous (secondary) | Underlying lung disease (COPD, asthma, CF, PCP, TB) | Older, diseased lungs | Chest tube; treat underlying disease |
| Tension pneumothorax | One-way valve → air accumulates under pressure → mediastinal shift → cardiovascular collapse | Any; trauma, mechanically ventilated patients | EMERGENCY: immediate needle decompression (2nd ICS, MCL) → chest tube |
🎯 Boards Pearl — Tension PTXTension PTX is a clinical diagnosis — DO NOT wait for imaging. Signs: respiratory distress, absent breath sounds ipsilateral, tracheal deviation away, hypotension, JVD. Treat immediately with large-bore needle at 2nd intercostal space, midclavicular line, followed by chest tube (5th ICS, anterior axillary line).
Acute Respiratory Distress Syndrome (ARDS)
Berlin Definition Criteria
- Acute onset (within 1 week of known insult)
- Bilateral opacities on CXR not fully explained by effusion, atelectasis, or nodules
- Not fully explained by cardiac failure or fluid overload
- PaO2/FiO2 ratio: Mild 201–300; Moderate 101–200; Severe ≤100 (all with PEEP ≥5 cmH2O)
Pathophysiology
Diffuse alveolar damage (DAD): direct (pneumonia, aspiration, inhalation) or indirect (sepsis, trauma, pancreatitis, transfusion/TRALI) insult → neutrophil activation → endothelial and epithelial injury → protein-rich edema → hyaline membranes → impaired gas exchange → refractory hypoxemia.
🏥 Management — ARDSnet ProtocolLow tidal volume ventilation: 6 mL/kg ideal body weight (lung-protective: prevents ventilator-induced lung injury). Plateau pressure ≤30 cmH2O. Permissive hypercapnia (allow pH 7.2–7.45). PEEP to optimize oxygenation. Prone positioning >16 hours/day (reduces mortality in severe ARDS — PaO2/FiO2 <150). Conservative fluid strategy (avoid excess fluids). Neuromuscular blockade (cisatracurium) for severe ARDS. Corticosteroids: methylprednisolone reduces duration of mechanical ventilation. Prone positioning reduces 28-day mortality by 16% in severe ARDS (PROSEVA trial).