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One. OK. Hello, good afternoon, sir. Today, welcome to the me uh year three written literature series. My name is Kaiser Field. So today we had a change to plan. So we'll be doing the end of the bones lecture first followed by the headaches lecture. So I just share my powerpoint with you guys. Can you see the slides? All right. So, so I'll be taking you guys to the endocrinology and post lecture. My name is, and there is my email address in case if you have any questions by the end of this lecture. So we can, I can address it by email or if you have any questions, we can address this at the end of this presentation as well. That's the main code if anyone would like to join in for some of the S pa that we have. So this is the content that we're covering today. So before we start off with some endocrinology topics, mainly P th related such as hyper P TH and Hypo, th we also cover osteomalacia and then we go on to some of the topics related bones uh which are encompassing within malignancies. And we talk about some bone diseases such as and osteoporosis at the end of the lecture. So let's start off with the endocrinology side of things. So basically, for the conditions, we've had a look at the specification on what is required for each of the conditions. And we've tried our best to cater the ation to that. So this is the learning objectives for each of the conditions that we're gonna cover in this presentation to start off. Let's just give some background to physiology with regards to P TH. So P th as you guys already know, is secreted as pre pro PTH by sheep cells in the parathyroid glands. And what happens is the, the PTH is released in response to calcium in the blood. So what happens is the calcium in the blood uh with extracellular fluid, it binds to the G protein coupled calcium sensing receptor. There's a lot of it, what it does is it inhibited inhibits the release of P TH. So the higher the concentration of calcium, the lower the concentration that would be released me? Yeah, I don't think we can see your slides moving on for some reason. Can you see it? No, I can, we can see your slight um set up but we can't see, we can see if you've not changed it. Do you mind going into present a moment? No, I wasn't in prison. I just shared the car window but I'll just share my entire screen with us. Yeah, thanks. Sorry to try that. Ok. You can start again if you want and we can recording if you want. All right, great. So, hello guys. So my name is fifth year medical students. I'll be taking you guys to the endocrinology and bones topic. Uh For this lecture. We'll cover these conditions. We focus on P TH and the diseases or the conditions related to it. We'll cover osteomalacia on some malignancy related topics as well as some bones diseases. Uh We start off with the endocrinology side of things and start with uh this is a learning objective through which we have catered this uh presentation and to begin with, I just wanna talk, talk about some physiology related to P TH. So P TH is secreted as a pre pro PTH by the she cells, the parathyroid glands and it is released in response to the concentration of calcium and the extracellular fluid. So, if the calcium concentration is high, the release of PTH would be inhibited. If calcium concentration is low, then PTH would be released. This, this I've adapted it from Professor Neve Martins and uh if you wanna go by it and then this is some of the functions of PTH. As you can see, it has a role in the resorption of calcium from the bones, also in excretion of fate from the kidneys as well as absorption of calcium from the kidneys as well. And also has a role in enhancing the activity of uh one alpha hydroxylase activity, which then creates the 1 to 5 or uh hydroxy D3 synthesis, which is Vitamin D which then acts up on the plans to increase calcium absorption and phosphate absorption. And this is basically the negative feedback that we ask PTI described earlier. But it's a schematic way to understand it better for those who are visual learners. Now, moving on to our very first condition, this is hyper pth or hyperthyroidism. So, in essence, it is high levels of P TH which leads to increased levels of calcium and decreased amount of phosphorate. It is more common in females and usually usually presents over 50 years of age. And so the pauses are three main types. So we have primary HPT with secondary hyperparathyroidism, we have tertiary hyperparathyroidism. So primary is basically an adenoma of the parathyroid glands which results in excessive secretion of P TH. Secondary hyperparathyroidism is basically a state of malnutrition or Vitamin D deficiency. So this is basically a physiological response to malnutrition or deficiency in Vitamin D on cases when there is damage to the kidneys and the scenario of chronic kidney disease. However, secondary H PT can progress and can lead to chronic increase in P TH which is then termed tertiary H PT or tertiary hyperparathyroidism, which is essentially due to hyperplasia of the parathyroid glands which leads to excessive secretion of PTH. So now just going through the clinical features, what to look out for. So, these are some of the signs and symptoms. You will see constipation, nausea, anorexia, polydipsia, polyurea, bone pain, renal stones, low mood, which can all be simplified and condensed into this really great knot stands for bone stones grows. So this is what you would get in hyperparathyroidism and this is the signs of bone pain. It will be skinny stones, there will be abdominal growths and there will be psych bones. So low mood, feeling slightly depressed at times as well. However, in practice, most patients will be uh asymptomatic. Uh but this is just something to be mindful when you go out there, examination patients as well as taking histories with regards to secondary and tertiary hyperparathyroidism. Uh would those symptoms are related to the underlying cause in case of a renal failure, exhibit some renal uh symptoms and signs uh where they exhibit some bone pain in terms of deficiencies of Vitamin D or malnutrition. Now, making a diagnosis, uh of course, we have to think of investigations. What sort of investigations would you carry out? You have to check the calcium levels, of course P th Vitamin D phosphate. And what you can also do is do an ultrasound to check for parathyroid. I don't know much to rule out primary hyperparathyroidism due to uh a tumor. You can also do a dexa scan to look at the bone health to see if there's any other underlying pathologies to rule out other differentials that you may have and the hair just given some parameters that you see in the different types of hyperparathyroidism. So, primary para para sorry, primary hyperparathyroidism, you have increased PTH, increased calcium but decrease in phosphate. The Vitamin D levels would be low one and secondary HPT because this is a malnutrition state or a state of low Vitamin D you have an increase PT for low cal and increased P uh phosphate are also decreased Vitamin D in terry. When secondary progresses to a pathological form, this is where you would see, you see elevated levels of calcium, elevated levels of P TH but lower levels of Vitamin D Now we just wanna briefly talk about the management of hyperthyroidism. So for primary uh hyperparathyroidism, the definitive management would be parathyroidectomy. So you get rid of the gland. In the meantime, you can also try some mimetics uh which inhibit the release of P TH. But of course, before you initiate any of those, you have to give some fluids for the patients. If they're hypoglycemic, you wanna correct the electrolytes imbalances and then treat secondary H PT. You have to trace down the line called with with. It's it is Vitamin D deficiency or C KD. You would approach and fixing that and tertiary H PT. The definitive treatment there would be para parathyroidectomy as well. So I've got uh SBA here and that's the code there. Uh I don't know if you have anyone here but I'll just give it 30 seconds for those who want to attempt this and then I'll give back, uh, after 30 seconds have a read. So which one of the following is the most likely there's a leading to the elevated p th that you see?