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Thyroid gland and parathyroid glands

Last updated: February 22, 2021

Summarytoggle arrow icon

The thyroid gland is a butterfly-shaped endocrine gland located inferior to the larynx and anterior to the trachea. The thyroid gland develops from the fusion of the median thyroid anlage with the two lateral thyroid anlages, which are derived from the pharyngeal pouches. The thyroid gland is contained by the pretracheal fascia and internal capsule. It receives its arterial supply from the superior and inferior thyroid arteries and drains into the superior, middle, and inferior thyroid veins. The lymphatics drain into the paratracheal and deep cervical lymph nodes. It receives sympathetic innervation via the cervical ganglion and parasympathetic innervation via the vagus nerve. The thyroid gland secrets thyroid hormones, which regulate body metabolism and growth, and calcitonin, which lowers serum calcium and phosphate through inhibition of osteoclasts. Hormone synthesis occurs in the epithelial lining of the thyroid follicles. The epithelial lining consists of follicular (thyroid epithelial) cells, which synthesize thyroid hormone, and parafollicular (C) cells, which synthesize calcitonin.

The parathyroid glands are four, oval-shaped endocrine glands located on the posterior surface of the thyroid gland. They are derived from the third and fourth pharyngeal pouches. The parathyroid glands receive their arterial supply from the inferior thyroid arteries and drain into the thyroid venous plexus. The lymphatics drain into the paratracheal and deep cervical lymph nodes. The parathyroid glands are innervated by the thyroid branch of the cervical ganglia. The parathyroid chief cells secrete parathyroid hormone, which maintains serum calcium and phosphate homeostasis and, furthermore, antagonizes the effect of calcitonin by increasing serum calcium and decreasing serum phosphate. The recurrent laryngeal nerves, parathyroid glands, sympathetic trunks, and the nerves of the carotid sheath are at risk of injury during thyroid surgery.

Overview

Damage to the recurrent laryngeal nerves, parathyroid glands, sympathetic trunks, and even the nerves of the carotid sheath is possible during thyroidectomy because of the thyroid's location in the anterior neck.

Gross anatomy

Vasculature and innervation

Overview of arterial supply and venous drainage
Vessel Supplies
Arterial supply
Venous drainage

The inferior thyroid artery runs close to the recurrent laryngeal nerve and the superior thyroid artery close to the superior laryngeal nerve. Both nerves are at risk during thyroid surgery.

Lobules of thyroid gland

Overview of thyroid cells
Cell type Characteristics Function

Thyroid epithelial cell (follicular cells)

C cells (parafollicular cells)

The thyroid gland produces thyroid hormones, which stimulate metabolism and growth, as well as calcitonin, which decreases bone resorption and is involved in plasma calcium homeostasis.

Calcitonin

Thyroid hormones

Thyroid hormone synthesis

Detailed steps of thyroid hormone synthesis
Steps Description Site

1. Synthesis of thyroglobulin (TG)

  1. Thyroglobulin (TG) is produced in the rough ER of the follicular cells.
  2. TG is packed in vesicles in the Golgi apparatus.
  3. TG is released into the follicular lumen via exocytosis.

2. Uptake of iodide

  1. Basolateral transport
  2. Apical transport

3. Iodination of thyroglobulin

4. Storage

5. Release

  1. Reuptake of iodinated TG in thyrocytes via endocytosis
  2. Fusion of endocytosis vesicles with lysosome
  3. Proteolytic enzymes cleave TG to release T3, T4, DIT, and MIT
  4. T3 (∼ 20%) and T4 (∼ 80%) are released into the blood (via the MCT8 transporter)
  5. Deiodinase removes the iodine from the MIT and DIT, which is then redistributed to the intracellular I- pool (iodine salvage).

Thyroxine hormone is produced from tyrosine and iodine.

Transport and degradation

Thyroid hormones are lipophilic; most of the circulating thyroid hormones are inactive and bound to transport proteins. Only a very small fraction (∼ 0.3%) is unbound and biologically active.

Effect

In general, thyroid hormones increase the metabolic rate: oxygen and energy consumption as well as thermogenesis increase under their influence.

Overview of thyroid hormone effects
Target organ Effect
Heart
Lungs
Nervous system
  • Maturation of the nervous system
    • Brain maturation
    • Myelin formation
    • Axonal growth
Musculoskeletal system
Reproductive system [2]
Metabolism
Thermoregulation

Regulation

TPO is stimulated by TSH and inhibited by PTU, methimazole, and excess iodine (Wolff-Chaikoff effect), resulting in, respectively, high and low thyroid hormone levels.

Thyroid-stimulating hormone (TSH) from the pituitary gland stimulates the basolateral uptake of iodine as well as the biosynthesis and release of thyroid hormones.

TSH levels are very sensitive to thyroid hormone dysfunction. If thyroid hormone levels are very high, TSH can fall below detection limits and if they are very low, TSH increases markedly. Therefore, serum TSH is an important parameter for assessing thyroid function and is usually the first step in thyroid diagnostics.

Overview

The thyroid gland develops in the first trimester of pregnancy from the fusion of the median thyroid anlage with the two lateral thyroid anlages derived from the pharyngeal pouches. Both follicular cells and C cells arise from pharyngeal endoderm [3][4][5]

Follicular cells arise mainly from the median thyroid anlage.
Parafollicular C cells arise mainly from the lateral thyroid anlage.

Thyroid diverticulum

During embryological thyroid migration, remnants of thyroid tissue can remain in the tongue (lingual thyroid) or elsewhere along the migration path. Incidental removal of ectopic thyroid tissue may result in hypothyroidism if the ectopic tissue is the only functioning thyroid tissue in the body.

Overview

Microscopic anatomy

Function of PTH

  • PTH increases serum calcium and decreases serum phosphate (see “Calcium homeostasis”).
    • High extracellular calcium → activation of calcium-sensitive receptors → PTH excretion
    • Low extracellular calcium → inhibition of calcium-sensitive receptors → PTH excretion

Embryology

DiGeorge syndrome is a congenital T-cell immunodeficiency that is caused by microdeletion at chromosome 22 (22q11.2). The deletion leads to defective development of the third and fourth pharyngeal pouches, resulting in aplastic parathyroids and hypocalcemia due to PTH deficiency.

Clinical significance

Surgery of the thyroid and parathyroid glands can result in destroyed or removed parathyroid glands due to their variable position. This may result in hypoparathyroidism and hypocalcemia.

  1. Costanzo LS. Physiology Board review series. Lippincott Williams & Wilkins ; 2014
  2. Dittrich R, Beckmann MW, Oppelt PG et al. Thyroid hormone receptors and reproduction. J Reprod Immunol. 2011; 90 (1): p.58-66. doi: 10.1016/j.jri.2011.02.009 . | Open in Read by QxMD
  3. Nilsson M, Williams D. On the origin of cells and derivation of thyroid cancer: C cell story revisited. Eur Thyroid J. 2016; 5 (2): p.79-93. doi: 10.1159/000447333 . | Open in Read by QxMD
  4. Thyroid Gland - General Embryology. http://www.pathologyoutlines.com/topic/thyroidembryology.html. Updated: July 18, 2018. Accessed: November 24, 2018.
  5. Nilsson M, Fagman H. Development of the thyroid gland. Development. 2017; 144 (12): p.2123-2140. doi: 10.1242/dev.145615 . | Open in Read by QxMD