A goiter is a goiter that can be visualized or palpated and can be generalized (diffuse or nodular) or focally enlarged. Goiter is a common clinical occurrence, but the prevalence and type varies widely in different populations. The appropriate clinical management of this includes discussing with the patient the diagnosis of the type of goiter, planning what treatment to take, and follow-up. In-depth discussion of the pathogenesis of goiter formation and environmental factors is important for preventive care programs for related diseases. Common types of goiter: More than 5% to 10% of school-age children have endemic goiter, depending on their geographic location. It is usually associated with severe iodine deficiency and occurs by a physiological mechanism that involves a decrease in iodine suppression of the thyroid gland (iodine self-regulation) and an increase in TSH stimulation of the thyroid gland (decreased thyroid hormone production and reduced TSH feedback regulation due to a lack of the substrate iodine). This type of goiter is caused by maladaptation to iodine deficiency and is initially compensatory enlargement in order to adapt to iodine deficiency. However, this process later goes out of control, allowing the formation of heterogeneous goiter in some individuals. The pathogenesis of this uncontrolled process is not yet clear, and studies suggest that it may be identical to the onset of multinodular goiter disseminated in iodine-rich areas. In addition to endemic goiters, many non-endemic goiters can be seen clinically. Non-endemic goiters are of various types and may have overlapping pathogenesis, and multiple types of goiters may be seen in the same patient, thus requiring caution in the diagnosis. The most common cause of an isolated thyroid lesion is a neoplastic goiter. The typical presentation of this type is a benign monoclonal process, and malignancy is rare. Isolated benign thyroid tumors have autonomic synthesis and secretion of thyroid hormones, and most have somatic mutations. Autoimmune thyroid disease can also lead to goiter. Most patients with Graves’ disease have diffuse goiter, presumably due to autoantibodies to TSH receptors that stimulate TSH receptors and cause thyroid cells to proliferate. It has also been found that the larger the size of the thyroid gland, the worse the response to medications in patients with hyperthyroid Graves’ disease. In contrast, about 15% of patients with autoimmune hypothyroidism have goiter. In these patients, the thyroid follicular cells are more or less stimulated by TSH, and their response to stimulation is similar to that of Graves’ disease. Thus, the functional defect in autoimmune hypothyroidism is due to a reduction in the number of functional thyroid cells rather than a functional defect in individual cells. The third type of goiter is multinodular goiter. It occurs most often in women, the elderly, and people with a genetic background. The pathogenesis of this type of goiter is more complex and the process of development is more difficult to understand.