Thyroid: Wikis


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Illu endocrine system.jpg
Endocrine system
Illu thyroid parathyroid.jpg
Thyroid and parathyroid.
Latin glandula thyroidea
Gray's subject #272 1269
System endocinal jubachina system
Artery superior thyroid artery, inferior thyroid artery, thyreoidea ima, accessory thyroid arteries from oesophageal and tracheal branches
Vein superior thyroid vein, middle thyroid vein, inferior thyroid vein, kocher's vein or 4th thyroid vein
Nerve sympathetic system middle cervical ganglion, inferior cervical ganglion
Lymph prelaryngeal, pretracheal, jugulo-diagastric groups of lymph nodes
Precursor Thyroid diverticulum (an extension of endoderm into 2nd Branchial arch)
MeSH Thyroid+Gland
Dorlands/Elsevier Thyroid gland

The thyroid is one of the largest endocrine glands in the body. This gland is found in the neck, inferior to (below) the thyroid cartilage (also known as the Adam's apple) and at approximately the same level as the cricoid cartilage. The thyroid controls how quickly the body uses energy, makes proteins, and controls how sensitive the body should be to other hormones.

The thyroid participates in these processes by producing thyroid hormones, principally thyroxine (T4) and triiodothyronine (T3). These hormones regulate the rate of metabolism and affect the growth and rate of function of many other systems in the body. Iodine and tyrosine are used to form both T3 and T4. The thyroid also produces the hormone calcitonin, which plays a role in calcium homeostasis.

The thyroid is controlled by the hypothalamus and pituitary. The gland gets its name from the Greek word for "shield", after the shape of the related thyroid cartilage. Hyperthyroidism (overactive thyroid) and hypothyroidism (underactive thyroid) are the most common problems of the thyroid gland.



The thyroid gland is a butterfly-shape organ and is composed of two cone-like lobes or wings, lobus dexter (right lobe) and lobus sinister (left lobe), and is also connected with the isthmus. The organ is situated on the anterior side of the neck, lying against and around the larynx and trachea, reaching posteriorly the oesophagus and carotid sheath. It starts cranially at the oblique line on the thyroid cartilage (just below the laryngeal prominence or Adam's apple) and extends inferiorly to the fifth or sixth tracheal ring.[1] It is difficult to demarcate the gland's upper and lower border with vertebral levels because it moves position in relation to these during swallowing.

The thyroid gland is covered by a fibrous sheath, the capsula glandulae thyroidea, composed of an internal and external layer. The external layer is anteriorly continuous with the lamina pretrachealis fasciae cervicalis and posteriorolaterally continuous with the carotid sheath. The gland is covered anteriorly with infrahyoid muscles and laterally with the sternocleidomastoid muscle. On the posterior side, the gland is fixed to the cricoid and tracheal cartilage and cricopharyngeus muscle by a thickening of the fascia to form the posterior suspensory ligament of Berry[2][3]. In variable extent, Lalouette's Pyramid, a pyramidal extension of the thyroid lobe, is present at the most anterior side of the lobe. In this region, the recurrent laryngeal nerve and the inferior thyroid artery pass next to or in the ligament and tubercle. Between the two layers of the capsule and on the posterior side of the lobes there are on each side two parathyroid glands.

The thyroid isthmus is variable in presence and size, and can encompass a cranially extending pyramid lobe (lobus pyramidalis or processus pyramidalis), remnant of the thyroglossal duct. The thyroid is one of the larger endocrine glands, weighing 2-3 grams in neonates and 18-60 grams in adults, and is increased in pregnancy.

The thyroid is supplied with arterial blood from the superior thyroid artery, a branch of the external carotid artery, and the inferior thyroid artery, a branch of the thyrocervical trunk, and sometimes by the thyroid ima artery, branching directly from the brachiocephalic trunk. The venous blood is drained via superior thyroid veins, draining in the internal jugular vein, and via inferior thyroid veins, draining via the plexus thyroideus impar in the left brachiocephalic vein.

Lymphatic drainage passes frequently the lateral deep cervical lymph nodes and the pre- and parathracheal lymph nodes. The gland is supplied by sympathetic nerve input from the superior cervical ganglion and the cervicothoracic ganglion of the sympathetic trunk[citation needed], and by parasympathetic nerve input from the superior laryngeal nerve and the recurrent laryngeal nerve.


Embryological development

In the fetus, at 3–4 weeks of gestation, the thyroid gland appears as an epithelial proliferation in the floor of the pharynx at the base of the tongue between the tuberculum impar and the copula linguae at a point latter indicated by the foramen cecum. The thyroid then descends in front of the pharyngeal gut as a bilobed diverticulum through the thyroglossal duct. Over the next few weeks, it migrates to the base of the neck. During migration, the thyroid remains connected to the tongue by a narrow canal, the thyroglossal duct. The fetus starts making its own thyroid-stimulating hormone (TSH) by week 8, and the follicles of the thyroid begin to make colloid and thyroxine by the 10th week.This article was originally based on an entry from a public domain edition of Gray's Anatomy. As such, some of the information contained within it may be outdated.

The portion of the thyroid containing the parafollicular C cells, those responsible for the production of calcitonin, are derived from the 4th pharyngeal pouch endoderm. This is first seen as the ultimobranchial body, which joins the primordial thyroid gland during its decent to its final location in the anterior neck.

Floor of pharynx of embryo between 18 and 21 days.


At the microscopic level, there are three primary features of the thyroid: [4]

Feature Description
Follicles The thyroid is composed of spherical follicles that selectively absorb iodine (as iodide ions, I-) from the blood for production of thyroid hormones. Twenty-five percent of all the body's iodide ions are in the thyroid gland. Inside the follicles, colloid serve as a reservoir of materials for thyroid hormone production and, to a lesser extent, act as a reservoir for the hormones themselves. Colloid is rich in a protein called thyroglobulin.
Thyroid epithelial cells
(or "follicular cells")
The follicles are surrounded by a single layer of thyroid epithelial cells, which secrete T3 and T4. When the gland is not secreting T3/T4 (inactive), the epithelial cells range from low columnar to cuboidal cells. When active, the epithelial cells become tall columnar cells.
Parafollicular cells
(or "C cells")
Scattered among follicular cells and in spaces between the spherical follicles are another type of thyroid cell, parafollicular cells, which secrete calcitonin.


Hashimoto's thyroiditis is an autoimmune disorder whereby the body's own immune system reacts with the thyroid tissues. At the beginning, the gland is overactive, and then becomes underactive as the gland is destroyed. Hashimoto's is most common in middle-age females and tend to run in families. Also more common in individuals with hashimoto's thyroiditis are type 1 diabetes and celiac disease. [5]

Postpartum thyroiditis occurs in some females following delivery. The gland gets inflamed and the condition initially presents with over activity of the gland followed by under activity. In some cases, the gland does recover with time and resume its functions.

Graves' disease is also a common cause of thyroid gland over activity. The disorder results from excess stimulation of the thyroid gland. Graves' disease is sometimes known as diffuse toxic goiter and is much more common in women than men. It usually presents with symptoms in the 2-3rd decade of life. The majority of individuals will present with an enlarged thyroid, protruding eyes, palpitations, excess sweating, diarrhea, weight loss, muscle weakness and unusual sensitivity to heat.

Cancers do occur in the thyroid gland and, in general, are more common in females. In most cases, the thyroid cancer presents as a painless mass in the neck. It is very unusual for the thyroid cancers to present with symptoms, unless it has been neglected. One may be able to feel a hard nodule in the neck. Diagnosis is made using a needle biopsy and various radiological studies. All thyroid cancers are treated with surgery. [6]

Many individuals may find the presence of small masses (nodules) in the neck. The majority of these thyroid nodules are benign (non cancerous). The presence of a thyroid nodule does not mean one has thyroid disease. Most thyroid nodules do not cause any symptoms, and most are discovered on an incidental exam. Doctors usually perform a needle aspiration biopsy of the thyroid to determine the status of the nodules. If the nodule is found to be non-cancerous, no other treatment is required. If the nodule is suspicious, then surgery is recommended.


The primary function of the thyroid is production of the hormones thyroxine (T4), triiodothyronine (T3), and calcitonin. Up to 80% of the T4 is converted to T3 by peripheral organs such as the liver, kidney and spleen. T3 is about ten times more active than T4.[7]

T3 and T4 production and action

The system of the thyroid hormones T3 and T4.[8]

Thyroxine (T4) is synthesised by the follicular cells from free tyrosine and on the tyrosine residues of the protein called thyroglobulin (Tg). Iodine is captured with the "iodine trap" by the hydrogen peroxide generated by the enzyme thyroid peroxidase (TPO)[9] and linked to the 3' and 5' sites of the benzene ring of the tyrosine residues on Tg, and on free tyrosine. Upon stimulation by the thyroid-stimulating hormone (TSH), the follicular cells reabsorb Tg and proteolytically cleave the iodinated tyrosines from Tg, forming T4 and T3 (in T3, one iodine atom is absent compared to T4), and releasing them into the blood. Deiodinase enzymes convert T4 to T3.[10] Thyroid hormone that is secreted from the gland is about 90% T4 and about 10% T3.[7]

Cells of the brain are a major target for the thyroid hormones T3 and T4. Thyroid hormones play a particularly crucial role in brain maturation during fetal development.[11] A transport protein that seems to be important for T4 transport across the blood-brain barrier (OATP1C1) has been identified.[12] A second transport protein (MCT8) is important for T3 transport across brain cell membranes.[12]

Non-genomic actions of T4 are those that are not initiated by liganding of the hormone to intranuclear thyroid receptor. These may begin at the plasma membrane or within cytoplasm. Plasma membrane-initiated actions begin at a receptor on the integrin alphaV beta3 that activates ERK1/2. This binding culminates in local membrane actions on ion transport systems such as the Na(+)/H(+) exchanger or complex cellular events including cell proliferation. These integrins are concentrated on cells of the vasculature and on some types of tumor cells, which in part explains the proangiogenic effects of iodothyronines and proliferative actions of thyroid hormone on some cancers including gliomas. T4 also acts on the mitochondrial genome via imported isoforms of nuclear thyroid receptors to affect several mitochondrial transcription factors. Regulation of actin polymerization by T4 is critical to cell migration in neurons and glial cells and is important to brain development.

T3 can activate phosphatidylinositol 3-kinase by a mechanism that may be cytoplasmic in origin or may begin at integrin alpha V beta3.

In the blood, T4 and T3 are partially bound to thyroxine-binding globulin, transthyretin, and albumin. Only a very small fraction of the circulating hormone is free (unbound) - T4 0.03% and T3 0.3%. Only the free fraction has hormonal activity. As with the steroid hormones and retinoic acid, thyroid hormones cross the cell membrane and bind to intracellular receptors1, α2, β1 and β2), which act alone, in pairs or together with the retinoid X-receptor as transcription factors to modulate DNA transcription[1].

T3 and T4 regulation

The production of thyroxine and triiodothyronine is regulated by thyroid-stimulating hormone (TSH), released by the anterior pituitary. The thyroid and thyrotropes form a negative feedback loop: TSH production is suppressed when the T4 levels are high, and vice versa. The TSH production itself is modulated by thyrotropin-releasing hormone (TRH), which is produced by the hypothalamus and secreted at an increased rate in situations such as cold (in which an accelerated metabolism would generate more heat). TSH production is blunted by somatostatin (SRIH), rising levels of glucocorticoids and sex hormones (estrogen and testosterone), and excessively high blood iodide concentration.

An additional hormone produced by the thyroid contributes to the regulation of blood calcium levels. Parafollicular cells produce calcitonin in response to hypercalcemia. Calcitonin stimulates movement of calcium into bone, in opposition to the effects of parathyroid hormone (PTH). However, calcitonin seems far less essential than PTH, as calcium metabolism remains clinically normal after removal of the thyroid (thyroidectomy), but not the parathyroids.

Significance of iodine

In areas of the world where iodine is lacking in the diet, the thyroid gland can be considerably enlarged, resulting in the enlarged thyroid glands of endemic goitre. In this situation, women with severe iodine deficiency can give birth to infants with thyroid hormone deficiency, who will have physical growth and development problems. Brain development can be severely impaired. This is a condition called endemic cretinism, and it is one cause of congenital hypothyroidism. Newborn children in many developed countries are now routinely tested for congenital hypothyroidism as part of newborn screening. Children with congenital hypothyroidism are treated by supplementation with levothyroxine, which enables them to grow and develop normally.

Thyroxine is critical to the regulation of metabolism and growth throughout the animal kingdom. Among amphibians, for example, administering a thyroid-blocking agent such as propylthiouracil (PTU) can prevent tadpoles from metamorphosing into frogs; in contrast, administering thyroxine will trigger metamorphosis.

Because the thyroid concentrates this element, it also concentrates various radioactive isotopes of iodine produced by nuclear fission. In the event of large accidental releases of such material into the environment, the uptake of radioactive iodine isotopes by the thyroid can, in theory, be blocked by saturating the uptake mechanism with a large surplus of non-radioactive iodine, taken in the form of potassium iodide tablets. While biological researchers making compounds labelled with iodine isotopes do this,November 2009 in the wider world such preventive measures are usually not stockpiled before an accident, nor are they distributed adequately afterward.[citation needed] One consequence of the Chernobyl disaster was an increase in thyroid cancers in children in the years following the accident.[13]

The use of iodised salt is an efficient way to add iodine to the diet. It has eliminated endemic cretinism in most developed countries, and some governments have made the iodination of flour, cooking oil or salt mandatory. Potassium iodide and sodium iodide are typically used forms of supplemental iodine.

As with most substances, either too much or too little can cause problems. Recent studies on some populations are showing that excess iodine intake could cause an inceased prevelence of autoimmune thyroid disease resulting in permanent hypothyroidism.[14] Some governments are reviewing the quantity of iodine added to salt using local salt consumption data.[citation needed]

Treatment for Hyperthyroidism

Beta blockers are used to decrease symptoms like fast heart rate, tremors, anxiety and chest palpitations, and are sometimes anti thyroid drugs used to block thyroid hormones. These medications take several months to take full effect and have side effects like skin rash or a drop in white blood cell count, which decreases the ability of the body to fight off infections. Because of the side effects of drugs, many patients choose to undergo surgery or the use of radioactive iodine. Sometimes, radioactive iodine is administered to destroy the gland; the radioactive iodine is selectively taken up by the gland and gradually destroys the tissues. The treatment has been noted to be safe and effective.

Individuals that have underactivity of the thyroid gland require hormone replacement therapy. Several types of thyroid hormone replacements are available and all are very safe but need to be taken for the rest of one's life. Thyroid hormone treatment is given under the care of a physician and may take a few weeks to become effective. [15]

Surgery is often used to treat overactive thyroid, thyroid nodules, and thyroid cancers. The surgery is quite effective but can have a few side effects:

  • The nerves controlling the vocal cords can be damaged.
  • The glands that produce calcium can be destroyed and one can develop bleeding.
  • If the entire thyroid gland is removed, one develops hypothyroidism, which entails taking hormone supplements for the rest of one's life. [16]


There are several findings that evidence a great interest for thyroid disorders just in the Medieval Medical School of Salerno (XII Century). Rogerius Salernitanus, the Salernitan surgeon and author of "Post mundi fabricam" (around 1180) was considered at that time the surgical text par excellence all over Europe. In the chapter "De bocio" of his magnum opus, he describes several pharmacological and surgical cures, some of which nowadays are reappraised quite scientifically effective.[17]

In modern times, the thyroid was first identified by the anatomist Thomas Wharton (whose name is also eponymised in Wharton's duct of the submandibular gland) in 1656.[18]

Thyroxin was identified only in the 19th century.

In other animals

The thyroid gland is found in all vertebrates. In fishes, it is, in general, located below the gills and is not always divided into distinct lobes. However, in some teleosts, patches of thyroid tissue are found elsewhere in the body, associated with the kidneys, spleen, heart, or eyes.[19]

In tetrapods, the thyroid is always found somewhere in the neck region. In most tetrapod species, there are two paired thyroid glands - that is, the right and left lobes are not joined together. However, there is only ever a single thyroid gland in most mammals, and the shape found in humans is common to many other species.[19]

In larval lampreys, the thyroid originates as an exocrine gland, secreting its hormones into the gut, and associated with the larva's filter-feeding apparatus. In the adult lamprey, the gland separates from the gut, and becomes endocrine, but this path of development may reflect the evolutionary origin of the thyroid. For instance, the closest living relatives of vertebrates, the tunicates and Amphioxus, have a structure very similar to that of larval lampreys, and this also secretes iodine-containing compounds (albeit not thyroxine).[19]

Additional images

See also


  1. ^ Clinical Case - Anterior Triangle of the Neck.
  2. ^ Yalçin B., Ozan H. (February 2006). "Detailed investigation of the relationship between the inferior laryngeal nerve including laryngeal branches and ligament of Berry". Journal of the American College of Surgeons 202 (2): 291–6. doi:10.1016/j.jamcollsurg.2005.09.025. PMID 16427555. 
  3. ^ Lemaire, David (2005-05-27). "eMedicine - Thyroid anatomy". Retrieved 2008-01-19. 
  4. ^ Fawcett, Don; Jensh, Ronald (2002). Bloom & Fawcett's Concise Histology. New York: Arnold Publishers. pp. 257-258. ISBN 0-340-80677-X. 
  5. ^ Treatment for Thyroid disease Retrieved on 2010-02-07
  6. ^ Thyroid Disorders overview Merck Sharpe & Dohme. Retrieved on 2010-02-07
  7. ^ a b The thyroid gland in Endocrinology: An Integrated Approach by Stephen Nussey and Saffron Whitehead (2001) Published by BIOS Scientific Publishers Ltd. ISBN 1-85996-252-1 .
  8. ^ References used in image are found in image article in Commons:Commons:File:Thyroid_system.png#References.
  9. ^ Ekholm R, Bjorkman U (1997). "Glutathione peroxidase degrades intracellular hydrogen peroxide and thereby inhibits intracellular protein iodination in thyroid epithelium". Endocrinology 138 (7): 2871–2878. doi:10.1210/en.138.7.2871. PMID 9202230. 
  10. ^ Bianco AC, Salvatore D, Gereben B, Berry MJ, Larsen PR (2002). "Biochemistry, cellular and molecular biology, and physiological roles of the iodothyronine selenodeiodinases". Endocr Rev 23 (1): 38–89. doi:10.1210/er.23.1.38. PMID 11844744. 
  11. ^ Kester MH, Martinez de Mena R, Obregon MJ, Marinkovic D, Howatson A, Visser TJ, Hume R, Morreale de Escobar G (2004). "Iodothyronine levels in the human developing brain: major regulatory roles of iodothyronine deiodinases in different areas". J Clin Endocrinol Metab 89 (7): 3117–3128. doi:10.1210/jc.2003-031832. PMID 15240580. 
  12. ^ a b Jansen J, Friesema ECH, Milici C, Visser TJ (2005). Thyroid hormone transporters in health and disease. Thyroid 15;757-768. PMID 16131319.
  13. ^ BBC NEWS | Science/Nature | Chernobyl children show DNA changes
  14. ^ Patrick L (June 2008). "Iodine: deficiency and therapeutic considerations" (PDF). Altern Med Rev 13 (2): 116–27. PMID 18590348. 
  15. ^ Thyroid Disorders Information MedicineNet. Retrieved on 2010-02-07
  16. ^ Thyroid Problems eMedicine Health. Retrieved on 2010-02-07
  17. ^ Bifulco M, Cavallo P (2007). "Thyroidology in the medieval medical school of salerno". Thyroid 17 (1): 39–40. doi:10.1089/thy.2006.0277. PMID 17274747. 
  18. ^ Thomas Wharton at Who Named It?
  19. ^ a b c Romer, Alfred Sherwood; Parsons, Thomas S. (1977). The Vertebrate Body. Philadelphia, PA: Holt-Saunders International. pp. 555-556. ISBN 0-03-910284-X. 

External links

1911 encyclopedia

Up to date as of January 14, 2010

From LoveToKnow 1911

THYROID (Gr. Oupo€Cli)s, shield-shaped, from Ovpcbc, a large oblong shield, shaped like a door, Om pa, and Eibos, form), in anatomy, a term applied (i) to the largest of the cartilages of the larynx (see Respiratory System), (2) to one of two arteries which lie near the thyroid cartilage and gland (see Arteries), and (3) to a vascular ductless gland, which rests on the larynx and upper part of the trachea (see Ductless Glands). The thyroid gland is used in medicine in two forms. Thyroideum siccum is a light dull brown powder, prepared by drying the thyroid gland of a sheep. Its chief constituent is a proteid known as thyreoglobulin, the active principle of which contains 9.3% of iodine and 0.5% of phosphorus, and is known as iodothyrin or thyroiodin. The dried gland easily becomes damp and deteriorates. Liquor thyroidei is a pink turbid liquid made by macerating the fresh gland of a sheep with glycerin and phenol.

XXVI. 29 a Thyroid gland administered to man increases the pulse rate, causes increased and enfeebled cardiac beat and leads to increased metabolism, consequently excess of urea, uric acid and phosphates are excreted in the urine; it therefore reduces the body weight. Glycosuria develops from the inability of the body to ingest glucose. Overdoses of thyroid cause rapid pulse, headache and vomiting, together with diarrhoea and pruritus, emaciation and weakness. These symptoms are known as thyroidism. Thyroid gland was introduced for the treatment of patients suffering from goitre, myxoedema and cretinism, in which diseases it has been remarkably successful, cretins growing rapidly under the thyroid treatment and developing intelligence. It has also been used in dwarfism, excessive obesity, psoriasis and scleroderma. When used in obesity an excess of nitrogenous food should be taken to balance the destruction of proteid. In certain forms of insanity, melancholia and climacteric insanities it has given good results. Full doses of thyroid are valuable in the prevention and relief of eclampsia. It should not be given to patients suffering from exophthalmic goitre, for which an anti-thyroid serum (antithyreoidin of Moebius), which is the serum of thyroidectomized animals, has been. introduced.

Rodagen is a white powder consisting of the dried milk of thyroidectomized goats, mixed with 50% of milk sugar. In exophthalmic goitre this preparation causes a reduction of the swelling and of the pulse rate, and an increase of body weight.

<< Thymol

Thyrostraca >>

Simple English

s. (Male left, female on the right.) 1. Pineal gland 2. Pituitary gland 3. Thyroid gland 4. Thymus 5. Adrenal gland 6. Pancreas 7. Ovary 8. Testes]]

The thyroid is one of the largest endocrine glands in the body. This gland is found in the neck below the mouth (see number 3 in the picture on the right). The thyroid controls how quickly the body burns energy, makes proteins, and how sensitive the body should be to other hormones.



Hyper- and hypofunction (affects about 2% of the population)

  • Hypothyroidism (underactivity)
    • Hashimoto's thyroiditis / thyroiditis
    • Ord's thyroiditis
    • Postoperative hypothyroidism
    • Postpartum thyroiditis
    • Silent thyroiditis
    • Acute thyroiditis
    • Iatrogenic hypothyroidism
  • Hyperthyroidism (overactivity)
    • Thyroid storm
    • Graves-Basedow disease
    • Toxic thyroid nodule
    • Toxic nodular struma (Plummer's disease)
    • Hashitoxicosis
    • Iatrogenic hyperthyroidism
    • De Quervain thyroiditis (inflammation starting as hyperthyroidism, can end as hypothyroidism)

Anatomical problems

  • Goitre
    • Endemic goitre
    • Diffuse goitre
    • Multinodular goitre
  • Lingual thyroid
  • Thyroglossal duct cyst



  • Cretinism

Additional images

Other pages

Other websites

Endocrine system
Adrenal gland - Corpus luteum - Hypothalamus - Ovaries - Pancreas - Parathyroid gland - Pineal gland - Pituitary gland - Testes - Thyroid gland - Hormone


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