Thyroid
Anatomy of the thyroid gland.
Is one of the largest 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 controls how sensitive the body should be to other hormones.
The thyroid participates in these processes by producing thyroid hormones, principally thyroxine (T4) and triiodothyronine (T3). These hormones regulate the rate of metabolism and affect the growth and rate of function of many other systems in the body. Iodine and tyrosine are used to form both T3 and T4. The thyroid also produces the hormone calcitonin, which plays a role in calcium homeostasis.
The thyroid is controlled by the hypothalamus and pituitary. The gland gets its name from the Greek word for "shield", after the shape of the related thyroid cartilage. Hyperthyroidism (overactive thyroid) and hypothyroidism (underactive thyroid) are the most
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), and is also connected with the isthmus. The organ is situated on the anterior side of the neck, lying against and around the larynx and trachea, reaching posteriorly the oesophagus and carotid sheath. It starts cranially at the oblique line on the thyroid cartilage (just below the laryngeal prominence or Adam s apple) and extends inferiorly to the fifth or sixth tracheal ring.[1] It is difficult to demarcate the gland s upper and lower border with vertebral levels because it moves position in relation to these during swallowing.
The thyroid gland is covered by a fibrous sheath, the capsula glandulae thyroidea, composed of an internal and external layer. The external layer is anteriorly continuous with the lamina pretrachealis fasciae cervicalis and posteriorolaterally continuous with the carotid sheath. The gland is covered anteriorly with infrahyoid muscles and laterally with the sternocleidomastoid muscle. 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 brachiocephalic trunk. The venous blood is drained via superior thyroid veins, draining in the internal jugular vein, and via inferior thyroid veins, draining via the plexus thyroideus impar in the left brachiocephalic vein.
Lymphatic drainage passes frequently the lateral deep cervical lymph nodes and the pre- and parathracheal lymph nodes. The gland is supplied by sympathetic nerve input from the superior cervical ganglion and the cervicothoracic ganglion of the sympathetic trunk[citation needed], and by parasympathetic nerve input from the superior laryngeal nerve and the recurrent laryngeal nerve.
Embryological development
In the fetus, at 3–4 weeks of gestation, the thyroid gland appears as an epithelial proliferation in the floor of the pharynx at the base of the tongue between the tuberculum impar and the copula linguae at a point latter indicated by the foramen cecum. 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.This article was originally based on an entry from a public domain edition of Gray s Anatomy. As such, some of the information contained within it may be outdated.
The portion of the thyroid containing the parafollicular C cells, those responsible for the production of calcitonin, are derived from the 4th pharyngeal pouch endoderm. This is first seen as the ultimobranchial body, which joins the primordial thyroid gland during its decent to its final location in the anterior neck.
Histology
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
T3 and T4 production and action
The system of the thyroid hormones T3 and T4.[6]
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)[7] and linked to the 3 and 5 sites of the benzene ring of the tyrosine residues on Tg, and on free tyrosine. Upon stimulation by the thyroid-stimulating hormone (TSH), the follicular cells reabsorb Tg and proteolytically cleave the iodinated tyrosines from Tg, forming T4 and T3 (in T3, one iodine atom is absent compared to T4), and releasing them into the blood. Deiodinase enzymes convert T4 to T3.[8] Thyroid hormone that is secreted from the gland is about 90% T4 and about 10% T3.[5]
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.[9] A transport protein (OATP1C1) has been identified that seems to be important for T4 transport across the blood brain barrier.[10] A second transport protein (MCT8) is important for T3 transport across brain cell membranes.[10]
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 (?1, ?2, ?1 and ?2), which act alone, in pairs or together with the retinoid X-receptor as transcription factors to modulate DNA transcription[1].
T3 and T4 regulation
The production of thyroxine and triiodothyronine is regulated by thyroid-stimulating hormone (TSH), released by the anterior pituitary. The thyroid and thyrotropes form a negative feedback loop: TSH production is suppressed when the T4 levels are high, and vice versa. The TSH production itself is modulated by thyrotropin-releasing hormone (TRH), which is produced by the hypothalamus and secreted at an increased rate in situations such as cold (in which an accelerated metabolism would generate more heat). TSH production is blunted by somatostatin (SRIH), rising levels of glucocorticoids and sex hormones (estrogen and testosterone), and excessively high blood iodide concentration.
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 is lacking in the diet, the thyroid gland can be considerably enlarged, resulting in the enlarged thyroid glands of endemic goitre. In this situation, women with severe iodine deficiency can give birth to infants with thyroid hormone deficiency, who will have physical growth and development problems. Brain development can be severely impaired. This is a condition called endemic cretinism, and it is one cause of congenital hypothyroidism. Newborn children in many developed countries are now routinely tested for congenital hypothyroidism as part of newborn screening. Children with congenital hypothyroidism are treated by supplementation with levothyroxine, which enables them to grow and develop normally.
Thyroxine is critical to the regulation of metabolism and growth throughout the animal kingdom. Among amphibians, for example, administering a thyroid-blocking agent such as propylthiouracil (PTU) can prevent tadpoles from metamorphosing into frogs; conversely, administering thyroxine will trigger metamorphosis.
Because the thyroid concentrates this element, it also concentrates various radioactive isotopes of iodine produced by nuclear fission. In the event of large accidental releases of such material into the environment, the uptake of radioactive iodine isotopes by the thyroid can, in theory, be blocked by saturating the uptake mechanism with a large surplus of non-radioactive iodine, taken in the form of potassium iodide tablets. While biological researchers making compounds labelled with iodine isotopes do this,November 2009 in the wider world such preventive measures are usually not stockpiled before an accident, nor are they distributed adequately afterward.[citation needed] One consequence of the Chernobyl disaster was an increase in thyroid cancers in children in the years following the accident.[11]
The use of iodised salt is an efficient way to add iodine to the diet. It has eliminated endemic cretinism in most developed countries, and some governments have made the iodination of flour, cooking oil or salt mandatory. Potassium iodide and sodium iodide are typically used forms of supplemental iodine.
As with most substances, either too much or too little can cause problems. Recent studies on some populations are showing that excess iodine intake could cause an inceased prevelence of autoimmune thyroid disease resulting in permanent hypothyroidism.[12] 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.[13]
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.[14]
Thyroxin was identified only in the 19th century.
In other animals
The thyroid gland is found in all vertebrates. In fishes it is generally 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.[15]
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.[15]
In larval lampreys, the thyroid originates as an exocrine gland, secreting its hormones into the gut, and associated with the larva s filter-feeding apparatus. In the adult lamprey, the gland separates from the gut, and becomes endocrine, but this path of development may reflect the evolutionary origin of the thyroid. For instance, the closest living relatives of vertebrates, the tunicates and Amphioxus, have a structure very similar to that of larval lampreys, and this also secretes iodine-containing compounds (albeit not thyroxine).[