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Costanzo Physiology (Chapter 9F) Endocrine Physiology: Calcium Regulation || Study This!
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hello and welcome to the final portion of the endocrine physiology chapter of costanzo's physiology textbook in this video we're going to go over the regulation of calcium and phosphate mainly going over the actions of pth or parathyroid hormone if you enjoyed the video please don't forget to give it a like and more importantly if you haven't subscribed yet please consider doing so as it does help the channel grow otherwise let's jump straight into talking about calcium and how it's moved around in the blood starting off with the calcium that's actually bound to plasma proteins about 40 of the total calcium within our blood is bound to proteins the rest is ultra filtratable meaning that it can actually go into our nephron because remember proteins don't cross that glomerular membrane out of that 60 that gets ultra filtrated 50 is ionized so the majority of that 60 is ionized calcium the remaining 10 is complex to anions like phosphate now this ionized portion this 50 percent this is what is metabolically active and this is what the parathyroid hormone is regulating it's trying to regulate the ionized calcium if we are hypocalcemic or hypercalcemic to the point of causing clinical signs it's because of a change in our ionized calcium we may get a change in our total calcium due to a change in our protein levels within our bloodstream but it's important to focus on the level of the ionized calcium so we do have some factors that once again alter our total calcium so plasma proteins alter it anion concentration alter it so if we have increased phosphate within our system within our bloodstream and that's going to increase the amount that's complex to iron ions so then our ionized calcium is going to decrease relatively and then our acid-base abnormalities can change things in acidemia albumin actually binds to more of those hydrogen ions so it displaces the calcium bound to plasma proteins so then our ionized calcium is actually going to increase and vice versa for alkalemia so you may actually notice some clinical signs of hypocalcemia during an alkalotic state now the clinical signs associated with calcium abnormalities hypocalcemia we end up with excitability of tissues and cells that's because we actually lower the threshold potential basically we make those sodium channels more twitchy to open so now it's going to open much more readily and therefore we need a lower stimulus for an action potential to be fired so hypocalcemia results in increased action potential firing in cells and basically causes twitches and excitability hypercalcemia on the other end so high calcium is going to cause the opposite and slow things down so we end up with constipation we end up with hyporeflexia lethargy coma potentially even death we also end up with polyuria and diptyo with hypercalcemia because we're increasing the amount of calcium going into our urine which takes with it water so getting to overall calcium homeostasis this figure down the bottom here depicts it nicely we have our extracellular fluid concentration so our plasma calcium level and you can see we have three organ systems contributing to it we've got our intestine our kidney and our bone our bone is constantly remodeling so our osteoblasts are constantly adding bone to bone and our osteoclasts are constantly removing old bone so we're constantly recycling old bone for new bone and that can be altered to increase resorption to increase our calcium levels within our blood or increase deposition to reduce our calcium levels within our blood we'll get to the hormones that are able to do that shortly when it comes to the intestine we can increase our absorption of calcium from our intestine but we can't alter secreting additional so mainly in the intestine we're trying to absorb more calcium during hypocalcemic states in the kidney we're able to reabsorb more calcium as well so we are able to increase the amount of calcium getting reabsorbed from the nephron so we lose less in the urine so that's able to also increase our calcium during hypocalcemic states so you'll also see these little plus signs which mean that they are activating and you'll see that pth and 125 dihydroxycholine calciferol which is a mouthful we're going to call this just activated vitamin d they activate the reabsorption of calcium from each of these organs so that increases calcium when we have low body calcium levels you'll notice that the only other hormone here is calcitonin which we'll touch on right at the end this is an inhibitory effect on boner's absorption so that's actually going to be secreted when we have high calcium levels within the bloodstream but we're not going to focus on that one too much because this chapter is mainly about the parathyroid hormone so a parathyroid hormone gets released whenever we have changes and now ionized calcium and you'll see in this graph here that we have the sigmoidal shape to pth secretion compared to our total plasma calcium so this shows that calcium wants to be maintained right in the middle here and one minor change of calcium in either direction will result in a dramatic change in our pth secretion if we slightly reduce our ionized calcium we get a remarkable change with an increase in pth secretion instantly if we slightly increase our calcium then we get instantly a reduction in our pth secretion so we finely tune our calcium level and try to keep it as constant as possible parathyroid hormone is actually released from the chief cells within the parathyroid glands it's called parathyroid because there are these four tiny little glands right next to the thyroid gland itself if we have chronic hypocalcemia so low calcium levels then we're going to get a constant stimulus to produce pth and the actual cells themselves the chief cells will be told to transcribe more of that gene that's going to synthesize pth so you actually see hypertrophy of your parathyroid glands and a hyperparathyroid state with chronic hypocalcemia and that's called secondary hyperparathyroidism it's a little teaser for what we're going to be talking about later on in this video now it does touch very briefly on magnesium basically magnesium has similar effects to calcium or pth secretion so if we have hypomagnesemia then we'll have some pth secretion as well it's not really the focus of this video or this chapter but just a little side note there so the actions of parathyroid hormone it mainly works through the adenylyl cyclase secondary messenger system by increasing cyclic amp and by doing that we increase the resorption of bone and we increase the reabsorption of calcium within the kidney it also works on the intestines in an indirect manner by activating vitamin d active vitamin d then actually increases the reabsorption of calcium from the intestines so pth works on those three organs but in an indirect manner works on that intestine so in bone the first thing pth does is actually interestingly this is going to be confusing it actually increases the activity of the osteoblasts so it actually slightly increases the deposition of bone initially but the long-term effects through the increased production of cytokines from the osteoblasts it's actually going to be a marked increase in the osteoclastic activity to reabsorb bone so really the net effect is a resorption of both calcium and phosphorus from the bone into your extracellular fluid space in the kidney remember we talked about pth in the kidney how it inhibits phosphate reabsorption from that proximal convoluted tubule so we increase the amount of phosphorus excretion in the kidney resulting in phosphateuria but not only that it increases the reabsorption of calcium within the kidney and this is important because since the parathyroid hormone has increased the resorption of both calcium and phosphate from bone if it keeps reabsorbing both of these together then calcium will just get complexed with phosphate and our ionized calcium wouldn't increase as much so it needs to actually excrete some phosphate and just increase the amount of ionized calcium within the bloodstream because that's what it's trying to maintain that is the metabolically active form of calcium so in the kidney it increases phosphate secretion or excretion and also increases calcium reabsorption from that distal convoluted tubule in the small intestine once again it works indirectly via activated vitamin d to increase the absorption of calcium from the intestine and we'll get into more details and exactly how it's able to activate vitamin d in the kidney but at least for now just remember small intestine is going to increase the calcium absorption in the presence of pth indirectly due to activated vitamin d now how about some issues of parathyroid hormone we've got a couple conditions here number one primary hyperparathyroidism think about this logically primary means that the issue is the parathyroid gland itself so the parathyroid gland is increasing the secretion of pth this is going to occur due to a tumor that's producing pth if we have excessive pth that means we're going to reabsorb a lot of calcium and excrete a lot of phosphorus from the kidneys so we're going to have hypercalcemia and hypophosphatemia our bones are going to also become very very weak because we are absorbing a lot of those minerals so you end up with the saying of stones bones and groans stones because you start to produce calcium stones within your urine although there's increased reabsorption in your kidneys there's still so much calcium in the bloodstream that there's a high filtered load so you still end up technically with more calcium being in the urine along with that phosphorus so you end up with calcium stones within the urine your bones become weakened because they're getting resolved and groans because of the constipation from hypercalcemia the treatment for this is parathyroidectomy secondary hyperparathyroidism means that there is a hypocalcemic state that is chronic that's causing the parathyroid gland to increase its secretion so something is causing calcium deficiency and that occurs due to vitamin d deficiency so we're unable to reabsorb enough calcium from our intestines and we have a reduced response with bone resorption because our activated vitamin d helps to resolve calcium from the bones or from chronic renal failure so we're just excreting a lot of calcium we're unable to reabsorb that calcium from the kidneys so secondary hyperparathyroidism means that we have high pth due to a chronic low calcium hypoparathyroidism is exactly as it says we have low parathyroid hormone either due to autoimmune destruction surgery removing the thyroid gland also indirectly removing the parathyroid glands or congenital hypoparathyroidism if we have low pth levels that means we're going to have low calcium within our bloodstream because we are unable to resolve our bones unable to reabsorb calcium as effectively from the kidneys and unable to absorb more calcium from our intestines so we are able to treat this with a combination of oral calcium supplement with activated vitamin d so then we are able to absorb more calcium from our intestines pseudo pseudohypoparathyroidism is named this way because we have what seems to be hypoparathyroidism with hypocalcemia and hyper phosphatemia however circulating levels of pth are actually increased and the reason behind that is because of a defective receptor within the kidney and the bone so we can't actually reabsorb that calcium so pth is trying to do its work but it's just not binding to its receptor last thing we'll mention here when it comes to calcium is humeral hypercalcemia of malignancy this is when tumors start to release parathyroid hormone related peptide so this is like a pth analog and it does the same actions as pth to increase our calcium levels within our bloodstream and reduce our phosphorus levels this means that regular pth is going to be chronically low because it's not going to be secreted in the presence of high calcium and you treat this by giving furosemide to reduce our calcium absorption from our kidneys and by giving medications that inhibit bone resorption so talking about calcitonin very briefly here we don't talk about this much because it seems like it's probably got a pretty minor role it gets released from cells or c cells within the thyroid gland so not the parathyroid gland within the thyroid gland itself and it gets released whenever we have high calcium levels within our bloodstream now works on osteoclasts by inhibiting them so then we stop resorption of bone and that's trying to reduce the amount of calcium entering the blood because of bone resorption it doesn't seem to have that much role in the minute to minute regulation of plasma calcium but we do mention here with our calcium homeostatic mechanisms now vitamin d plays a role in calcium homeostasis but it's important to distinguish how it's different to pth pth is role is to maintain a normal plasma calcium level vitamin d's role however is to promote the mineralization of new bone so it's trying to increase the amount of both calcium and phosphorus within the bloodstream so then that's available for bone to be able to be deposited now if you're a student you're able to pick up initially this issue of well i thought activated vitamin d actually resolved our bone you would be correct and i'll touch on that right now just to avoid that confusion activated vitamin d although its role is to mineralize new bone it does increase bone resorption but the key point is that it's increasing the resorption of old bone so it's trying to shuttle the old calcium and phosphorus away from the old bone and make it available for deposition of new bone so that is important vitamin d's role is to increase the environment for the mineralization of new bone by increasing calcium and phosphorus whereas our parathyroid hormone is only concerned about our calcium levels so it's trying to regulate calcium at the expense of phosphorus so talking about vitamin d its form is cholecalciferol and it's either obtained from your diet or is converted from cholesterol via uv light on your skin polycalciferol then gets metabolized in the liver and then finally in the kidneys by one alpha hydroxylase into our activated vitamin d now this one alpha hydroxylase is what gets manipulated by parathyroid hormone to increase the levels of activated vitamin d but this is also going to be activated by reduced calcium all together and then also reduce phosphorus because if we've reduced phosphorus then we do not have an environment for new bone formation so one alpha hydroxylase gets activated to produce more activated vitamin d so then activated vitamin d once it is produced it goes to the intestines the kidneys and the bone to increase the reabsorption of both calcium and phosphorus so in the intestine it does that via this figure 9.4 here by increasing this protein called calbindin it's not quite clear what this does whether it's buffering our calcium so then the calcium levels seem low in the cell so then we increase the electrochemical gradient from calcium to enter the cell or whether it's acting like a shuttle to shadow it all the way out into the blood but we increase calcium and phosphorous reabsorption within our intestine via this mechanism in the kidneys we increase the reabsorption of both calcium and phosphate and then in the bone we increase the resolution of old bone so then calcium and phosphorus is available for new bone formation so then that gets us to the pathophysiology of vitamin d if we have low vitamin d what's going to occur our bones are clearly going to become weak and not grow appropriately so if you're a child then you're going to get rickets and rickets is characterized by a failure of growth and particularly some skeletal deformities as well in adults that results in osteomalacia which is basically really weak or poorly mineralized bones because you're unable to mineralize new bone so that is our calcium homeostasis we do have this portion here of a summary which i have highlighted if you want the key points of this chapter otherwise we do also have the chapter questions feel free to pause it at this point if you want to get these summaries and then also we have another page of the questions too over here the answers of these questions are going to be supplied in the description once again if you haven't subscribed please consider doing so as it does help out the channel otherwise i hope you enjoyed it feel free to drop a comment
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