The thyroid gland , or just thyroid , is an endocrine gland in the neck, consisting of two lobes connected by an isthmus. It was found on the front of the neck, under the Adam's apple. The thyroid gland secretes thyroid hormone, which mainly affects the metabolic rate and protein synthesis. The hormones also have many other effects including those on development. Thyroid hormone triiodothyronine (T 3 ) and thyroxine (T 4 ) are made from iodine and tyrosine. The thyroid also produces the hormone calcitonin, which plays a role in calcium homeostasis.
Hormonal output from the thyroid is governed by thyroid-stimulating hormone (TSH) secreted from the anterior pituitary gland, which is itself regulated by thyrotropin-releasing hormone (TRH) produced by the hypothalamus.
The thyroid may be affected by some diseases. Hyperthyroidism occurs when the gland produces excessive amounts of thyroid hormone, the most common cause of Graves' disease, an autoimmune disorder. Conversely, hypothyroidism is a condition of inadequate production of thyroid hormones. Around the world, the most common cause is iodine deficiency. Thyroid hormones are important for development, and hypothyroidism secondary to iodine deficiency remains a major cause of preventable intellectual disability. In the iodine-sufficient region, the most common cause of hypothyroidism is Hashimoto's thyroiditis, as well as autoimmune disorders. In addition, the thyroid gland can also develop several types of nodules and cancer.
Video Thyroid
Structure
The thyroid gland is a butterfly-shaped organ that sits in front of the neck. It consists of two lobes, left and right, connected by a narrow isthmus. The thyroid weighs 25 grams in adults, with each lobe about 5 cm long, 3 cm wide and 2 cm thick, and isthmus about 1.25 cm in height and width. Glands are usually larger in women, and size increases in pregnancy.
The thyroid is near the front of the neck, lying in front of and around the front of the larynx and trachea. Thyroid cartilage and cricoid cartilage lie just above the gland, under the Adam's apple. Isthmus extends from the second to the third tracheal ring, with the uppermost part of the lobe extending to the thyroid cartilage, and the lower one around the fourth to sixth tracheal ring. The thyroid gland is covered by a thin fibrous capsule, which has an inner and outer layer. The outer layer continues with the pretracheal fascia, attaching the glands to the cricoid cartilage and thyroid, through the thickening of the fascia to form the posterior suspensory ligament of the thyroid gland also known as Berry ligament. This causes the thyroid to move up and down by swallowing. The inner layer is extruded into the gland and forms a septa that divides the thyroid tissue into microscopic lobules. Usually four parathyroid glands, two on each side, are located on each side between two layers of the capsule, at the back of the thyroid lobe.
The infrahyoid muscles lie in front of the glands and sternocleidomastoid muscles to the side. Behind the outer wings of the thyroid lies two carotid arteries. Trachea, larynx, lower pharynx, and esophagus are all located behind the thyroid. In this region, the laryngeal larynx is repeated and the inferior thyroid artery passes over or in the ligaments.
Blood, lymph and nerve supply
The thyroid is given with arterial blood from the superior thyroid artery, the branch of the external carotid artery, and the inferior thyroid artery, the branch of the thyrocervical trunk, and sometimes by the anatomic variant of the thyroid ima artery, which has a variable origin. The superior thyroid artery is divided into the anterior and posterior branches that supply the thyroid, and the inferior thyroid artery is divided into superior and inferior branches. The superior and inferior thyroid arteries join together behind the outside of the thyroid lobe. Venous blood is dried through the superior and middle thyroid veins, which flow into the internal jugular vein, and through the inferior thyroid vein. The inferior thyroid vein is derived from the venous tissue and flows into the left and right brachiocephalic veins. Both arteries and veins form the plexus between two layers of the thyroid gland capsule.
Lymphatic drainage often passes through prelaryngeal lymph nodes (located just above the isthmus), and pre-parake and paratracheal lymph nodes. The glands receive the sympathetic nervous supply of the superior, middle and inferior cervical ganglion of the sympathetic stem. The glands receive a supply of parasympathetic nerves from the superior laryngeal nerves and recurrent laryngeal nerves.
Variations
There are many variants in the size and shape of the thyroid gland, and in the position of the embedded parathyroid gland.
Sometimes there is a third lobe called the pyramidal lobe . Currently, this lobe often stretches the hyoid bone of the thyroid isthmus and may be one to several lobes divided. The presence of this lobe revolves around the reported study from 18.3% to 44.6%. It is proven more often arising from the left side and sometimes separately. The pyramidal lobe is also known as the Lalouette pyramid. The pyramidal lobes are the remnants of the thyroglossal duct which are usually wasted as long as the thyroid gland goes down. The small accessory thyroid gland may actually occur anywhere along the thyroglossal duct, from the foramen of the caecum to the thyroid position in an adult. A small horn behind the thyroid lobe, usually close to the recurrent laryngeal nerve and the inferior thyroid artery, is called the Zuckerkandl tubercle.
Other variants include levator muscles of the thyroid gland, connecting isthmus to the body of the hyoid bone, and the presence of small thyroid thyroid arteries.
Microanatomy
At the microscopic level, there are three main features of the thyroid - follicles, follicular cells, and parafolicular cells, first discovered by Geoffery Websterson in 1664.
- Follicles
Thyroid follicles are a small group of round cells with a diameter of 0.02-0.9mm that play a major role in thyroid function. They consist of a rim that has a rich supply of blood, nerves and lymphatic presence, which surrounds a colloidal core composed mostly of thyroid hormone precursor proteins called thyroglobulins, iodized glycoproteins.
- Follicular cells
The core of the follicle is surrounded by a single layer of follicular cells. When stimulated by thyroid stimulating hormone (TSH), this hormone secretes thyroid hormones T3 and T4. They do this by transporting and metabolizing thyroglobulin contained in colloids. The follicular cells vary in form from flat to cube form to column, depending on how active they are.
- Parapholycular cells
Spread between the follicle cells and in the space between the spherical follicles is another type of thyroid cell, parafollicular cells. These cells secrete calcitonin and are also called C.
Maps Thyroid
Development
In embryonic development, at 3-4 weeks gestational age, the thyroid gland appears as an epithelial proliferation at the base of the pharynx at the base of the tongue between the implanted tubercle and the copulal linguae. The cymbals soon become obscured by the hypopharyngeal eminence at a later point indicated by the foramen cecum. The thyroid then descends in front of the pharyngeal intestine as a bilobed diverticulum through the thyroglossal duct. Over the next few weeks, he migrates to the base of the neck, passing in front of the hyoid bone. During migration, the thyroid remains connected to the tongue through a narrow channel, the thyroglossal duct. At the end of the fifth week the thyroglossal ductus degenerates and the thyroid dislocates to its final position for the next two weeks.
The hypothalamus of the fetus and pituitary begin to release thyrotropin release hormone (TRH) and thyroid stimulating hormone (TSH). TSH was first measured at 11 weeks. At 18-20 weeks, the production of thyroxine (T 4 ) reaches a clinically significant and self-sustaining level. Fetal triiodothyronine (T 3 ) remains low, less than 15 ng/dL to 30 weeks, and increases to 50 ng/dL in full time. The fetus needs to be self-sufficient in the thyroid hormone to guard against neurodevelopmental disorders that will arise from maternal hypothyroidism. The presence of sufficient iodine is essential for healthy neurological development.
The parafollicular neuroendocrine cell, also known as C cell, is responsible for the production of calcitonin, derived from neural crest cells, which migrate to the pharyngeal arch. This part of the thyroid then first forms as the ultimopharyngeal body, which begins in the fourth ventral ventral pouch and joins the primordial thyroid gland as it descends to its final location.
Deviations in prenatal development may result in various forms of thyroid dysgenesis which may cause congenital hypothyroidism, and if untreated this may cause cretinism.
Function
Thyroid hormone
The main function of the thyroid is the production of thyroid hormones containing iodine, triiodothyronine (T 3 ) and thyroxine (T 4 ) and calcitonin peptide hormone. T 3 is so named because it contains three iodine atoms per molecule and T 4 contains four iodine atoms per molecule. Thyroid hormones have various effects on the human body. These include:
- Metabolic. Thyroid hormones increase basal metabolic rate and have an effect on almost all body tissues. Appetite, absorption of substances, and intestinal motility are all affected by thyroid hormones. They increase absorption in the intestines, generation, cell absorption, and breakdown of glucose. They stimulate the breakdown of fat, and increase the amount of free fatty acids. Despite increasing free fatty acids, thyroid hormones lower cholesterol levels, perhaps by increasing the rate of cholesterol secretion in bile.
- Cardiovascular. Hormones increase the rate and strength of the heartbeat. They increase respiratory rates, intake and oxygen consumption, and increase mitochondrial activity. Combined, these factors increase blood flow and body temperature.
- Developments. Thyroid hormone is essential for normal development. They increase the growth rate of young people, and the developing brain cells are the main target for thyroid hormone T 3 and T 4 . Thyroid hormones play a very important role in brain maturation during fetal development.
- Thyroid hormones also play a role in maintaining normal sexual function, sleep patterns, and mindset. Increased levels are associated with an increased speed of mind formation but a decrease in focus. Sexual function, including libido and maintenance of normal menstrual cycles, is affected by thyroid hormones.
After secretion, only a small part of the thyroid hormone runs freely in the blood. Most are bound to thyroxine binding globulin (about 70%), transthyretin (10%), and albumin (15%). Only 0.03% of T 4 and 0.3% T 3 are freely traveling have hormonal activity. In addition, up to 85% of T 3 in blood is generated after conversion of T 4 by iodothyronine deiodinase in organs around the body.
The thyroid hormone works by traversing the cell membrane and binding to the intracellular intracellular hormone receptor hormone TR -? 1 , TR -? 2 , TR -? 1 and TR -? 2 , which binds to the element of the hormonal response and transcription factor to modulate DNA transcription. In addition to this action on DNA, thyroid hormones also act in cell membranes or in the cytoplasm through reactions with enzymes, including calcium ATPase, adenylyl cyclase, and glucose transporters.
Hormone production
Thyroid hormones are made from thyroglobulin. This is a protein in the follicular space that was originally made in the rough endoplasmic reticulum of follicle cells and then transported to the follicle space. Thyroglobulin contains 123 units of tyrosine, which react with iodine in the follicle space.
Iodine is essential for the production of thyroid hormones. Iodine (I 0 ) moves in the blood as an iodide (I - ), which is taken into follicle cells by a sodium-iodide sympathizer. It is an ion channel on a cell membrane which in the same action transports two sodium ions and an iodide ion into the cell. The Iodide then moves from within the cell into the follicle space, through the action of pendrin, the iodide-chloride antiporter. In the follicular space, the iodide is then oxidized to iodine. This makes it more reactive, and iodine is attached to the active tyrosine unit in thyroglobulin by the thyroid peroxidase enzyme. It forms the precursor of thyroid hormone monoiodotyrosine (MIT), and diiodotyrosine (DIT).
When the follicle cells are stimulated by the thyroid-stimulating hormone, the follicle cells reabsorb the thyroglobulin from the follicle space. Iodine tyrosine is cleaved, forming the thyroid hormone T 4 , T 3 , DIT, MIT, and traces of reverse triiodothyronine. T 3 and T 4 are released into the blood. Hormones secreted from the gland are about 80-90% T 4 and about 10-20% T 3 . Enzyme deiodinase in peripheral tissue removes iodine from MIT and DIT and converts T 4 to T 3 and RT 3. This is the main source of either RT < sub> 3 (95%) and T 3 (87%) in peripheral tissue.
Rule
The production of thyroxine and triiodothyronine is mainly regulated by thyroid-stimulating hormone (TSH), secreted by the anterior pituitary gland. The release of TSH is in turn stimulated by thyrotropin releasing hormone (TRH), released by pulsatil from the hypothalamus. Thyroid hormones provide negative feedback to thyrotropes TSH and TRH: when thyroid hormone is high, TSH production is suppressed. This negative feedback also occurs when TSH levels are high, causing the production of TRH to be suppressed.
TRH is secreted at an elevated level in situations such as cold exposure to stimulate thermogenesis. In addition to being suppressed by thyroid hormone, TSH production is collected by dopamine, somatostatin, and glucocorticoids.
Calcitonin
The thyroid gland also produces the hormone calcitonin, which helps regulate blood calcium levels. Parafollicular cells produce calcitonin in response to high blood calcium. Calcitonin decreases the release of calcium from the bone, by reducing the activity of osteoclasts, the cells that break the bone. Bone is constantly reabsorbed by osteoclasts and is created by osteoblasts, so calcitonin effectively stimulates the movement of calcium into bone. The effects of calcitonin are in contrast to the parathyroid hormone (PTH) produced in the parathyroid glands. However, calcitonin appears to be much more important than PTH, because clinical calcium metabolism remains normal after thyroid extraction (thyroidectomy), but not the parathyroid gland.
Gene and protein expression
About 20,000 protein-encoding genes are expressed in human cells and 70% of these genes are expressed in normal thyroid. About 250 of these genes are more specifically expressed in the thyroid with about 20 genes that are very specific to the thyroid. Suitable specific proteins are primarily involved in the synthesis of thyroid hormones, such as thyroglobulin, TPO and IYD, and expressed in follicle cells. Other thyroid-enhancing proteins are calcitonin-related proteins such as CALCA and CALCB, expressed in parafollicular cells.
Clinical interests
Symptoms
Hyperthyroidism
Excessive production of thyroid hormones is called hyperthyroidism, most commonly caused by Graves' disease, multinodular toxic goiter, solitary thyroid adenoma, or inflammation. Other causes include drug induced iodine excess, especially from amiodarone, antiarrhythmic drugs; excess caused by preferenceal iodine removal by the thyroid after imaging of iodinated contrast; or from pituitary adenomas that can lead to overproduction of thyroid stimulating hormone. Hyperthyroidism often leads to various non-specific symptoms including weight loss, increased appetite, insomnia, decreased heat tolerance, tremors, palpitations, anxiety and anxiety. In some cases it can cause chest pain, diarrhea, hair loss and muscle weakness. These symptoms can be temporarily managed with drugs such as beta blockers.
Management of long-term hyperthyroidism may include drugs that suppress thyroid function such as propylthiouracil, carbimazole and methimazole. Radioactive iodine-131 â € <â € The less active thyroid gland produces hypothyroidism. Typical symptoms are abnormal weight gain, fatigue, constipation, heavy menstrual bleeding, hair loss, cold intolerance, and a slow heartbeat. Iodine deficiency is the most common cause of hypothyroidism worldwide, and autoimmune thyroiditis Hashimoto disease is the most common cause in developed countries. Other causes include congenital abnormalities, diseases that cause temporary inflammation, surgical removal or thyroid radioablation, amiodarone and lithium drugs, amyloidosis, and sarcoidosis. Some forms of hypothyroidism can cause myxedema and severe cases can cause myxedema coma. Hypothyroidism is administered by the replacement of thyroxine hormone. These are usually given daily as an oral supplement, and can take several weeks to become effective. Some of the causes of hypothyroidism, such as postpartum thyroiditis and subacute thyroiditis may be temporary and pass through, and other causes such as iodine deficiency may be corrected with dietary supplementation. Nodul
Thyroid nodules are often found in the gland, with a prevalence of 4-7%. The majority of nodules cause no symptoms and are non-cancerous. Non-cancerous cases include simple cysts, colloid nodules, and thyroid adenomas. Malignant nodules, which occur only in about 5% of nodules, include follicular, papillary, medullary and metastatic carcinomas from other sites. Nodules are more likely in women, those exposed to radiation, and in those with iodine deficiency.
When the nodule is present, a thyroid function test is performed and reveals whether a person has normal amounts of thyroid hormone ("euthyroid") or hormone excess, usually secreted by nodules, causing hyperthyroidism. When the thyroid function tests normally, ultrasound is often used to investigate nodules, and gives information as to whether the nodule is filled with fluid or solid mass, and whether its appearance indicates benign or malignant cancer. A needle aspiration biopsy can then be performed, and the sample undergoes cytology, in which the appearance of a cell is seen to determine whether the cell resembles a normal cell or cancer cell.
There are many nodules, called multinodular goitre, and this can sometimes be a toxic multinodular goiter.
Swelling
The enlarged thyroid gland is called mumps. Goitres are present in some forms in about 5% of people, and are the result of a large number of causes, including iodine deficiency, autoimmune diseases (both Grave's disease and Hashimoto's thyroiditis), infections, inflammation, and inflammatory diseases such as sarcoidosis and amyloidosis. Sometimes no cause can be found, a condition called "simple goitre".
Some forms of mumps are associated with pain, while many cause no symptoms whatsoever. The enlarged goiter can extend beyond the normal position of the thyroid gland to the lower sternum, around the airway or esophagus. Goitres may be associated with hyperhyoidism or hypothyroidism, related to the underlying cause of goiter. Thyroid function tests can be performed to investigate the causes and effects of goiter. The underlying cause of mumps can be treated, but many untreated goitres are only monitored.
Disease
Functional thyroid disorders are caused by dysfunction in hormone production, and both benign and malignant glands and tumors. Functional disorders can cause inflammation like some other forms of thyroiditis. Functional disorders can lead to overproduction or lack of hormone production. One functional thyroid disorder can cause enlargement of the gland and cause swollen neck termed as goiter.
Inflammation
Thyroid inflammation is called thyroiditis. An inflamed kidney may cause symptoms of hyperthyroidism or hypothyroidism. Two types of thyroiditis initially present with hyperthyroidism and are sometimes followed by periods of hypothyroidism - Hashimoto's thyroiditis and postpartum thyroiditis. There are other disorders that cause thyroid inflammation, and these include subacute thyroiditis, acute thyroiditis, silent thyroiditis, Riedel's thyroiditis and traumatic injury, including palpation of thyroiditis.
Hashimoto's thyroiditis is an autoimmune disorder in which the thyroid gland is inflamed by B-cell and T-cells lymphocytes. This further destroys the thyroid gland. In this way, Hasimoto's thyroiditis may have taken place secretly, and only be noticed when the production of thyroid hormone declines, causing symptoms of hypothyroidism. Hashimoto is more common in women than men, much more common after age 60, and has known genetic risk factors. Also more common in individuals with Hashimoto's thyroiditis is type 1 diabetes, pernicious anemia, Addison's disease vitiligo.
Postpartum thyroiditis occurs in some women after delivery. After delivery, the gland becomes inflamed and the condition initially comes with a period of hyperthyroidism followed by hypothyroidism and, usually, returns to normal function. The course of the disease lasts for several months, and is characterized by a non-painful goiter. Antibodies to thyroid peroxidase can be found in the test. Inflammation usually disappears without treatment, although thyroid hormone replacement may be necessary during the period of hypothyroidism.
Cancer
The most common neoplasm affecting the thyroid gland is a benign adenoma, usually appearing as a non-painful mass in the neck. Malignant thyroid cancer is most commonly carcinoma, although cancer can occur in any tissue consisting of thyroid, including C-cell cancer and lymphoma. Cancer from other sites also rarely gets into the thyroid gland. Head and neck radiation is a risk factor for thyroid cancer, and cancer is more common in women than men, occurring at a rate of about 2: 1.
In many cases, thyroid cancer appears as a painless mass in the neck. Very unusual for thyroid cancer comes with other symptoms, although in some cases cancer can cause hyperthyroidism. The vast majority of malignant thyroid cancers are papillary, followed by follicular, medullary, and thyroid lymphomas. Because of the superiority of the thyroid gland, cancer is often detected earlier in the course of the disease as a cause of nodules, which may have fine needle aspiration. The thyroid function test will help reveal whether the nodule produces excess thyroid hormone. A radioactive iodine absorption test can help reveal the activity and location of cancer and metastasis.
Thyroid cancer is treated by lifting the whole or part of the thyroid gland. Radioactive Iodine 131 may be administered for thyroid radioablates. Thyroxine is given to replace the lost hormone and to suppress the production of TSH, because TSH can stimulate recurrence. With the exception of rare anaplastic thyroid cancers, which carry a very poor prognosis, most thyroid cancers carry a very good prognosis and can even be considered curable.
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Persistent thyroglossal duct is the most common clinical congenital disorder in the thyroid gland. Persistent sinus ducts may remain as remnants of progression of thyroid gland tubules. Part of this tube can be eliminated, leaving a small segment to form a thyroglossal cyst. Premature neonates are at risk of hypothyroidism because their thyroid gland is insufficiently developed to meet their postnatal needs. To detect hypothyroidism in newborns, to prevent future growth and developmental abnormalities, many countries have newborn screening programs at birth.
Infants with thyroid hormone deficiency (congenital hypothyroidism) can manifest the problem of physical growth and development and brain development, called cretinism. Children with congenital hypothyroidism are supplemented with levothyroxine, which facilitates normal growth and development.
Mucosal and clear secretions may converge in this cyst to form a spherical mass or a fusiform swelling, rarely greater than 2 to 3 cm. It is present in the midline of the anterior neck to the trachea. Segments of ducts and cysts that occur high in the neck are enclosed by stratified squamous epithelium, which is essentially identical to that covering the posterior portion of the tongue in the foramen region of the caecum. Disorders occurring in the lower neck are more proximal to the thyroid gland fenced by epithelials that resemble thyroidal epithelium. Characteristically, in addition to epithelial lining, there is intense infiltration of lymphocytes. Overlapping infections can turn these lesions into abscess cavities, and rarely, cause cancer.
Another disorder is thyroid dysgenesis that can produce various presentations from one or more of the misplaced accessory thyroid glands. It can be asymptomatic.
Iodine
Iodine deficiency, most common in inland and mountainous areas, may predispose to goiter - if it is widespread, known as endemic goitre. Pregnant women with iodine deficiency can deliver babies with thyroid hormone deficiency. The use of iodized salt used to add iodine to the diet has eliminated endemic cretinism in most developed countries, and more than 120 countries have made mandatory salt iodination.
Because the thyroid concentrates iodine, it also concentrates the various isotopes of radioactive iodine produced by nuclear fission. In the case of a large release of such material to the environment, the absorption of radioactive iodine isotope by the thyroid may, in theory, be blocked by saturating the absorption mechanism with a large surplus of non-radioactive iodine, taken in the form of potassium iodide tablets. One consequence of the Chernobyl disaster was the increase in thyroid cancer in children in the years after the accident.
Like most substances, too much or too little can cause problems. Recent studies in some populations indicate that excess iodine intake may lead to an increased prevalence of autoimmune thyroid disease, resulting in permanent hypothyroidism.
Graves' disease
Graves' disease is an autoimmune disorder that is the most common cause of hyperthyroidism. In Graves' disease, for no apparent reason, autoantibodies develop against thyroid stimulating hormone receptors. These antibodies activate receptors, leading to the development of goiter and symptoms of hyperthyroidism, such as heat intolerance, weight loss, diarrhea and palpitations. Sometimes such antibodies block but do not activate receptors, leading to symptoms associated with hypothyroidism. In addition, a gradual eye-projection may occur, called Graves' ophthalmopathy, as does swelling in front of the shin. Graves' disease can be diagnosed with pathomnomonic features such as eye and shin involvement, or autoantibody isolation, or with uptake radiolabelled scan results. Graves' disease is treated with anti-thyroid drugs such as propylthiouracil, which decreases thyroid hormone production, but has a high recurrence rate. If there is no eye involvement, then the use of radioactive isotopes to dilate the glands may be considered. Gland removal surgery with subsequent thyroid hormone replacement may be considered, but it will not control symptoms associated with the eyes or skin.
Checkout
Doctors who specialize in the treatment of thyroid disorders are known generally as endocrine experts, thyroid specialists or thyroid specialists. Thyroid surgeons or otolaryngologists can play a role in surgical management of thyroid disease and general practitioners and family doctors can play a role in monitoring and identifying symptoms associated with thyroid disease.
The thyroid itself is examined by observing the surrounding glands and neck for swelling or enlargement. Then it is felt, usually from the back, and a person is often asked to swallow to better feel the gland against the radius of the testers. This gland moves up and down by swallowing due to its attachment to thyroid and cricoid cartilages. In a healthy person the gland is not seen as clear as a soft mass. Examination of the thyroid gland includes abnormal mass search and thyroid size assessment as a whole. Thyroid characters, swelling, nodules, and their consistency can all be felt. If there is a goiter, a tester may also feel his neck, consider tapping the top of the chest to check the extension. Further tests may include lifting the arm (Pemberton's sign), listening to the gland with a stethoscope for a bruit, reflex testing, and palpation of lymph nodes in the head and neck. Thyroid medical examination will also include the observation of people as a whole, to look for systemic signs such as weight gain or weight loss, hair loss, and signs at other locations - such as an eyelid or swelling of a calf in grave disease.
Testing
A number of tests can be used to test thyroid function, for the presence of the disease, and for the success or failure of treatment. Blood tests generally aim to measure thyroid function or determine the cause of thyroid dysfunction. Thyroid function tests include blood test batteries including T3 and T4 thyroid hormone measurements, as well as TSH measurements. They may reveal hyperthyroidism (high T3 and T4), hypothyroidism (low T3, T4), or subclinical hyperthyroidism (normal T3 and T4 with low TSH).
TSH levels are considered the most sensitive markers of thyroid dysfunction. However they are not always accurate, especially if the cause of hypothyroidism is thought to be associated with insufficient secretion of TRH, in which case it may be low or normal counterfeits. In such cases the TRH stimulation test, in which TRH is administered and the TSH level measured at 30 and 60 minutes thereafter, may be performed.
T3 and T4 can be measured directly. However, since two thyroid hormones move in ties to other molecules, and that is a biologically active "free" component, free T3 levels and free T4 can be measured. T4 is preferred, because at T3 levels hypothyroidism may be normal. The ratio bound to the unbound thyroid hormone is known as the thyroid hormone binding ratio (THBR). It is also possible to directly measure the primary carriers of the thyroid hormone, thryoglobulin and throxine binding globulin. Thyroglobulin will also be measurable in a healthy thyroid, and will increase with inflammation, and can also be used to measure the success of thyroid gland ablation or ablation. If successful, thyroglobulin should be undetectable. Finally, antibodies to the thyroid component, especially anti-TPO and anti-thyroglobulin, can be measured. It may be present in normal individuals but is very sensitive to autoimmune diseases.
Thyroid ultrasound can be used to reveal whether the structure is solid or filled with fluid, helping to distinguish between nodules and mumps and cysts. It can also help distinguish between malignant and benign lesions. A fine needle aspiration biopsy may be taken together with the thyroid tissue to determine the nature of the lesion. This biopsy is then sent for histopathology and cytology. When further imaging is required, iodine-123 or technetium-99 iodine uptake can be performed. It can determine the size and shape of the lesion, reveal whether the nodule or goiter is metabolically active, and reveal and monitor sites of thyroid disease or cancer deposits outside the thyroid.
History
The presence and disease of the thyroid have been recorded and treated for thousands of years, though the glands themselves have only been described and named since the renaissance. The first recorded mention of thyroid is in terms of goiter in Chinese manuscripts around 2700 BC, where there is general agreement. In 1600 BC burned sponges and seaweed were used in China for treatment of goiter, a practice that has been developed in many parts of the world. In Ayurvedic medicine, Sushruta Samhita's book written around 1400 BC describes hyperthyroidism, hypothyroidism, and mumps. Aristotle and Xenophon in the 5th century BC described cases of Grave's disease, which received its name over two millennia later because of the description given by Robert James Graves in 1834, Hippocrates and Plato in the 4th century BC provided some of the first descriptions of such glands. alone, proposed its function as a salivary gland. Pliny the Elder in the first century BC refers to the goitarian epidemic in the Alps and proposes treatment with seaweed being burned, a practice also referred to by Galen in the 2nd century, referring to the burning sponges for thyroid treatment.
In 1500 polymath Leonardo da Vinci gave the first illustration of the thyroid. In 1543, Anatomist Andreas Vesalius gave a description of the first anatomy and gland illustration. In 1656, the thyroid received its name, by the anatomist Thomas Wharton. The gland is called thyroid, which means a shield, because it resembles a shield commonly used in Ancient Greece. The English name thyroid gland is derived from the medical Latin used by Wharton - glandula thyreoidea . Glandula means gland in Latin, and thyreoidea can be traced back to the ancient Greek word ??????????, which means like a shield / shield .
French chemist Bernard Courtois discovered Iodine in 1811, and in 1896 Eugen Baumann documented it as a key ingredient in the thyroid gland. He does this by boiling the thyroid gland of a thousand sheep, and naming the sediment, the combination of thyroid hormone, 'iodothyrin'. David Marine in 1907 provided the iodine needed for thyroid function. Thyroxine itself was first isolated in 1914 and synthesized in 1927, and trirodothyroxine in 1952. The conversion of T4 to T3 was discovered in 1970. The process of TSH discovery occurred in the early to mid-twentieth century. TRH was discovered by the Polish endocrinologist, Andrew Schally in 1970, who partly contributed to the Nobel Prize in Medicine in 1977.
Either Aetius in the sixth century AD or Persia Ali ibn Abbas al-Magusi in 990 CE performed the first thyroidectomy listed as a treatment for goitre. The operation remained risky and generally unsuccessful until the 19th century, when the description emerged from a number of authors including Prussian surgeon Theodor Billroth, Swiss surgeon and physiologist Theodor Kocher, American physician Charles Mayo, William Halsted and George Crile. This description provides the basis for modern thyroid surgery. Theodor Kocher went on to win the Nobel Prize in Physiology or Medicine in 1909 "for his work on physiology, pathology and thyroid gland surgery".
Many authors describe cretinism, myxoedema their association with thyroid in the nineteenth century. Charles Mayo coined the term hyperthyroidism in 1910, Hakaru Hashimoto documented a case of Hashimoto's thyroiditis in 1912, and autoantibodies were shown in 1956. Knowledge of the thyroid and its condition evolved throughout the nineteenth and twentieth centuries, with many modern treatments and investigative modalities evolving throughout mid-20th century, including the use of radioactive iodine, tiouracil, and fine needle aspiration.
Other animals
The thyroid gland is found in all vertebrates. In fish, it is usually located under the gills and is not always divided into different lobes. However, in some teleosts, patches of thyroid tissue are found elsewhere in the body, associated with the kidneys, spleen, heart, or eyes.
In tetrapod, the thyroid is always found somewhere in the neck region. In most tetrapod species, there are two paired thyroid gland - that is, the right and left lobes do not join together. However, there is only one thyroid gland in most mammals, and the form found in humans is common to many other species.
In lamp lamps, the thyroid originates as an exocrine gland, secretes its hormones into the intestine, and is associated with a larval feeding apparatus. In adult lamprey, the gland separates from the gut, and becomes endocrine, but this developmental pathway may reflect the origin of thyroid evolution. For example, the closest relatives of vertebrates, tunicates and Amphioxus , have very similar structures to lampreys (endostyle) larvae, and this also excludes iodine-containing compounds (though not thyroxine)..
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