Autoimmune thyroid diseases represent a spectrum of immune-mediated thyroid dysfunction caused by loss of self-tolerance to thyroid antigens. Hashimoto thyroiditis (chronic lymphocytic thyroiditis) is the most common cause of hypothyroidism in iodine-sufficient regions. CD4+ T-helper cells (TH1) infiltrate the thyroid gland, and cytotoxic CD8+ T-cells directly destroy thyrocytes. Anti-thyroid peroxidase (anti-TPO) antibodies (present in 90-95%) and anti-thyroglobulin (anti-Tg) antibodies serve as diagnostic markers but also contribute to complement-mediated cellular destruction. Progressive destruction of thyroid follicles leads to fibrosis and eventual gland atrophy with clinical hypothyroidism. Graves disease is caused by thyroid-stimulating immunoglobulins (TSI) — IgG autoantibodies that bind and activate the TSH receptor, producing unregulated thyroid hormone synthesis and secretion independent of TSH feedback. TSI also stimulate retroorbital fibroblasts expressing TSH receptors, causing glycosaminoglycan deposition, inflammation, and extraocular muscle enlargement (Graves ophthalmopathy). The NP distinguishes these conditions through clinical presentation, TSH/free T4 levels, antibody profiles, and radioactive iodine uptake patterns (diffuse uptake in Graves vs decreased/absent uptake in thyroiditis-induced thyrotoxicosis).