thyroid gland

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thyroid gland

anterior view (Carlyn Iverson)

A two-lobed endocrine gland found in all vertebrates, located in front of and on either side of the trachea in humans, and producing various hormones, such as triiodothyronine and calcitonin.

An endocrine gland found in all vertebrates that produces, stores, and secretes the thyroid hormones. In humans, the gland is located in front of, and on either side of, the trachea. Thyrocalcitonin, one hormone of the thyroid gland, assists in regulating serum calcium by reducing its levels. The iodine-containing hormones thyroxine and triiodothyronine regulate metabolic rate in warm-blooded animals and are essential for normal growth and development. To produce these, the thyroid gland accumulates inorganic iodides from the bloodstream and unites them with the amino acid tyrosine. This activity is regulated by thyrotropic hormone from the anterior lobe of the pituitary gland. See also Thyroid hormone; Thyroxine.

The thyroid gland secretes hormones which are necessary for normal growth and development from fetal life onwards, and for maintenance of normal metabolism in the adult body.

The gland is located just below the larynx and attached to the front of the trachea. The adult gland weighs 10-20 g and consists of two relatively flat oval lobes linked by an isthmus. It is so named because of its resemblance to the classical shield (thureos) used by the ancient Greeks. However, unlike the shield, in any one individual the thyroid is generally asymmetric, with the right lobe being significantly larger than the left. The gland is usually larger in women than in men and it increases slightly in size during pregnancy. This is exploited as an early pregnancy test in some African communities: the neck of a bride is adorned with a tight necklace and pregnancy is indicated when in due course the necklace is broken by the swelling thyroid gland.

The embryonic thyroid originated in the floor of the pharynx and it can be detected as a midline thickening, as early as day 24. By weeks 6-7 the characteristic bilobed structure can be distinguished. At about this time, the gland becomes detached from the pharynx and the developing tissue mass descends into the neck. The two lobes finally come to rest on either side of the trachea with the joining isthmus lying across the front of it. Occasionally the thyroid fails to descend, or may descend too far; the fully developed gland is then found below the root of the tongue or within the thorax. Such developmental abnormalities do not necessarily affect thyroid function.

During its descent down the neck the developing thyroid incorporates ‘C-cells’ into its tissue mass; also two pairs of discrete parathyroid glands become attached to the back surface of the thyroid gland itself. These secrete hormones which regulate the concentration of calcium in the blood: the C-cells secrete the protein calcitonin, and the parathyroids the protein parathyroid hormone. Neither of these are regarded as thyroid hormones since they are not produced by the main mass of thyroid tissue; the latter consists of spherical follicles where the thyroid hormones are synthesized and stored.

The major functional and structural unit of the thyroid is the thyroid follicle. There are many thousands of follicles, and their individual sizes vary considerably, ranging in diameter from 20 to 100 μm (2/100-1/10 mm). A rich network of fenestrated capillary blood vessels surrounds small groups of follicles and there is an impressively high rate of blood flow through the gland as a whole (per unit mass, the flow is twice the flow through the kidneys, which themselves have a much greater blood supply than other organs relative to their size). The even greater flow through an overactive thyroid produces a ‘bruit’ which can be heard when a stethoscope is placed over the gland. The high blood flow ensures an adequate supply of blood-borne nutrients to the follicles — in particular the delivery of iodide derived from the diet — as well as uptake of the thyroid hormones into the bloodstream.

The unique biochemical characteristic of thyroid follicular cells is their ability to concentrate and to utilize dietary iodide. The cell possesses an iodide ‘pump’ which enables it to accumulate iodide internally, so that it can achieve a concentration twenty- to a hundred-fold higher than that in the circulating blood. Two other tissues which share a closely related embryonic origin with the thyroid (some cells of the stomach lining and the salivary glands) also possess this pumping mechanism, but the thyroid is unique in its ability to retain and utilize the iodide for the biosynthesis of its hormones. These hormones are small molecules derived from the amino acid tyrosine and they have iodine incorporated into their structures. There are two thyroid hormones, which have either 3 or 4 atoms of iodine per molecule; they are known respectively as T₃ (tri-iodothyronine) and T₄ (thyroxine). Both are synthesized within the thyroid follicles and secreted into the bloodstream when the cells are stimulated to extrude them by the thyroid stimulation hormone (TSH) from the pituitary gland. The thyroid hormones in the circulation in turn regulate the production of TSH by the pituitary, switching off TSH production when the appropriate level of T_3/T₄ is attained in the blood. Thus the ‘pituitary-thyroid axis’ is a classical example of a negative feedback system.

Following the accumulation of iodine in the follicular cells, the T₃ and T₄ are first synthesized separately and are then incorporated into a much larger molecule known as thyroglobulin. This large glycoprotein, which is sometimes referred to as ‘colloid’ is stored in the hollow interior of each follicle. If a thyroid gland which has been removed is cut across and gently squeezed, the colloid can be observed leaking from the transected follicles as a glistening yellowish fluid. TSH stimulates the release of the T₃ and T₄ from the thyroglobulin so that the hormones can be secreted from the cells into the bloodstream in a regulated fashion. This hormone storage system is unique in endocrine physiology; it ensures that there is a two-month supply of thyroid hormones in the event that a person encounters an iodine deficient environment. This occurs in many parts of the world, such as some mountainous regions in China and India. However, this capacity to store thyroid hormones within the follicles as thyroglobulin becomes disadvantageous if an individual inadvertently ingests radioactive iodine. This occurred after the huge release into the atmosphere of radioactive isotopes, including radioiodine, during the week following the Chernobyl accident on 26 April 1986. The natural storage of the radioiodine in the follicles delays clearance of the ingested radionuclide and concentrates the damaging radiation on the thyroid. In Belarus and the Ukraine this resulted in a major increase in the incidence of thyroid cancer in the 1990s amongst children born before the accident.

Thyroid hormones circulate in the blood in minute concentrations (nanomolar — of the order of 10^-9 × molecular weight per litre). Although this is very low compared with many blood constituents such as glucose or sodium ions, which circulate at millimolar concentrations (a million times greater), it is high relative to hormones in general. The blood concentrations of the thyroid hormones are tightly regulated by TSH and remain very stable in a healthy individual over prolonged periods. Thyroid hormones are relatively insoluble in water and this has two important consequences. Firstly, in the circulation more than 99% of them are linked to specific ‘binding proteins’; this prolongs their half-life in blood, and since the binding is reversible, maintains a biologically active ‘reservoir’ in the circulation. Secondly, on arrival at a target cell, the hormones, being relatively soluble in lipid, are able to cross the plasma membrane of the cell and then bind to specific receptors associated with gene regulation in the nucleus of the cell.

Thyroid hormones regulate the activities of almost all cells in the body. They exert three main classes of action. Firstly they control the basal metabolic rate (BMR). Secondly they influence cell differentiation and growth. Thirdly they may modify the action of other hormones, extending their importance still more widely. Thus a lack of thyroid hormones is manifested in diverse ways. In the developing fetus an inadequate supply leads to impaired brain development with the danger of the infant being borne a cretin. In an adult there is a depressed BMR with attendant lethargy. By contrast, excess thyroid hormones raise the BMR and may lead to cardiac problems due to potentiation by thyroid hormone of the effects of adrenaline.

T₃, the form of thyroid hormone which contains only 3 atoms of iodine per molecule, is now considered to be the physiologically active hormone, and T₄ to be a precursor of T₃, which can be converted to T₃ by specific enzymes within the target cells. Since T₄ circulates at a concentration about a hundred-fold higher than that of T₃, it can therefore be considered to be a storage form of the active hormone. Thus the thyroid system as a whole is designed to buffer any possibility of a reduction in the adequate supply of T₃ to target cells: large reserves are maintained in the thyroglobulin stored in the follicles, in the T₃ and T₄ attached to the circulating binding proteins, and in T₄ itself.

— N. J. Marshall

See endocrine. See also goitre; hormones; hyperthyroidism; hypothyroidism.

A highly vascular organ at the front of the neck, consisting of bilateral lobes connected in the middle by a narrow isthmus. The thyroid gland secretes the hormone thyroxine directly into the blood. It is essential to normal body growth in infancy and childhood. It also regulates the metabolic rate in adults.

Thyroid gland. (Thibodeau/Patton, 2002)

For more information on thyroid gland, visit Britannica.com.

A large, bilobed endocrine gland located along the midline of the neck, immediately below the larynx (Adam's apple). The thyroid gland secretes the hormones triiodothyronine and thyroxine, which regulate metabolic rate, and calcitonin, which helps regulate calcium metabolism.

For other uses, see Thyroid cartilage.

This article needs additional citations for verification. Please help improve this article by adding reliable references. Unsourced material may be challenged and removed. (June 2008)

thyroid
Endocrine system
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 in men) and at approximately the same level as the cricoid cartilage. The thyroid controls how quickly the body burns energy, makes proteins, and 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.

Contents 1 Anatomy 1.1 Embryological development 1.2 Histology 2 Physiology 2.1 T3 and T4 production and action 2.2 T3 and T4 regulation 2.3 Calcitonin 2.4 Significance of iodine 3 History 4 Additional images 5 See also 6 References 7 External links

Anatomy

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 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 fourth or fifth 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. Posteriorly, 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^{[citation needed]}.

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 aortic arch. 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

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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. Subsequently the thyroid 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.

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.

Histology

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

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.

Physiology

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.^[4]

T3 and T4 production and action

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)^[5] 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 is absent compared to T4), and releasing them into the blood. Deiodinase enzymes convert T4 to T3.^[6] Thyroid hormone that is secreted from the gland is about 90% T4 and about 10% T3.^[4]

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.^[7] A transport protein (OATP1C1) has been identified that seems to be important for T4 transport across the blood brain barrier.^[8] A second transport protein (MCT8) is important for T3 transport across brain cell membranes.^[8]

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 receptors (α₁, 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 (that is in turn released as a result of TRH release by the hypothalamus). 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.

Calcitonin

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, but not the parathyroids.

Significance of iodine

In areas of the world where iodine (essential for the production of thyroxine, which contains four iodine atoms) is lacking in the diet, the thyroid gland can be considerably enlarged, resulting in the swollen necks of endemic goitre.

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; conversely, administering thyroxine will trigger metamorphosis.

In humans, children born with thyroid hormone deficiency will have physical growth and development problems, and brain development can also be severely impaired, in the condition referred to as cretinism. Newborn children in many developed countries are now routinely tested for thyroid hormone deficiency as part of newborn screening by analysis of a drop of blood. Children with thyroid hormone deficiency are treated by supplementation with synthetic thyroxine, which enables them to grow and develop normally.

Because of the thyroid's selective uptake and concentration of what is a fairly rare element, it is sensitive to the effects of 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, in the wider world such preventive measures are usually not stockpiled before an accident, nor are they distributed adequately afterward. One consequence of the Chernobyl disaster was an increase in thyroid cancers in children in the years following the accident.^[9]

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 or salt mandatory. Potassium iodide and Sodium iodide are the most active forms of supplemental iodine.

Contradictory, recent studies on some populations are showing that excess of iodine could be related to the raise of autoimmune disease driving to permanent Hypothyroidism.^[10]. Some governments are reviewing the quantity of iodine added to salt using local salt consumption data.^{[citation needed]}

History

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.^[11]

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.^[12]

Thyroid hormone (or thyroxin) was identified only in the 19th century.

Additional images

Position of the Thyroid in Males and Females		Section of the neck at about the level of the sixth cervical vertebra.	Muscles of the neck. Anterior view.
The arch of the aorta, and its branches.	Superficial dissection of the right side of the neck, showing the carotid and subclavian arteries.	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.	The position and relation of the esophagus in the cervical region and in the posterior mediastinum. Seen from behind.	Section of thyroid gland of sheep. X 160.	The thymus of a full-term fetus, exposed in situ.
Thyoid histology

See also

• Thyroid disease
• Thymus
• Academy of Clinical Thyroidologists

References

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, http://www.emedicine.com/ent/topic532.htm, retrieved on 2008-01-19 
4. ^ ^{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 .
5. ^ 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. 
6. ^ 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. 
7. ^ 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. 
8. ^ ^{a b} Jansen J, Friesema ECH, Milici C, Visser TJ (2005). Thyroid hormone transporters in health and disease. Thyroid 15;757-768. PMID 16131319.
9. ^ BBC NEWS | Science/Nature | Chernobyl children show DNA changes
10. ^ Patrick L (June 2008). "Iodine: deficiency and therapeutic considerations" (PDF). Altern Med Rev 13 (2): 116–27. PMID 18590348. http://www.thorne.com/altmedrev/.fulltext/13/2/116.pdf. 
11. ^ 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. 
12. ^ Thomas Wharton at Who Named It?

External links

• American Thyroid Association (Thyroid Information and professional organization)
• Histology at KUMC epithel-epith03 "Thyroid Gland"

v • d • e Human anatomy, endocrine system: endocrine glands Hypothalamic/ pituitary axes Thyroid axis Thyroid gland (Parafollicular cell, Thyroid epithelial cell, Thyroid isthmus, Lobes of thyroid gland, Pyramid of thyroid) Parathyroid gland (Oxyphil cell, Chief cell) Adrenal axis: Adrenal gland Medulla Chromaffin cells Cortex Zona glomerulosa · Zona fasciculata · Zona reticularis Paraganglia Organ of Zuckerkandl · Aortic body · Carotid body Gonadal axis Testes · Ovaries · Corpus luteum Pituitary Posterior pituitary Pars nervosa · Median eminence · Infundibular stalk · Pituicyte · Herring bodies Anterior pituitary Pars intermedia · Pars tuberalis · Pars distalis Acidophils (Somatotropes, Lactotropes) · Basophils (Corticotropes, Gonadotropes, Thyrotropes) · Chromophobe Pineal gland Pinealocyte · Corpora arenacea Islets of pancreas Alpha cell · Beta cell · Delta cell · PP cell · Epsilon cell

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