## Mechanism and Onset of Action **Key Point:** ICS have a SLOW onset of action (hours to days for symptom relief, weeks to months for full anti-inflammatory effect) and are NOT suitable as reliever agents in acute exacerbations. ### Why ICS Are Not Acute Relievers Inhaled corticosteroids: - Require time to bind glucocorticoid receptors, translocate to the nucleus, and modulate gene transcription - Peak effect is achieved over **7–14 days** of regular use - Do NOT provide rapid bronchodilation needed in acute asthma attacks - Are **maintenance therapy**, not rescue therapy ### Correct Properties of ICS | Property | Details | |----------|----------| | **Anti-inflammatory mechanism** | Reduce eosinophils, mast cells, T lymphocytes; decrease mucus production | | **Airway remodeling** | Prevent collagen deposition and smooth muscle hypertrophy over weeks–months | | **Genomic action** | Bind cytoplasmic GR → translocate to nucleus → alter gene transcription | | **First-line status** | Recommended for all persistent asthma (mild, moderate, severe) | | **Onset** | Slow (hours to days for symptom relief) | | **Acute use** | NOT indicated for acute exacerbations; use SABA + systemic corticosteroids instead | **Clinical Pearl:** A patient with acute asthma exacerbation should receive a **short-acting beta-2 agonist (SABA)** like salbutamol for immediate relief, NOT an ICS. ICS are continued as background therapy. **High-Yield:** The distinction between ICS (maintenance, slow onset) and SABA (acute relief, rapid onset) is a frequent NEET PG trap. ICS do NOT replace SABA in acute settings. [cite:Harrison 21e Ch 297]
Sign up free to access AI-powered MCQ practice with detailed explanations and adaptive learning.