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OK. All right. So I've got some input that like you can see and hear me. Sorry. Um So I'm just gonna share my presentation if you just give me one moment, hopefully you can see um my screen. Um And I'm gonna start the presentation now as well. So, uh welcome to the part two of the endocrinology core conditions as part of the uh the beam a teaching program. Uh like I said, or like truth, you mentioned, my name is K Patel. I'm a final year um medical student at UC at the moment. So my sixth year and today the focus is gonna be on core conditions in endocrinology, um in particular, focusing on diabetes and the adrenal axis. I've tried to include uh things which I think will be really important in terms of exams. Um things which in my experience seem to pop up in SBA S and OSS. Um And I've included a mix of SBA questions and OY stations that we can discuss and talk about. Um But it'd be really good if we could engage in discussion and if you guys could interact in the chat, I have got access to the chat. Um So it, it's a lot better, I think. Um if you guys uh input into the chat, what you think and I will be asking loads of questions throughout. So please don't hesitate or don't feel worried about putting anything um into the chat. Um because I think it will be a lot more beneficial for you. Um So we've got a mix of emergency presentations for all of these conditions but also chronic conditions, um and the management for, for those. So hopefully it's um a good introduction or a good crash course into everything that you need to know uh for diabetes and the axis. So, um I created this in a case based way. So we'll start with the first case. So we have a 22 year old university student who has presented to the emergency department with a two day history of generalized abdominal pain and vomiting. He is brought in by his housemates who explain, he has, uh been increasingly drowsy today. He's other otherwise feeling well. Um And there is are his observations. So if you guys just wanna have a look at the observations, um and read again the presentation and I'm gonna open up to the chat, please do, input something if you, um think you can input something. But is there any differentials that you think might be going on or what, what do you think might be going on in this situation? There's not much information that I've given you, I've just given you a very short history and then a few observations. Um, so there's actually no right or wrong answer for this and it could be literally 1015, 20 different differentials. Um Maybe some are more likely given the fact that this is an endocrinology talk. Um But any input would be, would be valuable if anyone has any thoughts. Yeah, absolutely. So DK is uh a good differential and then appendicitis is absolutely another really good differential as well. Um So anyone with any sort of generalized abdominal pain who's young appendicitis definitely needs to be up there. Er, and DK A is a good er differential as well considering the context of this um this talk as well. Um So there could be all sorts of different things that are going on in this patient and just from what I've given you, um you could have a septic patient, you could have a patient who has gastroenteritis. Uh This could be a patient who's presented in Adison crisis. Um There could be anything to do with an acute surgical abdomen going on here. Um This patient could have gallstones, for example, or an affected gallbladder as well. Um But the most important thing is how you approach the a patient like this who has these sorts of presentations. Um and these observations. So how would you approach any sort of patient like this? Is there any method that you would use or um what would the first thing that you, you, you do be any thoughts on how to approach this patient? Yeah, absolutely. So full history and ABDO exam would be really, really important. Um So they come in with abdominal pain. So abdominal examination is gonna be something really valuable. Um And the history for this patient will be really valuable as well. Um So I guess the, the, the, the observations aren't that worrying, to be honest and they are quite young. So you might not necessarily um do it for ABCD E assessment. Um, but one of the things that I was thinking was taking an ABCD E approach to an acutely unwell patient. And um this is something which um is very likely to come up in, in an osk situation perhaps. Um and it's really good to know how to do one of these. Well, so um following a look, feel, listen, measure and treat method is always really useful. Er, and the first thing you wanna do is check the airway, er, the reason it's an ABCD E is because the airway is gonna kill first, you definitely want to check the danger before and a response. Um because if you, it will, if we ignore danger, but if you don't have a response, then you need to be looking at checking for signs for life uh and then moving down ABL S or a LS pathway. Um, but if they are responsive, but just drowsy, then you wanna check the airway. Um, why are we particularly concerned about the airway in this patient, given the presentation and what we think might be going on. Um, he's, he's got abdominal pain and he's vomiting. Um, what is one of the biggest concerns that we might have about the airway? So I'll let you guys warm up with the, um, yeah, absolutely. So, aspiration is absolutely one of the, the biggest things that we're concerned about with the airway in this, in this situation. So he's vomiting up, uh, and he's confused and drowsy. So a is he able to maintain his airway? Cos we know that as your G CS dwindles down, uh, your ability to maintain your airway and a safe swallow becomes greatly reduced in particular below G CS eight. but also he's vomiting. So we need to make sure the vomit isn't being aspirated and that's something which is really, really important. So, yeah, well done for that, um, suggestion. So, how do we actually deal with vomit? So that's, does anyone know what that is or what you can use to, um, deal with that or what these two things are? So, I'll just explain, this is a gel. So this is, um, an oropharyngeal airway. So that's gonna help support the airway, especially if they're, they're drowsy and, um, that they've got some vomiting as well. Um, and this is a Anker sucker and that's gonna, um, help remove the vomit. So, breathing, um, the next thing you wanna check is breathing. So, something which I think is really important for an ABCD assessment is, is tailoring it to the particular presentation which you're you're concerned about. So, because we mentioned the DK is one of our differentials, I'm just gonna put that in, in your mind. Is there anything that you think you might see on general inspection or look, which is specific to DK, which might be really impressive to, to mention or, or something that um you might find on examination in terms of breathing in a patient who has DK? Yes. Yeah. So um patients with Yeah, absolutely. Yeah. Good. Yeah. So acetic breath is something which is really, really uh important to mention actually or not important, but it's something really valuable I think that, that you can mention and it's small things like that which you add on to AAA classic ABCD E assessment um which really shows that you, you understand what you're looking for. Um And that you're trying to think of different differentials. Um So sweet smelling ketotic breath is, is something really valuable. Um I wasn't even thinking about that, but that's something really valuable, but also something called cosmo breathing. So this is deep labored um and more rapid breathing and this is something which is specific to patients who present with diabetic ketoacidosis. So you'll see them really having an increased respiratory effort and that's something which you might find on ree so with circulation, what might you see in particular with your look section or what can we add to our assessment? So, these patients are probably gonna be really dehydrated and, and you'll know that that forms a part of um your uh your, your management for diabetic ketoacidosis. So it's really important to add on a fluids assessment uh as part of your um circulation assessment. So you might wanna have a look at the mucous membranes, see what they're saying in terms of the dehydration sta or the hydration status of the, the patient as part of your circulation. When you're looking at the capillary refill time, you might even want to assess the skin tiger. Um And you can mention that um because I'm worried about diabetic he acidosis and subsequent dehydration. I'm also gonna check the skin tiger and I'm gonna look at the mucous membranes to make a hydration assessment. So they're important bloods which you might need um for your measurements. Um And how are you gonna justify each one? Um So one of the, some of the most important ones would be uh you know, a venous blood gas that will give you lots of information about the acidity of the blood, the extent of diabetic kato, the level of ketones in the blood uh and, and so on and so forth. Um And it's really important to insert a catheter. So um a catheter can be really uh valuable because especially in a dehydrated patient, we want to know the fluid input and output. Um and these DKA patients are gonna be particularly important to do this for. So, disability might be the thing which er is gonna yield the diagnosis and um it's often ABCD E FG. So don't ever forget the glucose. Um that's gonna be something which is really important for this patient and you would expect a really high glucose. So an abdominal examination is essential. Um Again, um the the person who has come in with acute abdominal pain, we don't know what it is yet, we haven't got investigations back. So doing an abdominal examination alongside a full history is something which is gonna be really valuable here. If there's any localization, the abdominal pain in someone with diabetic he acidosis might be quite generalized. Um So here it might not be that helpful. Um But if there's a man presenting with abdominal pain, what's really important that, that, that you add on to your assessment for every male who presents with abdominal pain. So for example, a female presenting with abdominal pain by default, in emergency department will have uh a urine urinary B to HCG. So they will have a, a pregnancy test. Um And that's something which you, you should add to your assessment for every woman who's presenting with abdominal pain of childbearing age. Um What is something which is really important to, to, to include as part of your assessment for a male. Does anyone have any ideas? Ok. Ok. So um as part of an abdominal examination for a male, anyone presenting with acute pain um needs to have a testicular exam um as part of that and that's also for um boys and in, in pediatrics as well. Um And finally, you're gonna expose the patient, see if there's any signs of bleeding. We don't want, we want to rule out um any sort of kind of hemorrhage or anything like that, especially with the low BP and dehydration. Um And yeah, testing glut is, is um one of the most important things to rule out for a male with um abdominal pain. So this is the venous blood gas that um has come back and, and the critical parts of this is um as part of the diagnosis of diabetic ketosis is um an alkalosis um sorry, an acidosis of the blood. So, Ph which is under the 7.35 the patient is gonna have a low P OC OP CO2. Why might that be happening? And it comes into something we mentioned earlier, why does the patient have a low P CO2? Um Other things which might be valuable um in a DK A diagnosis is there really high glucose levels? So you can hopefully see here that the glucose is 33. Um and most people will also give you a a ketone level, but I couldn't find a picture which I couldn't find, uh, you know, evidence of one which had that. Um, but yeah, those are the three components that you were looking at out for. So, lower ph, high glucose and evidence of ketones either in the urine. Yeah. Absolutely. So, um, the patients are breathing fast and they're blowing off CO2. So, the reason why we have Kal breathing and, and, um, the reason why the breathing becomes deep labored and rapid um is because of the ketosis in the blood that's causing an acidosis and causing the PH to drop. And therefore, as a physiological response, the breathing is becoming more deep and more labored. Um in order to almost or in order to cause a respiratory compensation of this metabolic acidosis. So something apa a V VG or a blood gas like this um might be interpreted as as saying um well, there is some sort of type on respiratory failure. But if we ignore the, the, the oxygen, um this would be a metabolic acidosis with evidence of respiratory compensation because the carbon dioxide is, is being lowered. So the patient is trying to blow it off. Um in order to raise the ph back to normal uh in the form of K breathing. So, the diagnosis of diabetic acidosis um has three components. So the test that you would want to do as part of your ABCD assessment would be an ECG chest X ray, uh urine dipstick, urine, mcu capillary lab, blood glucose ketones, uh ph blood, um, and using s um does anyone have any forms of, of ways that it's good to? So if you've been, if you were asked in an examination situation or in or in real life, what tests you would do? Is there any methods that anyone has to kind of categorize them to, in order to explain what might be most important or um, the order that you would do them? Does anyone have any ideas? Because there's quite a lot of essential tests for each condition that you might need to do? Um So it's important to um have a bit of an organization when you're, when you're talking about stuff like this. No. So um it's always good to, to start off with history and examination. So, uh like I said, I II wanna do a full abdominal examination for the patient, including a testing through exam. And then I want to move on to bedside tests. So that might include doing a urine dipstick and doing some capillary uh blood glucose levels. And then I want to um do stuff uh like an EKG which is happening. Um Yeah, absolutely. I said bedside. So an EC G which can happen at the bedside, then I want to take some bloods. So that might include the ketones are using a full blood count. Um And then I finally want to move on to imaging such as a chest X ray. So, the diagnosis of DKA can be in three components. So you need um acidosis, so, acidemia, say a blood ph less than 7.3 you need diabetes. So, hyperglycemia, evidence of hyperglycemia or known di uh diabetes and you need evidence of ketones. Um and these are the, the thresholds absolutely definitely worth memorizing them and learning them, maybe less er useful as the categorization of DK A into mild, moderate or severe. But um definitely worth learning these three components of diagnosis. Um So the treatment is uh taking an ABCD E approach. So you still, you've always still want to first stabilize a patient um if they have a dwindling airway, um then that's the first thing that you need to take care of before you worry about giving um the treatments for the actual DKA. But say we've resuscitated the patient. We've done the ABCD E assessment. What are the, what are the main components of DK A treatments? What are the main main principles? Yeah. So fluid is, is one of the most important things. So you definitely want to hydrate the patient. Um As you, you'll notice in, in your ABCD E assessment, they're gonna be really dehydrated because um they have these, these ketones in their blood, they have higher blood glucose. Yeah, absolutely. So you want to give them glucose? So, um why do you want to give them glucose though? Because I thought they had um high glucose why do we need to replace uh the glucose? Good. So, these are really good answer. So, fluid replacement is, is, is the most important thing. Um, we're missing one component. Yeah, absolutely. So you want to give fluid replacement and that's gonna hydrate the patient. Uh You want to give insulin because that's gonna drop the hyperglycemia. Um And then, um, the reason we'll talk about that in a second, but, um, ABCD EE is always resuscitating and stabilize the patient. So IV fluids is the most important thing. Um And I wouldn't worry too much about the nitty gritty of the, of the actual amounts that you should be giving. But um maybe just to start the, the starting um treatments because that can be quite helpful, especially in an ABCD E assessment to, to mention so a liter of a normal saline over an hour. But unless the patient is shocked, then you, you would give a bolus of 500 you can repeat that up to two times. Um And you want to give insulin to drop the um drop the glucose and again, really important um units, remember 0.1 units per kilo per hour. Uh And you wanna give dextrose because that insulin is gonna drop the blood glucose. So once you see it hit 14, uh you should be doing regular regular gasses and compare your blood measurements. Uh You want to drop it. Um And really importantly, you want to continue your long acting insulin, but stop the short acting insulin. So it's really important that the long acting insulin is continued. Uh So I think someone mentioned the fact that you do need potassium. Um So it's because insulin causes a huge intracellular shift of potassium. So you're gonna end up with a hypokalemia. So you, you, you want to introduce potassium chloride into the second bag of fluids if there is evidence of hypokalemia and that might be through cardio monitoring EKG monitoring or just doing a eutheia or a blood gas to, to get evidence of that. So you want to treat the underlying cause, something would have triggered this. So that's something which you definitely need to consider after. Um and there are some complications of treatment. Um we already mentioned aspiration pneumonia, which is a really good um suggestion. Um at the beginning, we know hyperkalemia, we've talked about that cerebral edema is something which is um a complication to definitely be aware of. How might you want to monitor this? How might if you, if you have a patient in, in front of you? Um How are you, how are you getting to monitor if, if you're causing a cerebral edema? Is there anything that you might want to to do? Ok. Ok. So um if you're worried about causing cerebral edema um then regular. Um so I've just, I've just seen these uh chat messages say um why do we have 1 L of um N ACL. So, so again, um one of the main reasons why DKA can be quite um quite devastating is because it causes a massive dehydration for the patient. So um as part of our diagnosis, um the hyperglycemia and the keton causes this dehydration for the patient. Um So, the main principles of, of treatment is hydration, rehydration. And again, we saw it here and there will be evidence of dehydration in the patient. Um So that's why that needs to be started first. Um Yeah, hopefully that answers your questions. And again, they're probably likely to have a low BP. So we just want to be pushing fluids in them, especially for anyone who's acutely unwell. Um They're likely to have fluids. Um Yeah, so headache, vomit nausea. So those are really good um signs and measure the blood, blood pressure and heart rate is a really good um thing to, to talk about as well. Yeah, absolutely. So you don't want to. Um So I think you said Cushing's syndrome, I think you might mean Cushing's uh Cushing's reflex. So Cushing's syndrome is something else and we are gonna talk about that in, in just a moment and that's something to do with the adrenal axes. But yeah, absolutely. Cushing's um Oh yeah, you did mention Cushing's trial. Um and yeah, monitoring for evidence of neurological dysfunction. So, headache, vomiting, nausea. Um What you could add is I want, I want to do regular neurological observations. And I would like to do regular lower limb and upper limb examinations and that can be a really easy way to, to monitor if there is any evidence of neurological damage um or space occupying lesion in the form of cerebral edema. Yeah. Um So in terms of why it's a liter rather than the, the 500 mL first, so they're not acutely shocked and if they're stable in terms of their BP, you just want to rehydrate them. Um in terms of the intricacies of actually like fluid replacement and DK, you can read about it. It is quite uh detailed and it is quite intricate. That's why I wouldn't be bogged down too much about um about, you know, the fluid therapy. Um But more so the principles of rehydration, um I maybe learn one controlled fluid therapy that you, you, you can learn one of them. Um At least for me, for II just learned that if they're shocked, then you, you need to get that bonus a lot quicker. But if, if, if not, then you can um be a little bit longer with, with the 1 L. So just on the talk of potassium, um I thought it might be really relevant just to bring this in if, if someone's not aware of this. So these are two really uh not, not common, but these are really two important signs that you might see on, on ECG. So potassium is a really important electrolyte in terms of um cardiac function. Um in particular, hyperkalemia can really be devastating and is a medical emergency. Um So it's really important that you're aware of um the signs which are associated with both hypo and hyperkalemia on an ecg. Um they're almost kind of opposite of each other. But hyperkalemia will have a classic tall tented T waves which should be pinched upwards and you're gonna have a wide QR s and you might have ap wave flattening and apr prolongation. And hypokalemia is gonna be the opposite. So you're gonna have T wave inversion. Um and some ST depression, it's really important to especially learn hyperkalemia and associated treatments. So, hypokalemia, you just want to replace the potassium hyperkalemia is a really important treatment. Does anyone know the the treatment of hyperkalemia? If anyone's already done like a renal rotation or uh a cardiology rotation, you might have come across this, but it's really a valuable one to definitely memorize for um exams and, and in general as well. Yeah, good. So uh yeah, calcium gluconate. So um 10 mL of 10% calcium gluconate, 10 units of insulin with 10% dextrose, uh calcium resonium and salbutamol. So those are really four really important aspects of, of treatment which I think um is worth uh remembering 1010, 1010, it's quite easy to remember, I think. OK. So the patient who's been stabilized, resuscitated is now comfortable. What is the single next best step in the management for this patient. Any ideas just put in the chat, what you think might be the case? Yeah. Any suggestions. Yeah. So you've got b Yeah, absolutely. So b is, um, the correct answer. So anyone well done. So anyone who's, um, who's presenting with, uh, diabetic he acidosis is a very common presentation of type one diabetes. Uh, and it's really important that they stay in hospital and they, they've got a review with a specialist diabetes team within 24 hours in the hospital that's for adults. Um and for Children as well, probably more importantly for Children um in pediatric DK. But um still on the guidelines for adults as well. So, um the bit bit of a busy slide, but if, if a patient is presenting with DK A, you're definitely considering um a diabetes diagnosis. So with DK A, that's often the type one presentation. Um but I thought we'd go through kind of the, the diagnostics for both type one and type two because there's a lot of similarities between the two. So learning them together makes sense, I think. So you're always gonna have symptoms of hypoglycemia um in both type one and type two. So that's gonna be um peeing a lot. Um being very thirsty, having problems with your eyes, um weight loss in particularly with type one, having loads of infections and being really tired and the mechanism for for diabetes in both of these cases is a bit different. So, in, in type one, you're lacking that endogenous insulin in the first place to lower your blood sugar. Whereas in type two, the problem is that there's enough insulin but the tissues are resistant to it and aren't really um using up that glucose. So you're gonna have signs of high insulin in patients with type two. and that might be presented as acanthosis, groans, So darkening of the skin um underneath the, the armpits. So, if a patient comes symptomatic, um then a single reading of either of these um is a suffice, will suffice to diagnose diabetes. Um And these are, these are some numbers that I would um definitely recommend uh HBA1C. So it shouldn't be on the type one side. It's not routinely used for type one diagnosis, but something to, to include for type two. Um if the patient doesn't have any symptoms and two of the same readings of these numbers, so a random plasma glucose are greater than seven, fasting, less than 11.1 or a HBA1C, greater than 48. Um on two different occasions, um is enough to yield a di di uh diabetes diagnosis. Um And so some features of type one diagnose uh type one diabetes which might point towards that um would be a rapid onset of symptoms, presentation under 50 ketoacidosis or DKA presentation, rapid weight loss BMI under 25 or a personal family history of autoimmune condition cos that and that can be all sorts of things. So in the nice guidelines, it says that if the diagnosis isn't particularly clear whether it's type one or type two, so you've done all the, the numbers, but you need to get a diagnosis of type one, type two. So they might have um they might have, you know, s some type one features but you're not completely sure if it's type one or type two, it's not very clear, then you can move on to some specialist tests. Um and some auto antibodies um such as the ones written here. So, c peptide anti il antibodies, et cetera. Um are some important ones that you can test. Um and the presence of these might suggest type one. Um OK, so I'm not gonna talk too much about the actual uh chronic management of type one or type two diabetes just because I think it's something which can be learned and some something which is, is should be learnt to be honest. Um But some principles is that Metformin is always first line. Um it's often gonna cause gi disturbance and at that point, you want to um offer mod modified release as opposed to a standard release. Um New guidelines say that um SGR T two inhibitors should pretty much be offered to everybody um who has established CBD S that's be hypertension, ischemic heart disease, et cetera or they have a QS score of 10% or higher. So, definitely have a look at a look at that and those are your flosin, er, drugs after that. You have, um, quite a lot of, uh, kind of leeway to see which ones you kind of wanna pick. But there are some contraindications to each and we'll talk about that in just a moment and that can help guide your choice. Um, and here we've got some HBA1C targets, which are worth learning as well. Um So there's loads of antihypoglycemics for uh type two diabetes and it will take longer if I, if I ask you about every single one of them. Um So we won't do that, but um some common ones are um biguanides. So that might be your Metformin. You've got sulfur urea, um You've got ma gluttons DPP four inhibitors, GLP agonists, se LT two inhibitors ACARS. Um And uh I'm not going to try and say the, the name of that one. But there's all sorts of antihyperglycemic and it's really important to also learn, I think um the action of, of how they happen. Um So um some drugs can increase, increase uh insulin secretion to try and drop the blood. Um some mess around with incretins, um which is closely related to insulin metabolism. Um You've got se ot two inhibitors which blocks the reuptake of glucose from the uh the PCT in the kidneys. So you end up peeing out a lot of glucose. Er, and then you've got stuff that works in the gi tract as well. Um, again, it's also really important to learn some, um, side effects of the most important or the most common oral antihyperglycemic. And that can help guide which one you might want to introduce. Um, so these are the ones which I think were most important. Uh, the things which I think, um, are worth learning. There's a long side effect list for literally every single drug. So we don't worry about learning everything under the sun. Um, but these are the most critical ones which I think, um, are relevant to, to learn. Um, and particularly definitely worth learning. Uh, for these ones. I thought it could be a good opportunity to counsel, uh, talk about counseling patients. This is something which likely comes up in OS stations and, and, and something which, um, I, in our case, both in our fourth year and our fifth year exams, we had to counsel er patients um on diabetes diagnosis. So in, in fourth year, uh, we had, we had to counsel patient on a type two diagnosis. Uh, and in fifth year we had to counsel pediatric, a 12 year old. Uh, I think it was or maybe 15 year old, sorry, on a type one diagnosis. Um, so definitely something which is likely to come up but not just in the context of diabetes, but in any chronic condition. So I thought we could talk about maybe, um, the way you would, you would come across cessation or the way that you would, you would tackle something like this, um, because it's very likely to come up. So the first thing you might want to do is always start by getting a quick history, um, of the condition. So, gauge how much the patient already knows about the condition. Um, the way that I like to do it is is always ask them what you're about to tell them. So I like to always say so how much do you already know, um, about what's been going on? Um And that, what that does is it really um, activates the patient. It makes, it makes it seem like you're getting them involved or it does get them involved. Um, and uh it makes the conversation a lot more engaging rather than speaking out to the patient for, for, you know, 10 minutes in the station or, or in a, in a GP appointment, 12 minutes. So I would always phrase it as. So what is diabetes? What do you understand about diabetes? Um, do you know what organ it affects? And then they would say, oh, I think it's something about high sugar and it might affect the pancreas and you say, oh yeah, absolutely. So this is, this is what happens when the pancreas doesn't quite work and you would fill in the gaps in their knowledge or correct them. Um, and that opens up a really good conversation and then you might ask why is it important that we control your blood sugar? Uh, and they say, well, it might be, I know it's important for my heart and you can say, well, yeah, actually it's important for your eyes as well. It's important for your kidneys. It's really important to stop you getting infections. And in the long term, it can be important in stopping you, um, from losing sensation because of your nerves. Um Again, throwing back the question in the patient's face, how are you gonna, or how are we gonna control your blood sugar? Do you, do you know any kind of ways that we can do this? Have you heard any of anything? And do you feel confident in doing this? Um And then they might say, well, maybe you can give me a pill and you can, you can come back and say, yeah, absolutely. So we can give you a pill. But first we might wanna start conservative. So it's really important that you, um, you know, improve your diet. Can we stop you smoking? Can we, um, have you, you know, drinking less perhaps, then we might consider doing some medications and then surgical. It's not too relevant in this case, but I thought it might, might be relevant. So if you were talking about Metformin in this case, and you were talking about, uh, you know, the medical management for Metformin Athletic is a really good acronym to use, not just for Metformin, but for every drug and this will ensure that you basically got everything down. So you wanna talk about the action which you now know um it basically decreases the amount of glucose that the liver um puts out. You wanna tell the patients when to take it. So, you know, at night time, how to take it. Yeah. Take it with a glass of water length of time. Well, this is something which you're probably gonna have to take for a very extended period of time if not the rest of your life. Um and a positive effect of this is that it's gonna lower your blood sugar, improve your eyesight or prevent damage from your eyes to your heart, et cetera. Uh There might be some tests that you need to do and important side effects. Um Is there any, does anyone know the most important side effects which um patients should be told about? Um for Metformin, it was on the previous slide. But um does anyone wanna mention it in the chat if anyone has any thoughts? Yeah. So gi upset is, is a really important one that's very common as well and that can be easily fixed by uh causing change into a modified release. Um importantly, there's also lactic acidosis and that's a rare but very serious complication. Um Look up the signs and symptoms for that, but if a patient feels really lethargic muscle cramps, um, feeling really under the weather. That's something which you want to, um, safety net. The patient about, um, and tell them where to seek help. So, with counseling, a patient, you want to address their concerns and offer support. So the patient might, you might say you need to improve your diet, but they say, I don't really know how to do that. There's no point just saying, ok, and then moving on, uh, can I offer you support with diabetes? UK, a charity? Um, they have a magazine which sends out recipes to patients. Um, can I support you in referring you to a dietician? There's a charity group in Camden Council which, um, where type two diabetes get, get together each week and, um, talk about different recipes and, and really try and be proactive with the support that you can offer. Cos that, that's something which goes quite a long way and, and I feel seems to set you apart when, when talking about things like this. Um, so I've got some specifics here for either type one or type two diabetes but, um, I should say type one, sorry, but freestyle Libra um, is a new technology for gluco sensing diabetes support groups. Um, you can give leaflets for healthy eating certain charities, er, and then certain sick day rules. Er, and as for any station, you always, always, always need a safety net, there will always be something which is important. So, uh for diabetes patients, it's DK A so vomiting, abdominal pain, um or hypoglycemia symptoms. Um, and that's some, some more stuff that you can talk about. So this is the next um, ba so if you guys want to um, have a go answering that, does anyone have any suggestions? So, uh just to summarize, it's an 18 year old woman who's presented with 30 minute history of left sided hemiplegia and weakness, some onset who's got a bit of an odd behavior and is confused. Um and she experienced a tonic chronic seizure in the ambulance. Um She was found on the kitchen floor with um her mother's insulin and she's got a past medical history of borderline personality disorder. What was the most appropriate action? Mhm Bye. Any suggestions in the chart renal impairment is a good uh suggestion for Metformin as well? Ok. So we've got uh take three blood glucose measurement. Any other suggestions, what are we gonna see? Yeah. So, um I think this one's difficult and I II think in all the sums that we've had, we've always had questions like this. Um So yeah, I II would go for D so it's always, always, always imperative that you secure the airway, especially even when you're doing SBA questions. Um The airway is always the first thing and you always want to talk about the airway first. So if you've got an option where you've got ABCD E Airways gonna kill first and securing the airway will always be the right answer. Really. Um Then if you're taking an ABCD E approach, then I think this falls into sea. So you wanna call the ICU, take a full blood panel, including cultures. Um And you can't rule out something like encephalitis meningitis. Um I guess with a history, it's less likely but it's something you probably might do. Um then you might move on to D which is don't have glucose. So then you would take the complete blood glucose and I think that would um yield you the diagnosis. What is the diagnosis in this case? What do we think is happening? Any suggestions? So this is um quite a quite AAA common presentation, it seems quite stroke or tia a. Um but yeah, hyperglycemia is the um the most important diagnosis here. Um And it's really important to know that hypoglycemia ie low blood sugar um especially with a history of kind of maybe a psychiatric uh history and an insulin overdose. Um Then uh yeah, hyperglycemia is the most uh likely. So the single most appropriate action. Um Yeah, I would say the initial action or the most important action. Um maybe I should rephrase that. What was the single most important action? And then I think securing the air, it will always be that um in terms of um yeah, I think, I think uh initial, yeah. Um so just the management of hyperglycemia. So it depends if the patient is conscious again, if they're unconscious or confused and you're worried about their swallow, like we mentioned with the DK A, we don't want them to aspirate. Um So you can give or glucose if they're conscious. Um If they are conscious but uncooperative, you can spread some gel on their gums. But if they're unconscious, we're worried about their airway, we're worried about them aspirating. So you would give IV glucose and then you wanna recheck blood pressures. Um And you can read about insul insulinomas if you, if you'd like to. Um but that's um a cause of hypoglycemia due to uh a, a tumor in the pancreas. Um And that can be um that can be checked by using the C peptide. Does anyone know how you would um differentiate if there is or I'll mention I'll tell you now, um if someone's overdosed with insulin or there's endogenous. So, a natural reason why the insulin's raised, um the C peptide will be raised um in a natural form of insulin. So, if the patient did have a pancreatic tumor that was doing this, um then the C peptide would be raised. Um But uh if it was uh if she was given insulin um by injection by overdose, then it wouldn't be raised and then uh the urine tox screen and a CT head would be important as well. So, you've got a 30 year old woman who presents to the ed acutely confused and irritated, she's complaining of abdominal pain and has vomited in the department. Um There's evidence, of course, crackles in the right lung base dog percussion. Uh You find a red card in a pocket and evidence of vitiligo on the skin and pigmented palmar creases. And those are the observations. Um So what is the most important immediate management for this patient? Any suggestions? Yeah, absolutely. So, I think c is, is absolutely what I was um going for. Um So uh does anyone want to suggest what might be going on here? So this is um the red card that was gonna be in the patient's pocket. So this is a steroid emergency card. Um And an anyone with uh a chronic diagnosis of this condition will have this emergency card because it can very likely precipitate into crisis. Um And the treatment for this is giving 100 mg of hydrocortisone IV bolus stats. So that needs to be immediately done. Um What are we thinking? The, the diagnosis is here? Yeah. Does anyone have any suggestions about the diagnosis? So, uh I think in this case, we're thinking about an Addisonian crisis. So an Addisonian crisis is um a state where there's um you know, a sudden uh or on a back maybe on a background of Addisonian disease or Addison's disease. Addison's disease is uh a reduced steroid level in the blood. So, uh corticosteroid and mineralocorticoid level is gonna be both reduced. So, the same patient? What is the most likely electrolyte balance seen on blood results? So, now that we know it's Addison's disease, which we said um is both mineralocorticoid uh reduction or, or a, you know, a deficiency mine Mineralcorticoid and a deficiency in Glucocorticoid. What is the likely blood test result? Does anyone wanna have a go? This one's a bit of a hard one, I guess. Yeah. Yeah. Absolutely. Yeah. So cc is the correct answer. So uh in this patient, we've got an Addisonian crisis. So like we said, low Glucocorticoid, so Glucocorticoid is your cortisol. So it's gonna be a low cortisol er and there's gonna be a high ACTH trying to cause the adrenal gland to release more cortisol in response to this low cortisol. So that's why you're gonna have a negative feedback mechanism there. Um And then because of the mineralocorticoid er deficiency, you're gonna have a low sodium level and a high potassium level. Er and those are the most important findings on uh blood test results. So in a patient with uh who's presenting like this, you might need ACTH or you will need ACTH and cortisone readings, you definitely wanna support with IV fluid bolus to bring up the BP. It's very low in this case. And that's because they're lacking the the um the sodium to maintain the BP. But also um the steroid effect of from Glucorticoid of of increase in BP and minera corticoids, they're likely to have a low blood uh blood sugar level. So you wanna give some glucose to support them. Um And like I said, they will have hyperkalemia due to the electrolyte imbalance. So we've already talked about the, the, the treatments for it and you wanna find the underlying cause which might have precipitated this. Um you want, after you give them the initial dose of hydrocortisone, you want to continue the infusion but you can change this to steroids um after, if they're in good condition. So, moving on to the adrenal gland, I think in the interest of time we will run over, but hopefully, we can finish it within the next 15 minutes and be done by, by 10 pass if that's OK. Um But just looking at the adrenal gland and, and thinking about the, the dysfunctions of the adrenal axes, um bringing it back to the anatomy, you've got your four zones. Um And in particular, we're gonna be focusing on er axes which are all or diseases, disease process of minera corticoids and glucocorticoids um and the, the medulla as well. Um So, Addison's disease uh or primary adrenal insufficiency um is when the adrenal cortex isn't producing sufficient er amounts of your corticosterone and your androgens as well. Er In particular, we'll just focus on the glucocorticoids and the um mineralocorticoids, but it's worth mentioning about the androgens as well. So, this is essentially failure of the adrenal gland to produce its hormones and these are the reasons why it happens. What is the most common cause in the UK? Uh Does anyone know why does this happen? Very, why does this happen the most in the UK? Why is this, um why does Addison's disease happen? What's the etiology behind it? Or if anyone knows the infectious disease which causes it, which causes the most common uh which causes it most commonly worldwide? No. So um autoimmunity. So that's Addison's disease. So, autoimmune destruction of the adrenal gland is the most common cause of this. Well, uh in the UK um but infectious disease, so, tuberculosis is the most common cause of this worldwide. Um You've also got bilateral adrenal hemorrhage, which might be worth mentioning. So this is when you've got meningococcal septicemia and this is particularly Waterhouse Friederich Syndrome syndrome, which might be worth reading about. So this mean you've got bilateral adrenal hemorrhage secondary to meningococcal septicemia. And that's why you've got a, a adrenal insufficiency. Um So this is primary adrenal insufficiency when the adrenal gland isn't working or the cortex isn't working. In particular. Secondary adrenal insufficiency makes sense when you look at the axes, but that's something a bit more upstream. Um also downstream. So this is commonly due to suppression of this axis due to long term uh steroids. So you might be producing lots of cortisol. Um And then you're suppressing the hypothalamus and anterior pituitary. Um And then when you withdraw these, these are just being chronically um suppressed and it doesn't go back to its normal state. So the C Rh and ACTH is um uh decreased. Um And then you get this very typical tanning of the skin which were pigmented palmic creases. So, just um will you find this, this, this, this tanning both in secondary and primary adrenal insufficiency or would you find it in just one? And why does anyone know? Sure. So, um so yes, sure. So, increased steroid use leads to secondary adrenal insufficiency. Um So if you, if you imagine that steroids are basically just cortisol. So when you take oral steroids, you're increasing the cortisol level just because of feed negative feedback mechanisms which happen in um all kind of endocrinology, er or in los of the axes, um high levels of cortisone will cause a suppression of the ACTH and suppression of the C Rh levels. So, there's gonna be a suppression of the hypothalamus and a suppression of the anterior pituitary. So, if you're taking steroids for so long, um there's gonna be a chronic suppression of both the anterior pituitary and the hypothalamus. Um and therefore, when you withdraw these steroids, actually, these, these um structures are gonna be in such a state of, of um suppression for so long that they're not gonna be able to bounce back uh to create more C Rh and AZT H to cause er the endogenous release of cortisol. So you've kind of just damaged the negative feedback mechanism if that makes sense. Um So, yeah, absolutely. So this tanning is only gonna happen in primary because um in the secondary case, you, like we said, we have less ch less ACTH and this ACTH is what's causing the tanning for this patient. So it's similar and buys the melanin receptors. But because um this th this loop that we're making has low ACTH, um it's going to er not cause that tanning so busy slide necks, but these are some of the symptoms that you might experience um as part of adrenal insufficiency. So just think of, you know, the opposite of having a steroid crisis. So you wanna be, you're gonna have a low BP, uh you're gonna be tired, dizzy, fainting, um vomiting, abdominal pain, anyone who presents with vomiting and abdominal pain, this needs to be AAA an important um differential that you put up there. So even the first patient I mentioned uh right at the beginning with DK definitely could have um this a crisis definitely could have been a a valid differential for that. It causes lots of mood symptoms which are often forgotten a depression or psychosis. Um just like um yeah, sorry. Er and it can go cause shock coma, raise temperature. That's the a so crisis that we just saw. So in the test, you're gonna see a low sodium and high potassium because there's less mineralocorticoid, low glucose because you've not got glucocorticoids and then there's some other blood findings there. Um But diagnostically, you, you want to do a short ACTH stimulation stimulation test. So you give ACTH um and then you measure the cortisol before and after you give that synthetic ACTH and because the adrenal gland or the adrenal cortis isn't working um in uh Addison's disease, um you'll have a low cortisol but if it rises um up above 550 then you know that, that actually the adrenal gland is functioning as normal. So you, you think of other reasons why it might be, might not be primary adrenal insufficiency. Um and you can also do a serum a ACTH, it will be high in primary and low in secondary. As we just mentioned, uh specific test for Addison's disease. 21 hydroxylase adrenal autoantibodies, which might be worth mentioning. Uh The long term treatments is hydrocortisone daily or, or 2 to 3 times a day. This is really important treatment. And if a patient is sick, um it's really important that we continue this. Um you want to give them mineralocorticoid as well to correct their BP. But essentially, if their adrenal glands aren't working, you just need to give hormone replacement therapy just like you would. Um for a type one diabetic, you'd give insulin or for someone with hypothyroidism, you would give them thyroxine. Uh It's really important to give steroids. Um If they've got a period of illness or febrile febrile sickness, then you add uh hydrocortisone or double it. Sorry. Um And if you are counseling a patient on Anderson's disease, you always wanna give them II M hydrocortisone if they've got, you know, uh food poisoning and they can't take oral steroids and that's um important. Uh and then some long term things is you wanna check their BP review for other autoimmune diseases and always give a steroid card because these patients can get unwell very quickly. Ok. We'll speed move through but we've got a 45 year old man with known men two A syndrome. Um, and he's admitted because of a pneumonia, he complains of severe pulsating headaches and feels dizzy as if about to die. What is the most appropriate initial management, given the most likely diagnosis? Yeah. Ok. Ok. Does anyone have any ideas about this one? Mhm. Right. So, um, this one we're kind of thinking, um, was kind of the opposite. So he's got a really bad headache. Um, maybe it was with me, not, not giving you um uh kind of uh, um observation. Sorry. Um, but if the patient had a really high BP, if I added that onto it, um, and it got men to a syndrome, I think both in combination. So if you know, if you know your men syndrome, which are worth learning, uh you'll know that pheochromocytoma is, is the most common or, or the most likely diagnosis in this case. So, um, these are the symptoms. So you're definitely gonna have hypertension. So I probably should have given the BP in this case. Um, you're gonna have sweating, you're gonna be a headache, a headache and you're gonna have, um, quite, you're gonna be quite anxious and panicky. Um, and that's because of what, uh, fair. So one of the most important things is they have a really high BP which you need to stabilize. So, once we stabilize the BP, um with an alpha blocker, which is the first thing that you always want to um give in in these patients. Um Often a second drug can be added. And the indication for that is if the patient has tachycardia. So you would give um IB uh propranolol. So you would give a beta blocker after giving an alpha blocker. Um And that's because um it doesn't necessarily need to be given. Um but it always needs to be given after you give an alpha blocker. Um So we know it's fair chromic and we'll talk about what that is in just a moment. But what investigation is gonna confirm the diagnosis, what it's gonna be a 24 hour urine metanephrine. And this is gonna be the gold standard to diagnose this condition. So what exactly is a pheochromocytoma? So it's catecholamine. So I just think of it as adrenaline producing tumor. Um It happens in the adrenal medulla and this is a sympathetic paraganglionic cells or chromaffin cells in the adrenal medulla. Er, and that's gonna cause a surge of adrenaline um or your catecholamines and that's gonna give you these symptoms like a headache. Um, a really high BP and feeling really anxious. Uh It's kind of just thinking, imagine if you had lots of adrenaline pumping through you at all times. So it's often in the adrenal or medulla because that's the area that actually secretes the catecholamines, but 10% extra adrenal and they might be at the aortic bifurcation, for example. Um, and in terms of the diagnosis, so this, um, once you've confirmed it with 24 hour urine metanephrines, you want to localize a lesion with a CT or MRI and you're likely to see some sort of lesion in the adrenal medulla or somewhere around there. Er, and the treatment is to actually cut it out. So, because it is a tumor, you just want to do some surgery after you've controlled the BP with alpha and beta blockers. Um, so that can be a matter of 4 to 6 weeks even, um, after first presentation. But if someone's come to with this, this presentation, you're, you're suspecting that and then you do these, these tests and then you need to be really sure that the, the BP is controlled and then worry about the surgery after, um, I guess the main learning point, which I would say at this point is, er, alpha is er, really important to give first alpha receptor blockers and then beta blockers, er, only if there's a reflex tachycardia. Uh And then after this operation, you wanna mo monitor the BP and the urine metanephrines following the operation to ensure that you've actually got everything out and there is no reoccurrence. Ok. So we have um a 35 year old woman who's being investigated for secondary hypertension. After, after presenting with muscle weakness and raised BP, you've got hypokalemia and hypernatremia which for the following er which the following is not a possible cause I think just for the in the interest of of time, I'm gonna answer this one. but maybe some of you can have a think about this. Um but the answer that I've got is Bartter syndrome. So, um the kind of the, the diagnosis that we're thinking um uh about here is hyperaldosteronism. So that's when we've got a mineralocorticoid excess in the body. Um And that's what gives you the hypokalemia hypernatremia. So this is the opposite to Addison's disease. So, Addison's disease is a deficiency in those um mineralocorticoids, whereas uh hyperaldosteronism is an excess of aldosterone, uh ie or mineralocorticoids. So you get that hyponatremia and hypokalemia on on blood readings. Um And I think all the four other four options um ex are, are kind of self explanatory about why that might be the case of bilateral hyperplasia of the adrenal glands. Of course, they're gonna be um they're gonna be um releasing more aldosterone and you just want to use a aldosterone receptor antagonist to treat that. Um If you've got an adenoma of the adrenal gland, you just wanna cut it out. Um Bartter syndrome uh is, is not a cause of hyperkalemia, hypernatremia. Uh Again, with a car with a adrenal carcinoma, you would just want to cut it out if that's causing um the hypoaldosteronism. Um and this is just a, a niche cause which I thought I might add on to um the choices. Ok. So we've got a low renin, high aldosterone level. What is the next best investigation to confirm the diagnosis? So, again, looking at our negative feedback loops on your r renin angio renin angiotensin aldosterone system, um we know that a low renin will lead to a high aldosterone. Um And that's because uh the hy aldosterone will inhibit the renin secretion and, and it will be decreased. Um So, yeah, we know that there's a problem with the adrenal glands and the best way to um diagnose that would be doing a ct abdomen and that might help differentiate between the different causes of um excess uh mineralocorticoids. Uh If that is um that doesn't yield any particular uh you know, diagnosis or doesn't, doesn't make anything clearer, then you can do adrenal vein sampling. So, taking the output from both the adrenal glands and measuring the aldosterone levels, seeing if the left or the right has a particularly higher level of aldosterone that is secreting and therefore, you can help localize the lesion and know. Well, actually it's the left adrenal gland which is causing the problem, er and then go onto some further imaging from that. Um Again, so this is just a normal axes. Um So again, in hyperaldosteronism, uh you've got a lesion in the adrenal gland in the adrenal cortex and that's causing an increased aldosterone and that's going to inhibit the kidneys release of renin. So you're going to get the classic increased aldosterone with uh a low renin ratio. Um and these are some of the er symptoms that you get so hyponatremia with hypokalemia uh with uh you know, a raised BP hypertension uh and potentially volume overload as well. Um So, just to finish off, I'm really nearly finished. Um after this, I think it's in the last couple of slides. Um But I thought just to wrap up on the Cushing's Syndrome, um it could be a good idea to talk about how to approach an examination, you're less confident. So, if you were asked in an exam to perform a focused Cushing's Syndrome examination, I don't think many people would know how to do it. Um including, you know, if I walked into an exam and I saw that I would, I would be pretty shocked, but also um would have no idea what to, what to do, but it is a valid examination and there could be stuff like that that comes up. Um So it's always important just to take a really systematic review. So ju just like a Parkinson's exam or hydration status and not the thyroid exam, just the, the kind of niche exams simply just be very symptomatic systematic. Sorry. Um So wipe a QQ, so wash your hands, introduce yourself as a patient. Um, ask if they're in any pain, expose them adequately. Um, you want to reposition them and ask them if there are any pain or discomfort. Um, and that's always the, the, the, the way to start any exam. Look at them from the bedside. Is there any medications around, is there any steroids around that I might be taking and then look at the patient themselves. Are they acutely unwell or are they comfortable? Um, some things which you might see in someone with, uh Cushing's syndrome is they might be particularly large in habit, central obesity in terms of the distribution as well. Um, they might be particularly red and have this buffalo hump with this, which is a supraclavicular fat hump. Um, on the top of the, er, on the top of the neck and then what I like to do is start with the hands, go to the neck, look at the face and then do the chest, do the abdomen and basically just take a systematic way um over your, the whole body. So in the hands, you wanna check the pulse and the BP, which you might expect to be raised in Cushing's syndrome, which is an excess of cortisol. Um The the skin might be thin, you might have hyperpigmentation because of raised ACTH um fingerprint marks if they're diabetic, check their arms for their movement because uh we know they can cause muscle weakness, uh then you can move onto the face. Um So they might have moon faces, facial acne has seism because they have access to the androgens. Um the inside of the mouth or thrush for steroid use. Um visual fields assessment is really important and we'll talk about that in just a moment. But uh biotemper or hemianopias are likely uh cause of, of of Cushing's syndrome in the form of Cushing's disease. So, doing a quick visual fields assessment, which is part of a cranial nerves assessment. So it's when you ask them to c uh cross their eyes and, and do this this on each eye. Um that can be really valuable and something which you should definitely include in a Cushing's Syndrome. Uh assessment, check the chest for gyne capacity again with uh androgens uh and the abdomen can have purple, abdominal stray. So these are some of the classical symptoms of Cushing's syndrome. Is there an abdominal mass that you can palpate? So, again, Cushing's syndrome is because of an excess of cortisol. So there could be an adrenal adenoma which is causing that. So is there something that you can actually feel. Um And then these are some of the, the, the symptoms you should also talk about again on the, the legs. Is there any bruising or thin skin, any weakness? Um But the, the point here is I just wanted to explain all the symptoms of and signs of adrenal. Oh Sorry Cushing's syndrome. Um But also just explain how to do it in a systematic way. And if you're unsure about any sort of examination, it's always good to start from the hands and make your way up and then back down. Uh and that can be really helpful um mood exams. So we know that Cushing's Syndrome patients because of the cold, so excess uh can be irritable depression uh and often psychosis as well. Um So you might want to perform a, a mental state examination or mention that you're gonna perform a mental state examination. Uh And then these are some further tests that you want to do. So, er, very nearly finished, but just talking about what exactly is Cushing's syndrome. So Cushing's syndrome is an excess of cortisol. So we talked about the adrenal gland and we talked about each of the sections and what happens with an excess of it and a uh a, a deficiency of the cortisol is when we, we've got an excess of cortisol in the Cushing's Syndrome. Um So there's all sorts of different causes. Um, but I think because ii in things when there's so many different causes, it's always really good to categorize your answer into certain different ways. Um Because then it becomes a lot more organized in, in the way that you're presenting it. And it's a lot easier, easier to follow when you categorize things. So there's ACTH dependent causes and ACTH independent causes. So, dependent causes would mean essentially there's an increased ACTH for whatever reason and that's causing the adrenal gland to release a lot more cortisol. So that will, that's what we call ACTH dependence. So that's when the ACTH is raised. And therefore, the cortisol is already ra a also raised and anything upstream of that. So if the C Rh is, is raised, that's also gonna cause the ACTH to be raised, et cetera. Um independent causes are causes where ach isn't really the isn't really, you know, bothering the adrenal gland to cause it to release more cortisol. Um And we'll just talk about some of the reasons why, why this happened. So, ac ACTH dependent causes, you can have the classic Cushing's disease. So this is when you've got ACTH secreting pituitary, adenoma and the on the anterior pituitary which causes adrenal hyperplasia. And then that's what's gonna give you that bitemporal hemianopia. So it's gonna be pressing on the optic chiasm in the middle of the brain and then you're not gonna be able to see on both sides. Um And that's your classic um presentation and it can be imaged er with pitu MRI. Uh another ACTH dependent cause is um when there's ACTH being produced from somewhere else. So not the anterior pituitary. Um that's when. Yeah, in Cushing's disease, the anterior pituitary is causing an increased A th which is causing increased cortisol. There are some causes of small lung, small lung, uh small cell lung cancer, which can um or some small lung cancers which have paraneoplastic features which greatly increase the amount of ectopic um ACTH. So they'll release it from the cancer in the lungs and this is cause causes a greater uh lots of pigmentation. So that is something which um is similar to er Addison's disease. Um and very rarely, you can have increased C Rh production ectopically from particularly medullary thyroid cancers and prostate cancers. Um So those are your in. So your dependent causes. So they're basically upstream of ACTH. Uh but then you also have um independent causes. So, again, quite as you would expect if there's an adrenal adenoma or hyperplasia, particularly of the adrenal gland, um that's not really being caused by ACTH. So that's an ACTH independent cause um and oral steroids. Um If, if patients are on long term oral steroids, this can be a common cause um of uh Cushing's syndrome, of everything there. What is the most common cause of Cushing's Syndrome? Does anyone want to suggest this? And this will be the last um question I present after we after a year. Does anyone want to suggest what the most common um cause is? Ok. So we've got bilateral adrenal hyperplasia. Um So that's Cushing's disease. Ok. Yeah, that's valid. Anyone else wanna have some suggestions? No. So, so of everything that's on the screen at the moment, the absolute most common cause of Cushing's syndrome, iatrogenic. So it is oral steroids for a long period of time. So the most common cause of Cushing's syndrome is exogenous steroid use. So, patients who are on long term steroids, um particularly maybe for rheumatological conditions, uh patients with polymyalgia, for example, er will be on oral steroids for a long period of time. Um and it's often iatrogenic. So, I iatrogenic meaning caused by, by medicine, it's caused by, by healthcare. Really? Ok. So that's the most common cause of all of them. Does anyone know of the green ones? So, ACTH dependent causes which one's the most common? No. So Cushing's disease um of the ach dependent causes er is the most important one. Yeah, or not most important. So the most common but again, these, these um are this this and so all four of these other than oral steroids are exceedingly rare. Um but Cushing's disease is the most common of the rare ones but oral steroids is, is the the principal cause for Cushing's uh syndrome. So finally, uh actually actually the last slide um how to diagnose Cushing's disease or Cushing's syndrome? Sorry. Er and understand the etiology for it. So just generally this summary, I always got confused about it. So I think it's worth mentioning but the dexamethasone suppression test. So this is the way that we diagnose Cushing's syndrome and get an idea about why um there is a cortisol excess. So, dexamethasone ordinarily causes acr h decrease from the hypothalamus and that leads to a decreased ACTH from the anterior pituitary, which leads to a decreased called cell from the adrenal gland in the dexamethasone suppression test. Uh The first line is always a low dose dexamethasone test. So you always want to start with, uh you always want to start with low dose um dexamethasone. This is a screening test and we'll confirm Cushing's syndrome. So if you're given low dose dexamethasone, uh and you end up with low cortisol, um that's normal because if you, if, if you think about it, it's gonna cause less C IH which causes less ACTH and less cortisol, that's expected if you give dexamethasone. Um and the cortisone ends up being high. That's strange. And then you, you know that you've got Cushing's syndrome. So, Cushing's syndrome is uh the syndrome of all the symptoms and signs of increased cortisol. But then you need to think of like what is the cause of the Cushing's syndrome uh out of all of these options here and that's where the high dose test comes on. So if you've got a positive result or a confirmation from low dose dexamethasone that you've got Cushing's syndrome, you then move on to giving high dose dexamethasone. And if you're given high dose dexamethasone, um and you end up, uh you end up with a low cortisol, you end up with Cushing's disease on as the diagnosis. And that's because um even if you give a lot of dexamethasone, it's gonna actually end up causing um a downstream reduction in ACTH. Um because it's, it's still, the pituitary adenoma is still responsive to C IH and still sensitive to it. Um However, if you give a high dose dexamethasone and you end up with um a high cortisol, then you're worried that actually it's not ACTH dependent and you're, it's still kind of um coming from somewhere else. So, um if you have a low ACTH, that means that the adrenal gland is causing this increased cortisone and that's causing a negative feedback back onto the hypothalamus. Um sorry, back onto the anterior pituitary. Um And if you have a high ACTH like super high, then you think that the ACTH is coming from somewhere ectopic ie more so, lung cancer or so or somewhere else. Um This is something really important to, to learn um something to get your head around. But once you get a around, put your head around it a couple of times you, you, you, you'll definitely understand it but understand it in relation to er this diagram cos this really helps. Um and it means that you don't end up memorizing it, but rather you understand it physiologically. Ok. Well, I think that's the end, sorry for, uh, overrunning, I think. Um, yeah, I think, I think I spent a bit too much time at the beginning but, um, it'd be really good to get some feedback.