Thyroid - Wikipedia, The Free Encyclopedia

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Not to be confused with the parathyroid glands

In vertebrate anatomy, the thyroid gland or simply, the thyroid (pronounced /ˈθaɪrɔɪd .../), is one of thelargest endocrine glands. The thyroid gland is found in the neck, below (inferior to) the thyroid cartilage(which forms the laryngeal prominence, or 'Adam's Apple'). The isthmus (the bridge between the two lobesof the thyroid) is located inferior to the cricoid cartilage.

The thyroid gland controls how quickly the body uses energy, makes proteins, and controls how sensitive thebody should be to other hormones. It participates in these processes by producing thyroid hormones, theprincipal ones being triiodothyronine (T

3) and thyroxine (T

4). These hormones regulate the rate of

metabolism and affect the growth and rate of function of many other systems in the body. T3 and T4 are

synthesized from both iodine and tyrosine. The thyroid also produces calcitonin, which plays a role incalcium homeostasis.

Hormonal output from the thyroid is regulated by thyroid-stimulating hormone (TSH) produced by theanterior pituitary, which itself is regulated by thyrotropin-releasing hormone (TRH) produced by thehypothalamus.

The thyroid gets its name from the Greek word for "shield", after the shape of the related thyroid cartilage.The most common problems of the thyroid gland consist of an overactive thyroid gland, referred to ashyperthyroidism, and an underactive thyroid gland, referred to as hypothyroidism.

Thyroid - Wikipedia, the free encyclopedia http://en.wikipedia.org/wiki/Thyroid_gland

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1 Anatomy1.1 Evolution1.2 Embryological development1.3 Histology

2 Disorders2.1 Hyperthyroidism2.2 Hypothyroidism2.3 Initial hyperthyroidism followed by hypothyroidism2.4 Cancers2.5 Non-cancerous nodules2.6 Other disorders

3 Physiology3.1 T3 and T4 production and action

3.2 T3 and T4 regulation

3.3 Thyroid function tests3.4 Significance of iodine

4 History5 In animals6 Additional images7 See also8 References9 External links

The thyroid gland is a butterfly-shaped organ and is composed of two cone-like lobes or wings, lobus dexter(right lobe) and lobus sinister (left lobe), connected via the isthmus. The organ is situated on the anteriorside of the neck, lying against and around the larynx and trachea, reaching posteriorly the oesophagus andcarotid 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 approximately the fifth or sixth tracheal ring.[1] Itis difficult to demarcate the gland's upper and lower border with vertebral levels because it moves positionin relation to these during swallowing.

The thyroid gland is covered by a fibrous sheath, the capsula glandulae thyroidea, composed of an internaland external layer. The external layer is anteriorly continuous with the lamina pretrachealis fasciaecervicalis and posteriorolaterally continuous with the carotid sheath. The gland is covered anteriorly withinfrahyoid muscles and laterally with the sternocleidomastoid muscle also known as sternomastoid 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] The thyroid gland's firm

attachment to the underlying trachea is the reason behind its movement with swallowing.[4] In variableextent, Lalouette's Pyramid, a pyramidal extension of the thyroid lobe, is present at the most anterior side ofthe lobe. In this region, the recurrent laryngeal nerve and the inferior thyroid artery pass next to or in theligament and tubercle.

Between the two layers of the capsule and on the posterior side of the lobes, there are on each side twoparathyroid glands.

The thyroid isthmus is variable in presence and size, and can encompass a cranially extending pyramid lobe


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(lobus pyramidalis or processus pyramidalis), remnant of the thyroglossal duct. The thyroid is one of thelarger endocrine glands, weighing 2-3 grams in neonates and 18-60 grams in adults, and is increased inpregnancy.

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

Lymphatic drainage passes frequently the lateral deep cervical lymph nodes and the pre- and parathracheallymph nodes. The gland is supplied by parasympathetic nerve input from the superior laryngeal nerve andthe recurrent laryngeal nerve.

Evolution

Thyroid cells phylogenetically derived from primitive iodide-concentrating gastroenteric cells (endostyle)which, during evolution, migrated and specialized in uptake and storage of iodine in follicular cellular

structures, also in order to adapt the organisms from iodine-rich sea to iodine-deficient land. Venturi et al.[5]

suggested that iodide has an ancestral antioxidant function in all iodide-concentrating cells from primitivealgae to more recent vertebrates. In 2008, this ancestral antioxidant action of iodides has been

experimentally confirmed by Küpper et al.[6] Since 700 million years ago thyroxine is present in fibrousexoskeletal scleroproteins of the lowest invertebrates (Porifera and Anthozoa), without showing anyhormonal action. When some primitive marine chordates started to emerge from the iodine-rich sea andtransferred to iodine-deficient fresh water and finally land, their diet became iodine deficient. Therefore,during progressive slow adaptation to terrestrial life, the primitive vertebrates learned to use the primitivethyroxine in order to transport antioxidant iodide into the cells. Therefore, the remaining triiodothyronine(T

3), the real active hormone, became active in the metamorphosis and thermogenesis for a better adaptation

of the organisms to terrestrial environment (fresh water, atmosphere, gravity, temperature and diet). In fact,the U.S. Food and Nutrition Board and Institute of Medicine recommended daily allowance of iodine rangesfrom 150 micrograms /day for adult humans to 290 micrograms /day for lactating mothers. However, thethyroid gland needs no more than 70 micrograms /day to synthesize the requisite daily amounts of T4 and

T3. These higher recommended daily allowance levels of iodine seem necessary for optimal function of a

number of body systems, including lactating breast, gastric mucosa, salivary glands, oral mucosa, thymus,

epidermis, choroid plexus and brain,[7] etc.[8][9][10]

Embryological development

In the fetus, at 3–4 weeks of gestation, the thyroid gland appears as an epithelial proliferation in the floor ofthe pharynx at the base of the tongue between the tuberculum impar and the copula linguae at a point laterindicated by the foramen cecum. The thyroid then descends in front of the pharyngeal gut as a bilobeddiverticulum 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.

Thyrotropin-releasing hormone (TRH) and thyroid-stimulating hormone (TSH) start being secreted from thefetal hypothalamus and pituitary at 18-20 weeks of gestation, and fetal production of thyroxine (T4) reach a

clinically significant level at 18–20 weeks.[11] Fetal triiodothyronine (T3) remains low (less than 15 ng/dL)

until 30 weeks of gestation, and increases to 50 ng/dL at term.[11] Fetal self-sufficiency of thyroid hormones

protects the fetus against e.g. brain development abnormalities caused by maternal hypothyroidism.[12]

However, preterm births can suffer neurodevelopmental disorders due to lack of maternal thyroid hormones

due their own thyroid being insufficiently developed to meet their postnatal needs.[13]


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The portion of the thyroid containing the parafollicular C cells, those responsible for the production ofcalcitonin, are derived from the neural crest. This is first seen as the ultimobranchial body, which joins theprimordial thyroid gland during its descent to its final location in the anterior neck.

Aberrations in embryological development can cause various forms of thyroid dysgenesis.

Histology

At the microscopic level, there are three primary features of the thyroid:[14]

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, but also forstorage of iodine in thyroglobulin, in fact iodine is necessary for other importantiodine-concentrating organs as breast, stomach, salivary glands, thymus etc. (seeiodine in biology).

Twenty-five percent of all the body's iodide ions are in the thyroid gland. Insidethe follicles, colloid serves as a reservoir of materials for thyroid hormoneproduction and, to a lesser extent, acts as a reservoir for the hormonesthemselves. 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, whichsecrete T3 and T4. When the gland is not secreting T3/T4 (inactive), the

epithelial cells range from low columnar to cuboidal cells. When active, theepithelial cells become tall columnar cells.

Parafollicular cells(or "C cells")

Scattered among follicular cells and in spaces between the spherical follicles areanother type of thyroid cell, parafollicular cells, which secrete calcitonin.

Thyroid disorders include hyperthyroidism (abnormally increased activity), hypothyroidism (abnormallydecreased activity) and thyroid nodules, which are generally benign thyroid neoplasms, but may be thyroid


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cancers. All these disorders may give rise to goiter, that is, an enlarged thyroid.

Hyperthyroidism

Main article: Hyperthyroidism

Hyperthyroidism, or overactive thyroid, is the overproduction of the thyroid hormones T3 and T

4, and is

most commonly caused by the development of Graves' disease,[citation needed] an autoimmune disease inwhich antibodies are produced which stimulate the thyroid to secrete excessive quantities of thyroidhormones. The disease can result in the formation of a toxic goiter as a result of thyroid growth in responseto a lack of negative feedback mechanisms. It presents with symptoms such as a thyroid goiter, protrudingeyes (exopthalmos), palpitations, excess sweating, diarrhea, weight loss, muscle weakness and unusualsensitivity to heat.

Beta blockers are used to decrease symptoms of hyperthyroidism such as increased heart rate, tremors,anxiety and heart palpitations, and anti-thyroid drugs are used to decrease the production of thyroidhormones, in particular, in the case of Graves' disease. These medications take several months to take fulleffect and have side-effects such as skin rash or a drop in white blood cell count, which decreases the abilityof the body to fight off infections. These drugs involve frequent dosing (often one pill every 8 hours) andoften require frequent doctor visits and blood tests to monitor the treatment, and may sometimes loseeffectiveness over time. Due to the side-effects and inconvenience of such drug regimens, some patientschoose to undergo radioactive iodine-131 treatment. Radioactive iodine is administered in order to destroy aproportion of or the entire thyroid gland, since the radioactive iodine is selectively taken up by the gland andgradually destroys the cells of the gland. Alternatively, the gland may be partially or entirely removedsurgically, though iodine treatment is usually preferred since the surgery is invasive and carries a risk ofdamage to the parathyroid glands or the nerves controlling the vocal cords. If the entire thyroid gland is

removed, hypothyroidism results.[15]

Hypothyroidism

Main article: Hypothyroidism

Hypothyroidism is the underproduction of the thyroid hormones T3 and T

4. Hypothyroid disorders may

occur as a result of congenital thyroid abnormalities (see congenital hypothyroidism), autoimmune disorderssuch as Hashimoto's thyroiditis, iodine deficiency (more likely in poorer countries) or the removal of thethyroid following surgery to treat severe hyperthyroidism and/or thyroid cancer. Typical symptoms areabnormal weight gain, tiredness, baldness, cold intolerance, and bradycardia. Hypothyroidism is treated withhormone replacement therapy, such as levothyroxine, which is typically required for the rest of the patient'slife. Thyroid hormone treatment is given under the care of a physician and may take a few weeks to become

effective.[16]

Negative feedback mechanisms result in growth of the thyroid gland when thyroid hormones are beingproduced in sufficiently low quantities as a means of increasing the thyroid output; however, where thehypothyroidism is caused by iodine insufficiency, the thyroid is unable to produce T

3 and T

4 and as a result,

the thyroid may continue to grow to form a non-toxic goiter. It is termed non-toxic as it does not producetoxic quantities of thyroid hormones, despite its size.

Initial hyperthyroidism followed by hypothyroidism

This is the overproduction of T3 and T

4 followed by the underproduction of T

3 and T

4. There are two types:

Hashimoto's thyroiditis and postpartum thyroiditis.


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Hashimoto's thyroiditis or Hashimoto's Disease is an autoimmune disorder whereby the body's own immunesystem reacts with the thyroid tissues in an attempt to destroy it. At the beginning, the gland may beoveractive, and then becomes underactive as the gland is damaged resulting in too little thyroid hormoneproduction or hypothyroidism. Some patients may experience "swings" in hormone levels that can progressrapidly from hyper-to-hypothyroid (sometimes mistaken as severe moodswings, or even being bipolar,before the proper clinical diagnosis is made). Some patients may experience these "swings" over a longerperiod of time, over days or weeks or even months. Hashimoto's is more common in females than males,usually appearing after the age of 30, and tends to run in families meaning it can be seen as a geneticdisease. Also more common in individuals with Hashimoto's Thyroiditis are type 1 diabetes and celiac

disease.[17]

Postpartum thyroiditis occurs in some females following the birth of a child. After delivery, the glandbecomes inflamed and the condition initially presents with overactivity of the gland followed byunderactivity. In some cases, the gland may recover with time and resume its functions. In others it may not.The etiology is not always known, but can sometimes be attributed to autoimmunity, such as Hashimoto'sThyroiditis or Graves' Disease.

Cancers

Main article: Thyroid cancer

Cancers do occur in the thyroid gland and are more common in females.[citation needed] In most cases, thethyroid cancer presents as a painless mass in the neck. It is very unusual for the thyroid cancers to presentwith 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.[18]

Non-cancerous nodules

Further information: Thyroid nodule

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

Other disorders

Limited research shows that seasonal allergies may trigger episodes of hypo- or hyperthyroidism.[19][20]

A ectopic thyroid is an entire or parts of the thyroid located in another part of the body than whatis the usual case.

The primary function of the thyroid is production of the hormones triiodothyronine (T3), thyroxine (T

4), and

calcitonin. Up to 80% of the T4 is converted to T

3 by peripheral organs such as the liver, kidney and spleen.

T3 is several times more powerful than T4, which is largely a prohormone, perhaps four[21] or even ten times

more active.[22]


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The system of the thyroid hormones T3 and T

4.[23]

Synthesis of the thyroid hormones, as seen on an individual thyroid

follicular cell:[24]

- Thyroglobulin is synthesized in the rough endoplasmic reticulum

and follows the secretory pathway to enter the colloid in the lumen of

the thyroid follicle by exocytosis.

- Meanwhile, a sodium-iodide (Na/I) symporter pumps iodide (I-)

actively into the cell, which previously has crossed the endothelium

by largely unknown mechanisms.

- This iodide enters the follicular lumen from the cytoplasm by the

transporter pendrin, in a purportedly passive manner.[25]

- In the colloid, iodide (I-) is oxidized to iodine (I0) by an enzyme

called thyroid peroxidase.

- Iodine (I0) is very reactive and iodinates the thyroglobulin at tyrosyl

residues in its protein chain (in total containing approximately 120

tyrosyl residues).

T3 and T4 production and action

Thyroxine (T4) is synthesised by the follicular cells from

free tyrosine and on the tyrosine residues of the proteincalled thyroglobulin (Tg). Iodine is captured with the"iodine trap" by the hydrogen peroxide generated by the

enzyme thyroid peroxidase (TPO)[26] and linked to the3' and 5' sites of the benzene ring of the tyrosine residueson Tg, and on free tyrosine. Upon stimulation by thethyroid-stimulating hormone (TSH), the follicular cellsreabsorb Tg and cleave the iodinated tyrosines from Tgin lysosomes, 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.[27]

Thyroid hormone secreted from the gland is about

80-90% T4 and about 10-20% T

3.[21][22]

Cells of the developing brain are a major target for thethyroid hormones T

3 and T

4. Thyroid hormones play a

particularly crucial role in brain maturation during fetal

development.[28] A transport protein that seems to beimportant for T4 transport across the

blood-brain barrier (OATP1C1(http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=gene&cmd=Retrieve&dopt=full_report&list_uids=53919) ) has

been identified.[29] A second transportprotein (MCT8(http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=300095) ) is importantfor T3 transport across brain cell

membranes.[29]

Non-genomic actions of T4 are those that

are not initiated by liganding of thehormone to intranuclear thyroid receptor.These may begin at the plasmamembrane or within cytoplasm. Plasmamembrane-initiated actions begin at areceptor on the integrin alphaV beta3that activates ERK1/2. This bindingculminates in local membrane actions onion transport systems such as theNa(+)/H(+) exchanger or complexcellular events including cellproliferation. These integrins areconcentrated on cells of the vasculatureand on some types of tumor cells, whichin part explains the proangiogenic effects


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- In conjugation, adjacent tyrosyl residues are paired together.

- The entire complex re-enters the follicular cell by endocytosis.

- Proteolysis by various proteases liberates thyroxine and

triiodothyronine molecules, which enters the blood by largely

unknown mechanisms.

of iodothyronines and proliferativeactions of thyroid hormone on somecancers including gliomas. T4 also acts

on the mitochondrial genome viaimported isoforms of nuclear thyroidreceptors to affect several mitochondrialtranscription 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 (TBG), transthyretin, and albumin.

Only a very small fraction of the circulating hormone is free (unbound) - T4 0.03% and T

3 0.3%. Only the

free fraction has hormonal activity. As with the steroid hormones and retinoic acid, thyroid hormones crossthe cell membrane and bind to intracellular receptors (α

1, α

2, β

1 and β

2), which act alone, in pairs or together

with the retinoid X-receptor as transcription factors to modulate DNA transcription[1](http://arbl.cvmbs.colostate.edu/hbooks/pathphys/endocrine/thyroid/receptors.html) .

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: TSHproduction is suppressed when the T4 levels are high. The TSH production itself is modulated by

thyrotropin-releasing hormone (TRH), which is produced by the hypothalamus and secreted at an increasedrate in situations such as cold exposure (to stimulate thermogenesis). TSH production is blunted bysomatostatin (SRIH), rising levels of glucocorticoids and sex hormones (estrogen and testosterone), andexcessively 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 ofcalcium into bone, in opposition to the effects of parathyroid hormone (PTH). However, calcitonin seems farless essential than PTH, as calcium metabolism remains clinically normal after removal of the thyroid(thyroidectomy), but not the parathyroids.

Thyroid function tests

Main article: Thyroid function tests

Test Abbreviation Normal ranges[30]

Serum thyrotropin/thyroid-stimulating hormone TSH 0.3–3.0 μU/ml

Free thyroxine FT4 7–18 ng/l = 0.7–1.8 ng/dl

Serum triiodothyronine T3 0.8–1.8 μg/l = 80–180 ng/dl

Radioactive iodine-123 uptake RAIU 10–30%

Radioiodine scan (gamma camera) N/A N/A - thyroid contrasted images

Free thyroxine fraction FT4F 0.03–0.005%


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Serum thyroxine T4 46–120 μg/l = 4.6–12.0 μg/dl

Thyroid hormone binding ratio THBR 0.9–1.1

Free thyroxine index FT4I 4–11

Free triiodothyronine l FT3 230–619 pg/d

Free T3 Index FT3I 80–180

Thyroxine-binding globulin TBG 12–20 ug/dl T4 +1.8 μg

TRH stimulation test Peak TSH 9–30 μIU/ml at 20–30 min.

Serum thyroglobulin l Tg 0-30 ng/m

Thyroid microsomal antibody titer TMAb Varies with method

Thyroglobulin antibody titer TgAb Varies with method

μU/ml = mU/l, microunit per milliliterng/dl, nanograms per deciliterμg, microgramspg/d, picograms per dayμIU/ml = mIU/l, micro-international unit per milliliterSee [2] (http://www.aruplab.com/Testing-Information/key-to-units.jsp) for more information onmedical units of measure

Significance of iodine

In areas of the world where iodine is lacking in the diet the thyroid gland can become considerably enlarged,a condition called endemic goiter. Pregnant women on a diet that is severely deficient of iodine can givebirth to infants who can present with thyroid hormone deficiency (congenital hypothyroidism), manifestingin problems of physical growth and development as well as brain development (a condition referred to asendemic cretinism). In many developed countries, newborns are routinely tested for congenitalhypothyroidism as part of newborn screening. Children with congenital hypothyroidism are treatedsupplementally with levothyroxine, which facilitates normal growth and development.

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

Because the thyroid concentrates this element, it also concentrates the various radioactive isotopes of iodineproduced 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 uptakemechanism with a large surplus of non-radioactive iodine, taken in the form of potassium iodide tablets. Oneconsequence of the Chernobyl disaster was an increase in thyroid cancers in children in the years following

the accident.[31]

The use of iodised salt is an efficient way to add iodine to the diet. It has eliminated endemic cretinism inmost developed countries, and some governments have made the iodination of flour, cooking oil, and saltmandatory. 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 somepopulations are showing that excess iodine intake could cause an increased prevelence of autoimmune

thyroid disease, resulting in permanent hypothyroidism.[32]


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There are several findings that evidence a great interest for thyroid disorders just in the Medieval MedicalSchool of Salerno (12th century). Rogerius Salernitanus, the Salernitan surgeon and author of "Post mundifabricam" (around 1180) was considered at that time the surgical text par excellence all over Europe. In thechapter "De bocio" of his magnum opus, he describes several pharmacological and surgical cures, some of

which nowadays are reappraised quite scientifically effective.[33]

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.[34]

Thyroxine was identified only in the 19th century.

The thyroid gland is found in all vertebrates. In fish, it is, in general, located below the gills and is notalways 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.[35]

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

species.[35]

In larval lampreys, the thyroid originates as an exocrine gland, secreting its hormones into the gut, andassociated 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. Forinstance, the closest living relatives of vertebrates, the tunicates and Amphioxus, have a structure verysimilar to that of larval lampreys, and this also secretes iodine-containing compounds (albeit not

thyroxine).[35]

Position of the Thyroidin Males and Females

Section of the neck atabout the level of thesixth cervical vertebra.

Muscles of the neck.Anterior view.


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The arch of the aorta,and its branches.

Superficial dissection ofthe right side of theneck, showing thecarotid and subclavianarteries.

Diagram showingcommon arrangementof thyroid veins.

Sagittal section of nosemouth, pharynx, andlarynx.

Muscles of the pharynx,viewed from behind,together with theassociated vessels andnerves.

The position andrelation of theesophagus in thecervical region and inthe posteriormediastinum. Seenfrom behind.

Section of thyroid glandof sheep. X 160.

The thymus of afull-term fetus, exposedin situ.

Thyoid histology

Thyroid diseaseThyroid disease in pregnancyAcademy of Clinical Thyroidologists


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^ Clinical Case - Anterior Triangle of the Neck. (http://anatomy.med.umich.edu/nervous_system/antneck_case.html)

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^ Kamath, M. Aroon. "Are the ligaments of Berry the only reason why the thyroid moves up with deglutition?"(http://www.doctorslounge.com/index.php/blogs/page/13485) . Doctors Lounge Website.http://www.doctorslounge.com/index.php/blogs/page/13485. Retrieved August 24, 2010.

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^ Küpper FC; Carpenter LJ; McFiggans GB et al. (2008). "Iodide accumulation provides kelp with an inorganicantioxidant impacting atmospheric chemistry" (Free full text). Proceedings of the National Academy of Sciencesof the United States of America 105 (19): 6954–8. doi:10.1073/pnas.0709959105 (http://dx.doi.org/10.1073%2Fpnas.0709959105) . PMC 2383960 (http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=2383960) . PMID 18458346 (http://www.ncbi.nlm.nih.gov/pubmed/18458346) .

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^ Spitzweg, C., Joba, W., Eisenmenger, W. and Heufelder, A.E. (1998). "Analysis of human sodium iodidesymporter gene expression in extrathyroidal tissues and cloning of its complementary deoxyribonucleic acid fromsalivary gland, mammary gland, and gastric mucosa". J Clin Endocrinol Metab. 83 (5): 1746.doi:10.1210/jc.83.5.1746 (http://dx.doi.org/10.1210%2Fjc.83.5.1746) . PMID 9589686(http://www.ncbi.nlm.nih.gov/pubmed/9589686) .

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^ Banerjee, R.K., Bose, A.K., Chakraborty, t.K., de, S.K. and datta, A.G. (1985). "Peroxidase catalysediodotyrosine formation in dispersed cells of mouse extrathyroidal tissues". J Endocrinol. 2: 159.

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^ Hidaka Y, Amino N, Iwatani Y, Itoh E, Matsunaga M, Tamaki H (December 1993). "Recurrence of20.


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^ Ekholm R, Bjorkman U (1997). "Glutathione peroxidase degrades intracellular hydrogen peroxide and therebyinhibits intracellular protein iodination in thyroid epithelium". Endocrinology 138 (7): 2871–2878.doi:10.1210/en.138.7.2871 (http://dx.doi.org/10.1210%2Fen.138.7.2871) . PMID 9202230(http://www.ncbi.nlm.nih.gov/pubmed/9202230) .

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^ Bifulco M, Cavallo P (2007). "Thyroidology in the medieval medical school of salerno". Thyroid 17 (1): 39–40.doi:10.1089/thy.2006.0277 (http://dx.doi.org/10.1089%2Fthy.2006.0277) . PMID 17274747(http://www.ncbi.nlm.nih.gov/pubmed/17274747) .

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^ Thomas Wharton (http://www.whonamedit.com/doctor.cfm/2046.html) at Who Named It?34.^ 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.

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EndocrineWeb.com for more information on thyroid disease, hormones, and surgery(http://www.EndocrineWeb.com)American Thyroid Association (http://www.thyroid.org) (Thyroid Information and professionalorganization)Histology at KUMC epithel-epith03 (http://www.kumc.edu/instruction/medicine/anatomy/histoweb/epithel/epith03.htm) "Thyroid Gland"

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