6.6 Respiratory Pharmacotherapy: Asthma, COPD, and Inhaled Therapy

6.6 Respiratory Pharmacotherapy: Asthma, COPD, and Inhaled Therapy

Exam Focus: Respiratory conditions appear on the Evaluating Examination inside the Pharmacotherapeutics subcategory of Pharmacy Practice. Expect items that ask you to distinguish asthma from COPD on objective data, choose the next therapeutic step, recognise the traps of reliever overuse, and identify device-technique failures.

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Asthma: Assessment and Control

Asthma is a chronic inflammatory airway disorder producing variable expiratory airflow limitation. Diagnosis in adults requires objective confirmation of variable obstruction, most commonly a post-bronchodilator increase in forced expiratory volume in one second (FEV1) of at least 12% and 200 mL.

Control, not severity, drives day-to-day therapeutic decisions. The Canadian Thoracic Society control criteria a pharmacist can assess at the counter are:

A patient failing any single criterion has uncontrolled asthma. Before escalating drug therapy, work through the four reversible causes in order: adherence, inhaler technique, trigger exposure (smoke, occupational agents, pets, non-steroidal anti-inflammatory drugs in aspirin-exacerbated respiratory disease), and comorbidity (rhinitis, reflux, obesity).

Reliever strategy: the anti-inflammatory reliever shift

The most heavily tested change in modern asthma care is the move away from short-acting beta-2 agonist (SABA) monotherapy. Because every symptom episode reflects underlying inflammation, current Canadian guidance positions as-needed budesonide-formoterol (an inhaled corticosteroid combined with a fast-onset long-acting beta-2 agonist) as the preferred reliever in patients 12 years and older, either alone in mild disease or as both maintenance and reliever therapy (MART) in moderate to severe disease.

The practical dispensing signal is quantitative: filling more than two salbutamol inhalers in a year predicts exacerbation risk and, at higher volumes, mortality. Treat it as a hard trigger for assessment, not a routine refill.

Controller escalation

1. Low-dose inhaled corticosteroid (ICS) daily, or as-needed ICS-formoterol in mild disease.
2. Low-dose ICS plus a long-acting beta-2 agonist (LABA), ideally as MART.
3. Medium-dose ICS-LABA.
4. Add a long-acting muscarinic antagonist (tiotropium) or a leukotriene receptor antagonist.
5. Refer for biologic therapy phenotyped by blood eosinophils and immunoglobulin E (omalizumab, mepolizumab, benralizumab, dupilumab).

A LABA is never dispensed as monotherapy in asthma. It relieves bronchoconstriction while leaving inflammation untreated, and this combination is associated with increased asthma-related death.

Montelukast carries a boxed warning for serious neuropsychiatric events including agitation, sleep disturbance, aggression, and suicidal ideation. Counsel on this explicitly and document the discussion.

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Chronic Obstructive Pulmonary Disease

COPD requires post-bronchodilator spirometry with an FEV1/FVC ratio below 0.70. Symptoms alone are not diagnostic; a pharmacist who recommends therapy for "smoker's cough" without spirometry is skipping the diagnostic step the examination expects.

Pharmacotherapy escalation in COPD

• Low symptom burden, low exacerbation risk: short-acting bronchodilator as needed.
• Persistent breathlessness: a long-acting muscarinic antagonist (LAMA) or LABA, then dual LAMA-LABA.
• Recurrent exacerbations: add an ICS, giving triple ICS-LAMA-LABA therapy. Benefit is greatest with a history of exacerbations or blood eosinophils of roughly 0.3 x 10^9/L or higher.
• Further exacerbations despite triple therapy: consider roflumilast in chronic bronchitis with an FEV1 below 50%, or long-term azithromycin.

Inhaled corticosteroids increase pneumonia risk in COPD, so the decision to add or continue them is an explicit risk-benefit judgement and a legitimate deprescribing target in a patient who has never exacerbated.

Only three interventions alter COPD mortality: smoking cessation, long-term oxygen therapy in documented chronic hypoxemia, and lung volume reduction surgery in selected patients. Pharmacotherapy improves symptoms and reduces exacerbations. Smoking cessation is therefore a therapeutic intervention, not an aside, and pharmacists in every province can support it with varenicline, bupropion, and nicotine replacement combinations.

Managing an acute exacerbation

Increase short-acting bronchodilators, add prednisone 40 mg daily for 5 days, and add an antibiotic when sputum becomes purulent and increases in volume alongside worsening dyspnea. Extended corticosteroid courses provide no additional benefit and increase harm.

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Cystic Fibrosis

Cystic fibrosis results from mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene, producing viscous secretions, obstructive lung disease, chronic Pseudomonas aeruginosa infection, and pancreatic insufficiency. Pharmacist-relevant therapy includes airway clearance with dornase alfa and hypertonic saline, inhaled tobramycin for chronic Pseudomonas, pancreatic enzyme replacement taken with every meal and snack, fat-soluble vitamin supplementation (A, D, E, K), and CFTR modulators such as elexacaftor-tezacaftor-ivacaftor, which are selected by genotype rather than by symptoms.

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Device Selection and Technique

Device technique is a therapeutic variable, not a courtesy.

Counsel every patient on an ICS-containing product to rinse and spit after use to prevent oropharyngeal candidiasis and dysphonia. A spacer reduces both oropharyngeal deposition and systemic exposure.