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Costanzo Physiology (Chapter 9C) Endocrine Physiology: Thyroid Hormone || Study This!
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hello and welcome to the next portion of the endocrine physiology chapter going over the thyroid hormones in the thyroid gland if you enjoy the video please don't forget to give it a like and subscribe to the channel so going over our thyroid hormones this is produced by the follicular epithelial cells within the thyroid gland itself we have two types of thyroid hormones we've got t4 and t3 t3 is the metabolically active hormone within the actual cell itself but t4 is more abundant in the plasma so it's almost stored as t4 and the plasma goes into the cell and it gets converted to t3 within the cell to then have its actions the difference between t3 and t4 is just the amount of iodine within the molecule so t4 means that there's four iodine molecules within that hormone whereas t3 has three iodine molecules so that's the major difference between the two so going into how the thyroid hormone gets produced within the thyroid gland first we should look at the anatomy of the thyroid gland within the thyroid gland we have these thyroid follicles which is essentially a ring of follicular epithelial cells which secrete colloid into the lumen this colloid contains thyroid hormone attached to a molecule called thyroglobulin when the gland gets stimulated to secrete thyroid hormone that thyroid hormone within the colloid then gets endocytosed into the cell and then excreted via the follicular cells into the blood vessels so now we should talk about how thyroid hormone actually gets produced within the follicular epithelial cell that's shown here in figure 9.18 here and all the specific steps so the first step is actually getting iodine into the cell since that's the major component of thyroid hormone interestingly the thyroid gland is the only gland that actually uses iodine so all your dietary iodine goes to your thyroid gland to get incorporated into thyroid hormone so via the sodium co-transporter here iodine gets transported into the follicular epithelial cell and this transporter actually gets upregulated if we have iodine deficiency to help shuttle even more iodine into the cell this is against its concentration and electrical gradient so it's quite a push it requires a lot of energy to actually get the iodine into the cell clearly if there is a severe iodine deficiency then we will have a lack of iodine going into the cell and then a reduced production of our thyroid hormone but this transporter tries to combat it initially by up regulating in the presence of mild deficiency now once iodine enters the cell it then gets oxidized into an i2 molecule via what's called a thyroid peroxidase this thyroid peroxidase is going to come up a couple times but you'll see that within the follicular lumen now we have our oxidized iodine as i2 now this i2 will then bind with a thyroglobulin molecule which comes from the cell being synthesized from a tyrosine molecule so the combination of iodine with thyroglobulin is called organification and then that creates this molecule which is thyroglobulin with either an mit or dit mit stands for mono iodine tyrosine and then dit stands for diado tyrosine basically mit means there's one iodine with that tyrosine molecule on the thyroglobulin dit means there's two iodines so at this stage we then have another peroxidase reaction which will combine these molecules to create t4 and t3 so if we combine two dits then we're going to end up with t4 if we combine the dit with an mit then we're going to end up with t3 because that's simple maths we're just adding on iodine together so then we end up with four iodines in the case of t4 and then three iodines in the case of t3 there is also some residual mit and dit molecules left on this thyroglobulin so this is the kind of final product that sits within the follicular lumen which is this thyroglobulin with attached t4 and then some mit and dit so this just sits in the follicular lumen waiting for the stimuli to secrete t4 so once that stimulus occurs which predominantly is the secretion of thyroid stimulating hormone from that anterior pituitary gland then this thyroglobulin complex is going to get endocytosed into the follicular cell and then it's going to release its t4 and t3 into circulation that thyroglobulin tyrosine molecule is going to get recycled so is the mit and dit releasing its iodine to then get recycled back into this equation again so that is the entire production of thyroid hormone remember t4 is the most prevalent molecule in the plasma but then t3 is the more metabolically active so once in the circulation these thyroid hormones actually bind to something called thyroxine binding globulin so the majority of our thyroid hormone is actually bound to proteins within the plasma and that means that it's almost stored in the plasma for the cells the free hormones are the only physiologically active hormones so if we have less of this globulin molecule that means more of the thyroid within the plasma is going to be in the free active form so we may have less globulin and hepatic failure which is the organ that actually produces these globulins which means we have more of the active t4 t3 in the plasma that actually gets sensed by the anterior pituitary gland which means that we secrete less thyroid stimulating hormone as a negative feedback mechanism so we actually reduce the amount of thyroid gland secretion in that situation whereas if we have an increased level of globulins so then it's actually holding more of that thyroid hormone in the plasma as non-active or protein-bound thyroid hormone which is going to happen let's say in pregnancy which inhibits hepatic breakdown of this globulin that means that there is less active t43 that is free within the blood the anterior pituitary gland senses that and thinks that we have a relative thyroid deficiency so then it's going to release more tsh to increase the secretion of thyroid hormone once the thyroid hormone actually enters the cell remember predominantly it's going to be t4 that enters the cell since that is more abundant in our plasma the target tissue will then convert that t4 into active thyroid hormone as in t3 using the enzyme 5-ironase now that will also produce some of this reverse t3 which is inactive but the active component is t3 now during starvation when you don't have many nutrients and you are not producing that much energy and you need to reduce your metabolic rate then you will inhibit this five iodine enzyme to reduce your metabolic rate by reducing the amount of active thyroid hormone in your target cells because thyroid hormone the whole thing about it is that it actually increases our metabolic rate so if you're in the starvation state you need to conserve energy you're going to produce less active thyroid hormone so then your cell is going to have a lower basal metabolic rate that gets us to the regulation of hormone secretion we've already talked about the globulin levels so if you have increased globulin levels then you're going to increase the secretion of your thyroid hormone because there's less free hormones and vice versa thyroid stimulating hormone is clearly the main stimulation for secretion from the thyroid glands and then thyroid stimulating immunoglobulins is another molecule which basically acts like tsh at the receptor of the thyroid gland and that's actually a cause for hyperthyroidism called graves disease which is just excessive production of this thyroid stimulating immunoglobulin which tells the thyroid gland to produce a lot of thyroid hormone so you end up in a hyperthyroid state in terms of inhibitory factors obviously if you have severe iodine deficiency you don't have enough iodine to incorporate into your thyroid hormones you could have deficiency of that drnas which releases t4 and t3 from your thyroglobulin ironically excessive iodine intake actually inhibits the organification of iodine to a thyroglobulin which is also an inhibitory factor and then lastly any medications that's going to inhibit the movement of iodine into the cell or inhibit those peroxidase enzymes which create the thyroid hormone themselves so next up we're going to talk about the actual actions of thyroid hormones the easiest way to think about this is that thyroid hormone gets into the cell activates the nuclear receptor via t3 and then that causes the increased synthesis of new proteins via transcription and translation so thyroid hormone will get into the cells and increase the metabolism of that cell so whatever that cell may be it's just going to increase the metabolic rate of that cell so it's going to cause growth of our organs it's going to cause bone maturity it's going to cause maturation of our central nervous system in our cardiovascular system it's going to increase our cardiac output because it gets into the myocardial cells basically increases the enzymes or calcium recycling increases our contractions increases the beta receptors on the cells so then they're more likely to get stimulated by the sympathetic nervous system and increase cardiac output it increases metabolism just because it increases the cycling of glucose we're increasing the protein production to increase glucose absorption to produce glucose increase lipolysis increase protein synthesis and degradation ultimately it actually has a net catabolic effect on protein degradation because your entire body is basically just churning through its metabolic processes it's just trying to work as hard as possible it increases our basal metabolic rate by increasing the production of our sodium potassium atpase transporters which just increases the amount of oxygen consumption because we need to produce a lot of atp to now feed these increased sodium potassium atpases so oxygen consumption goes up a lot of energy gets used we increase our heat production due to that increased use of energy and then our basal metabolic rate increases so the typical clinical signs of someone with excessive thyroid hormone which is up regulating all of these cells basal metabolic rate is going to be an increased hunger but yet weight loss because you're just chewing through all that extra energy and excitability or irritability obviously the opposite is also true if you don't have enough thyroid hormone then your basal metabolic rate is going to reduce everything's going to reduce so you're going to become lethargic sluggish and gain weight now it does go into some of the causes of hyperthyroidism and hypothyroidism for people the main cause of hyperthyroidism so high thyroid gland is that graves disease remember we increase the level of our thyroid stimulating immunoglobulins if you have high of those that means that you're going to produce a lot of t4 and t3 that's going to have a negative feedback on your anterior pituitary gland so your tsh is going to be low and that's the same if you have a thyroid gland neoplasia that's producing excessive thyroid hormone so you can sometimes use thyroid stimulating hormone levels as a telltale to see what's going on obviously if you've got something that's increasing t43 production independent of tsh that's going to have a negative feedback on tsh and you'll have low tsh levels obviously if you have hyperthyroidism however due to increased tsh levels then your tsh is going to be high in addition to your thyroid hormones but that happens much less commonly when it comes to hypothyroidism the most common reason is immune disruption of our thyroid glands or thyroiditis so that's going to reduce your t4 and t3 levels which via negative feedback is going to increase your tsh levels because tsh is going to say why aren't we producing any t4 and t3 so tsh is going to be high t4 t3 is going to be low another clinical sign associated with hypothyroidism is mixed edema which is increased filtration of fluid out of your capillaries causing edema of the subcutaneous tissues because of increased osmotically active muco-polysaccharides within your interstitial fluid when it comes to treatment it's rather self-explanatory for hypothyroidism you're just going to do hormone replacement therapy by giving thyroid hormone for the treatment of hyperthyroidism high thyroid hormone then there's three real options medications to inhibit the synthesis of thyroid hormones surgical removal of the thyroid gland or radioactive ablation that's when you give radioactive iodine since the thyroid gland is the only gland that uses iodine then you just only have radioactivity within the thyroid gland which kills off only the thyroid gland so those are our treatment options now the last thing we'll talk about here is goiter goiter just means that the thyroid gland has enlarged and that's going to occur whenever we have high levels of trophic hormones which includes tsh and also thyroid stimulating immunoglobulin so any thyroid abnormality where we have increased tsh or increased thyroid stimulating immunoglobulin is going to stimulate the growth of the thyroid gland usually we have increased tsh either because of a tumor in the anterior pituitary gland which is uncommon or because we have low t4 tsh levels with very low negative feedback to our interior pituitary gland so that's going to be the end of this video for today i hope you enjoyed it feel free to join in for the next one where we are going to talk about our adrenal glands feel free to drop a comment otherwise we'll see in the next one
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