- The thyroid gland is a butterfly-shaped structure that sits slightly below the larynx, anterior to the trachea. The isthmus, or central portion, is bordered by wing-shaped left and right lobes. The parathyroid glands are embedded in each of the thyroid lobes, mainly on the posterior sides. Thyroid follicles make up the majority of the thyroid gland’s tissue.
- The follicles have a core chamber that is filled with a sticky substance known as colloid. The colloid, which is surrounded by epithelial follicle cells and is the focus of thyroid hormone production, is dependent on the hormones fundamental and distinctive component iodine.
Synthesis and Release of Thyroid Hormones
- Hormones are created in the colloid when atoms of the mineral iodine bind to a glycoprotein known as thyroglobulin, which is released into the colloid by follicle cells. When TSH binds to its receptors in thyroid follicle cells, the cells actively transfer iodaide ions (I–) through their cell membrane from the circulation into the cytosol.
- As a result, the concentration of iodide ions “locked” in follicular cells is many times larger than the bloodstream concentration. Iodide ions subsequently travel to the follicle cells’ lumens, which border the colloid. There, the ions are oxidised (their negatively charged electrons are removed). Iodine (I2) is formed when two iodide ions (2 I–) are oxidised and pass past the follicular cell membrane into the colloid.
- Peroxidase enzymes in the colloid link iodine to thyroglobulin’s tyrosine amino acids to form two intermediaries: a tyrosine connected to one iodine and a tyrosine attached to two iodines. Triiodothyronine (T3), a thyroid hormone with three iodines, is formed when one of each of these intermediates is joined by covalent bonds. Two copies of the second intermediary bond are much more common, resulting in tetraiodothyronine, often known as thyroxine (T4), a four-iodine thyroid hormone. TSH causes endocytosis of colloid back into the follicle cells, therefore these hormones stay in the colloid centre of thyroid follicles until TSH stimulates endocytosis of colloid back into the follicle cells. Lysosomal enzymes degrade the thyroglobulin colloid there, releasing free T3 and T4 that diffuse past the follicular cell membrane and into the bloodstream.
- Less than 1% of the circulating T3 and T4 remain unbound in the bloodstream. Free T3 and T4 are able to pass through the lipid bilayer of cell membranes and be absorbed by cells. The remaining 99 percent of T3 and T4 in circulation is bound to thyroxine-binding globulins (TBGs), albumin, or other plasma proteins. This “packing” inhibits them from freely diffusing into the cells of the body. When T3 and T4 levels in the blood drop, bound T3 and T4 are liberated from plasma proteins and easily penetrate the membrane of target cells. T3 is more powerful than T4, and many cells convert T4 to T3 by removing an atom of iodine.
Regulation of TH Synthesis
- Thyroid-stimulating hormone controls the release of T3 and T4 from the thyroid gland (TSH). Low T3 and T4 levels in the blood cause the hypothalamus to release thyrotropin-releasing hormone (TRH), which causes the anterior pituitary to secrete TSH. TSH causes the thyroid gland to produce T3 and T4 as a result. TRH, TSH, T3, and T4 levels are regulated by a negative feedback loop in which rising T3 and T4 levels reduce TSH synthesis and release.
Functions of Thyroid Hormones
- Thyroid hormones T3 and T4 are known as metabolic hormones because their levels affect the body’s basal metabolic rate, or how much energy the body uses at rest. When T3 and T4 attach to mitochondrial intracellular receptors, they trigger an increase in nutritional breakdown and oxygen usage to make ATP. T3 and T4 also start the transcription of genes that help with glucose oxidation. Although these pathways cause cells to make more ATP, the process is inefficient, and the reactions emit an excessively high amount of heat as a consequence.
- The calorigenic effect (calor =”heat”) causes the body temperature to rise. Thyroid hormone levels must be adequate for protein synthesis as well as prenatal and childhood tissue development and growth. They’re notably important for appropriate nervous system development in gestation and early childhood, and they’re still important for adult neurological function.
- Thyroid hormones have a complicated interaction with reproductive hormones, as previously mentioned, and deficits can affect libido, fertility, and other aspects of reproductive function. Finally, thyroid hormones up regulate receptors in the blood vessels, making the organism more sensitive to catecholamines (epinephrine and norepinephrine) from the adrenal medulla.
- This impact accelerates the heart rate, intensifies the beating, and raises blood pressure when T3 and T4 hormone levels are too high. Thyroid diseases can have serious and extensive repercussions because thyroid hormones regulate metabolism, heat production, protein synthesis, and many other physiological activities.
- The thyroid gland secretes calcitonin, which is produced by parafollicular cells (also known as C cells) that stud the tissue between follicles. When blood calcium levels rise, a hormone called calcitonin is secreted.
- However, the importance of calcitonin is uncertain because these activities are often minor in maintaining calcium homeostasis. Patients with osteoporosis and osteoarthritis may be given calcitonin pharmaceutical formulations to reduce osteoclast activity and cartilage degradation.
The Parathyroid Glands
- The parathyroid glands are small, spherical structures that are normally found lodged in the thyroid glands posterior side. The glands are separated from the thyroid tissue by a strong connective tissue capsule. The average person has four parathyroid glands; however there are occasionally more in the neck or chest tissues.
- The function of oxyphil cells, one type of parathyroid cell, is unknown. The main cells are the parathyroid glands’ major functioning cells. The parathyroid hormone (PTH), a key hormone involved in the regulation of blood calcium levels, is produced and secreted by these epithelial cells.
- In reaction to low blood calcium levels, the parathyroid glands generate and emit PTH, a peptide hormone. PTH secretion stimulates osteoclasts, which secrete enzymes that disintegrate bone and release calcium into the interstitial fluid, causing calcium to be released from the bones. PTH also inhibits osteoblasts, the cells responsible for bone formation, allowing blood calcium to be conserved.
- PTH increases the reabsorption of calcium (and magnesium) from the urine filtrate in the kidney tubules. PTH also causes the kidneys to produce the steroid hormone calcitriol, which is the active form of vitamin D3. Calcitriol then promotes the intestines to absorb more calcium from the food they eat. PTH levels are regulated by a negative feedback loop, with rising blood calcium levels preventing further PTH release.
- Hyperparathyroidism is a condition caused by an excess of PTH produced by the parathyroid gland, which leads in excessive calcium reabsorption from the bones. Hyperparathyroidism lowers bone density, which can lead to spontaneous fractures or deformities. When blood calcium levels rise, cell membrane permeability to sodium decreases, and nervous system reactivity decreases.
- Calcium deposits may form in the body’s tissues and organs at the same time, limiting their function. Hypoparathyroidism, or a lack of parathyroid hormone, can produce unusually low blood calcium levels. Hypoparathyroidism can develop after a thyroid gland injury or surgery.
- Low blood calcium causes muscle twitching, cramping, spasms, and convulsions via increasing membrane permeability to salt. Severe deficits can cause muscles to become paralysed, particularly those involved in breathing, which can be fatal. Calcitonin is generated and secreted by the thyroid glands parafollicular cells when blood calcium levels are high. As previously stated, calcitonin suppresses osteoclast activity, limits dietary calcium absorption in the intestine, and signals the kidneys to reabsorb less calcium, resulting in higher calcium excretion in the urine.