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The thyroid gland is a vital butterfly-shaped endocrine gland situated in the lower part of the neck. It is present in the front and sides of the trachea, inferior to the larynx. It plays an essential role in regulating the basal metabolic rate (BMR) and stimulating somatic and psychic growth, besides having a vital role in calcium metabolism. It is a gland consisting of two lobes, the right, and the left lobes, joined together by an intermediate structure, the isthmus. Sometimes a third lobe called the pyramidal lobe projects from the isthmus. It has a fibrous/fibromuscular band, i.e., levator glandulae thyroideae running from the body of the hyoid to the isthmus.[1] The lobes are 5 x 2.5 x 2.5 cm in dimension and weigh around 25 gm. It extends from the fifth cervical to the first thoracic vertebrae. The lobes extend from the middle of the thyroid cartilage to the fifth tracheal ring. The isthmus is 1.2 x 1.2 cm in dimensions and extends from second to third tracheal rings. It grows larger in females during the period of menstruation and pregnancy. The lobes are conical in shape and have an apex, a base, three surfaces – lateral, medial, and posterolateral, and two borders – the anterior and posterior. The isthmus, however, has two surfaces – anterior and posterior and two borders – superior and inferior. The lobes are related anteriorly to the skin, superficial and deep fascia, and platysma.  Posteriorly, the lobes are associated with the laminae of the thyroid cartilage and tracheal rings and laterally to the external carotid artery and internal jugular vein.[2] The thyroid gland is a richly vascular organ supplied by the superior and inferior thyroid arteries and sometimes by an additional artery known as the thyroidea ima artery (see Image 1). The Thyroid Artery).[3] The venous drainage is by superior, middle, and inferior thyroid veins. Sometimes a fourth thyroid vein might be present, called the vein of Kocher. The nerve supply is mainly from the middle cervical ganglion and partly from the superior and inferior cervical ganglia. Two capsules completely cover the thyroid gland. The true capsule is made up of fibro-elastic connective tissue. The false capsule comprises the pre-tracheal layer of the deep cervical fascia. It consists of a deep capillary plexus, deep to the true capsule. Hence, it is crucial to remove the plexus with the capsule during thyroidectomy.[4]

The follicular cells take up the iodinated thyroglobulins from the colloid present within the lumen of the thyroid follicle. This process is under the influence of follicle-stimulating hormone (FSH). Afterward, lysosomal digestion and intracellular proteolysis release the thyroid hormone in the form of T3 and T4. These amino acid derivatives are so small that they can easily escape the follicular cells and enter the bloodstream through fenestrations present in the capillaries. The thyroid-stimulating hormone (TSH) secreted by the anterior pituitary gland affects not only the changes in the follicular cells but also the thyroid follicles and the activity of the gland itself. TSH stimulation occurs when there is a low iodine level in the diet by a negative feedback mechanism on pituitary thyrotrophs. TSH increases the size of the follicular cells (hypertrophy) and increases the number of follicular cells (hyperplasia). Thus under the influence of the TSH, the follicular cells become tall and columnar, demonstrating the heavy activity of the follicular cells and the follicles. The TSH also enhances the exocytosis, synthesis, and iodination of thyroglobulin. It also enhances endocytosis and intracellular breakdown of colloid. Thus the intraluminal colloid is greatly reduced, which manifests externally by the enlargement of the thyroid gland. Usually, enlargement of the thyroid gland is called goiter, which is a diseased state. But in this condition, the enlargement of the thyroid gland is because of the hypertrophy and hyperplasia of the parenchyma. Hence it is called parenchymatous goiter.[37] This condition differentiates from another type of goiter where the enlargement is not because of the hypertrophy and hyperplasia of the parenchyma but due to an increase in the production of colloid within the thyroid follicle. This condition is known as colloid goiter.[38][39] If this condition becomes longstanding with recurrent stages of hyperplasia and involution, it leads to a more irregular enlargement as a multinodular goiter [40]. They later also show fibrosis, calcification, cystic changes, and hemorrhagic spots. If there is no stimulation of TSH, it leads to a decrease in the size of follicular cells to the cuboidal and later squamous cells.

The thyroid-stimulating hormone (TSH) secreted by the anterior pituitary gland affects not only the changes in the follicular cells but also the thyroid follicles and the activity of the gland itself. TSH stimulation occurs when there is a low iodine level in the diet by a negative feedback mechanism on pituitary thyrotrophs. TSH increases the size of the follicular cells (hypertrophy) and increases the number of follicular cells (hyperplasia). Thus under the influence of the TSH, the follicular cells become tall and columnar, demonstrating the heavy activity of the follicular cells and the follicles. The TSH also enhances the exocytosis, synthesis, and iodination of thyroglobulin. It also enhances endocytosis and intracellular breakdown of colloid. Thus the intraluminal colloid is greatly reduced, which manifests externally by the enlargement of the thyroid gland. Usually, enlargement of the thyroid gland is called goiter, which is a diseased state. But in this condition, the enlargement of the thyroid gland is because of the hypertrophy and hyperplasia of the parenchyma. Hence it is called parenchymatous goiter.[37] This condition differentiates from another type of goiter where the enlargement is not because of the hypertrophy and hyperplasia of the parenchyma but due to an increase in the production of colloid within the thyroid follicle. This condition is known as colloid goiter.[38][39] If this condition becomes longstanding with recurrent stages of hyperplasia and involution, it leads to a more irregular enlargement as a multinodular goiter [40]. They later also show fibrosis, calcification, cystic changes, and hemorrhagic spots. If there is no stimulation of TSH, it leads to a decrease in the size of follicular cells to the cuboidal and later squamous cells. In Graves's disease, the follicular cells are tall, columnar, and overcrowded, resulting in small papillae formation. These papillae will project into the follicular lumen. The colloid is pale and shows scalloped margins. The interstitium becomes infiltrated with T lymphocytes.[41][42]

If there is no stimulation of TSH, it leads to a decrease in the size of follicular cells to the cuboidal and later squamous cells. In Graves's disease, the follicular cells are tall, columnar, and overcrowded, resulting in small papillae formation. These papillae will project into the follicular lumen. The colloid is pale and shows scalloped margins. The interstitium becomes infiltrated with T lymphocytes.[41][42] In the case of adenoma, the follicular cells are uniform and contain colloid in the lumen. They show atypia, prominent nucleoli, and focal nuclear pleomorphism. They are well encapsulated in an intact capsule, which distinguishes them from follicular carcinoma. The papillary carcinoma shows typical "Orphan Annie eye" nuclei, which are due to finely dispersed chromatin.[43][40] It also shows a papillary architecture with the papillae and psammoma bodies (calcified concentric structures; see Image 3. Papillary Thyroid Cancer, Psammoma Bodies)[44][45]. The cytoplasm of follicular cells also shows invaginations, which give an intranuclear inclusions-like appearance. Anaplastic carcinomas present with large, pleomorphic giant cell lesions, spindle cells, etc. The parafollicular cells secrete calcitonin whenever the plasma calcium level exceeds its normal limit. The target site for calcitonin in the bone is the osteoclast cells, thus reducing their number and action. Calcitonin also promotes the excretion of phosphate and calcium through urine. However, no significant clinical manifestations have been observed due to an increase or decrease of calcitonin levels in humans, leaving its role in humans unclear. In parathyroid adenomas, the predominant cells will be chief cells, with few nests of oxyphil cells.[33] The chief cells are larger and show variability in nuclear size compared to the normal. Some cells also show bizarre and pleomorphic nuclei. Parathyroid carcinomas are difficult to distinguish from adenomas based on microscopic features, and hence only local and metastatic features are conclusive in making a diagnosis.