PT
● MODULE 11 / 20
Respiratory Pharmacology
Separate airway inflammation, bronchoconstriction and secretion management when choosing a drug class.
Quick revision ↓ Medical Dictionary
FULL CHAPTER EXPLANATION
Deep Learning — Module 11
Read this section in sequence. It moves from drug targets to therapeutic effects, adverse reactions and safe use.
01
Airway disease mechanisms
Asthma combines variable airflow limitation with airway inflammation; bronchodilation and anti-inflammatory control address different parts of the disease. COPD has distinct pathological and clinical features, so treatment choices are not copied automatically from asthma. Inhaled delivery concentrates medicine in airways but depends on device technique and inspiratory ability. Poor technique can imitate drug failure. Assess adherence, exposures and the diagnosis before assuming that a higher dose is the answer.
02
Beta-2 agonists and antimuscarinics
Salbutamol produces relatively rapid bronchodilation through beta-2 signaling. Long-acting beta agonists provide longer bronchodilation but should not be used without inhaled corticosteroid treatment in asthma. Inhaled ipratropium and tiotropium reduce muscarinic bronchoconstriction and have roles that vary by disease and setting. Beta agonists can cause tremor, tachycardia and hypokalemia; antimuscarinics can cause dry mouth and other class effects. Onset and duration differ among products.
03
Corticosteroids and other controllers
Inhaled corticosteroids suppress airway inflammatory gene expression and reduce exacerbation risk, but they are not immediate smooth-muscle relaxants. Oral candidiasis and dysphonia can be reduced with appropriate technique and mouth rinsing. Systemic corticosteroids have broader adverse effects and are used in selected circumstances. Leukotriene receptor antagonists such as montelukast target a different inflammatory pathway; potential neuropsychiatric effects require discussion and review. Biologics target defined inflammatory phenotypes in selected severe disease.
04
Methylxanthines and cough medicines
Theophylline has bronchodilator and other actions but a narrow therapeutic margin and many kinetic interactions. Toxicity may cause vomiting, arrhythmias or seizures. Dextromethorphan suppresses cough centrally and can interact with serotonergic medicines. Acetylcysteine can reduce mucus viscosity by disrupting disulfide bonds; expectorants aim to facilitate clearance. Treating a cough symptom does not establish its cause, and suppressing a protective cough may be inappropriate in some settings.
05
Device teaching and clinical integration
Ask the learner to demonstrate the inhaler rather than merely confirm ownership. A spacer may improve delivery from a compatible metered-dose inhaler; device-specific instructions still matter. Distinguish reliever response from long-term inflammatory control and provide a clinician-directed action plan. Marked breathlessness, fatigue or altered consciousness requires urgent assessment. This chapter explains drug principles; exact asthma or COPD regimens should follow current local guidance and supervised clinical assessment.
High-Yield Revision
- Inhaler technique is part of the effective dose.
- Bronchodilation and inflammation control are separate treatment targets.
- Theophylline toxicity may present with arrhythmias or seizures.
Common Exam & Concept Pitfalls
- Long-acting beta agonist monotherapy is inappropriate in asthma.
- Inhaled corticosteroids are not immediate rescue bronchodilators.
Sources & Further Reading
Curriculum scope checked 23 September 2026. These original study notes summarize established principles; current institutional guidance and product information govern clinical use. Faculty review is pending.
RAHBAR study structure: target → drug action → therapeutic use → adverse effects → monitoring. Use institutional curriculum and faculty guidance for local sequencing, practical requirements and assessment specifications.