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Welcome to another of our Learn Nurses sessions. Some of you, I can see your names are already there on the one that we just did at seven o'clock which was understanding BP. Now we're going to go. Hi, Rachel. You were the first one to say hello. Um Now we are going to be talking a little bit about chronic kidney disease. O2, Rachel's lovely. Um Understanding C KD. Excuse me, chronic kidney disease. Lots of hellos back. Lovely. Lovely. Remember? Oh, come on brain. Think, think it's getting dark. I'm not really good when it gets dark, you know, um it's better in the summer and the sunshine when I, my brain gets a little bit slower. So if I peddle a bit that will make my brain work a bit better. So tonight's session the second. Hi, Joyce back again. Lots of lovely hellos again. Hi, shea, understanding chronic kidney disease at learn with nurses or at LW nurses. Hashtag learn with nurses and I'm on, this is Michaela. Do follow us, do feel free to take screenshots, do tag us in anything you want to. Um And I was just quickly reading the feedback from the last session. And somebody had said, oh, copy of the slides, you do get a copy of the slides. Actually, it is part of something called catch up content. Um So when you've done your evaluation that gets you the certificate and it gets you access to the slides now, whilst you're all here as well and obviously thinking about this but have a ponder for me and think about what else you might want from low with nurses at Rachel's everywhere. You're the third Rachel lovely. And think about what else you might want from loan with nurses, not necessarily the clinical content, but different ways you might want to develop your training. So there might be different types you say, ok, well, it's all very well listening here and we've already got some on demand stuff. So you might want to watch more stuff on demand. You might want to have, what about if you collect badges and you did 10 sessions and you've got a badge saying I've accumulated this amount of time, you know, just think all if different ways um that you might want to be able to develop your learning and how you learn and how you interact. Um pop it on your, you can either pop it in the chat or you can pop us an email uh or you can chat to us on social media however you want to do. But let us know, I just thought I'd quickly ask you here. But obviously don't think too hard because really what I want you to do now is think about chronic kidney disease. Now, C KD has the potential to be really complicated because it is really complicated. And I couldn't, I couldn't remember kidneys for ages. I couldn't remember them. I always struggled. And just when I thought I got CKD, it went again and then I thought I got CKD and it went again and I kept having to relearn it. I was a bit rubbish at remembering it and, but now I've got it now I've got it cos a bit like what I did with the BP one and we, we've turned it into quite simple stuff again and that's what we're gonna be looking at now making KD more memorable, easier to remember. And it's really important that we do that because it's a really big problem. So it's estimated based by how it's been increasing on what the rate of death is. So back in 2013, it was the 19th cause of death across the world. Ok. 19. So that's quite a low way down, but it's estimated by 2040. It will be the fifth cause of death. Ok. It's on its way, it's really on its way more than ever. And you'll be feeling that where you're working, you'll be finding more and more people with KD. Now, from remembering from the last one, I'm an old fashioned nurse. And I can remember before we had CKD. Ok. I can remember a time before CKD, our kidneys might have got a bit older, but also we didn't live as long. You know, if I went back 35 years ago, we didn't live as long as what we did now. And we have much less diabetes and much less hypertension that was out there. And these are the two things that are really causing it. But the last time we properly counted how many people have got C KD around the world was in 2017. And look at that, I can't even say, say the number, what's that? 8436 million people have got CKD. That's approximately one in every 10 people. So it, it's all over the place. Think of your road you live on. There's a lot of people with CKD, diagnosed or undiagnosed and it's more common in people with hypertension with type two diabetes as we get older. And it's more common in women. And certainly for people's ethnicity can put them more at risk of CKD. And for some countries, it's in the top 10 causes of death. And that is Greece, Israel and Singapore. So if you're not up to speed with CKD, now you will be. So what we're gonna do with KD, we're gonna look at the function of the kidney. Ok. How does it do? What, what, what does it do? And then once we know what and how, what, how it works. Then we're gonna look at how does the kidney go wrong, then we're gonna look at how we get it diagnosed and then we look at the impact that CKD has on the kidney function and that's, and, and this sort of lets us think. So that's why we do this sort of monitoring here. Ok. That's why we're gonna break it down. If you look at the nice guidelines, it jumps straight in with and this is how we categorize it. I'm not gonna look at that, ok? I'm not gonna look at that until later till we start to understand what is an EGFR and what is an ACR and, and, and, and then we can start to look at the categorizing of it baroreceptors for those of you when there was a lot of you that were on the last session. Um I'm just giving up but for anyone who wasn't on the last session and that was a BP one just going to remind us who baroreceptors are. Baroreceptors in my world are like dinner ladies and dinner ladies are just, well, they were women when I was growing up. Maybe we get dinner men there, maybe they're not even called dinner ladies anymore, but they are, they were people who not only did they serve the food but at play time, they would hang around the playground, looking around at high risk areas, waiting for it to kick off or someone to fall down the stairs or someone to fall over and they would intervene and they would blow away and make something happen. And we have these barer receptors in our bodies and they hang around parts of our bodies. Uh Absolutely carry, we, I do the hypertension one every few months and I'm actually thinking we might put one on, catch up as well so people can put it on demand and watch it whenever you want to. Absolutely. So those barer receptors are there, they hang around in our neck, they hang around in our heart, they hang around in our kidney waiting to see a drop in BP. That's what they're hanging around to do. So when we are lying flat and this is where it comes from, we're lying flat. Gravity doesn't do anything to us. When we stand up, when we stand up, gravity pulls the blood down and the baroreceptors kick in to push the blood back up to our brain. So they will say things like make the heartbeat faster, make the body keep in some salt, maybe squeeze up our arteries to cause vaso constriction. Push the. But that's what the baroreceptors do. They trigger all those responses, pushing blood back up to our brain, keeping the brain perfused because it's really important to have your brain perfused. We can't live, we can live without an arm, we can live without a leg. You can chop your liver in half, we don't live without our brain. So there are so many systems, our bodies designed to keep that brain looked after and keeping it perfused and baroreceptors is one of those systems. And it's, it's important that we understand this system to be able to look at. Si, I don't know why I'm shaking piglets, but we are to make sure we understand CKD. And that system is the renin angiotensin system. We've got our liver. Our liver does lots of fantastic things. I think of the liver as a factory and it does lots of different things. And one of the departments produces angiotensinogen and angiotensinogen is always in the, it's always in our body. It's always there hanging around. It's a bit of a, it's a bit of an old Wimpy Disney princess. Ok. Snow White. The first Disney film I ever watched was Snow White. And she's not those like kick ass modern princesses nowadays. She was a bit wimpy and she didn't do much and most of the time she was just waiting for Prince Charming to come along and save her. That's what angiotensinogen does. It's a very inert, very inert chemical in our body. Hi, Lindsay, the kidney. Once the dinner ladies have given them a little tickle produces RNA and renin I think of is Prince Charming. So he's going to get released from time to time. Ok? And when he gets together with snow, right? So when angiotensinogen and renin get together, they make angiotensin one and angiotensin one is full of potential. It doesn't do anything but it's full of potential. And then in the presence of an ace, which is an angiotensin converting enzyme, it goes from potential to action and action means it will either vasoconstrict, ok, making less space for the blood to be in helping to put our BP up. But that angiotensin two also tickles, our adrenal glands that sit on top of our kidneys that produce aldosterone and aldosterone. Help with the balance of salt and water. Ok? Help with that balance of salt and water. We know that if you eat a salty meal, you're really thirsty and you want more fluid afterwards, our body does exactly the same inside. Keeps more water in our body. All increases our BP, a fantastic system that has looked afterwards for many, many years. So we've got that ran and angiotensin system there. So now we're going to come back to that in a moment. But now we're going to look at our kidneys and our kidneys do lots of things and look at the happy little creatures. Most of most of us have got two, some people have got three, some people have got one but they do on average five different things. They help to balance out the salt and water. They get rid of waste from the blood. They help to control our BP. They make strong bones and they boost the production of red blood cells. Now, here is a happy kidney, do out my artwork. I do that all by myself. So here is a happy kidney. And what happens is blood enters the renal art through the renal artery into the kidney. And then inside that kidney there is um there is I have to see what my next slide was. So the happy kidney blood enters inside the kidney. Things happen on the inside blood leaves the renal vein. Ok? And the ureter brings away everything that is filtered out. That's a happy kidney. That's a sad kidney. Ok. This is a kidney with CKD. So what makes our kidneys sad? Well, there are lots of different things. There are things like cardiovascular disease, toxins, long term nonsteroidals. It could be something structural that we've got there. It could be genetic in our family. But our two big reasons and our two big increasing reasons is diabetes and hypertension and never before have we had so much hypertension and so much diabetes out there. So that's really what we're going to focus on tonight is just how do diabetes and hypertension make CKD happen because we know that particularly for people with diabetes and hypertension, they are way more likely to have CKD. So there's that happy kidney. There we go. Let's go back to the happy kidney. The blood flows inside the renal artery. So I want you to start thinking about size Now, think about the size of your kidney. Ok. Your kidney is smaller than your fist stuck up here. Tuck down to your rib cage and the renal artery goes in and it's not very big. But inside there, we've got about, between the two kidneys, about 150,000 of these fellas and these fellas are our nephrons. So you can imagine that big artery going into the kidney, then it divides down, down, down, down, down into smaller, smaller, smaller arteries and then goes into our nephrons. Now, the neph is where blood uh gets filtered stuff pass over with osmosis. We're not going to think about how they work. We're just going to think about. It's where the magic happens. Ok. Nice and easy. It's where the magic happens inside those kidneys where it all filters everything out. So, hypertension. So with hypertension, we've got raised BP and that BP creates extra pressure on the inside of our arteries. It creates turbulence, it creates blockages in our arteries, but not just on that big artery that we can see entering the kidney. We in all those little arteries inside. So imagine each kidney has got 750,000 nephrons. Imagine how small those little arteries are that we've got and it's under higher pressure, much higher pressure than it should be. Remember that is where the magic happens. That's where the filtering happens. So it causes damage, damage, not just on that big artery, but on all the little arteries inside and when they're damaged and it's not working so well. And we've got all of that turbulence and the blockages are building up. It means there is less blood and therefore less oxygen getting to the nephrons, they're becoming ischemic. Ok. They like when your heart muscle doesn't get enough blood supply, they're becoming ischemic and therefore not working as they should do. Remember, our kidneys have got those high functions. So the impact in the kidney on doing those five things. Now, diabetes. Now, I want you to think for people with diabetes, they've got a bit of extra sugar, a bit of extra protein floating around in our bloodstream. So the blood enters our kidneys in that renal artery. Again, all of the filtering starts to happen on the inside, but it's more in the venous side of the kidneys where the diabetes affects things. I want you to think about those little sugary molecules, those little protein molecules sticking to the inside of the veins, sticking to the inside of the veins, not just on that big fat vein, we can see there but all those little tiny veins in those nephrons where the magic happens. And for diabetes, what that does is it means that the blood can't flow out of the kidneys in quite the same way. So normally it would flow in fil to f to flow out, it's gone in, it's filtering, not so well, because hypertension and then it can't get out because of diabetes and that causes something called hyperfiltration. It damages the nephrons and they're quite delicate creatures. It damages them and it makes the kidneys filter stuff that it shouldn't do because it blows holes in the nephrons. It's hyperfiltration, forcing more things through the filtering system. Now, all of that, those two processes, those two process of the ischemia with not enough blood getting into the nephrons and this hyperfiltration that happens because of diabetes. And they've got this back, this sort of back pressure with inside the kidneys means that the kidneys don't filter as well, which means our function drops down and we get the low egfr the low filtering function, the estimated glomerular filtration rate drops. Now this is where our dinner ladies come back in. Remember our dinner ladies are there for when we've got big blood loss for when we're bleeding all over the place and they start to notice this drop in the filtration. Ok. It's not necessarily in the neck that it gets noticed because they won't know because they're looking for high BP. But the ones in the kidneys, the the the dinner ladies that are hanging around the kidneys, they're looking for the filtering way. And when they see this drop in filtration, the dinner ladies only know one thing you must have had your leg bitten off by a big animal and you know, from years and years ago, you must have had your leg bitten off and you're losing blood everywhere. We've got to protect the brain. How do we protect the brain? Well, we do everything we can to push the BP up and everything we can. And that means it triggers our renin angiotensin system. So we might already have hypertension, but our body doesn't know that really doesn't know. It just knows our kidneys aren't functioning as they should do. And so this kicks in and it says we've gotta keep that brain protected. Come on, the angiotensin is already there. Snow white's already there. Bang out some renin. Let's get that angiotensin one which is full of potential. Let's get it converted to angiotensin two. Let's get that vasoconstriction up. Let's keep in the salt and water. Let's get that of that. Aldosterone keeps in the salt. Let's get that BP up because that's what they were designed to do. It was to protect us. And so we're all the time driving up our BP. When we've got CKD, our body systems are working against us to keep the BP up. That's why it's harder to get BP down. No, in a happy kidney, blood enters the kidney, the magic happens, it gets filtered, blood leaves the renal artery and we pee out some and that when we do, when we have a sad kidney, we get stuff that you can tell my, my hours clearly didn't do art, we have stuff in the bloodstream that shouldn't be there and we have stuff that should be in the way that isn't there. And that's how we test for it. This is where the filtering has gone wrong and this is how we test. So we do, oh, the EGFR, we do them all the time. Standard stuff all the time. Check your creatinine. Look for the EGFR. Now the EGFR we get, as I said from, there were other blood tests we can look at which might make us suspicious about the kidney function. So whether that's your urea or your sodium or your potassium. But really what I want to look at tonight is your creatinine that if we just measure somebody's creatinine, which is fine, we can measure it. It doesn't really give us much. It might give us a bit of a mm. I wonder if there's something going on but it can't tell as much because we have ranges for creatinine. Ok. We have total these big ranges. You can see between men and women and it also can make a difference with what we've eaten. So if we've eaten meat in the last 12 hours, it will change our creatinine level. Don't worry about all those blood tests where people have gone off for a, for an EGFR and you haven't told them don't eat meat the night before, but it's really good. Uh A good practice going forward to say, don't eat meat, just don't eat meat for 12 hours before. Then we can be sure that what we're measuring is your body of creatinine, not just the hamburger, ok? Because it's a byproduct of muscle metabolism. Um uh that becomes e ex you know, excreted. It just the kidneys don't change the muscle bit when we've eaten them, when we've eaten meat. Now, we do see as, as the creatinine goes up, it can be a marker of, of chronic kidney disease or kidney damage. But we don't just go by that. We go and look at the EGFR. So the E for EGFR stands for estimated. So we're not really measuring it. Ok, we're estimating it. So it takes the creatinine and because of creatinine can change according to our age and our muscle mass and our size and, and, and our ethnicity, then that's why when we submit and you know, when we do the blood test, we have to make sure the age, the sex and the ethnicity is also included on there because there's a calculation that happens up in the laboratory that comes up with this estimation and that gives us a much easier number to work with. Otherwise we'd be saying, oh, so what should the creatinine be for someone who is 34 South Asian and male versus what should the creatinine be for someone who is 38? And so it would just be messy. Whereas now we have a sort of a number that we can compare and we just have one number, although it's an estimated number because it's an estimate. It does mean it's subject to error. So if you've got a big bodybuilder, ok, a big bodybuilder that takes a lot of creatinine. There's a lot of high protein diets out there at the moment, then that's going to alter the creatinine. If you've got somebody with an amputation, well, they'll just have less muscle mass and we don't use it in women who are pregnant or Children. So we get that number. Now you do your first creatinine and if it's less than 60 I'm not gonna say the millimoles per minute per 1.73. Well, I've just said it, but if it's less than 60 then we repeat within 14 days, we repeat very quickly because that's where we're trying to exclude acute kidney injury. We're not in acute kidney injury session. Today, we're chronic, what we're looking at and then what we wanna do is think about progression. So we don't go by a single test. So that's why it's fine. Don, we're about the ones with the hamburgers in the past, but we wanna do at least three eg fr s over 90 days. That's why we repeat and we repeat and repeat. We're trying to get a bit of a picture of that kidney. And alongside that, we do the ACR OK. Now the ACR I want your brain to go back to the picture where I had the wii in the different places. So when we do the blood test, we're looking for what's in the blood test. Ok. The bit that's leaked and should have gone in there. So albumin, ok. Albumin is a healthy protein that should be in the bloodstream. It should be in the bloodstream and it's absolutely fine. But when our kidneys don't work so well, then the albumin ends up in the way, some of the Albumin goes in the way, the creatinine that should go out in the way doesn't always go out of the way and stays in the bloodstream. So that's what we're doing. When we do the blood test, we're looking for more creatinine in the bloodstream than should be because we should have excreted it out. And then when we're doing the ACR, we're going ok. So it's gonna be less creatinine in the way, but there's gonna be more albumin because the kidneys aren't working well and it's letting it go out in the way and it shouldn't be there. And that's what our ACR is. We're looking at the ratio between the two and ideally we do it early morning. So it's nice and concentrated and that's how we get to diagnose KD. That's where our, our categorization comes from. So we have the ACR and as the ACR gets higher, then our kidneys are becoming more impaired, the dysfunction gets worse. And as our EGFR goes down, gets lower, shows us of that progression. And you can see as we go down to that bottom right corner, the, um, the, the, the CKD becomes worse and worse, the risk starts to increase. Now, of course, we can have a reduced ACR with quite a normal EGFR. So we can have all of those ones as well. But we can see how we start to categorize those, but the majority, they, they start to slip down. And what we want to do is find out where somebody is, find out where they are as quickly as possible and then get to manage it. And we want to slow down that progression, slow it down and, and, and improve kidney function if at all possible. Now we've got our CKD diagnosed, what are we gonna do? Well, we start to look at the impact that CKD has on our bodies and has on those five functions that it does. So remember, balance salt and water, get rid of waste, help to control BP, make strong bones and produce the production of red blood cells. So because it helps to balance the salt and water, we keep an eye on our salts. We keep an eye on the sodium and the potassium. You've already heard me talk about aldosterone and that's part of our renin angiotensin and we have the antidiuretic hormone and they're the ones that will keep more salt back in the body. Keep more salt in. Let's get because remember they think that you've got blood loss and it's trying to increase our BP. So the kidneys all the time are saying, drink, keep that salt on board. Let's get that salt in which means we keep an eye on the sodium and the potassium. Now, the frequency of all of this monitoring is all dependent on the previous result and what level of CKD they're at. So for some people, it will be every year, for some people, it will be every two months. It's all dependent on previous levels. We know the kidneys are there to filter an excrete waste. So we monitor that process the EGFR. So we know what the EGFR now is. Yeah, that's how much creatinine that is in the bloodstream that shouldn't be there. And we know as our EGFR goes down, the filtering system goes down, the worse it is the creatinine goes up. EGFR goes down and the ACR, that's the albumin that should be in the bloodstream that's sitting in the weight and the creatinine that should be in the way. But it's in the bloodstream, we're looking at that ratio and we keep an eye on that one. Again, the frequency is all to do with what level of KD somebody's at and what the previous results look like. The control BP. So we measure and we try and control BP, but it's really hard to control BP really hard to control BP in people with CKD. We'll come back to that in a moment. They help to make strong bones. So we keep an eye on that as well. And that's looking at the calcium, the thyroid levels. And my mom always says I'm on the old lady tablets. I mean, bless her. She's only 77. And uh, so yeah, she's on a calcium, a thyroxine and a statin. Um, and that's really good. I mean, ii don't need to tell you a life story, but those are her kidneys are fine but they're less good. So, but that's what we want to keep an eye on because they make bones, strong bones. This is how we can see how things are going. They help to produce, produce pro boost the production of red blood cells. So we keep an eye out for anemia. That's why we're always doing for blood counts. Again. Frequency, all depends on at least annually, possibly more, depending on the status of those kidneys. And we keep an eye. We try and address what makes our kidneys sad. So yes, I mean, we can't get rid of cardiovascular disease if we've got it, but we've got long term nonsteroidals, get to get people off that if there's any toxins that we can do all of that. We can't say let's get rid of your family history. We're not going to do that. But let's focus on diabetes and high BP getting better control of the HBA1C is, is essential for so many things. And what that will be able to do just when you've got less sugar and less proteins floating around that are gonna stick to the inside of those veins, which causes that backflow, that hyperfiltration because the blood can't flow out of the kidneys in quite the same way. And more and more now we're seeing really good renal responses, really better control of KD with some of the more modern sugar weaning out diabetes medicines. And of course, we've got to get on top of hypertension. And that's why for people with CKD, they have tighter targets, but it's so hard to get there because all the time you're trying to get people's BP down the kidneys. The dinner ladies are trying to keep it up because they don't know that it's CKD. They just think, oh, you know, you've, you've, you've had your leg bitten off and there's blood flowing everywhere and it's trying to protect the brain. So it's quite a battle with CKD to try and get on top of it because our body is working against us. And so ideally don't get CKD to start with is what I'd say. And we do that by early diagnosis of type two diabetes, early diagnosis of hypertension because the sooner we can get those things diagnosed, the sooner we can get them managed, the sooner we can get better control or ideally don't get diabetes or hypertension in the first place. And we know that our lifestyle for the majority of is what's driving our diabetes and our hypertension, which is a bit sad, but that's going back to using our bodies the way it was designed to be used. So, not smoking, don't put tobacco in by eating the right fuel and, uh, by moving a lot more than what we really are. And that will reduce our hypertension and diabetes. They reduce our CKD. But that's the long term strategy for a lot of us. It's getting good control of the diabetes and the high BP and keeping an eye out really regularly for chronic kidney disease. Now, there might be other times when we think, hm. Should I look for it? So we should be proactively almost screening for it. You know, all those annual blood tests for people with type two diabetes and hypertension always looking for it. But when might we be suspicious? Well, these are some of the sort of classic symptoms of CKD. You might be a bit tired, you might feel a bit breathless, your hands and feet might get a bit swollen. You might have a bit of weight loss, poor appetite. You might find you weeing a bit more at night. I mean, some of these things might not be CKD at all, but it's often thinking, ok, you have tired, you've got a bit of that. Let me just check your kidneys and I think more and more we should becoming more suspicious of the kidneys, particularly if there's hypertension type two diabetes, female older or, um, or, or, or black or South Asian. Ok. There that, so I had a brain moment then. And so, um, yeah, so we should be more suspicious when we get these symptoms and they're not very exciting symptoms for people to present with, but let's just do things to exclude what it might be. So, in summary, kidneys are really precious. Most of us only got two of them and they do lots of different things. Remember, they do pretty much five different things and we need to look after our kidneys. They are just delicate creatures where the magic happens inside of them. And if we don't look after them, how they were designed to be looked after they won't function so well for us going to pop the feedback in the chat while I just finish off here. So it is time for any questions that you've got. But my brain is getting slower and slower. So I'll be careful with the questions. Remember to do your evaluation at the end. That's where if you, we've already, well, I'll be put the slides up in a moment for the catch up content. That means you just can get a copy of the slides, just go and look for the latest version of the slides that are for you and you get your certificate as well. And um if you want to join us any of the social media, please do so. Um ok. So Lorraine wants to know why does KD increase the risk of CHD? It's all connected, it's all connected. And remember as a, as often like a KD, well, CHD increases our risk of CKD and CKD increases our risk of that because it's all down to those arteries. It's all down to the arteries which will, uh which have the same problems of that, the, of forming on the inside of their arteries. It's all that damage to our endothelium. Thank you guys. See. Don't you remember? Kidneys? Now, I struggled with kidneys for years. Like I struggled with baroreceptors until I turn them into dinner ladies and just always try and break things down as easy as we can. Making CKD A, a bit easier to understand. So, um, yeah, Lorraine and I hope that makes sense. It's the risk factors for CKD are the same as the risk factors. They're all interconnected. They all overlap. And if you've got CKD, you've probably got type two diabetes, you've probably got hypertension which increases your chances of um things. Um So why else do you need to repeat, egfr like when drops? And um I like when drops, like when drops. So repeat it. So if they repeat it, so you just have to go back on what your previous one was, what the previous one and what the history was like, so if you've had one that looks a bit weird, you might want to retest it again. Just to see. Is that an errant one? Are I finding a trend what's going on? Um So the retest of the normal A cr if the patient has got a normal EGFR, but an elevated A cr again, I'm trying to remember the frequency of retesting. I just follow whatever template and guidelines are going there. But I think it depends on what it was and how far along your acr is and then keep an eye on everything else that's there. Ok? So I am going to leave it there. We do have some more sessions coming up for you and oh, first time you've joined. Thank you, Jane. Thank you. We all have our own styles of doing things I will say at, at here at learn with nurses. So we've got some, we've got some really exciting ones. Well, I don't know how, I don't know how exciting you find management of fecal incontinence, but it's really important and Lola does that one. I've got some about chest pain coming up. We've got management of urinary incontinence. We've got one coming up for menopause. So we've only got them booked up until the, until end of March, but we will be putting some more on as well for you for after March. Um But we might be having um oh, a first time for you too. Debbie? Oh, loads of first time sessions. Brilliant. Brilliant. Oh, loads of first timers. So, for you, first timers, how did you find out about us? That's what we want. That's what I want to know. Maybe you put that in your sign up. How did you find out about us? Because, um, it's always good to know where you find us. Sometimes people find us from, um, ah, Facebook. Ok. Cool. Ok. It's always interesting. We, we get it, we get it from different places. Well, everybody, I am going to love you and leave you. Uh, sh, I do do sessions on cholesterol, uh, just like this. Oh, colleagues and Charlene, the cholesterol ones, we kind of do these cycles once every two or three months. So you'll find cholesterol will come up. I usually do, I do this BP bit. I do a couple on cholesterol and I do a couple on atrial fibrillation and they cycle around and I do chest pain and I do chest pain when it's traditional heart attacks that we think about. And then, um, if you didn't click onto the last session, how can you get? Just wait, just wait for, because you'll be sent an email reminder. So if you didn't click on the link before Laura and for anybody else, an email will be sitting in your email box saying you've watched it and you've participated, please do your feedback, um, a diabetes session yet. David we need to nudge Judy because she's our one that does the diabetes and she normally blocks them all in. So, for you, first timers and for anybody who wants more sessions just to let you know, um, it always comes as a bit of a shock to people. This is not our day job. Ok. We do learn with nurses in our spare time. So, um, yeah, so if we don't always seem like we're doing as many or as quickly as that you want, it's, yeah, it's in our spare time that we do this stuff which, you know, makes me sound like amazing. But um, but we love doing it and we get so much out of trainers, get so much out of actually delivering these sessions as well. And I've learned loads doing it myself because, you know, you have to learn it to teach it, don't you?