Inhaled corticosteroids (ICS) are the cornerstone of persistent asthma management and play an important role in COPD treatment when combined with long-acting bronchodilators. Understanding their mechanism, device-specific pharmacokinetics, and clinical application is essential for NP prescribing. ICS exert their anti-inflammatory effect by crossing the cell membrane and binding to intracellular glucocorticoid receptors (GR) in airway epithelial cells, macrophages, eosinophils, and lymphocytes. The activated GR-ICS complex translocates to the nucleus where it suppresses inflammatory gene transcription through two mechanisms: trans-repression (binding to NF-κB and AP-1 transcription factors, preventing their activation of pro-inflammatory cytokine genes including IL-4, IL-5, IL-13, TNF-α, and GM-CSF) and trans-activation (inducing anti-inflammatory proteins including lipocortin-1/annexin A1, which inhibits phospholipase A2 and thus blocks the entire arachidonic acid cascade). The net result is: reduced mucosal edema and microvascular permeability, decreased mucus hypersecretion, reduced eosinophilic infiltration and mast cell proliferation, restored beta-2 receptor responsiveness (preventing tachyphylaxis to beta-2 agonists), and decreased airway hyperresponsiveness (BHR). ICS pharmacokinetics are influenced by the delivery device. Metered-dose inhalers (MDIs) deliver medication as an aerosol propelled by HFA (hydrofluoroalkane); only 10-20% reaches the lower airways...