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So, hi guys. My name is Preet and I am the Vicepresidente of Maddie Path International. We are excited to start our lecture series today, which is sponsored by M D U and it is CBD approved. So today we're gonna start with our very own co founder, Lola Bello on endocrinology emergencies. So please welcome Lola, Doctor Lola. Hi, guys. Hope everyone as well. I'll just quickly introduce myself. My name is Lola. I'm one of the co founders of Med, a Path International. I graduated from Medical University in Sofia. I graduated about two years ago after I graduated, I started working as an F one doctor, then went on to do my masters in. So that's like what I've done a bit to get to where I am now. Currently. Um I am going into GP training this August. Um And yeah, so I'm starting GP training this August. I'm really excited for that. Hope to be a GP in the future side, hustles and side things. I do. I'm quite into aesthetic medicine. So I also do aesthetics on the side. And tiktok, I love to tiktok. I don't know if you see my tiktok. So Yeah, I also love tick talking. But yeah, that's just a little bit about me. So today we're going to be talking about um, endocrine emergencies. I like to, I'm someone with a short attention span. So my lectures is not going to be me just talking at you rather I would prefer it if it's more interactive, we're talking to each other. I'm, or chatting to each other in the chat. It's going to be lots of questions thrown your way. No judgment. No, no question is the city question. Just answer the poll, say what you think, chat on the chat and then we'll just go through it that way. So my presentation is mainly going to be a few case studies. So pre if we could go to the next slide. Yeah. So this is the Yeah. All right. Okay. So this is basically what I've just said. So essentially what we're gonna have, we're gonna have two clinical cases. Both of them are gonna be common endocrinology, emergencies during the cases. We're going to have a discussion about the signs and symptoms, um guessing on the diagnosis or if you know from the clinical signs and symptoms, you get trying to identify the diagnosis, we'll talk about treatment and what we do after treatment. So monitoring after. So, but when it's the emergency, you kind of have to stabilize the patient burst and then you follow up after and then at the end, we'll just have a conclusion and a mini quiz. All right. If you could go to the next slide. All right. So this is the first, our first patient, next slide. All right. So here you have a female. She is 46 years old. Her initials R S P. She doesn't have any allergies. She lives in the UK. Now she presents with chest pain and palpitations. She has a three month history of, she's quite, where she's quite stable. She has a stable mood in the last three months. She's been quite anxious. She's been quite frightened. She's been sweating a lot. She's had a lot of weight loss despite a normal appetite and she's quite fatigued on examination. You find when the nurses do her obs, you find that she has a heart rate of 100 and 20 BP. Naturally you asked for an E C G and the E C G shows sinus tachycardia. All right. Next page. Now, I think there's a poll if everyone could just essentially guess or if you kind of know what it is already, just submit your answer. It's all anonymous. So, don't worry. Okay. It says you got one. Okay. Fine. I'll give it like 30 seconds more and then we'll go on to the next slide. We'll give you a bit more information to see what we think it is. All right. Ok. So from looking at the whole, so far, it seems majority think it's very toxic crisis. A few, somebody said, didn't choose the endocrine one because it's endo kind of emergencies. Yeah. And if people think it's a CS acute coronary syndrome, this is an interesting one. Okay. If we go to the next side, I'll give you a bit more information. All right. So here are her investigations. So her tear, I've got the results of the patient under result. And if you don't know the normal range is the next column is range which shows you the normal range. So where you can see the patient's result in the normal range, I'll give you guys a second or a minute just to look through that. So her TSH just reduced. Her F T four is elevated. Her F T three is elevated, white cells are elevated, neutrophils are elevated as well as cortisol. All right, let's go to the next side and give people a chance to guess again. Now, now seeing the results, what does everyone think it? Oh, wait, it's not this poll. Can we stop this poets? It's, wait, hold on. Oh, no. Don't answer the second poll. We're not there yet. Okay. We'll just move on. Let me just see. Pre can we have the first poll up again? Is that possible? One, second one? I will do it or if you can't, it's fine if people just want to chat now that they've seen the results of people want to just write in the chat, what they think it is Oh, I don't think we can. Sorry guys, technical issues. Let's just go to the next side. All right. So for everyone who basically said it was a thyrotoxic crisis, you are right. The patient came in with chest pain, um, weight loss, tachycardia, all of these are signs of a thyrotoxic storm. And then when we saw the blood results, you saw that her TSH was suppressed, her F T four was high. All indicating that her thyroid hormones are in excess in the bloodstream. So, as you can see here, I've just put a discussion summary, thyroid hormones control the body's metabolism. So I like to think of it because sometimes people get a bit confused between hyperthyroidism, hypothyroidism. When you think of the thyroid hormone controlling the body's metabolism. When you're hyperthyroid, just think of it like everything's going faster. So your heart rate goes faster. Um You metabolize things quicker. Therefore, as you're metabolizing things quite quickly, um and everything is on. It's like I like to imagine you're just like running and how everything's just going fast, fast, fast. When you run really fast, your heart rate goes fast. If you're continuously running, you'll lose weight. That's how I like to think of it as hyperthyroidism. Then I like to think of hypothyroidism is what happens when everything slows down. So you have the weight gain, you have the mood swings, things of that nature essentially if we go to the next slide. So here Yes. So again, some of the symptoms of the disease, you can see our difficulty, swelling, sleeping, sorry, sensitivity to heat, increased sweating and weight loss. And sometimes I think with, when I think of endocrinology, um disease is just as a whole with endocrine, I think typically because it presents because it's your hormones and it affects multiple body systems, it presents in a different way. So sometimes when you think of patient's coming into A and e if they come in with chest pain, everyone's mind immediately goes to cardiology acs but always have in the back of your mind, the endocrinology, signs and symptoms. If it's not that, what, what could it be like always have in your mind the differentials if you go to the next side. Yeah. So I just have a graph here where you can kind of see the signs and symptoms of hypothyroidism and hyperthyroidism just to kinda if you want to take a screenshot, you can take a screenshot just to have in the back of your mind. Really? Um Yeah, we can go on to the next side. So what's next? So now is meant to be the second poll. Know what's next, you want to go to the next side? All right. Ok. Is it possible to have the second poll up again or is it not? Okay? Fine. So now that you guys have seen it's a thyrotoxic storm, she's in thyrotoxic crisis. What do you think the immediate management would be. Do you think the first thing we do is to wait and watch and see what happens? Do you think we should do further investigations? Try and find the thyroid antibodies to try and identify the cause? Do you think we start the patient on anti thyroid medications and beta blockers? And then the steroids is a plus minus. It depends on your trust, not all trust you steroids or do you think we should give the patient beta blockers to slow down the heart rate and IV fluids to rehydrate them? What do you think the immediate management would be for this? I'll give a hint for this emergency for this endocrinological emergency. Mm. So I see we're getting the polls coming in. Some people are saying to do further investigations such as a trap to identify the primary course. Some people said to get beta blockers. Some people said to commence anti thyroid medication. All right. So I'll give you the answer. Can we go to the next slide, please? The people who said anti thyroid medication, beta blockers plus minus steroids are correct. The thing I want to reiterate is this is an emergency. So, whilst trying to find out the cause by doing a thyroid receptor antibody to see if it's graves' disease or to see if it's a thyroid itis or just to see what's going on that's causing this thyrotoxic storm. The first thing you need to do first is stabilize the patient because that antibody test can take a couple of days to come back and it's not fair to the patient to leave them in that state of hypothyroidism or thyrotoxicosis where everything's going quick, it's not fair to leave them in that state. Um Some people said eat a blockers and IV fluids. Yes. While beta blockers will provide symptomatic relief by slowing down the heart rate and IV fluids could give hydration if they are dehydrated, that management will not essentially stop the thyroid from going into overdrive. So you kind of have to think of it. Thyrotoxic storm. Your thyroid is producing excess amount of thyroid hormones and whereas you can and that those thyroid hormones are essentially what's going around your body and causing all the symptoms. So, if those thyroid hormones are going to your heart and making it beat faster, increasing your metabolism, causing the weight loss or weight loss, all those things. So, if you're just giving beta blockers to control the heart rate, you're not essentially treating the cause of the thing that's making the heart go fast in the first place. So the main management, if this patient comes into your A and E is to give them anti thyroid medication. Now, there's different types of regimes that can just be according to your trust, there's the block and replace regime, that is the titrations regime. So that would be the first thing you do. You give beta blockers as well too. You save down that heart rate and sometimes they give steroids next. Okay. So we, we don't have to do this one. We can go to the uh I've given the answer so we can just go on to the next slide. Yeah. So as we've said here, so basically the beta blockers, we give to control the symptoms induced by increased a genetic tone. We give the anti thyroid drugs. These are to block the new hormone synthesis. As I said earlier, the things that are cause it's these thyroid hormones that are causing all the havoc in the body. So what we want to do is give anti thyroid drugs to stop the synthesis of new or more thyroid hormones. And I say steroids is a plus a stash minus as not all trust use it, but essentially steroids can reduce the conversion of T F T 43, thyroxine 42 F T three. Now, when you have elevated F T four, that is not the active form, the active form, the most active form of your thyroid hormone is F T three. Now, um by preventing the conversion of F T 42 F T three, you're also reducing the effects of the thyroid hormone of F T three on the body. Does that make sense? If anything doesn't make sense? Just right in the chat box and I will answer. All right next. Now, here I'm just gonna talk. So I wanted to do talk about n technology emergency. So the first thing test was to stabilize the patient. But once you've stabilized the patient, the patient is on their anti thyroid medication, beta blockers and steroids. The next thing you need to do is kind of try and identify the court. What is causing this person to have Vira toxic Asus, what's causing them to have this storm? And that's when you think of your different differentials. So you've got different things that can cause that you've got parad itis. So, inflammation of the thyroid gland can cause excess um hormones to leak into the blood. You've got the most common thing of toxic osis graves' disease, which is an autoimmune disease, which causes excess thyroid hormone in the blood. So you kind of want to do a few um investigations. Number one you can do is a trap, which is known as the thyrotropin receptor antibodies. If that's positive, more than likely, your patient will have grave's disease. You can, you can determine by the uptick of a radioactive iodine test. You could also measure authority or blood flow on ultrasonography. So you can have a thyroid ultrasound, which if if it is grave's disease, you do see increased, you do see enlargement of the thyroid. So you can see a goiter. If it's not necessarily protruding outwardly, you can do a ultrasound to see how big it is. It could be enlarged but just not visible to your eye. Okay, next side. And here I just have like a little chart of essentially um how to kind of, I hope it's quite small my screen, I hope everyone else can see it, but it's almost like putting me a flow chart of like differentials and ways you can go to kind of see if what the diagnosis will be. So, first of all, you can look and see does the patient have any of the following new on new onset orbitopathy? Um large non nodular thyroid or moderate to severe hypothyroidism and then you would follow, follow, follow it down. So, if it's, yes, it says, does the patient have present some well consistent with graves' disease? One second, if your patient comes in on um urine and has a f how this modify the management. This is an important one because amiodarone is essentially it can cause hyperthyroidism due to the excess iodine that your thyroid home as a maid of. Now, I think it would affect the management for me. What I would do if I was in that situation where a patient came in with thyrotoxic osis. One thing I'd be thinking of is this thyrotoxicosis induced by the amiodarone. So again, my differentials we thinking whereas I'll have grave's disease and everything else in the back of my mind, I would also be thinking of amiodarone induced thyrotoxic osis. What I would do is hold the amiodarone refer to cardiology to kind of say, look this is our situation because they'll know the cardiac history of the reason why the patient is on amiodarone. Can we give another medication or what would you guys suggest? So it's not like somebody will have necessarily all the information in their head sometimes. Like if I wouldn't know that personally, I might not know another cardiology medication to switch them onto. So, what I would do is just refer to cardiology. I would hold the amiodarone and refer to cardiology all within the same time just to move forward with the management. Does that make sense? But then after you um model hold the amiodarone again, it would be treatment the same way. But you could also monitor to see if the hyperthyroidism will resolve or the thyrotoxicosis will resolve by itself. But yeah, that's what we would do. We definitely hold the amiodarone because that could be the cause of our issue. All right. Okay. If you go to the next slide. So just to conclude, thyrotoxicosis is a clinical emergency. You always be aware. It could have a clinical presentation for me personally, I do have grave's disease. And when I first presented to the hospital, I was admitted to the cardiology department because I had chest pain and I was tacky Cardiac. So they wanted to do investigations on me. And that's why you kind of always just have to be aware that whereas it can present looking one way, always, if somebody I would just say rule of thumb. If somebody comes in with sinus tachycardia, just do your, just, just add TFTs onto the patient's blood's, that's your thyroid function test on to the patient's blood. When you're requesting your usual um user knees, full blood count all of that, just add it on because you never know. And things do present with a very clinical presentation. So always have endocrinology, diseases in your, in the back of your mind. Remember, immediate management is with anti thyroid drug. So that's your copy muscle or your pro pro thyroid Euro sell a beta blocker, which is your like a bisoprolol plus minus steroids. According to your trust guidelines, there are many different etiologies for thyrotoxicosis such as toxic multinodular goiter to grave's arad itis to further investigation is required. Once the patient is stable, now these patient's can come to you appearing stable. So just always make sure they're on that. Don't just overlook it. Just always make sure they, you put start them on anti thyroid drugs before you start to investigate. All right. Any questions or not before we move on to the second clinical case. No. Okay. Let's go on to the next slide. So this is our second patient. All right, next side, we have a 40 year old male presenting to a and E with symptomatic hyperglycemia Exide. So I want you to have a look here. These are the investigations. So the patient's come in. You don't know much about their past medical history but they've had this A B G done. Uh No, sorry. They've just, yeah, they've had an A B G done plus they're bloods and you can kind of see here. The texting red is like your hints for what it potentially could be. Um So that's what I'm hinting to you guys, but otherwise just have a look at everything. You see the plasma glucose is elevated. You can see the annan graph is slightly raised, well raised. You can see the key tones, you can see the plasma hospitality, you see all these things. All right, next slide based on this, okay. We have a poll now based on this. What is the most likely diagnosis? H H S D K A sepsis A K I on CKD, acute, acute in the injury, on chronic in your injury and then watch and wait. You don't know what the diagnosis is. So I'll give you guys about a minute just to have a think and what this could be. These questions are anonymous. So feel free to answer whatever you think it is. Okay. All right. So from what I can see here, somebody's not sure. They said they'll watch and wait and see. Majority of the people said they think it's diabetic ketoacidosis. Some people have said they think it's ahh s hypoglycemia make hyperosmolar states. Okay. Quite interesting. All right, let's go to the next side. So for those of you who said DKA, that is the right answer. And we'll go into why we think that is. So if we go to the next side now, the people that said H H S, I do understand where you guys are coming from. Now, there is a difference between D K and H H S as a general rule of thumb, which is not always you do have your exceptions, but the way I like to think of it is you typically will have D K in your type one diabetics, then you typically will have ahh s in your type two diabetics and certain things you can use to determine which is, which is in your D K A. You have ketones present in your H S, you don't have ketones present. Now you, the way you can think of this as in, in type one diabetes, essentially, it's that autoimmune disease. Your insulin is, there's no insulin. You put, the body is pretty much destroyed. All insulin in type two diabetes, the body does produce insulin, but there's an insulin sensitivity syndrome. So that's pretty much why you kind of think of it is when you're, you've got a lot of sugar in your blood. When you're hypoglycemic, the body in type one diabetics doesn't have the insulin to um it doesn't have the insulin. Therefore, the body then produces ketones to kind of help with that. So that's why you have the elevated ketones. It breaks down your fatty acids and things like that to reduce ketones to help. Okay. If we go to the, oh, and also one thing I would say you can, sounds like one thing I also say about HS, you kind of have very severe dehydration, very severe hypoglycemia. So it's even more higher and worse than I would say. D K A next slide. All right. So from the dike, from the investigations and from the, the blood and stuff I showed you, you could see that if you looked at the ph, you can see that that person's ph was acidotic. Um There was high levels of ketone in the blood and they were also hypoglycemic. So this is the way you can kind of be able to diagnose DK if they are Sadat Ick, if they have key tones and if the hypoglycemic obviously clinically, you'll be able to tell some signs such as cosmo's breathing and things like that. But once you see these three things on your A B G or on your V G, you should start to think okay. This patient might have D K. Next. Now, common signs of symptoms of D K is nausea and vomiting. You have polydipsia. So they're quite thirsty high population. So that's that cosmos breathing abdominal cramps and polyuria next side. Now, so this is kind of a little bit about what I was talking about in the, in the earlier is the pathophysiology of um D K A now, the way I would just like to think of it, just on a general aspect is I like to think of insulin as the door that pretty much lets the glucose in your blood into the bloodstream. So it's the gateway, it basically acts to help take glucose from your blood and to your tissues. So it's that door, it just helps if you don't have insulin, there's nothing to take the sugar in your blood into your cells, right? And essentially your cells need glucose for just for normal metabolism. For normal energy, your cells need glucose for energy. And if the patient doesn't have insulin, there's no way to get the sugar from the blood vessels into the cells. So essentially your cells are not getting the energy they need. And you have all this increased glucose in the bloodstream, right? As a result of all these increased, increased glucose in your bloodstream, a lot of it's going to go out in your urine. So you're gonna have glycosuria, you're gonna have polyuria because water will follow where the glucose goes out of your kidneys. And then you're gonna have polydipsia. So the patient's gonna be quite thirsty as a result of this. So your tissues aren't still getting the energy they need. Your body's gonna then increase like policies, which is the breakdown of um fatty acids. So it's gonna have increased fatty acids, breakdown fatty acids to kind of produce the ketones in the liver So that's why you're gonna have your ketones, which you're gonna have the kitamura in your urine and you're also gonna have excess ketones in your blood ketones are acidic and that is why your blood ph goes down. Does that make sense? Okay. I hope so. Alright. If we go to the next slide. So now what does everyone think the immediate management would be for our patient with D K A? Just have a guess if you're not sure, just have a guess. Do you think the correct management would be for an insulin infusion? Do you think they should have Dextrose and IV fluids? Do you think they should have just IV fluids or do you think they should have IV fluids with continuous insulin infusion and electrolyte monitoring? So I will just give you guys a minute. All right. Oh, this is great. So most people said IV fluids, continuous insulin infusion, electrolyte monitoring. Um Yeah. Now stay with, that's where I just saw a question come in. Okay. I'll answer that often. So basically the reason why we give IV fluids continuous into the infusion and you monitor electrolytes. One is because this patient is having polyps, polyuria. So they're urinating a lot, they're going to become very dehydrated due to all the glucose in the bloodstream. Um which car passes out, they're gonna become quite dehydrated. So the first thing we want to do is rehydrate the patient. Now somebody said Dextrose an IV fluids. So yes, we would give IV fluids but essentially giving dextrose, it's just adding to the problem. They already have glucose in their bloodstream. Why would we give them more sugars in their bloodstream? It's only gonna make the TKA worse. So, what we want to do is give them the thing they're missing, which is the insulin, which is that door, which is that doorway from outside to the tissues, basically from the blood vessels of the tissue. So why when we give them that continuous infusion of Linton and we're treating the issue were helping the glucose in the bloodstream go into the cells. So that's why we do that. And then we also just make sure you also monitor your potassium whilst you're doing that okay. Now, the question are those, yeah, it says S dot G I, I'm guessing this is SGLT two medications at risk of you guys emmick keto acidosis. Now or your retesting my pathophysiology here. The the answer is yes, I'll need to cross check why the actual um mechanism for it. But yes, those on a CLT two inhibitors can be at risk of you guys. You make ketoacidosis. All right. Next slide. So yes, as I just mentioned, the management of DKA would be a fluid resuscitation. So that's just giving IV fluids insulin to help, basically move the glucose into the blood cell and as well just to suppress that hepatic gluco neogenesis as well as like pollicis and ketogenic icis, we always monitor the electrolytes just to make sure the potassium isn't too low. If that's the case, you should give potassium supplements. So typically, if you're giving IV fluids naturally, the hospitals, you can add um you can add um potassium chloride, that's it to your bag. So you can just do a bag of IV fluids alongside potassium chloride. So regular V B G monitoring is important to kind of monitor your um electrolytes. Next slide. So conclusions D K is a clinical emergency. D K is different from H H S to always remember to get that past medical history. Is this a type one diabetic is a type two diabetic. It presents with nausea and vomiting, abdominal cramping, hyperventilation, polyuria and polydipsia. Immediate management is with IV fluids, insulin and electrolyte monitoring. Now, common etiologies. So common things that can cause a patient to go into DKA is infection infarction, intoxication or inappropriate withdrawal of insulin. So typically in your young patient's try and look to see if they are compliant with taking their insulin. All right. So yeah, that's that for D K A next slide quiz time. Okay. So this is just to see if you guys pretty much got everything that we've been talking about next side. So this one you can put in the chat. What are three symptoms of thyrotoxic osis? Oh, I saw it. Yeah. Somebody said chest pain, palpitations, difficulty sleeping. Yep. Yep. Yep. Ok. Well, done guys. Okay. The next one, let's go into the. Yep. All right, we're getting the OS. Yep. Yep. People are saying it tachycardia, weight loss, sweating, heat, intolerance. Yep. Yep. So the next one, what are three symptoms of D K A? Yeah, that's a good one. Reduced ucs. That is a good one. Yeah, it was your vomiting update. Pain. Yeah. Polyuria, polydipsia nausea. Exactly. Okay. You guys, you guys are paying attention? Yeah. All right. Okay. Let's get you the next one. Next slide. Pre please. Oh, wait, go back. Sorry, go back. Um Yeah. What is the immediate management of D K A? So what's the first thing you need to do? IV. Fluids, insulin. Yes, exactly. We need to rehydrate the patient. Give insulin to help push glucose into the cells as well as stop future or potential. Um, ketone production. Yep. Yep. Monitor electrolytes. Yeah. Next slide. What is the immediate management of thyrotoxic osis? Who remembers this one? Yeah. Anti thyroid medications, beta blockers, anti thyroid. Yeah, those are your main to your main two. Would be your anti thyroid medications and your beta blockers. Yeah. Ok. Next slide. Okay. I'm glad everyone's getting it now. I think this is the last one. What is the difference between D K and H H S? Mhm. Say, yeah. Yeah. Well done guys. Yep. Yep. Yep. D K. You have excess ketones hatred. She, she won't hate. It says typically can present with severe dehydration. Severe hypoglycemia, things like that. And I think that was the end of the slide. Yeah, that was the end of the slide. There's my email. If you do have any questions, there was a question. I know somebody put in some medications on here. Oh, it was already said Dapagliflozin mpeg. Yeah. I don't know if you heard my answer to it. I said, um, SGLT two. It's rare but they can cause, um, uh an increased risk. They can cause you guys seem a keto acidosis just by their mechanism of action, but it is not as common but it can happen. Does anyone else have any questions? So with H H S, it would be the similar, it would be a similar management in the terms of you would need to give, you would need to give your fluids. You need to give a lot of IV fluids to rehydrate the patient. You could also give insulin to help with that um, glucose because the body's not essentially very sensitive to what they have just as just to stabilize. So it's a similar treatment, similar treatment, similar management. Two D K A. The only difference is afterwards, after you stabilize the patient, you can put them by back on their normal type two diabetic medications. But I think first things first, you would need to see is what, what caused them to go into this state. Was it an infection or is it just lack of compliance? If it is lack of compliance, you can then do further investigations to see the HBA one C, um, to see if you would need to, um, up titrate their normal medications. So according to the guidelines, you would start off with Metformin, then if they meet the criteria, you can start them on the SGLT two or you can start them on self in your or whatever. And then I think the last stage is actually, I know they're doing the G R P ones now, but then you can also up titrate them back to insulin. So that would be after they're stable, you would then again reassess their normal medications and then see if you need to up titrate it if what they were on currently was not managing it. Any other questions rather than your master's. Did you do that during your Yeah. So, yeah. Okay. So the way I did it, so I studied medicine and Bulgaria. So for those of you who are studying medicine abroad, um, I, technically, when we come back to the UK, we technically do not have to do an F one year. We technically just have to work three months and then go into GP training or specialist training. You have a specialty. Um, however, I would recommend people work at least a year or two before going to specialty training because the NHS is a different system and you need to get used to this different system. So what I did was when I finished in January, I took up an F one post. So I think someone dropped out of the F one program in the hospital near me. So I started in January and I just did, I did F one from January to August. I just did their rotations. Now after that, I then started low comming. So once I finished in August and everyone usually finishes, I started low coming and then picked up my master's when I was low comming. So I, I likened in the same trust in the same ward pretty much. But the way I um negotiated my contract was that to have Fridays off because Friday's, I needed to go to uni for my masters. So I would technically say I took a locum year and then during that locum year, I did my masters. It's quite difficult. Well, it depends on the masters. Some masters are all completely virtual so you can do them if you have time alongside. But for me, for me, I just um I just took off the local year just because it was 9 to 5 an easiest and easier, like an easier, just routine. And then I did my masters at the same time as I'm quite interested in endocrinology as well as going down the G P roots. Yeah. If you are looking for your masters, I would recommend the one in Queen Mary's in London. Bart's. They do a good masters in Clinical Endocrinology. They also do one part time, which I think is completely virtual and two years. So if you did want to do F one F two, you could do that one. Or if you did want to do like um year, you can just do the one year one um expression. Can we be a recording of this? Um I'm not sure. Yes, it's recording. They can have access of our recordings on our medical page. That's possible. And the last one, is it safe to use? Thank you. S SGLT two drugs in insulin dependent type one diabetics who have fluid overloaded. Oh, this is a worthy question type. Wonder who have fluid overloaded. Solich. Hopefully I will be reduced, haven't you? Yeah, it's a worthy question in synergistic. Cool. To be honest, I'm unsure with this question. It seems like there are a lot of parts to it to answer the beginning part. Is it safe to use SGLT two inhibitors drugs, insulin dependent type one diabetics who are fluid overload? I'm just, I don't really understand this question. If you're, if the patient is insulin dependent, why would we be giving them an SGLT two? I'm sorry, I don't understand this question but leave it with me. If you just email it to my email, I could go over again. I don't really understand the question but yes, if that, if there, if there are no further questions, if you do have any questions about doing a masters or anything like that. Feel free to email my email address on the screen or, you know, LA, which is my full name dot Bello one at NHS dot net. And I'll be happy to answer any further questions there. Okay. And that's pretty much the end of the presentation. Thank you so much guys for spending this 45 minutes with me and learning about just your, just the basics essentially on endocrine emergencies. I've enjoyed it. I've enjoyed teaching it. And yeah, if you have any questions you can email. But yeah, um I wish you guys all the best with if it's future studies or if it's work. Yeah. Okay. Thank you so much, Doctor Dola for the amazing lecture. And thank you all for joining us today. We would love to hear your feedback by the way. So please fill the forms, which will be you receiving automatically so you can receive the certificates, data with the CPD points which are approved by Royal College of Surgeons of Edinburgh. And also a reminder that our next Syria that we will continue next week, Thursday with spinal emergencies, which will be held by doctor. A naughty. He is a surgical trainee and he's graduated from uh the George, the ST George University of London. So please tune in next week and thank you again. Thank you.