PH5.1 | PH5.1 | Obstructive Airway Disease Pharmacotherapy — Summary & Reflection

KEY TAKEAWAYS

Obstructive Airway Disease Pharmacotherapy — Key Points:

• Asthma is driven by eosinophilic airway inflammation + bronchial hyper-reactivity; COPD by neutrophilic/macrophage inflammation with irreversible obstruction; rhinitis by IgE-mediated nasal mucosal inflammation with histamine as the primary mediator.

• SABA (salbutamol, terbutaline) = rescue bronchodilator in both asthma and COPD. LABA (salmeterol, formoterol, indacaterol) = long-acting bronchodilator. Critical rule: LABA + ICS mandatory in asthma (NEVER LABA monotherapy); LABA mono acceptable in COPD.

• ICS = cornerstone anti-inflammatory in asthma (all steps ≥2); add selectively in COPD (high exacerbation risk, eosinophilic features) — carries pneumonia risk in COPD. Rinse mouth after ICS to prevent oral candidiasis.

• SAMA (ipratropium) = short-acting add-on in acute asthma/COPD. LAMA (tiotropium) = once-daily COPD maintenance; add-on in severe asthma.

• Leukotriene modifiers: Montelukast/zafirlukast = CysLT1 receptor antagonists; zileuton = 5-LOX synthesis inhibitor. Montelukast: neuropsychiatric black-box warning.

• Theophylline: narrow TI (5–15 µg/mL), CYP1A2 substrate — monitor TDM; check smoking status and interacting drugs.

• Biologics: omalizumab (anti-IgE), mepolizumab/reslizumab (anti-IL-5), benralizumab (anti-IL-5Rα), dupilumab (anti-IL-4Rα). Reserved for Step 4–5 severe asthma.

• Rhinitis: INCS = most effective (all symptom domains); 2nd-gen H1 antihistamines (cetirizine, loratadine, fexofenadine) effective for all except congestion; topical decongestants ≤5 days only (rhinitis medicamentosa risk).

• GINA stepwise (Steps 1–5) for asthma; GOLD ABCD for COPD — both guide step-up/step-down decisions based on symptom burden and exacerbation risk.

REFLECT

Think back to the opening scenario of the student in respiratory distress who had stopped her 'brown inhaler.' Now that you have worked through this module:

1. What is the 'brown inhaler' most likely to be (what class, what mechanism), and why was stopping it the critical error?
2. If a patient asks you: 'The SABA reliever works immediately; why do I need to keep taking the ICS when I feel fine?' — how would you explain the difference between symptom relief and disease control using the pathophysiology concepts from this module?
3. Consider a middle-aged COPD patient who also has allergic rhinitis. How would the united-airway concept change your prescribing approach? Would you prescribe separately for each condition, or is there a single agent that addresses both?

Write a brief reflection (200–300 words) connecting at least two of these questions to a clinical reasoning principle you will carry forward into your clinical years.