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Oreos. Oh, brilliant. Um Sorry. Hello. My name is Sarah Lewis. I'm 1/4 year medical student at Manchester University. And today I have a presentation on endocrine lab tests and interpretation for OSK. So I've got a few slides to run through. Um We'll be going through thyroid function tests. It's just a few slides to start with. So, thyroid function tests, uh parathyroid hormones and the adrenal hormones. We've also got stuff on um differentials you might suggest if you were given a set of endocrine lab test results in an OSK. So we'll go through those and then just be some practice osk stations for you to run through to kind of practice what these slides are on and give it all a go. So to start off with. Um so the breakout sessions will be at about 40 minutes time. Um So these slides hopefully will run through quite quickly and then you get some time to practice, I think about an hour, 40 minutes or so in a small breakout room. So to start with thyroid function tests, so it's a blood test measuring three different things. You've got TSH, which is thyroid stimulating hormone. And then your free T three and free T four, which is also called thyroxine TSH is made by the anterior pituitary gland and T three and T four are made by the thyroid gland. Free T four is a more relevant marker than T three. So thyroid itself makes more T four than it does T three. But her 20 to 1 ratio, you don't really need to know that much detail for your osk. But, you know, looking at the T four, is probably a slightly better marker. And all that free means is that it's not bound to a protein in the blood. So the ones that you're gonna want to look at when you're in the station is your TSH, um T four T three as well if it's that. So what do the different thyroid hormones do? TSH is the hormone which tells the thyroid to make more thyroid hormones. So, T three and T four and it's under the control of a negative feedback loop. So when you've got high levels of T three and T four, your TSH is going to go down and vice versa. If you've got no T three or T four, your TSH is gonna go right up tongue, the thyroid to make more thyroid hormones. T three is the active thyroid hormone. Again, don't get too caught up on this. Um, because for the osk itself, you don't really need to know how much detail, but T three is what acts peripherally in your tissues. Whereas T four is the one, as I said, gets released more by the thyroid gland and then it then gets converted. But yeah, those are your thyroid hormones and what you need to look out for on your panel. T three and T four is when they're high, they're going to be causing hyperthyroidism and the kind of increased metabolism, the symptoms that you see when you look at something like grave's disease or other causes of hyperthyroidism. Whereas when the TSH is high, it's kind of the opposite of what you'd expect. It's kind of one of those tricky situations where you kind of learn it in medical school and you, you might remember it better because it's the opposite of what you expect. But II will go through kind of a, a strategy of how we're going to interpret T FT S. But I would always suggest that you look at the T three and T four first because it is, it's, it's more simple. If it's high, then the thyroid is working too much. Whereas if you look at TSH, you might get a bit confused. So this is a picture of what I've just described. So you can see that TSH acts on the thyroid causing it to make more T three and T four. So in AOK, apart from the general data interpretation, sort of question where you get all your blood test results, they might have a reference range of, is this normal or is this not normal? You might then be asked to suggest some differentials based on these, or it might be that you took a history and then they give you these panel of results, I'm not sure. But either way it's good to know what conditions are related to the thyroid gland. The main ones are hyperthyroidism and hypothyroidism. So hyper is when it works too much. Hypo is when it doesn't work well enough. And I've put under here, the thyroid hormone kind of results that you'd expect to have. So hyperthyroidism, if you look to start with at the thyroid hormone, T three and T four, they're too high hypo, they're too low, quite simple as I said. And then we see that TSH is the opposite of that. So kind of one's high, one's low. So if you've got t high T three, high T four, then you've got low TSH and vice versa. For hypothyroidism, I put here the most common causes. So, hyperthyroidism, it's, it's good to look through. Uh there's some good websites. So geeky Medics Xero to Finals is one I use quite a lot as well. But if you look at the um, conditions which cause cos hyperthyroidism itself isn't the full diagnosis. The most common cause of hyperthyroidism is Graves disease and the most common cause of hypothyroidism is hashimoto's. So just be aware of those sorts of things. Cos an examiner could ask you, well, you know, what might be causing that. You've also got subclinical hypo and hypothyroidism. And this is when your thyroid hormone. So, t three, t four is normal, however, your TSH is low or high depending on what's going on. So, it's kind of like a prestage hyper hypothyroidism. Um, the patient doesn't tend to have symptoms, they might have symptoms but they tend to have symptoms. But if you see that in an AK and you're like, oh, well, you know what's going on here, it's something to be aware of. I think hyper hypothyroidism, probably the more common things that could come up. But, you know, if you've got knowledge of that, then you're prepared, aren't you? There's also secondary, um, hyper and hypothyroidism and that's when this kind of pathology that isn't coming from the thyroid itself. Ok. And then if you've got secondary hypo or hyperthyroidism, as we see in the first two, so I've put up here low TSH and high T three T four. We can see there's one that's high, one that's low in secondary causes, they'll both be high or they'll both be low. I think I have a table, hopefully to describe that matter or maybe not. Ok. So how would we approach ATF T interpretation AY station? So I've said to look at T three and T four first, is this is what you'd expect to, you know, to be high. If it's hyperthyroidism, it's gonna be high hypo, it's going to be low and this can help you to avoid confusion. It certainly helps me to avoid confusion. And then after you've looked at your T three T four, look at TSH. Is it the same? So, is it, you know, is it high? And the TSH is um, sorry, if the T three and T four is also high, this then could be a secondary course. If one's high, one's low, then it's a primary course. So primary um hyperthyroidism is when there's a problem in the thyroid gland itself, primary just means it's the problems in the thyroid gland. Sorry, I thought I had a bad table for this unfortunately, but I don't. OK. So I've got an example question now. Um I'll give you a minute or so. Just have a think about it. So you've just performed a thyroid examination on the patient and an examiner passes you a sheet of paper with these lab results. So we can see the reference ranges are on your right. And then you've got your thyroid hormone results a few more seconds. So this would be a, oh, I'm not on the side. It would be a subclinical hyperthyroidism. So the way we've got to that is that the T three and T four are normal whereas your TSH is low. So as I said, it's negative feedback loop TSH acts and when there's a kind of a low level, normally TSH will show up, we can see th H is low. So there must be too much T four T three or some sort of pathology we're suggesting that way. So again, try not to get too caught up in subclinical. I put that in as a bit of a slightly nasty question just because it's what I found online. But yeah, it be aware of subclinical but mostly if you understand your T three and T four and your TSH and how that works, you should be OK for an interpretation on T FT S the next step. So an examiner could ask you, well, now, what would you like to do? You think this might be a, you know, hyperthyroidism? For example, you can do a thyroid exam and I haven't got slides today about how to do a thyroid examination. So you can look up some things on geeky medics afterwards. They've got some good results on there. But um you know, you might be looking for a goiter, you might be looking for some clinical signs of um hyperthyroidism. So a fine tremor or um bulging eyes, like weight loss, sweating, those sorts of signs. It could be something that you get asked in the osk. You can do other blood tests that relate to the thyroid. Again, I think this is slightly harsh. It would be quite harsh if it because I'm gonna ask you this upright, but there's different autoantibodies in some thyroid conditions. So, in graves disease, which is the most common cause of hyperthyroidism. There are TSH receptor autoantibodies and in hashimoto's disease, which is the most common cause of hypothyroidism. You've got anti TP O which is thyroid peroxidase. I believe. I can't quite remember. Cos I put TP O and also thyroglobulin antibodies. So those are good ones to be aware of. If you know those you might be able to I impress your examiner, but don't get too caught up on those revised drug management cos you might get asked about a management plan. So for hyperthyroidism, carbimazole is an antithyroid drug which is used or you might do a long term management. So radioiodine therapy, hypothyroidism, you do thyroid replacement with levothyroxine and then you can do repeat blood. So T FT S the H the hormones they take a while to be synthesized and could take effect. So you're not gonna do a repeat T FT in a couple of days. You do it in about 4 to 6 weeks. So you could suggest that as part of your action plan as well. So the next section is about parathyroid hormones. Are there any questions about TF TSI know I have run through that quite quickly. If anyone's put anything in the chart, I'd be happy to try and answer it. No. Ok. Well, if anyone thinks of anything, please do, put it in the chart and we can go through it as we go along, but moving forward then I'll continue on to parathyroid hormone. So, parathyroid hormone is unsurprisingly made by the parathyroid glands which are located near the thyroid. This tells the serum calcium levels to go up. It does that in three ways. So by making osteoclast activity increase osteoclast crunch. I like to think co um osteoblast is building up the bone and osteoclasts crunching on the bone but it breaks down bone and increases serum calcium from the bone. Um kidneys acts on kidneys as well. It tells the kidneys to not pee out calcium basically. So that's going to increase your serum calcium too. And finally, it acts on the intestine and increases Vitamin D activity. Vitamin D helps calcium absorption from the diet. So if you've got better Vitamin D it cos it converts Vitamin D into its active form, then you're gonna have more Vitamin D absorbed into your blood. Again, it's negative feedback. So if you've got a low serum calcium, then more P th will be secreted to tell that serum calcium to go up. And if you've got high serum calcium, then less P th will be secreted to tell that serum calcium to go down. There's a diagram illustrating all that. So we can see, I'm not sure if you're able to see my cursor, but so we've got the parathyroid glands which are these little yellow things that look a bit like grains of rice on the thyroid gland and they are secreting P th acting on those three ways that I outlined and altogether these increase serum calcium. So there some conditions to be aware of relating to parathyroid parathyroid hormone, there's primary secondary and tertiary hyperparathyroidism. So in primary um hyperparathyroidism, there is too much pth secreted and this is normally by a parathyroid tumor. I think for all these conditions, it's good to know and same for the thyroid ones, it's good to know the common causes because you might guess that as a question at the end of your station and that's why I put them on the slide. So I hope you find this helpful secondary hyperparathyroidism is when low Vitamin D levels causes reduced calcium absorption. And then because you've got low calcium, this causes the hyperparathyroid glands to go a bit crazy and they go up and it makes them really active. So then you get a hyperparathyroidism because of that tertiary hyperparathyroidism is what you can think of a secondary hyperthyroid, sorry, hyperparathyroidism. It's very long words, it's se it's secondary that goes on for a long time. And when your glands working too hard for a long time, you get gland hyperplasia. So increase in the number of cells. And then yeah, you've again, you've got a thyroid, a hyperparathyroidism. So pa ha parathyroid glands that are going a bit mad, then the course is fixed, but of course, hyperplasia is going to stay there, isn't it? So you fixed your low Vitamin D level or your chronic kidney disease, which was causing the secondary hyperparathyroidism. But you've still got para hyperplasia of your hy of your parathyroid glands. Goodness me. So you've still got hyperactive gland and therefore you're still going to have hyperparathyroidism. Sorry, that was a massive jumble of words. So I've got a little table here to demonstrate what goes wrong and what you can look out for on a data interpretation question related to P TH. So in all of these, it's hyperparathyroidism. So you're gonna have high P TH. So looking at the P TH isn't gonna be that helpful. Um It's not gonna tell you anything, it's not gonna tell you the cause. However, we look at the serum calcium and we can see that it's different. So primary, it's high. If we go back to this one here, we can see that P TH just keeps being secreted and sorry, let me find that picture again. So P TH is secreted and tells the serum calcium to go up. So continuous secretion of P TH is going to cause serum calcium to be high in secondary. You've got high P TH COS you've got um the glands that are working too hard, but actually you've got either low Vitamin D or um chronic kidney disease. So the serum calcium isn't going to be high as it normally would be because um if you've got low Vitamin D calcium is not being absorbed properly. So actually you don't have the effects of the P TH because something else in the body is going wrong for P TH to not be working. So your glands still gonna be keep going and making P TH like crazy trying to fix that course. But it's not going serum calcium isn't going to respond because something's not letting it. Um So in that case, you're going to have low or normal serum calcium. Finally, in tertiary hyperparathyroidism, it's going to be the same as primary. Um So again, looking at, I don't think you probably have data interpretation station just relating to the different types of hyperparathyroidism because there's not really that much to differentiate between, you can't differentiate between primary and tertiary hyperparathyroidism unless you've got the history. And I'll show you an example question in a second which illustrates that because often it will say if you've got like a progress test question or something that this is a patient who has normal Vitamin D they haven't got loads of Vitamin D levels or they have recently had C KD, but they've received a transplant and then you can kind of work based off that. And if they have got that kind of background history of low Vitamin D or C KD, which has been fixed, then you'll lean more towards tertiary. If you've not, none of that, I would always lean back towards primary. So I've got a question here. It's very grainy, I'm afraid. Um But I'll read it out and then give you a minute or so to have a think so, a 54 year old woman attends a clinic with a six month history of abdominal pain and excessive thirst, systemic inquiry and examinations were otherwise unremarkable. The patient has an remark, unremarkable past medical history in particular, there's no history of Vitamin D deficiency or C KD. So as I was saying, you know, you get that in the stem, I would hope in a exa like a osk examination station, you would get the same. Um But if you're aware of that, then you can kind of use that in your clinical reasoning. Are you able to see these, see these results? Cos I don't want to give you a minute if you're not able to, to read anything on this slide, it is a little bit pix, I'm afraid, could someone put in the chat if they were able to see it? We can just about see. OK, let me try and I've got it on my computer so I'll zoom in a little bit so I can see it. It is a little bit tricky to see. I appreciate. OK. So let's have a look. We have a normal platelet level. We have a normal white blood cell count. Sodium is 145. So the upper limits of normal, but it is within the normal range. Potassium's normal. Urea is high, creatinine is high C RP is normal and then looking at our parathyroid hormone panel, we've got a elevated serum calcium, a low phosphate and a elevated P TH. So I'll give you a minute. So just to reiterate those last three, you've got a high, high calcium, a low phosphate and a high P TH. So for this one, because calcium is high and P TH is high, I would put that as primary hyperparathyroidism. Um If you had so a few of the differential, I'm not sure. Again, if you're able to see those multiple choice questions, I got this off passed from my sister's laptop. So, apologies for the terrible quality, but we've got some drop down options. So one of them is myeloma which could cause a raised um serum calcium if you've got um bone metastases ca causing like um bone breakdown and high calcium because of that. But it would also um cause a low white blood cell count. So, and like an anemia. So I wouldn't, I wouldn't put it as like that. And it could also show a like a reduced ese we do have a slightly reduced uu ands there. But um again, you've got no anemia and you've got no thrombocytopenia. So I wouldn't be going towards the myeloma there. And then again, because it is not so secondary hyperparathyroidism because you've got a race serum calcium and it's not tertiary because we can see there's no history of Vitamin D or any or C KD. That's been fixed? Ok. So the next section is on the adrenal hormones and Cushing's disease, adrenal insufficiency. Are there any questions over those last slides about um hyperparathyroidism or am I OK? To continue? No? Ok. Again, if there's any questions that come up or pop up along, please do just pop it in the chart or say, and we can address those. So, oh, we've got a thing on these. Unfortunately, it's ok. I'll read out what was behind that massive picture of an adrenal gland. So what are the adrenal hormones? So you've got cortisol aldosterone, the sex hormone precursors and then adrenaline and noradrenaline. And in this picture, I've kind of tried to show the different zones of the gland which secrete each type of hormone. I hope this wouldn't come up in an osk examination because I don't know this off the top of my head. But just for your knowledge, there's different parts of the gland to secrete different hormones. Next slide. So conditions to be aware of relating to the adrenal glands. Cushing's syndrome is quite a big one. So the main cause of Cushing's syndromes is iatrogenic as in, we've caused it by giving them steroids for asthma or some sort of say vasculitis or something. Um So look out for that in the history, if someone's on these medications, that is the most common cause. So we've also got um other causes of Cushing's syndrome. So if you've ruled out your iatrogen causes. You've also got um your ACTH which stands for adrenocorticotrophic hormone dependent causes. Don't get too tied up over these classifications, but you've got some which um stem from tumors in the pituitary that was known cush as Cushing's disease. And you've also got um conditions where you've got a adenoma. So, a benign tumor from um the adrenal glands or adrenal gland hyperplasia causing too much cortisol to be produced. But overall Cushing's Syndrome, your main pathology is that there's too much cortisol, other conditions, you've got adrenal insufficiency. So you've got primary and secondary causes of this primary adrenal insufficiency is also called Addison's disease and it's primary. So there's a problem within the adrenal gland itself. Secondary causes, there's a problem with stimulation of the adrenal glands which comes from the pituitary. And I have got a diagram to illustrate this somewhere. So we can see that the pru gland releases, I'll just call it ACTH for easiness, but he has ACTH, it acts on the adrenal glands and then the adrenal glands make cortisol, these are all under negative feedback. So again, when we saw all of the T FT S with um P th kind of one goes up, the other goes down. So there's different tests in Cushing's syndrome. And I think Cushing's is probably the most likely condition I could see bring brought up in an AY and I do get quite confused with the Cushing's syndromes test. So I hope this will help clarify some of that. So there's a dexamethasone suppression test. So if you've ruled out that someone's not taking isogenic steroids, then you're going to be considering, well, what, why have they got high cortisol, what's going on here and to start with you give them a low dose of dexamethasone. No dexamethasone acts um kind of in the way of called so wood. So if you give that, it kind of acts on that negative feedback access and should cause everything else to go down. So the low dose of dexamethasone should, it should tell you if you've got Cushing's syndrome or not. So, in a normal person, you give them um cortisol. So you give them dexamethasone and their cortisol level, their serum cortisol will go down that as a normal result. If that doesn't happen, then you know there's something going wrong there and there's some sort of pathology. So I've got a table somewhere, hopefully bring this up for you. So you can give a high dose of dexamethasone as well. So if you've given it and you know, their, their cortisol doesn't go down, then as I said, there's pathology, then you would give them a high dose and depending on the course. So you can have OK back here. Um So if you've got Cushing's disease, you've got pituitary adenoma, which is secreting ACTH. So if you give them a really high dose of dexamethasone, then it is going to suppress the axis. I like to think of it as, you know, there's a pathology in the axis itself. There's a tumor on the pituitary which should be doing its job, but it's not. But if you give them a higher dose, you're kind of still acting within the axis and you can shut down that pathology. If you've got ACTH being produced from an adenoma somewhere else or there's something going wrong with the adrenal glands themselves. Your high dose dexamethasone isn't gonna do anything. It's not going to suppress the access, it's not going to cause a rejection in your serum cortisol. So hopefully this table summarize that a little bit better if you've got a pituitary adenoma. So third, calm down. Um we can see that the high dose causes low cortisol but adrenal adenoma. Well, that's not in the, I like to think of it as not in the H PX as it's not the pituitary going wrong itself. It's not going to be responsive to negative feedback no matter what dose of dexamethasone we throw at it, it's not going to affect it. So, cortisol is still gonna be high and then ectopic ACTH that can be produced by some tumors. Um Again, you're working outside of that axis, giving your dexamethasone at any dose, isn't going to squish that down. So, I don't know if that kind of idea helps anyone else, but it helps me to kind of process it. Um another hormone that you'll be given in the panel would be ACTH. So if you've got something, an omic, an ectopic production of ACTH, you're gonna have obviously a high level of that. A normal person isn't going to have high levels of ACTH. I don't know the reference ranges for ACTH. I don't know what um kind of value I can give you, but look at whether it's normal, whether it's high, whether it's low. Um, and it acts again within this feedback loop. So if someone's got a pituitary adenoma, they are gonna be having a high dose of ACTH because the adenoma itself produces ACTH and adrenal adenoma itself produces cortisol. So ACTH is going to be squished down because squad cells high A T ACTH is low, there's negative feedback will be, I hope that's makes a bit of sense. It is tricky stuff. Um If you just work within, looking at these negative feedback loops, this is from Gy Med's picture. If you learn this, you can kind of use reasoning to work out what's going on and which one should be high and what's going like, which one should be low? It takes some time. But I hope, I hope with time and with a bit of practice in the breakout session soon, that'll, that'll be a bit of help if you want that for reference. Um Again, I got that from Gy Medics. So I don't know if you want that on your screen when you're practicing just to have a reference. I find it helpful just to revise that for the exams. Um, and same for the thyroid hormone one as well. Revise it for the exams. And then even if you're given it and you don't quite remember what, what should be high and what should be low, you know, should serum calcium be high in this case or not. If you kind of know the causes and the axis itself, I find that helpful. OK. So at the end of your um station that you've interpreted your um panel for Cushing's tests, you might be then asked. Oh, well, now what are you gonna do? What would you like to do? So hopefully you'll have a bit of an idea based off the ACTH level and the cortisol level if it's suppressed or not of what the cause of Cushing's syndrome is. If you're suspecting a pituitary adenoma, you can do an MRI of the pituitary and hopefully you'll see the adenoma on there. And that is your answer. You can also do something called inferior pitu sinus sampling. That's not really done so much anymore. Cos it's quite an invasive test. But basically, you, you look at the um concentration of ACTH in the venous sinus and compare it to how it is in the rest of the blood. And if you've got like a adenoma which is secreting tons of ACTH, then the serum ACTH in that sinus will be really high compared to what it is in the rest of the body. So it kind of tells you that there's something there that's secreting it. But again, I don't think you'd have quite a mean examiner if they were pushing you into like, what's the second line test for Cushing's disease? Know that you can do some imaging of the pituitary and you'll be fine. Um, if you're sus suspecting pathology within the gland itself, you can do a ct of the abdomen, looking at the adrenals and you might see an adenoma there, a carcinoma, you might see something wrong with it basically. And then ectopic ACTH production. So I mentioned that that is produced by some tumors, mostly small cell lung cancer and bronchial tumors. So you could do a ct of the thorax. Um And you know, in your history, some of these things might, might come in like, especially I think whenever I'm doing past med questions, I always see something about like someone who's come in with a lung cancer and they've got a persistent cough or they've coughed that bled and then you might get these results and you're like, oh, well, it could be a small cell lung cancer. So history can help you. Um I don't know how kind your examiners will be, but I hope a bit of clinical history if you're really struggling can give you a few hints. So going on to adrenal insufficiency is the second condition I was talking about on those slides. So, um, the test that you do for that is something called the short Syn Actin test. And Synacthen is a, I don't know if it's a brand name or if it's just the a name but it's fake. ACTH. Basically, it's man made ACTH. And what you wanna do is give that to see if the adrenal glands are gonna wake up. So as you can see in the picture on the right, um ACTH acts on the adrenals cause them to spring into action, but only if you've got healthy adrenal glands. So if you've got Addison's disease, um like primary adrenal insufficiency, giving ACTH isn't going to cause a rise in your cortisol and same for secondary causes of ACTH, you know that that's process isn't working properly. You've got adrenal insufficiency. So you measure your course after giving you short snack then and if it doesn't rise, then you've got adrenal insufficiency. That is the first test that you do. Secondly, you're gonna wanna think, well, ok, you've got adrenal insufficiency but why like what's going wrong? And you can do that by measuring serum ACTH. So as I mentioned before, primary means that you've got a problem in the gland itself. Um the most common cause of Addison's disease is an autoimmune. It might be. Yeah. No autoimmune causes so that, you know, the, the glands aren't going to, to be working and making cortisol properly. So, the negative feedback loop isn't going to be suppressed and you've got high levels of ACTH because the ACTH keeps being produced, trying to stimulate the cort, trying to stimulate the glands and it's not gonna work. So you're gonna have low cortisol and you're gonna have high ach secondary causes. So, secondary causes of, um, sorry, I get my slides up here. Um, secondary causes of ta th so it's not actually a problem in the gland itself but more a problem with the pituitary. So you've not actually got ACTH being produced properly. So how can the adrenal gland, you know, function and make cortisol because nothing's stimulating it too. And therefore you're gonna have low ACTH because pituitary is not doing its job as well as the low cortisol because nothing's stimulating it, stimulating the gland to make cortisol. I've made that in a table here. Hope for that somewhere else. I don't mind if I take a picture or anything of these tables. Um online, it said that the um cortisol should increase by at least two times to make sure that that's like a normal um adrenal function. So if you've got a increase when you give shots and it s Anacin, but it's only by a little bit, it's not by at least two times the amount, then that is still adrenal insufficiency. Again, I think that would be a bit harsh to bring up in an ay on the spot. But if you're aware of it then you're prepared, aren't you? Ok. So moving on here. So I've just put a quick note about kind of. Now, what? So you've worked out that someone's got adrenal insufficiency, what else can you do? So, in some autoimmune causes, um So absence's disease, you can have antibodies which are raised and in secondary insufficiency, as I said, the problem is coming from the pituitary. So you could do some imaging MRI imaging of the pituitary to see if you can see any lesions. Um history may be suggestive of someone with secondary adrenal insufficiency. So there's a few different types, different causes of secondary adrenal insufficiency. So, trauma or surgery to the pituitary, something's basically happened to the pituitary where it's not working as it should lesions, as I said. So you could do the MRI scan as well. Um You might do some like some knees and see that there are other electrolyte abnormalities in absence disease. Notably, you'd have a low sodium and a high potassium. You could also have raised creatinine or urea because you're dehydrated. Um And you could also have hypoglycemia. So if you see a panel of someone with, you know, some suspected a disease, there might be a few things going on that are actually going wrong. Um So just to be aware of those, there's a couple of syndromes that I've not talked about today. Um Con syndrome is one of them. Um I think these are all covered in if you're a Manchester Medical student towards the end of this year. So I think it comes into the hypertension case Conn's syndrome is when you produce too much aldosterone. And that causes a reason in your BP. And there's also something called pheochromocytoma, which is a tumor um of the adrenals and you get too much adrenaline and also high BP. So those should come up in your future cases. They do kind of relate to endocrine lab tests, but I didn't do them knowing that it's December and you've not covered that case yet. So if you want some more information, I hope they will be covered in your TCD. Um If not, I'm sure there'll be another session from by code blue about those. So I hope that's been helpful. Um If there's any questions at all, please do ask. Um, I know I've run through this quite quickly and some of my slides have been a little bit grainy. So I apologize for those. But if there's any clarification I can give, please do, let me know. And I think there's a feedback QR code here. If you've got time and are able to do that, I'd really appreciate it. Um If there's any improvement can be made to the slides, that would be really helpful, please let me know. And apart from that, thank you for listening. And now I think you'll have some time to go through and do some obviously practice with a small breakout room. So, thanks.