 In this video, I will describe the structure and function of the thyroid gland and parathyroid glands, discuss the effects of the thyroid hormones T3 and T4, and describe the effects of hyperthyroidism and hypothyroidism, then discuss the regulation of calcium homeostasis by calcitonin and parathyroid hormone. The thyroid gland is a butterfly shaped organ located on the anterior cervical region, or it might help you to remember this, that it's sort of similar to the shape and location of a bow tie, there in the front of the neck where you would wear a bow tie, the thyroid gland has two larger lobes connected by a narrow isthmus on the midline. The thyroid gland produces the thyroid hormones T3 and T4 that stimulate metabolic rate. The production of the thyroid hormones is stimulated by a hormonal release mechanism in response to TSH thyroid stimulating hormone from the anterior pituitary as part of the hypothalamic pituitary thyroid axis. The hypothalamus produces the thyroid tropon releasing hormone TRH to stimulate the anterior pituitary to make TSH, which then stimulates the thyroid gland and TSH both stimulates the growth of the thyroid gland as well as stimulating the production of thyroid hormones T3 and T4, which then have the effects of increasing the metabolic rate, which helps warm our body. The thyroid gland also produces another hormone known as calcitonin, which is important for decreasing blood calcium levels. Calcitonin is released in response to a humoral release mechanism in response to low blood calcium concentration. The paraphilicular C cells of the thyroid gland secrete calcitonin to stimulate a decrease in the blood calcium concentration. On the posterior of the thyroid gland are four small round masses known as the parathyroid glands. The parathyroid glands secrete parathyroid hormone under a humoral release mechanism in response to low blood calcium concentration. The parathyroid glands secrete parathyroid hormone in order to increase blood calcium concentration. On the left we see the chemical structure of the thyroid hormones T3 on the top. T3 stands for triiodothyronine because the chemical structure of T3 contains three iodine atoms and T4, also known as thyroxin, contains four iodine atoms in its chemical structure. Because the thyroid hormones contain iodine, dietary iodine deficiency impairs the synthesis of thyroid hormones. This can lead to a goiter, an overgrowth of the thyroid gland, which is shown in the picture on the right. The function of the thyroid hormones T3 and T4 is to increase the basal metabolic rate and this stimulates an increase in body temperature. If the metabolic rate and body temperature are too low, the hypothalamus will release TRH, stimulating the anterior pituitary to release TSH, then TSH binds to receptors on the surface of thyroid follicle cells in the thyroid gland, and these cells then release T3 and T4, which then bind to receptors within cells all throughout the body, leading to increased metabolic rate and the calorogenic effect, increasing body temperature. T3 and T4 also bind to receptors within cells in the hypothalamus as a negative feedback mechanism T3 and T4 inhibit the production of TRH, leading to decreased TSH. Iodine deficiency, disrupting the production of T3 and T4, removes this negative feedback mechanism, leading to excessive TSH production, which causes the goiter. Insufficient thyroid hormone signaling is known as hypothyroidism. The most common cause of hypothyroidism is iodine deficiency. With insufficient levels of iodine, the thyroid gland cannot produce the thyroid hormones, thyroxin and triiodothyronine. This leads to disruption in negative feedback, causing elevated levels of TSH. And as TSH is a tropic hormone, TSH stimulates growth of the thyroid gland, producing a goiter in enlargement of the thyroid gland, as is shown in the picture here. Now, disruption of thyroid hormone signaling, hypothyroidism, will also slow the metabolic rate, leading to weight gain. And this disrupts the normal homeostatic mechanisms for thermal regulation, leading to cold intolerance. Other symptoms that can be associated with hypothyroidism include decreased heart rate, bradycardia, or a decreased stroke volume, constipation, depression, fatigue or weakness, feeling tired, facial swelling or puffiness, especially around the eyes. And while iodine deficiency is the most common form of hypothyroidism and is the easiest to treat using iodine supplementation, there's also an autoimmune disease known as Hashimoto's, which is an inflammatory disease that involves the immune system attacking the thyroid gland. And this disrupts the ability of the thyroid gland to produce the thyroid hormones. Now, in contrast to hypothyroidism, hyperthyroidism is excess thyroid hormone signaling. The most common cause of hyperthyroidism is known as Graves' disease, and this is an autoimmune disease where the body produces autoantibodies that bind to the receptors for TSH. And by binding to those receptors, these antibodies activate the TSH receptor much like TSH would. This stimulates growth of the thyroid gland producing a goiter and also stimulates an increased secretion of the thyroid hormones, leading to an increased metabolic rate, producing weight loss and disrupting the thermoregulation mechanism leading to heat intolerance. Other symptoms that are common in hyperthyroidism include an elevated heart rate, tachycardia, diarrhea, anxiety, insomnia, restlessness, and particularly in Graves' disease there are protruding eyes as well as a goiter. The protruding eyes results from inflammation of the orbital tissues surrounding the eyes causing the eyes to bulge out. Hyperthyroidism can also lead to elevation of the upper eyelid, which can also further contribute to hyperthyroidism, but the protruding eyes is specific to Graves' disease. There are other forms of hyperthyroidism, and aside from Graves' disease, the most common of these are tumors, these are tumors of glandular tissue in either the thyroid gland or the pituitary gland. The thyroid gland tumor could be uncontrolled growth of the cells in the thyroid gland that produce the thyroid hormones leading to hyperthyroidism, or it's also possible that you could have a tumor in the pituitary gland producing TSH that would then lead to a hyperthyroidism that would be associated with a goiter. And so you can see that a goiter is commonly found in both hyperthyroidism as well as forms of hyperthyroidism, although it's possible to have hypothyroidism without a goiter or hyperthyroidism without a goiter. The most common thyroid disorder is iodine deficiency, which is associated with a goiter, but the most common form of hyperthyroidism can also be associated with a goiter. In response to hypercalcemia, calcitonin released from C cells in the thyroid gland binds to receptors on osteoblasts in bone, stimulating osteoblasts to store calcium in the bone. Calcitonin also inhibits osteoclasts, reducing the rate of calcium reabsorption from the bone. Parathyroid glands are four small glands on the posterior of the thyroid gland that respond to hypocalcemia, that is low blood calcium concentration. When blood calcium concentration drops, the parathyroid gland releases the parathyroid hormone abbreviated PTH. Then PTH binds to receptors on the surface of cells in the bone and in the kidneys. Parathyroid hormone inhibits osteoblasts and stimulates osteoclasts in bone, leading to the release of calcium from the bone. This works to increase blood calcium concentrations. Parathyroid hormone also binds to receptors on the surface of cells in the kidney, stimulating the reabsorption of calcium, which lowers the loss of calcium in the urine as another mechanism working to increase blood calcium concentrations. Parathyroid hormone also stimulates the production of calcitrile in the kidneys. Calcitrile is the active form of vitamin D, which functions as a hormone produced in the kidneys that travels to the intestine, where vitamin D3 or calcitrile binds to receptors in cells lining the intestine and stimulates calcium absorption from the diet.