Hashimoto’s thyroiditis (HT), also known as chronic lymphocytic thyroiditis, is the most prevalent autoimmune thyroid disorder and a leading cause of hypothyroidism worldwide. It is characterized by immune-mediated destruction of thyroid follicles, often accompanied by elevated thyroid peroxidase (TPO) and thyroglobulin (Tg) autoantibodies. While genetic predisposition plays a significant role in disease susceptibility, epigenetic modifications and environmental factors—such as iodine intake, infections, and stress—also contribute to its pathogenesis. Beyond the classic form, several clinicopathologic variants of HT have been recognized, all of which typically progress to hypothyroidism, though patients may initially present as euthyroid or even hyperthyroid. In addition to thyroid dysfunction, HT has been increasingly associated with extra-thyroidal manifestations affecting multiple organ systems, including the neurological, cardiovascular, dermatological, gastrointestinal, and musculoskeletal systems. Its impact on pregnancy is particularly significant, necessitating early diagnosis and timely thyroid hormone replacement to optimize maternal and fetal outcomes. Standard treatment primarily involves levothyroxine therapy to correct hypothyroidism, while surgical intervention is reserved for cases of large goiters causing compressive symptoms or suspicious thyroid nodules with inconclusive cytology. Effective management of HT requires a multidisciplinary approach, with endocrinologists, primary care physicians, internists, and gynecologists playing a central role in diagnosis, treatment optimization, and monitoring for complications.