2 Artlabeling Activity Histology of the Thyroid Gland Quizlet
Learning Objectives
By the end of this section, you will be able to:
- Depict the location and anatomy of the thyroid gland
- Hash out the synthesis of triiodothyronine and thyroxine
- Explain the role of thyroid hormones in the regulation of basal metabolism
- Identify the hormone produced by the parafollicular cells of the thyroid
A butterfly-shaped organ, the thyroid gland is located anterior to the trachea, just inferior to the larynx (Figure ane). The medial region, called the isthmus, is flanked by wing-shaped left and right lobes. Each of the thyroid lobes are embedded with parathyroid glands, primarily on their posterior surfaces. The tissue of the thyroid gland is composed mostly of thyroid follicles. The follicles are made upward of a central cavity filled with a sticky fluid called colloid. Surrounded by a wall of epithelial follicle cells, the colloid is the center of thyroid hormone production, and that production is dependent on the hormones' essential and unique component: iodine.
Figure 1. The thyroid gland is located in the neck where it wraps around the trachea. (a) Inductive view of the thyroid gland. (b) Posterior view of the thyroid gland. (c) The glandular tissue is composed primarily of thyroid follicles. The larger parafollicular cells oftentimes appear within the matrix of follicle cells. LM × 1332. (Micrograph provided by the Regents of University of Michigan Medical School © 2012)
Synthesis and Release of Thyroid Hormones
Hormones are produced in the colloid when atoms of the mineral iodine attach to a glycoprotein, called thyroglobulin, that is secreted into the colloid by the follicle cells. The post-obit steps outline the hormones' associates:
- Binding of TSH to its receptors in the follicle cells of the thyroid gland causes the cells to actively transport iodide ions (I–) across their cell membrane, from the bloodstream into the cytosol. Equally a event, the concentration of iodide ions "trapped" in the follicular cells is many times higher than the concentration in the bloodstream.
- Iodide ions then move to the lumen of the follicle cells that border the colloid. There, the ions undergo oxidation (their negatively charged electrons are removed). The oxidation of ii iodide ions (2 I–) results in iodine (I2), which passes through the follicle cell membrane into the colloid.
- In the colloid, peroxidase enzymes link the iodine to the tyrosine amino acids in thyroglobulin to produce two intermediaries: a tyrosine fastened to one iodine and a tyrosine attached to ii iodines. When one of each of these intermediaries is linked by covalent bonds, the resulting compound is triiodothyronine (T3), a thyroid hormone with three iodines. Much more commonly, ii copies of the second intermediary bond, forming tetraiodothyronine, too known as thyroxine (T4), a thyroid hormone with 4 iodines.
These hormones remain in the colloid center of the thyroid follicles until TSH stimulates endocytosis of colloid back into the follicle cells. There, lysosomal enzymes interruption autonomously the thyroglobulin colloid, releasing gratuitous Tiii and Tiv, which diffuse beyond the follicle cell membrane and enter the bloodstream.
In the bloodstream, less than one percent of the circulating Tiii and T4 remains unbound. This costless T3 and T4 can cross the lipid bilayer of cell membranes and be taken up by cells. The remaining 99 percent of circulating T3 and T4 is bound to specialized ship proteins called thyroxine-binding globulins (TBGs), to albumin, or to other plasma proteins. This "packaging" prevents their free improvidence into body cells. When blood levels of T3 and T4 begin to decline, leap T3 and Tiv are released from these plasma proteins and readily cross the membrane of target cells. T3 is more than potent than T4, and many cells convert T4 to T3 through the removal of an iodine atom.
Regulation of Thursday Synthesis
The release of Tiii and Tfour from the thyroid gland is regulated by thyroid-stimulating hormone (TSH). Every bit shown in Figure 2, depression blood levels of T3 and T4 stimulate the release of thyrotropin-releasing hormone (TRH) from the hypothalamus, which triggers secretion of TSH from the anterior pituitary. In turn, TSH stimulates the thyroid gland to secrete T3 and Tfour. The levels of TRH, TSH, T3, and Tfour are regulated by a negative feedback arrangement in which increasing levels of T3 and T4 decrease the production and secretion of TSH.
Effigy 2. A classic negative feedback loop controls the regulation of thyroid hormone levels.
Functions of Thyroid Hormones
The thyroid hormones, T3 and T4, are often referred to as metabolic hormones because their levels influence the body'due south basal metabolic charge per unit, the amount of energy used past the body at rest. When T3 and Tfour bind to intracellular receptors located on the mitochondria, they cause an increment in nutrient breakdown and the use of oxygen to produce ATP. In addition, T3 and T4 initiate the transcription of genes involved in glucose oxidation. Although these mechanisms prompt cells to produce more ATP, the process is inefficient, and an abnormally increased level of heat is released every bit a byproduct of these reactions. This then-called calorigenic upshot (calor- = "heat") raises body temperature.
Adequate levels of thyroid hormones are also required for protein synthesis and for fetal and childhood tissue evolution and growth. They are especially critical for normal evolution of the nervous organisation both in utero and in early childhood, and they go on to support neurological function in adults. As noted earlier, these thyroid hormones have a complex interrelationship with reproductive hormones, and deficiencies tin can influence libido, fertility, and other aspects of reproductive function. Finally, thyroid hormones increase the body'southward sensitivity to catecholamines (epinephrine and norepinephrine) from the adrenal medulla by upregulation of receptors in the blood vessels. When levels of T3 and Tfour hormones are excessive, this upshot accelerates the heart charge per unit, strengthens the heartbeat, and increases blood pressure. Because thyroid hormones regulate metabolism, estrus product, protein synthesis, and many other body functions, thyroid disorders can have severe and widespread consequences.
Disorders of the Endocrine Arrangement
Iodine Deficiency, Hypothyroidism, and Hyperthyroidism
As discussed above, dietary iodine is required for the synthesis of T3 and T4. Just for much of the world's population, foods practise not provide adequate levels of this mineral, because the amount varies according to the level in the soil in which the food was grown, as well every bit the irrigation and fertilizers used. Marine fish and shrimp tend to have high levels considering they concentrate iodine from seawater, but many people in landlocked regions lack access to seafood. Thus, the primary source of dietary iodine in many countries is iodized salt. Fortification of salt with iodine began in the United States in 1924, and international efforts to iodize salt in the world's poorest nations continue today.
Dietary iodine deficiency can result in the impaired ability to synthesize T3 and Tfour, leading to a variety of severe disorders. When Tthree and T4 cannot exist produced, TSH is secreted in increasing amounts. As a upshot of this hyperstimulation, thyroglobulin accumulates in the thyroid gland follicles, increasing their deposits of colloid. The accumulation of colloid increases the overall size of the thyroid gland, a status called a goiter (Figure 3). A goiter is merely a visible indication of the deficiency. Other iodine deficiency disorders include impaired growth and evolution, decreased fertility, and prenatal and infant death. Moreover, iodine deficiency is the primary crusade of preventable mental retardation worldwide. Neonatal hypothyroidism (cretinism) is characterized past cognitive deficits, short stature, and sometimes deafness and muteness in children and adults born to mothers who were iodine-deficient during pregnancy.
Figure three. Goiter (credit: "Almazi"/Wikimedia Commons)
In areas of the world with access to iodized table salt, dietary deficiency is rare. Instead, inflammation of the thyroid gland is the more than common cause of low blood levels of thyroid hormones. Chosen hypothyroidism, the status is characterized by a depression metabolic rate, weight gain, cold extremities, constipation, reduced libido, menstrual irregularities, and reduced mental activity.
In contrast, hyperthyroidism—an abnormally elevated blood level of thyroid hormones—is often caused by a pituitary or thyroid tumor. In Graves' affliction, the hyperthyroid state results from an autoimmune reaction in which antibodies overstimulate the follicle cells of the thyroid gland. Hyperthyroidism can lead to an increased metabolic rate, excessive body heat and sweating, diarrhea, weight loss, tremors, and increased center rate. The person'south eyes may bulge (called exophthalmos) as antibodies produce inflammation in the soft tissues of the orbits. The person may also develop a goiter.
Calcitonin
The thyroid gland besides secretes a hormone called calcitonin that is produced by the parafollicular cells (as well called C cells) that stud the tissue betwixt distinct follicles. Calcitonin is released in response to a rise in blood calcium levels. It appears to have a office in decreasing claret calcium concentrations past:
- Inhibiting the activity of osteoclasts, bone cells that release calcium into the circulation by degrading bone matrix
- Increasing osteoblastic action
- Decreasing calcium assimilation in the intestines
- Increasing calcium loss in the urine
Even so, these functions are usually not meaning in maintaining calcium homeostasis, and so the importance of calcitonin is non entirely understood. Pharmaceutical preparations of calcitonin are sometimes prescribed to reduce osteoclast activeness in people with osteoporosis and to reduce the degradation of cartilage in people with osteoarthritis. The hormones secreted by thyroid are summarized in Table 1.
| Table one. Thyroid Hormones | ||
|---|---|---|
| Associated hormones | Chemic class | Result |
| Thyroxine (Tiv), triiodothyronine (T3) | Amine | Stimulate basal metabolic rate |
| Calcitonin | Peptide | Reduces claret Ca2+ levels |
Of course, calcium is critical for many other biological processes. It is a 2d messenger in many signaling pathways, and is essential for muscle contraction, nerve impulse manual, and claret clotting. Given these roles, it is not surprising that claret calcium levels are tightly regulated past the endocrine organisation. The organs involved in the regulation are the parathyroid glands.
Affiliate Review
The thyroid gland is a butterfly-shaped organ located in the neck anterior to the trachea. Its hormones regulate basal metabolism, oxygen use, food metabolism, the production of ATP, and calcium homeostasis. They also contribute to protein synthesis and the normal growth and development of trunk tissues, including maturation of the nervous system, and they increase the body's sensitivity to catecholamines. The thyroid hormones triiodothyronine (T3) and thyroxine (Tiv) are produced and secreted by the thyroid gland in response to thyroid-stimulating hormone (TSH) from the anterior pituitary. Synthesis of the amino acid–derived T3 and T4 hormones requires iodine. Insufficient amounts of iodine in the diet can lead to goiter, cretinism, and many other disorders.
Self Check
Answer the question(s) below to see how well yous understand the topics covered in the previous department.
Disquisitional Thinking Questions
- Explain why maternal iodine deficiency might lead to neurological damage in the fetus.
- Define hyperthyroidism and explain why one of its symptoms is weight loss.
Glossary
calcitonin:peptide hormone produced and secreted by the parafollicular cells (C cells) of the thyroid gland that functions to subtract claret calcium levels
colloid:viscous fluid in the cardinal crenel of thyroid follicles, containing the glycoprotein thyroglobulin
goiter:enlargement of the thyroid gland either as a event of iodine deficiency or hyperthyroidism
hyperthyroidism:clinically abnormal, elevated level of thyroid hormone in the blood; characterized by an increased metabolic rate, excess body rut, sweating, diarrhea, weight loss, and increased eye rate
hypothyroidism:clinically abnormal, depression level of thyroid hormone in the blood; characterized past depression metabolic rate, weight gain, common cold extremities, constipation, and reduced mental activeness
neonatal hypothyroidism:condition characterized by cognitive deficits, brusque stature, and other signs and symptoms in people built-in to women who were iodine-deficient during pregnancy
thyroid gland:large endocrine gland responsible for the synthesis of thyroid hormones
thyroxine:(also, tetraiodothyronine, T4) amino acid–derived thyroid hormone that is more abundant only less strong than Tthree and often converted to T3 by target cells
triiodothyronine:(also, Tiii) amino acid–derived thyroid hormone that is less abundant but more than potent than Tfour
Source: https://courses.lumenlearning.com/suny-ap2/chapter/the-thyroid-gland/
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