Amiodarone hydrochloride is an antiarrhythmic drug, with proven efficacy in prevention and treatment of numerous arrhythmias, atrial fibrillation especially, or ventricular arrhythmias, with a long half-life (55–60 days). The increased risk of developing amiodarone-induced pulmonary fibrosis is directly related to the dose and the duration of the intake. Amiodarone-induced pulmonary toxicity is conditioned by dose, patient’s age, and pre-existent pulmonary pathologies. The pattern for drug-induced lung injury may vary in many forms, but the amiodarone can cause polymorphous injuries such as diffuse alveolar damage, chronical interstitial pneumonia, organizing pneumonia, pulmonary hemorrhage, lung nodules or pleural disease. The pathological mechanism of pulmonary injury induced by amiodarone consists of the accumulation of phospholipid complexes in histocytes and type II pneumocytes. Differential diagnosis of pulmonary fibrosis induced by amiodarone is made mainly with idiopathic pulmonary fibrosis, left ventricular failure or infectious disease. Before starting treatment with amiodarone, patients should be informed of potential adverse effects and any new respiratory symptoms should promptly be reported to their family physician or attending physician. The assessment carried out at the initiation of amiodarone treatment should include at least chest X-ray and respiratory function tests and extrapulmonary evaluation.

Background: Cigarette smoking remains one of the most important preventable causes of respiratory morbidity, exerting detrimental effects even in young adults. Medical students represent a particularly relevant population, as the lifestyle habits they adopt during their training years may influence both their personal health and professional credibility. Methods: We conducted a cross-sectional analysis of 264 medical students from the University of Medicine, Pharmacology, Science and Technology of Târgu-Mures, aged 18–30 years, stratified according to smoking status, type of tobacco product used, and lifestyle characteristics (athletic vs. sedentary). Standardized spirometry was performed to assess FVC, FEV₁, FEV₁/FVC ratio, PEF, and small airway flow parameters (MEF₂₅, MEF₅₀, MEF₇₅). Statistical comparisons between groups were performed using t-tests, Mann–Whitney U tests, chi-square tests, and correlation analyses, with p < 0.05 considered statistically significant. Results: Smokers demonstrated significantly lower values for FEV₁, PEF, and MEF parameters compared with non-smokers, confirming early functional impairment of both large and small airways. Within the smoking group, users of e-cigarettes or heated tobacco products exhibited more favorable FEV₁ and small airway flow values than conventional cigarette smokers. However, differences in FVC were less pronounced. Significantly, athletes consistently outperformed their sedentary peers across all respiratory parameters, regardless of smoking status, with markedly higher FEV₁, FVC, and MEF values and a lower prevalence of obstructive patterns. Cumulative smoking exposure (pack-years) was inversely associated with small airway function, whereas higher levels of physical activity were independently linked to a pronounced protective effect. Conclusions: Even in early adulthood, smoking is related to measurable declines in lung function, particularly affecting small airway dynamics. Although alternative products may appear less harmful than conventional cigarettes, they cannot be considered risk-free. Conversely, regular physical activity demonstrated a protective association in the case–control analysis, attenuating functional decline and supporting the preservation of long-term respiratory health. These findings underscore the importance of integrated prevention strategies in medical universities, combining smoking cessation initiatives with the systematic promotion of physical activity to safeguard the health of future physicians and reinforce their role as credible health advocates.