Thyroid

Thyroid

The human thyroid as viewed from the front, with

arteries visible.
Note the superior thyroid artery, which supplies the
thyroid with much of its blood.

The thyroid as it may be seen from a posterior view,

from behind the trachea
Details
Latin

Glandula thyreoidea

Precursor Thyroid diverticulum (an extension of

endoderm into 2nd branchial arch)
System

Endocrine system

Identifiers
Gray's

p.1269

MeSH

A06.407.900

Dorlands
/Elsevier

Thyroid gland

TA

A11.3.00.001

FMA

9603

Anatomical terminology
The thyroid gland, or simply the thyroid /ard/, in vertebrate anatomy, is one of the
largest endocrine glands and consists of two connected lobes. The thyroid gland is found in
the neck, below the thyroid cartilage (which forms thelaryngeal prominence, or "Adam's apple").
The thyroid gland controls how quickly the body uses energy, makes proteins, and controls how
sensitive the body is to other hormones. It participates in these processes by producing thyroid
hormones, the principal ones being triiodothyronine (T3) and thyroxine(sometimes referred to as
tetraiodothyronine (T4)). These hormones regulate the growth and rate of function of many other
systems in the body. T3 and T4are synthesized from iodine and tyrosine. The thyroid also
produces calcitonin, which plays a role in calcium homeostasis.
Hormonal output from the thyroid is regulated by thyroid-stimulating hormone(TSH) produced
by the anterior pituitary, which itself is regulated bythyrotropin-releasing hormone (TRH)
produced by the hypothalamus.
Contents
[hide]

1 Structure
o 1.1 Prenatal development
o 1.2 Histology

2 Physiology
o 2.1 T3 and T4 production and action
o 2.2 T3 and T4 regulation

3 Clinical significance
o 3.1 Hyperthyroidism
o 3.2 Hypothyroidism
o 3.3 Thyroiditis
o 3.4 Cancers
o 3.5 Non-cancerous nodules
o 3.6 Congenital anomalies
o 3.7 Other disorders
o 3.8 Thyroid function tests
o 3.9 Significance of iodine

4 History

5 Other animals

6 Etymology

7 Additional images

8 See also

9 References

10 External links

Structure[edit]

The thyroid gland as present on the human trachea, here with a visible pyramidal lobe
(orLalouette's pyramid).
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 theisthmus. Each
lobe is about 5 cm long, 3 cm wide and 2 cm thick. 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
approximately 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. There is occasionally (28%-55% of population, mean 44.3%)[2] a third lobe present
called the pyramidal lobe of the thyroid gland. It is of conical shape and extends from the upper
part of the isthmus, up across the thyroid cartilage to the hyoid bone. The pyramidal lobe is a
remnant of the fetal thyroid stalk, or thyroglossal duct.[3] It is occasionally quite detached, or may
be divided into two or more parts. The pyramidal lobe is also known as Lalouette's pyramid.[4]
The thyroid gland is covered by a thin fibrous sheath, the capsula glandulae thyreoideae,
composed of an internal and external layer. The external layer is anteriorly continuous with
the pretracheal fascia and posteriorolaterally continuous with the carotid sheath. The gland is

covered anteriorly with infrahyoid 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 andcricopharyngeus muscle by a thickening of the fascia to
form the posterior suspensory ligament of thyroid gland also known as Berry's ligament.[5][6] The
thyroid gland's firm attachment to the underlying trachea is the reason behind its movement with
swallowing.[7] In variable extent, the pyramidal 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, can change shape and size, and can
encompass the pyramidal lobe (lobus or processus pyramidalis.[citation needed] 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.

Isthmus showing pyramidal lobe position

In a healthy patient the gland is not visible yet can be palpated as a soft mass. Examination of the
thyroid gland is carried out by locating the thyroid cartilage and passing the fingers up and down,
examining for abnormal masses and overall thyroid size. Then, place one hand on each of the
trachea and gently displace the thyroid tissue to the contralateral side of the neck for both sides
while the other hand manually palpates the displaced gland tissue; having the patient flex the
neck slightly to the side when being palpated may help in this examination. Next, the two lobes
of the gland should be compared for size and texture using visual inspection, as well as manual
or bimanual palpation. Finally, ask the patient to swallow to check for mobility of the gland;
many clinicians find that having the patient swallow water helps this part of the examination. In
a healthy state, the gland is mobile when swallowing occurs due its fascial encasement. Thus
when the patient swallows, the gland moves superiorly, as does the whole larynx.[8]

The thyroid is supplied with arterial blood from the superior thyroid artery, a branch of
the external carotid artery, and theinferior thyroid artery, a branch of the thyrocervical trunk, and
sometimes by the thyroid ima artery, branching directly from the subclavian artery. The venous
blood is drained via superior thyroid veins, draining in the internal jugular vein, and viainferior
thyroid veins, draining via the plexus thyreoideus impar in the left brachiocephalic vein.
Lymphatic drainage passes frequently the lateral deep cervical lymph nodes and the preand paratracheal lymph nodes. The gland is supplied by parasympathetic nerve input from
the superior laryngeal nerve and the recurrent laryngeal nerve.
Prenatal development[edit]

Floor of pharynx of embryo between 18 and 21 days

In the embryo, at 34 weeks of gestation, the thyroid gland appears as an epithelial proliferation
in the floor of the pharynx at the base of the tongue between thetuberculum impar and the copula
linguae at a point later 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, passing anterior to the hyoid bone. 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 the fetal hypothalamus and pituitary at 18-20 weeks of gestation, and fetal
production of thyroxine (T4) reach a clinically significant level at 1820 weeks.
[9]
Fetal triiodothyronine (T3) remains low (less than 15 ng/dL) until 30 weeks of gestation, and
increases to 50 ng/dL at term.[9] Fetal self-sufficiency of thyroid hormones protects the fetus
against e.g. brain development abnormalities caused by maternal hypothyroidism.
[10]
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.[11]
The portion of the thyroid containing the parafollicular cells, also known as C cells, responsible
for the production ofcalcitonin, are derived from the neural crest. This is first seen as

the ultimobranchial body, which joins the primordial thyroid gland during its descent to its final
location in the anterior neck.
Aberrations in prenatal development can cause various forms of thyroid dysgenesis.
Histology[edit]
At the microscopic level, there are three primary features of the thyroid:(first discovered by
Geoffary Websterson in 1664)[12]

Histological section through the thyroid of a horse. 1 follicles, 2 follicular epithelial cells, 3
endothelial cells
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, and also for storage of iodine in thyroglobulin. Twenty-five
percent of the body's iodide ions are in the thyroid gland. Inside the
follicles, in a region called the follicular lumen, colloid serves as a
reservoir of materials for thyroid hormone production and, to a lesser
extent, acts as a reservoir for the hormones themselves. Colloid is rich
in a protein called thyroglobulin.

The follicles are surrounded by a single layer of thyroid epithelial

Thyroid epithelial cell
cells, which secrete T3 and T4. When the gland is not secreting T3 and
s
T4 (inactive), the epithelial cells range from low columnar to cuboidal
(or "follicular cells")
cells. When active, the epithelial cells become tall columnar cells.
Parafollicular cells
(or "C cells")
Physiology[edit]

Scattered among follicular cells and in spaces between the spherical

follicles are another type of thyroid cell, parafollicular cells, which
secrete calcitonin.

The primary function of the thyroid is production of the hormones T3, T4 and calcitonin. Up to
80% of the T4 is converted to T3 by organs such as the liver, kidney and spleen. T3 is several
times more powerful than T4, which is largely aprohormone, perhaps four[13] or even ten times
more active.[14]
T3 and T4 production and action[edit]

The system of the thyroid hormones T3 and T4.[15]

Synthesis of the thyroid hormones, as seen on an individual thyroid follicular cell:[16]

- Thyroglobulin is synthesized in the rough endoplasmic reticulum and follows the secretory
pathway to enter the colloid in the lumen of thethyroid follicle by exocytosis.

- Meanwhile, a sodium-iodide (Na/I) symporter pumps iodide (I) activelyinto 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.[17]
- In the colloid, iodide (I) is oxidized to iodine (I0) by an enzyme calledthyroid peroxidase.
- Iodine (I0) is very reactive and iodinates the thyroglobulin at tyrosylresidues in its protein chain
(in total containing approximately 120 tyrosyl residues).
- In conjugation, adjacent tyrosyl residues are paired together.
- The entire complex re-enters the follicular cell by endocytosis.
- Proteolysis by various proteases liberates thyroxine andtriiodothyronine molecules, which
enters the blood by largely unknown mechanisms.
Thyroxine (T4) is synthesised by the follicular cells from free tyrosineand on the tyrosine
residues of the protein called thyroglobulin (Tg).Iodine is captured with the "iodine trap" by
the hydrogen peroxidegenerated by the enzyme thyroid peroxidase (TPO)[18] 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
cleave the iodinated tyrosines from Tg in 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.
[19]
Thyroid hormone secreted from the gland is about 80-90% T4 and about 10-20% T3.[13][14]
Cells of the developing 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.[20] A
transport protein that seems to be important for T4 transport across the bloodbrain
barrier(OATP1C1) has been identified.[21] A second transport protein (MCT8) is important for
T3 transport across brain cell membranes.[21]
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 (TBG), 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
receptors (1, 2, 1 and 2), which act alone, in pairs or together with the retinoid Xreceptor as transcription factors to modulate DNA transcription.[22]
T3 and T4 regulation[edit]
The production of thyroxine and triiodothyronine is happening by thyroid-stimulating hormone
(TSH), released by theanterior pituitary. The thyroid and thyrotropes form a negative feedback
loop: TSH production is suppressed when the T4levels are high.[23] 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 exposure (to stimulate thermogenesis).
TSH production is blunted by somatostatin (SRIH), rising levels of glucocorticoids and sex
hormones (estrogen andtestosterone), and excessively high blood iodide concentration.
An additional hormone produced by the thyroid contributes to the regulation of
blood calcium levels. Parafollicular cellsproduce 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.
Clinical significance[edit]
Main article: Thyroid disease
Thyroid disorders include

hyperthyroidism (abnormally increased activity),

hypothyroidism (abnormally decreased activity)

thyroiditis, inflammation of the thyroid

thyroid nodules, which are generally benign thyroid neoplasms (tumours), but may
be thyroid cancers.

All these disorders may give rise to a goiter, that is, an enlarged thyroid.
Hyperthyroidism[edit]
Main article: Hyperthyroidism

Hyperthyroidism, or overactive thyroid, is defined as an overproduction of the thyroid hormones

T3 and T4. This condition is most commonly caused by the development of Graves' disease, an
autoimmune disease in which anomalous antibodiesstimulate the thyroid to secrete excessive
quantities of thyroid hormones.[24] The disease can progress to the formation of a toxic goiter as a
result of thyroid growth in response to a lack of negative feedback mechanisms. It presents with
symptoms such as a thyroid goiter, protruding eyes (exopthalmos), palpitations,
excess sweating, diarrhea, weight loss, muscle weakness and unusual sensitivity to heat.
The appetite is often increased.
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 thyroid hormones, in particular, in the case ofGraves' disease. These medications
take several months to take full effect and have side-effects such as skin rash or a drop in white
blood cell count, which decreases the ability of the body to fight off infections. These drugs
involve frequent dosing (often one pill every 8 hours) and often require frequent doctor visits and
blood tests to monitor the treatment, and may sometimes lose effectiveness over time. Due to the
side-effects[clarification needed] and inconvenience of such drug regimens, some patients choose to
undergo radioactive iodine-131 treatment. Radioactive iodine is administered in order to destroy
a portion of or the entire thyroid gland, since the radioactive iodine is selectively taken up by the
gland and gradually destroys the cells of the gland. Alternatively, the gland may be partially or
entirely removed surgically, though iodine treatment is usually preferred since the surgery
is invasive and carries a risk of damage to the parathyroid glands or the nerves controlling
the vocal cords. If the entire thyroid gland is removed, hypothyroidism results.[25]
Hypothyroidism[edit]
Main article: Hypothyroidism
Hypothyroidism is the underproduction of the thyroid hormones T3 and T4.
Hypothyroid disorders may occur as a result of

congenital thyroid abnormalities (Thyroid deficiency at birth. See congenital

hypothyroidism),

autoimmune disorders such as Hashimoto's thyroiditis,

iodine deficiency (more likely in poorer countries) or

the removal of the thyroid following surgery to treat severe hyperthyroidism and/or
thyroid cancer.

Typical symptoms are abnormal weight gain, tiredness, baldness, cold intolerance,
and bradycardia. Hypothyroidism is treated with hormone replacement therapy, such

as levothyroxine, which is typically required for the rest of the patient's life. Thyroid hormone
treatment is given under the care of a physician and may take a few weeks to become effective.
[26]

Negative feedback mechanisms result in growth of the thyroid gland when thyroid hormones are
being produced in sufficiently low quantities, as a means of increasing the thyroid output;
however, where hypothyroidism is caused by iodine insufficiency, the thyroid is unable to
produce T3 and T4 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 produce toxic quantities of thyroid hormones, despite its size.
Thyroiditis[edit]
Main article: Thyroiditis
There are two types of thyroiditis where initially hyperthyroidism presents which is followed by
a period of hypothyroidism; (the overproduction of T3 and T4 followed by the underproduction of
T3 and T4). These are Hashimoto's thyroiditis and postpartum thyroiditis.
Hashimoto's thyroiditis or Hashimoto's Disease is an autoimmune disorder whereby the body's
own immune system reacts with the thyroid tissues in an attempt to destroy it. At the beginning,
the gland may be overactive, and then becomes underactive as the gland is damaged resulting in
too little thyroid hormone production or hypothyroidism. Some patients may experience
"swings" in hormone levels that can progress rapidly 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 longer period 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 genetic disease. Also
more common in individuals with Hashimoto's thyroiditis are type 1 diabetes and celiac disease.
[27]

Postpartum thyroiditis occurs in some females following the birth of a child. After delivery, the
gland becomes inflamed and the condition initially presents with overactivity of the gland
followed by underactivity. 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's thyroiditis or Graves' disease.
There are other disorders that cause inflammation of the thyroid, and these include subacute
thyroiditis, acute thyroiditis,silent thyroiditis and Riedel's thyroiditis.[28]
Cancers[edit]
Main article: Thyroid cancer

In most cases, thyroid cancer presents as a painless mass in the neck. It is very unusual for
thyroid cancers to present with symptoms, unless they have 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.[29]
Non-cancerous nodules[edit]
Further information: Thyroid nodule
Many individuals may find the presence of thyroid nodules on the gland. The majority of these
thyroid nodules are benign(non cancerous), and their presence does not necessarily indicate
disease. Most thyroid nodules do not cause any symptoms, and most are discovered on an
incidental examination. Often there can be many nodules, which is termed a multinodular goiter.
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.
Congenital anomalies[edit]
A persistent thyroglossal duct or cyst is the most common clinically significant congenital
anomaly of the thyroid gland. A persistent sinus tract may remain as a vestigial remnant of the
tubular development of the thyroid gland. Parts of this tube may be obliterated, leaving small
segments to form cysts. These occur at any age and might not become evident until adult life.
Mucinous, clear secretions may collect within these cysts to form either spherical masses or
fusiform swellings, rarely larger than 2 to 3 cm in diameter. These are present in the midline of
the neck anterior to the trachea. Segments of the duct and cysts that occur high in the neck are
lined by stratified squamous epithelium, which is essentially identical to that covering the
posterior portion of the tongue in the region of the foreamen cecum. The anomalies that occur in
the lower neck more proximal to the thyroid gland are lined by epithelium resembling the
thyroidal acinar epithelium. Characteristically, next to the lining epithelium, there is an intense
lymphocytic infiltrate. Superimposed infection may convert these lesions into abscess cavities,
and rarely, give rise to cancers.[citation needed]
Another anomaly is that of thyroid dysgenesis which can result in various presentations of one or
more accessory thyroid glands. These can be asymptomatic.
Other disorders[edit]

Limited research shows that seasonal allergies may trigger episodes of hypo- or
hyperthyroidism.[30][31]

Some rapid-cycling versions of bipolar disorder seem to have a complex relationship with
thyroid dysfunction, however the specifics of the relationship are poorly understood.[32]

Thyroid function tests[edit]

Main article: Thyroid function tests
Test

Abbreviatio
n

Normal ranges[33]

Serum thyrotropin/thyroid-stimulating
hormone

TSH

0.56.0 U/ml

Free thyroxine

FT4

718 ng/l = 0.71.8 ng/dl

Serum triiodothyronine

T3

0.81.8 g/l = 80180 ng/dl

Radioactive iodine-123 uptake

RAIU

1030%

Radioiodine scan (gamma camera)

N/A

N/A - thyroid contrasted

images

Free thyroxine fraction

FT4F

0.030.005%

Serum thyroxine

T4

46120 g/l = 4.612.0 g/dl

Thyroid hormone binding ratio

THBR

0.91.1

Free thyroxine index

FT4I

411

Free triiodothyronine l

FT3

230619 pg/d

Free T3 Index

FT3I

80180

Thyroxine-binding globulin

TBG

1220 ug/dl T4 +1.8 g

TRH stimulation test

Peak TSH

930 IU/ml at 2030 min.

Serum thyroglobulin l

Tg

0-30 ng/m

Thyroid microsomal antibody titer

TMAb

Varies with method

Thyroglobulin antibody titer

TgAb

Varies with method

U/ml = mU/l, microunit per milliliter

ng/dl, nanograms per deciliter

g, micrograms

pg/d, picograms per day

IU/ml = mIU/l, micro-international unit per milliliter

See [1] for more information on medical units of measure

As of early 2014, in the United States, new guidelines for TSH levels have been implemented as
endorsed by The American Association of Clinical Endocrinologists. the new range is a TSH of
0.3 to 3.0. Many testing facilities and doctors are still unaware of the change.[citation needed]
Listed below are some of the effects of drugs on thyroid function.
Effects of some drugs on Tests of Thyroid function[34]
Cause

Drug

Effect

Inhibit TSH secretion

Dopamine, L-dopa, Glucocorticoids,

Somatostatin

T4; T3; TSH

Inhibit thyroid hormone

synthesis or release

Iodine, Lithium

T4; T3; TSH

Inhibit conversion of
T4 to T3

Amiodarone, Glucocorticoids, Propranolol,

Propylthiouracil, Radiographic contrast agents

T3; rT3; , ,
T4and fT4; ,
TSH

Inhibit binding of
T4/T3 to serum proteins

Salicylates, Phenytoin, Carbamazepine,

Furosemide, Nonsteroidal anti-inflammatory
agents, Heparin (in vitro effect)

T4; T3; fT4E,

, fT4; TSH

Stimulate metabolism of
iodothyronines

Phenobarbital, Phenytoin, Carbamazepine,

Rifampicin

T4; fT4;
TSH

Inhibit absorption of
ingested T4

Aluminium hydroxide, Ferrous sulfate,

Cholestyramine, Colestipol, Iron sucralfate,
Soybean preparations, Kayexalate

T4; fT4; TSH

Increase in concentration Estrogen, Clofibrate, Opiates (heroin,

of T4-binding proteins
methadone), 5-Fluorouracil, Perphenzazine

T4; T3; fT4;

TSH

Decrease in

T4; T3; fT4;

Androgens, Glucocorticoids

concentration of T4binding proteins

TSH

: reduced serum concentration; : increased serum concentration; : non change; TSH:

Thyroid-stimulating hormone; T3: Total triiodothyronine; T4: Total thyroxine; fT4: Free
thyroxine; fT3: Free triiodothyronine; rT3: Reverse triiodothyronine
Significance of iodine[edit]
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 give birth to infants with thyroid hormone deficiency (congenital
hypothyroidism), manifesting in problems of physical growth and development as well as brain
development (a condition referred to as endemic cretinism). In many developed countries,
newborns are routinely tested for congenital hypothyroidism as part of newborn screening.
Children with congenital hypothyroidism are treated supplementally with levothyroxine, which
facilitates normal growth and development.
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. In amphibian metamorphosis, thyroxine and
iodine also exert a well-studied experimental model of apoptosis on the cells of gills, tail, and
fins of tadpoles. Iodine, via iodolipids, has favored the evolution of terrestrial animal species and
has likely played a crucial role in the evolution of the human brain. Iodine (and T4) trigger the
amphibian metamorphosis that transforms the vegetarian aquatic tadpole into a carnivorous
terrestrial adult frog, with better neurological, visuospatial, olfactory and cognitive abilities for
hunting, as seen in other predatory animals. A similar phenomenon happens in
the neotenic amphibian salamanders, which, without introducing iodine, don't transform into
terrestrial adults, and live and reproduce in the larval form of aquatic axolotl.[35]
Because the thyroid concentrates iodine, it also concentrates the 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. One consequence of the Chernobyl disaster was an
increase in thyroid cancers in children in the years following the accident.[36]
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, and 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 increased prevalence
of autoimmune thyroid disease, resulting in permanent hypothyroidism.[37]
History[edit]
Historical references to what we now know as the thyroid gland arise early in medical history. In
Ayurvedic System Of medicine,the book Susrut Samhita written about 1500 BC mentions the
disease goitre as 'Galaganda' along with its treatment. In 1600 BC the Chinese were using burnt
sponge and seaweed for the treatment of goitres (enlarged thyroid glands). Celsus first described
a bronchoceole (a tumour of the neck) in 15 AD. Around this time Pliny referred to epidemics of
goitre in the Alps and also mentioned the use of burnt seaweed in their treatment, in the same
way as the Chinese had done 1600 years earlier. In 150 AD Galen, an instrumental figure in the
transition from ancient to modern medicine, referred to 'spongia usta' (burnt sponge) for the
treatment of goitre. He also suggested (incorrectly, as it turns out) that the role of the thyroid was
to lubricate the larynx.
There are several findings that evidence a great interest for thyroid disorders just in the Medieval
Medical School of Salerno(12th 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 as scientifically
effective.[38]
It was not until 1475 that Wang Hei anatomically described the thyroid gland and recommended
that the treatment of goitre should be dried thyroid. Paracelsus, some fifty years later, attributed
goitre to mineral impurities in the water.
In modern times, the thyroid was first identified in 1656 by the anatomist Thomas
Wharton (whose name is alsoeponymised in Wharton's duct of the submandibular gland).[39] In
1656 Thomas Wharton named the gland the thyroid, meaning shield, as its shape resembled the
shields commonly used in Ancient Greece.
In 1909, Theodor Kocher from Switzerland won the Nobel Prize in Medicine "for his work on
the physiology, pathology and surgery of the thyroid gland".[40]
Other animals[edit]
The thyroid gland is found in all vertebrates. In fish, it is usually 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.[41]
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.[41]
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
(the endostyle), and this also secretes iodine-containing compounds (albeit not thyroxine).[41]
Etymology[edit]
The English name thyroid gland[42] is derived from Latin glandula thyreoidea.
[43]
Glandula means gland in Latin,[44] andthyreoidea can be traced back to the Ancient
Greek word , meaning shield-like/shield-shaped.[45] The Englishanatomist Thomas
Wharton was the first to coin the Latin expression for the thyroid gland.[46] However, he
introduced the incorrect spelling glandula thyroidaea [47] as the adjective thyroidaea is a faulty
rendering in Latin of Ancient Greek .[48] The Latin ending aea does not correspond to
Ancient Greek and more importantly the e after thyr is missing, creating a resemblance
between thyroidaea and Ancient Greek , that actually means like a door[45]instead of
the intended shield-like.
The first edition[43] of the official Latin nomenclature (Nomina Anatomica) of 1895 rightfully
included the e after thyr in the expression glandula thyreoidea as well as the subsequent editions
from 1936[49][50] and 1955.[51] Subsequent editions[52][53][54][55][56] as well as the most recent list
(Terminologia Anatomica)[57] replicated the mistake originally made by Wharton, i.e. incorrect
elision of e after thyr, and printed glandula thyroidea (= door-like gland).
The decision to elide the e from thyreo- is a gesture of the nomenclature committee of the
Nomina Anatomica to English-speaking anatomists, as they have difficulties in pronouncing this
specific sequence of letters,[58] thereby forcing a greater resemblance between Latin and English
orthography. Although the spelling thyroid is nowadays accepted in English, earlier English
medical dictionaries[59] remarked that thyroid was the less correct form of thyreoid.
The adjective thyreoidea in the expression glandula thyreoidea seems actually quite odd, as this
gland isnt clearly shield-like at all.[46] This name is however based on the fact that the thyroid
gland is in the close vicinity of the thyroid cartilage.[46]The English expression thyroid
cartilage is derived from the Latin expression cartilago thyreoides.[49][60] The latter is a translation
of Ancient Greek [45] attested in the writings of the Greek physician Galen.
[45]
In this case in refers to the shield-like appearance of the
thyroid cartilage.[46] As the thyroid gland itself is not shield-like at all, but refers to another
structure that is shield-like in appearance, using the same adjective to refer to both structures
might be confusing.[46] The proper rendering of Ancient Greek might be thyreoides in

Latin.[60]The edition of the Nomina Anatomica from 1936[49] uses the adjective thyreoides to refer
to shield-like structures, but uses the (additional) ending eus/ea/eum to refer to structures that are
related or in the close vicinity of shield-like structures, but not shield-like themselves.
[61]
Others[60] use the ending icus/ica/icum as in glandula thyreoidica as the Latin
endingeus/ea/eum does not correspond to a possible Greek form.
Alternatively, other names have been proposed for the thyroid gland like thyreaden,[48] derived
from Ancient Greek ,shield,[45] and , gland.[45]
Additional images[edit]

Thyroid and parathyroid.

Clearly visible pyramidal lobe of the thyroid

Section of the neck at about the level of the sixth cervical vertebra.


Diagram showing common arrangement of thyroid veins.

Sagittal section of nose mouth, pharynx, and larynx.

Muscles of the pharynx, viewed from behind, together with the associated vessels and nerves.

Thyroid


Thyroid gland

Thyroid gland

Thyroid cartilage lamina

Muscles, nerves and arteries of neck.Deep dissection. Anterior view.

Surgery to remove thyroids - known as athyroidectomy.

See also[edit]

Thyroid disease

Thyroid disease in pregnancy

Academy of Clinical Thyroidologists

Iodine in biology

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External links[edit]
Wikimedia Commons
has media related
to Thyroid gland.

EndocrineWeb.com for more information on thyroid disease, hormones, and surgery

American Thyroid Association (Thyroid Information and professional organization)

Histology at KUMC epithel-epith03 "Thyroid Gland"

[hide]

Anatomy of the endocrine system

Pituitary gland

Anterior

Pars intermedia

Pars tuberalis

Pars distalis

Acidophil cell

Posterior

Thyroid gland

Parathyroid
gland

Somatotropic cell

Prolactin cell

Basophil cell

Corticotropic cell

Gonadotropic cell

Thyrotropic cell

Chromophobe cell

Pars nervosa

Median eminence

Stalk

Pituicyte

Herring bodies

Thyroid isthmus

Follicular cell

Parafollicular cell

Chief cell

Oxyphil cell

Cortex
Adrenal gland

Medulla

Gonads

Islets of pancreas

Zona glomerulosa

Zona fasciculata

Zona reticularis

Chromaffin cell

Testicle

Leydig cell

Sertoli cell

Ovary

Theca interna

Granulosa cell

Corpus luteum

Alpha cell

Beta cell

Delta cell

PP cell

Epsilon cell

Pineal gland

Other

Pinealocyte

Corpora arenacea

Enteroendocrine cell

Paraganglia

Organ of Zuckerkandl

Placenta

Index of hormones

Glands

Hormones

thyroid

Description

Disease

intermediates

metabolism

mineralocorticoids

Physiology

Development

Diabetes

Congenital

Neoplasms and cancer

Other

Symptoms and signs

eponymous

Procedures

Drugs

Treatment

Authority control

calcium balance

corticosteroids

oral hypoglycemics

pituitary and hypothalamic

thyroid

Categories:

Thyroid

Glands

Endocrine system

Human head and neck

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