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Uh Bianca. Can you still hear me? Ok. Yeah, you're still ok. Um, yeah, that's ok. You can just make a start if you want. Yeah, for 37 participants and they'll, like, probably join as you present yourself. Yeah, that sounds good. All right. Um, hello everybody. I'm Craig. Uh I'm going to be talking a bit about endocrinology and so this even I'm gonna talk mostly about diabetes and thyroid. Like that's the main thing you need to worry about for your exams. Like if there's, I don't know, 10 questions, 8, 10 questions in your exams. Most of them are going to be about diabetes and thyroid. Um, the other stuff people find quite confusing and they'll go over that as well because it's quite difficult to get into your head. Um, Cushing's and steroids and like adrenal insufficiency is quite important for us as well. Um, so just a bit of physiology before we get into anything else. Um, just remember that if we talk about something that's primary, this is with the, the, the hypothalamic pituitary end organ axis. So if something's primary, we're talking about the effect, like it's usually an adenoma or a lack of, um, hormones coming out like the thyroid, the adrenal gland or the ovaries or something. Um, if it's secondary, if you can see a pointer, um, it's something that's in the pituitary itself and if it's tertiary, it's the level above the pituitary which are really rare. And again, pituitary and hypothalamus is usually again, adenomas. Um, the one exception which we'll talk about is hyperparathyroidism. It's sort of something you need to learn about by itself. But we'll, we'll talk about that at the end. Um, and just for terminology, we'll talk about things that are, are, are hormones that are endogenous. That's things that your body produces. Um, and exogenous is things we give to patients. Um, so diabetes again, I said is the most important thing we're going to talk about. So type one diabetes is the autoimmune beta islet destruction. So you've no insulin being produced, uh, type two diabetes as you get like later in life, it's um, higher peripheral insulin resistance. The w the wh O, checklist is, is on the screen there. So that's, er, so the numbers are, it's pretty hard to remember, but the numbers are 11.1 and 11.1 for your oral glucose tolerance test. And it makes sense like your blood sugar is gonna be low after you fast. That's less or greater than seven is diagnostic for diabetes. And remember if you're symptomatic, you need only one measurement and these are the symptoms like polyurea, polydipsia, um, unintentional weight loss, opportunistic infections, things you usually get with type one diabetes and type two diabetes as well. Um, and if you're symptomatic, you need two of those measurements just across different, usually weeks apart. Um, HBA1C, usually in type two diabetes is more commonly being used for diagnosis. And remember the number 48 is the golden number that's diagnostic for diabetes. This is sort of another one. It's difficult to remember the exact numbers. But again, just remember if you fast, your blood sugar should go down slightly. Um Obviously, whenever you eat your blood sugar goes up. So HBA1C, the numbers are 48 I said it's diagnostic for diabetes. 42 less than 42 is the normal range. Um So in between that is uh prediabetic for fasting for fasting blood sugars, it's greater than seven, as we said, is diabetic less than six, you should be as normal. And then in between that, so 6 to 7 is prediabetic or impaired fasting glucose makes sense. Um And then after your 75 g oral glucose tolerance test, it's 7.8 to 11.1. Uh and that's your impaired glucose tolerance. So I gt um pretty hard to remember, but this diagram makes it a little bit more straightforward. Just remember those sort of intermediate numbers. Um In type one diabetes, it's usually what we call a basal bolus. People are treated by it and it's usually that in exams, like people can be all sorts of things, but it's pretty straightforward here. So, um, in short acting. So this is like a mix of, you usually get short acting insulin, like novo, rapid pre meal and then you get your longer acting like Levemir post meal. Um, so it's, and then, yeah, this is usually four times a day. Usually get your Levemir, like at night time. Um, it says there it's the most common in type one diabetes. You can get anything like you can be on pumps, you can be on all sorts, but usually in exams like this will be what patients are on. Um on type the most common it says there in type two diabetes is, but again, you see anybody with it is what's like a mixed regime. So you, you're, you're on like twice daily insulin and this is a combination of short acting insulin and long acting insulin that's usually called Nova. Um in any patient with diabetes as well. Not just type one, it's just on this slide. Uh you need to remember that patients. And then again, for us, you can um find some patients on this. Um patients should attend or like it's usually annual every other year, especially later in life or if they have diabetic eye disease, they need to get retinal photographs from the optician and they need to get regular U and e usually like every year, every couple of years to assess their kidney function and then do as attend podiatry if relevant. Uh, this was a station in our third year. I was pretty terrible at it because I didn't know these questions. But if you know these questions, it is pretty straightforward. So, first of all, for us, I can't remember what it was. I think it was a patient. They either just had DKA or they just had a hypoglycemia episode and you needed to counsel them and figure out exactly why that happened and it turns out that they're control at home. They just were a pretty bad patient. Like they weren't controlling their diabetes well, at all. Um, so you need to think first. So, just the control, you need to think. Are they monitoring at home? How often? And when they monitor at home and like, what sort of readings do they get? Do they keep a booklet and that sort of thing that's helpful if they get an, a, like if they do keep a record, can I see it? Um, you need to consider, do they get hypos? Do they have what's called hypo awareness? Do they get that usual? Like, some people get confused, thirsty, um, a bit jittery whenever they get hypo, do they know what it feels like when they get one and then try and work out if they do get them? Why, um, do they know to self ajuste insulin? And, um, are they aware of, like how to do that. Um Need to ask, do they rotate injection sites? Remember some people with insulin, you need to inject in different areas in your body. So usually it's like both sides of your abdomen, your leg, your buttock, and all those sorts of things. If you keep injecting on the same side, usually if somebody's right hand and it's here, there is a preferred side, but you can get like hard lumps underneath your skin. Um And this is important because it, it affects the absorption of insulin subcutaneously. So people are having really bad control, but they're taking their insulin while it might not, it might not be um just absorbed under the skin. I need to ask as well. Do they have like, do they know their most recent HBA1C? Um In my station? I probably asked about one or two of those questions. I was terrible, but you know, at least you'd know that. Now um the sick day rules is a big thing in endocrinology for it's for insulin and for steroids, you need to know over steroids later. So the number one thing is do not stop insulin. So if somebody's sick, people think, oh I'm not eating and drinking, you still need insulin in your system because you'll always have like a baseline level of insulin. If you don't take insulin, your body will just go into DKA, which we'll talk about later. Um So you encourage people to eat and drink as much as they can. Um, and obviously if they're sick, like their blood sugars are going to go everywhere. They need to check that and then check ketones and be wary like they need to know what the EK A is and the risk of them going into it. Um, and then just safety net and the same with anything. Like if somebody's chest pain, like go to the hospital, if somebody's nausea, vomiting, if they're breathing, if they're confused, if they're showing signs essentially of going into DKA, send them to the hospital and make sure they know what to do. Um This was a final station a couple of years ago. It's probably quite advanced for a third year, but it's probably, it's something you should really be aware of anyway. Uh pretty much you're given like an inpatient insulin prescription sheet and you need to see whether, you know, you need to potentially adjust it. So you need to see, are they having any recorded hypo episodes or are they running too high? Um You can see there, do you see the, the column that says CBG that's capillary blood glucose and that's what the nurses or healthcare assistants will check before they get a meal and then they usually get them over it anyways. Um So you need to establish like, what's the baseline control in these sorts of stations using those questions we asked, you need to think like, why are they having bad blood sugar control. Um, in hospital, it's usually because people are on steroids, which we're going to talk about give you really bad hyperglycemia. Um People are usually septic people's diet in the hospital is terrible. Like you being on the ward, you usually see people's um side tables stacked with treats because the food's not very good. Um, you need to identify the pattern as well. This is the safety thing. So you need to think does the long acting or the short acting insulin need to be adjusted? So if it's high pre meal, you need to think what's the insulin that's acting on that. So if it was like before lunch, your insulin was high, you need to think the insulin is acting on. That is the green one is a color coded chart. It completely makes sense. Um If it's overnight, if you wake up and your blood sugar is, I don't know, like 23 that's way too high. So the insulin that needs to be adjusted is the long acting the left mir like we talked about earlier. Um, and again, safety people, it said in the feedback of your, of the station of this in third year and final year. Um, if the blood glucose is low, you need to reduce insulin and if it's too high, you need to give more insulin, you need to get that the right way around. It's hard to like it's easy to get rather than a that sort of thing. Um And as well, you need to think of the 10% rule this, it's a big safety thing, like you can adjust these incrementally over the space of several days. Um It's kind of, it's different for every patient, but a, a rough guide is the fact that one unit of insulin reduces glucose by two or three millimoles. So this patient here is on 10 units. Um So you'll only really like, you know, add one or two units on them. Um So to talk a bit about the treatment of type two diabetes, um it's quite complicated and I know there's a lot of drugs but and I say this about a lot of things so far, but it's something I just had to chuck into my short term memory like the day before I could never remember them. Um So I just try to remember like a few points for each things, for each, for each of the drugs. Sorry. Um So the, the number one, the the first line is obviously Metformin like everybody and their granny are on Metformin. Uh It's good because it's weight neutral. Um The the the main teaching point is it's contraindicated um in chronic kidney disease. So if your EGFR is less than 30 I haven't written it there. But you also need to remember um BC, you know, if somebody has an AK I do you know the damn drugs. So diuretics, ace inhibitors, Metformin and NSAIDS. Those are the four drugs or the four classes of drugs, not diuretics. Sorry. Yeah, it's diuretics. Ace inhibitors, Arbs, Metformin and Nsaids. You need to think about stopping. Uh, if somebody has an acute kidney injury. So, Metformin is one of those drugs. Uh, Sulfon aures is one of, there's a few of these drugs that are the second line drugs. Um, and it's the one that has a, a big hypo risks. Um, very few of the other ones do. Uh Pioglitazone is another one of those second line drugs and it's quite a, it works well but it's quite a dirty drug. Um, so it causes weight gain, which if somebody's already overweight you're not going to want to do. Um, it causes edema and heart failure. So somebody's already overloaded. Pioglitazone is contraindicated. Um, and there's a pretty substantial risk of bladder cancer as well. So you need to, to counsel a patient on that. Um, the rest of these drugs I got confused by because their names are similar and I'm sorry if I confuse you guys, but it, I II don't know, it just confused me. Um, the DPP fours which will usually be like SITagliptin. Um This is, it's another one of the second line choice drugs. It works well and it reduces weight. I think they're just quite expensive. Um, I might have made that up as well. Um, glutide like, or the G LP one analogs. This is like semaglutide, which you've heard the names like Ozempic. If you heard all it's a drug, all the celebrities are using to, to lose weight. Um It was originally a diabetic drug and it's useful for patients that are overweight for the same reason. And then it is the only of, of course, obviously insulin is given subcutaneously. All the others of these drugs are orals and then this is given subcutaneously. Um and then the S DLT two inhibitors are really, really important and you, you do need to know them. Uh So, II remember the names like Slozen, like dapagliflozin um flow is like, do you know urine flow you talk about? Um So that's how it works. It excretes sugars out through the urine, uh which is good because it's really good for treating type two diabetes. Uh It's really useful in cardiovascular disease as well. It's cardioprotective. Um The only thing is sugary urine is really good for diet for um like bacteria. So there's a quite a substantial risk of UTI S with SC LT two inhibitors. Um And you need to remember quite importantly now, the risk of you glycemic DKA in AK is so there's quite a move to it. I know I just told you about the damn drugs. Uh There's a move to, to teaching people about sad man um which includes SGL T two inhibitors. That's something you'll always see. I actually saw a couple of weeks ago, somebody had a, a, an acute loss of their, like their, I don't know, their creatinine rose substantially and their fr went down. So they, and they were on an SGL T inhibitor and it was held. So it makes sense. Um I know when, when people are giving these sorts of talks, everybody always talks about nice guidelines and they'll honestly, this one's pretty straightforward and it kind of makes sense. It's worthwhile passing your eye over. Um So pretty much just diet and exercise first, then Metformin, then any of these here, second line drugs that we were talking about. And if they have cardiovascular disease, that's when you want to get onto the SC LT two inhibitors. Um completely. Yeah, that makes sense. So for counseling, the long term risks of diabetes, we talk about microvascular and macrovascular complications. Um and yeah, so if somebody has poorly controlled diabetes, the the sort of things they can get, it's easy to remember as well. You know, we talked about the screening that you need to do for diabetes. That's what you do for microvascular complications. So your retinopathy is your like diabetic retinopathy. You screen for with your eyes. Nephropathy is what you screen for with people's kidneys. Um and then neuropathy again, the nerve damage and macrovascular complications is the things that really limit people's lives like heart attacks and strokes. So now to talk a bit about the d the diabetic emergencies. EK A is really high yield. Um This is how a lot of people end up being diagnosed with uh type one diabetes. Uh And again, I talked about it earlier, but just to remind you, so no insulin because your pancreas has been fried. Um It means no glucose gets into the cell, which means your blood sugars rise, which means ketones are used as body fuel and ketones are acidic or well, the breakdown products I think are acidic. I don't know. Um So that causes again, so it causes hyperglycemia because you're not utilizing your fuel. It causes ketosis and it causes acidosis. Um This is one of the, and that's the diagnostic criteria. It's one of the times in the hospital you'll see somebody with an uh an acidosis. Remember your normal range is 7.35 to 7.45. You'll see people in DK A with an acidosis of like 7.1 and usually that's approaching not compatible with life, but people can survive that with DK A. Um the treatment because of the laws of osmosis. If whenever people arrive in the hospital at DK, they're usually really, really fluid deplete. So your job as the F one will be to hang that 1 L bag of 0.9% saline over the first hour. And then I can't remember it's usually one hour, then two hours, then two hours, then four hours or whatever. Um And yeah, so also just try to try and find it whenever you're in the hospital to look at the, the DK A protocol. Um It's usually pretty laid out, it's usually pretty IOP proof. So it's worthwhile having a look at um the main risk to think about whenever you're treating somebody for DKA is cerebral edema. Um especially in page, you learn more about this, like giving that somebody that much fluid. Um you're at risk of um hipping somebody in cerebral edema, which is is can be fatal. So you need to think about and I think it might be on the DK protocol. I'm not sure um about looking at somebody's D CS. Um I'm trying to think if they have an altered mental status. Um if they're dropping D CS or they're becoming more confused for any reason, you need to think about this and try and prevent it. Um And yeah, so the fixed rate insulin infusion is what you give. So it's 0.1 units per kilogram per hour, it's on the sheet as well. So for the 70 kg man, in that first hour, you'll give seven units for the infusion and potassium is used in replacement. So um so if somebody has not to make it confusing, but somebody has hyperkalaemia, you give insulin, so insulin reduces potassium and reduces sugar. Um So whenever you're treating somebody for hyperkalemia, you need to give them sugar. And if you're treating somebody for AK A which is too much sugar, pretty much um you need to replace the potassium. Um which kind of makes sense. Uh hypoglycemia is pretty straightforward. Again, it could be an ay station. Uh The hypoglycemia kit and the algorithm are pretty idiot proof. Uh A few things you need to think about are stop anything. Like whenever somebody has an AK I, you need to stop giving drugs that are potentially going to make that worse. Um So therefore you need to stop any um, drugs that are gonna worsen your hypoglycemia. So if there's an IV insulin infusion, you need to stop that. I need to think about adjusting any subsequent subcut insulin. And you need to assess consciousness pretty much. The whole point of it is how conscious are they like, are they awake? You just give them like gluco tabs. If they're completely unconscious, you give them like Im Glucagon or IV glucose. Um And then once you've fixed that, once you've fix them, you don't walk away like, well, you, you, you, you try and encourage them to take something like longer acting like bread or something to, to keep their sugars going over a longer period of time. I'll not labor the point on HHS because it's quite complicated. Um, but pretty much it's just DKA but for patients with type two diabetes, um, the main difference is the mortality rate. It's really serious, like it's 10 to 20%. And actually, whenever I was in Antrim in third year, there was a patient there that um I saw in the ward that ended up dying from this like it's really, really bad. Um They usually like, you know, patients need to be treated in HD U with specialist care and all, um you'll see a lot of things in endocrinology is it's, it's usually picked off by like a physiological stressor. So that's usually like an infection or dehydration or something. Uh And the treatment, the, the, the concept is pretty much the same as DKA. So you need to replace fluids. Um And the big thing actually because this is, it's in hyperosmolar state. If you remember your blood being hyperosmolar, um makes it more likely to clot. So you a big part of the treatment of, of HHS is Cine. So you need to stop people from clotting. That's usually it can be what, what potentially kills people. So now to talk a bit about thyroid disease, uh we're gonna talk about your hyperthyroidism, your hypothyroidism, um some thyroid status exam stuff for acies and then the emergencies. Um So in hyperthyroidism, the features we talk about are obviously tachycardia heat intolerance. I've never seen somebody in a clinic, like they'll be absolutely sweating, like they're way too warm, they've lost weight, they'll be quite anxious and irritable and they'll have loose stools and the thing with periods can be quite confusing with hyper and hypothyroidism. But I always remember it like, do you know the, the um whenever you have like a young fit female with a low body fat percentage. Sometimes they, they can get like quite irregular absent periods. I think they're pretty much the same as hyperthyroidism. Um It's, it's the same idea. Um, and to talk a bit about the, the thyroid function tests, uh, secondary hyperthyroidism is really rare but it's just here for demonstration. So if you think there for primary, their T three T four is really high. So that's the thyroid gland going into overdrive and the low TSH is the obituary telling it to slow down pretty much. Um and secondary, they're both high, but as I say, secondary is really rare. Uh and the management is pretty much carbimazole. So you, you can give carbimazole as like a block therapy. So you titrate it down or you can block it fully and then titrate up with levothyroxine. Uh propylthiouracil is also used, but it's, it's used more in like an acute setting and there's a really severe risk of agranulocytosis which can be quite serious. Um In some circumstancess, you give people like radioactive iodine and I don't remember from physio like that's how the thyroid works. Is it up hiding? So if you give them radioactive iodine that pretty much slows down or destroys part of the thyroid gland and then if you think of your counseling, people for that, they can't be near pregnant women, they can't be pregnant themselves and they can't be near Children for like a few weeks. Um And then as well, it's important for symptomatic management. You need to give people propranolol because it can be serious. Like if somebody's in fast af you need to, you need to slow down their heart rate. That's also the thing that really bothers people about being hyperthyroid is their tachycardia and like being anxious and jittery. Um, the main causes of hyperthyroidism is or is graves. Um And this is the thing you find and it's kind of a pattern in exams is you get positive anti TSH antibodies. So, as we've seen in the last slide TSH is the, the pituitary hormone that says go to the thyroid. So it causes the pedal to go too far. Um So whenever there's your autoantibody, it's essentially doing the same thing. Um And it's an autoimmune condition. So you have a positive anti TPO titer as well. Uh The pathognomonic signs would be exophthalmos, you can see on the left. Uh I've never seen it, but like this is your thyroid eye disease, uh pretibial myxedema, which you're gonna look for in your thyroid status exam. Um And then your diffuse goiter, it's usually smooth, I think in exams we usually talk about and then toxic multinodular goiter is a bit rarer, but it's um or it's the second most common cause of hyperthyroidism, but it's not, you don't really stay in exams as much. Um Usually, I think the thyroids is described as lumpy or, or whatever. Um In hypothyroidism again, the clinical features, it is just the opposite of hyperthyroidism just when the pedal isn't done hard enough. Uh So you've low energy, like you gain weight, the periods are the opposite again. So they have heavy periods. Their mood is the other way, it's low and they're absolutely freezing. Um And the T FT S again, it's the complete opposite. So think of it with primary. So the TSH is trying to tell the thyroid come on, like work a little bit harder here. And the T three T four is, is not doing anything as low as a result. Um In secondary, this can be from like, I don't know, pituitary failure or something, the TSH is not working at all. So then the T three T four doesn't know to, to go up. Um management is just replacing the lack of endogenous um hormone with an exogenous levothyroxine. And it's, I can't remember, you need to look at the BF as I can't remember, like it's titrated up usually like over spaces six weeks and you, you judge this both by symptoms. Um and then the TSH levels of the patient. So, um well, in primary hypothyroidism, you adjust it based on like is there TSH responding? Because if it isn't like the, the TSH isn't going like, you know, telling it to, to go to work harder. And then obviously in T four, like the maturity is not working anyway. So we just based on the T four levels. Um Another concept in endocrinology is the fact that whenever you replace an endogenous steroid, you should get no side effects from it. So in this case, you know, levothyroxine doesn't actually or shouldn't have any side effects. The only side effects you get from it are, would be from if you're not titrating it to an appropriate level or it's not being taken correctly. So it's kind of an important thing to think about and we'll get to that with steroids as well. Um And then the main causes of hypothyroidism are hashimoto's thyroiditis in the developed world. One of my friends actually has this. Um and that's more of a fun fact that iodine deficiency is the most common cause in the developing world. Uh Again, hashimoto's is an autoimmune condition. So just remember that that any autoimmune thyroid um disease has anti TPO titers. Um As with anything autoimmune, it tends to affect women more commonly than men and the goiter is firm and nontender. Unlike the next conditions, Decor's Thyroiditis, which is the one in exams that has like a painful goiter. Um And this is like a viral illness. You don't actually. So it's you go from high to low to normal. And I usually like you don't treat this, you just leave it. So the two thyroid emergencies, thyroid storm as per the name, usually you think you have too much thyroid hormone um this is a medical emergency. Someone actually died from this in Belfast. Like last year, I think one of my friends in f one there, like, like really, really serious. The, the symptoms are like, you think too much thyroid hormone, it makes you really hot, it makes your heart go too fast and you get agitated and all. And again, as with anything in endocrinology, it's usually precipitated by acute illness and stress. Um the management are trying to sort out the things that are potentially gonna kill somebody which is um their dehydration and their, their really high body temperature. You need to bring down the heart rates, usually like IV propranolol. And then this is whenever you give propylthiouracil compared to carb rather than carb carbimazole because it's, it's more useful, I think, I don't know why it's just used in, in the emergency. And then los iodine, I don't know why. And then myxedema coma, myxedema would be like the old word for hypothyroidism and a myxedema coma is just like really severe hypothyroidism. Again, it's really severe and can be fatal and this is whenever you'd get like a bradycardia, um you have a low body temperature and you can get an altered mental status um and makes sense, you treat it with IV of, of the hormone you that they don't have, which is levothyroxine and IV steroids and then you just keep the patient warm. It's pretty much across the board, like they're just the opposite of each other. Um, somebody might have said this if you've had your surgical talk already. But just to, to quickly throw it in like the main types of thyroid cancer. I would always remember P FMA is the most common types. Um, and then just, it's the same with the type two diabetes, drugs, just a few of the main points, just of each type. So for papillary, it's, it's classically an exam. Like the young female patient is pretty good prognosis. Like the, the, the 10 year survival of papillary thyroid cancer is like 9090 to 100%. And follicular is the one that can be like either an adenoma or a carcinoma. Medullary is the one like you could get a, a pathology statement or pathology report saying there's C cells and there's a raised serum calcitonin that makes the medullary thyroid cancer. And then anaplastic is the one that's like older patients. And there's a really bad prognosis for uh thyroid status exams. This was uh I did it with my peers, share students last week and this was um my final year walk. I think it was um, it's pretty, it's pretty straightforward. Um But, well, actually it's not pretty straight where the problem is. There's like, do you know when you're doing like a chest exam? Everything kind of makes sense. Everything you do is part of the chest and this, you're kind of bouncing like from one system to the next to the next. So the way I've laid it out is the way I remember it and it, and it's trying to keep everything sort of in a bit more of a logical flow. So you on general inspection, you suggest like, are they dressed appropriately? You know, are they wearing a tshirt in the middle of winter? Um Are they really like wrapped up in a coat? Um Are they sweating? Are they their behavior as well? Are they tremulous? And then politely, you might want to suggest, like looking at their eyebrows, like is the outer third of their eyebrow thinned, um or is their hair thinned? Um You can get them to stick out their hands like, do they have a fine tremors? You get with hyperthyroid, um check their pulse. Um Do they have a tachycardia uh thyroid, a arthropathy thyroid nail disease and then feel their palms like, are they moist or are they dry or are they sweaty and then sort of move off the arms? And this is when you do your proximal myopathy, I think I can't remember which hypo or hyper, but it'll be in your books and then you do reflexes and it's exactly what you think it would be. So risk would be hyperthyroid and slower reflexes would be hypo, then pretibial myxedema. This is the, the rash we talked about earlier. You have a look at the legs and this would be before you get to the head and neck. So whenever you're, you're examining somebody's eyes, you have a look, go around the back of them look and see if they have a proptosis or an exophthalmos. Um and like look down their eyes and then you want to do extraocular movements. The important one is have them looking up and then looking down and follow. Like does do they have lid like does does their eyelid lag behind? Um then you inspect the neck. So have a look for the goiter, get them to usually be like a glass of water in the stations, get them to swallow water and they stick out their tongue and see if the, if they have a goiter, does it rise and fall, um palpate it. So the technique is to like hold one side of um the thyroid gland and then palpate the other with your fingers, then do the same thing, swallow in water and stick out your tongue and then you auscultate it. Um I've actually heard this before and if anybody is a go like you can usually hear a bruit on it. Um So now to move over to, I guess some of the the smaller illnesses um pushings, I would think of as like excess steroid or having too much steroids, the easiest way to remember it. So it's a pathological overproduction of cortisol. Um Remember in, in a especially that the most important features are not, you don't wanna say, like the most important like moon faces and the Buffalo hump. The things that are potentially important and potentially life threatening or hyperglycemia um are mood changes like you get a psychosis with this. Uh you can gain weight and osteoporosis. Um I kind of don't really, not that I don't understand the dex metho suppressant test. I didn't. And the best way I can, I can tell anybody to remember this, like is the, the zero to finals video taught me everything I know about this. So it's really good. The whole idea of it is um to diagnose somebody with cushing's and it helps you to find out where exactly the problem is. Um you pretty much just give a little bit of dexamethasone, see what that does and then give a lot of dexamethasone and see how much that affects their, their levels and their ACTH and whether it suppresses their, their cortisol. Um It makes sense and I would just watch a video like it, it's, it's 100 times better than anything I could say. And Addison's disease, I would think of as not enough steroid, which kind of makes sense. Um And recognizing this clinical picture was a station for us in our ay finals this year. So we had a patient, little hyperkalaemia, hyponatremia, hypoglycemia and, and hypotension, we had to take pretty much a false history. It was kind of hard to take a false history and then write out a prescription for IV hydrocortisone and we had the B NF page in front of us. Um And that was at the station like it was really hard. We just had to know those three things caused that pattern. Um So, primary insufficiency is when you have an autoimmune destruction of the gland and secondary insufficiency is when you have a failure of the pituitary. And that's the cause of the reduced ACTH, which is the pituitary hormone. Um So the features of the things we talked about are hyperpigmentation usually of the skin and like the mucosal membranes that would only really be in primary. Um And then the investigations are for exams would be your short syn actin test. It's, you can remember because you see that word syn actin has ACTH adrenocorticotrophic hormone in it. And yeah, it's pretty much synthetic and ACTH. When you give it to a healthy person, their cortisol level should rise, makes sense that adrenal glands are responding to that. But in medicines, they won't. Uh Addisonian crisis. This is the the acute presentation of it. And you need to, you need to remember like this can be, this is either the first presentation of Allison's or if you have somebody on high dose steroids for something like, I don't know, polymyalgia or something. If you abruptly stop them, you can uh you can cause an Adison crisis. And that's why like they, you're, you're on a tapering dose of steroids whenever they're done. And, and again, as I say, with anything, they're usually caused by a precipitating illness, especially in Addison's disease. Uh and the presentation, as I say is shock. So they collapse of Parex, they're shocked of a low BP and that little triad. You need to remember if you've done past med endocrinology, like you'll know this pattern. So it's hyperkalaemia, so high potassium hyponatremia and hypoglycemia. Um The reasons for this, I don't want to bore you with any of the physiology. If you remember from, from second year or whatever it was, it's like, you know, this cotransporter. Um that's from if you have addisons, like you've none of that aldosterone which cause that cotransporter. So you're not, you're not excreting any of the potassium and you're not reabsorbing any of the, the sodium which causes that those blood tests. Um And the management as you would expect is just reco like ad e and then high dose IV steroids. Uh steroid counseling would be a common Osk station and it's something always sort of worthwhile knowing. Um mm I would always consider why the patients are, you know, say in the stage, like why they need to be prescribed a steroid and learn off sort of 5 to 10 of the main side effects. And as I said, like the main ones being the most important things would be like hyperglycemia, psychosis and then fracture risk and weight gain. Um Always consider this is the thing I was talking about, do you know when you're giving somebody endogenous hormones, there shouldn't be any side effects. So, if somebody has Addison's, you're just giving the hormone that their body should have been producing anyway. Um, but if you're giving it a high dose for something, like, again, polymyalgia, you need steroids will wreck somebody's stomach. So you need to give somebody a PPI and then a bisphosphonate that if they're a, a fracture risk, um they need like a bracelet or a card to say that they're steroid dependent and then to give that to anybody through undergoing surgery. Uh And as I said, we go through the sick day rules. Um it kind of makes sense because cortisol is the stress hormone. And if you're dealing with a physiological stressor, your body will produce more cortisol. So if you're unwell, you need more cortisol or more steroid. Um if you are and similarly, if you're undergoing surgery, patients will, will have a sheet with them, it's usually like a guide. You know, if you are unwell, you need to take this sort of dose of steroid or this or like double your dose. Um The same with anything the same with insulin if it's severe. Um and you're not able to swallow your tablets, you need heavy steroids and people can have like a rescue pack like I am hydrocortisone at home that the relative can be trained to use. Um I said a talk about hyperparathyroidism. This is the exception to that rule about primary secondary tertiary. Uh So the, so for a basic refresher, parathormone releases calcium from the bones which and the symptoms are therefore hypercalcemia driven. So your usual bone stones moans and groans. Um primary is whenever there's a gland problem, that's the same. So you have an adenoma like in one of the, the parathyroid glands and you treat that by uh either a total or a subtotal parathyroidectomy secondary is a bit different. So this is any condition that causes hypocalcemia. It's almost always like D D. Um and this causes your body to have to produce more parathyroid hormone. Uh PS is even is slightly more confusing. This is as a result of long term hypocalcemia usually by CKD and the gland hypertrophies. Um due to uh and um so we have the gland hyper arteries and keeps producing way more hyperparathyroidism even if the hypocalcemia resolves itself. Um It, it's quite a difficult thing. I would just learn this table and once you again, once you do more questions on it, you kind of get a feel of the patterns. Uh diabetes insipid has really confused me when I rise in third year. Um Pretty much insipid means tasteless, which kind of means like the, the urine is tasteless, which is kind of weird. Somebody wants to figure that out. Um I tend to think of this. Do you know when it, so whenever you drink alcohol, alcohol pretty much gives you diabetes insipidus. So it inhibits the release of a DH, it gives you like an A DH deficiency. Um and it causes, I think whenever you, you're like, you're out drinking the night of you drinking, like you go to the bathroom loads and you urinate out like a really dilute urine and then you get up the next morning and you're really thirsty and your urine is like really dark. Like you wonder why that happens. It's because of ADH. So the features whenever somebody has diabetes insipidus, you have polydipsia and polyurea, people drink loads and loads of water each day. And if you did nothing about it, like you can cause a really fatal hypernatremia. Um The way A DH works is it, it's the aquaporin channels in your kidney. So it works almost independently from sodium. So it's you reabsorbing water like independently of sodium. So you can just dilute down your blood fatally or no, sorry, undilute your blood fail if you don't have a itch. Um So the the types of it. So you think there are two types. So you have cranial diabetes, insipidus, which has caused you, you're not releasing it um from your brain. So this is either from pituitary surgery or meningitis like any brain injury. Um and replacement. The, the management is pretty straightforward like it's replacing it with exogenous desmopressin, which is just another word for a DH um nephrogenic is this was actually a question on our, on our finals paper. Um it was a patient with lithium. So, so, so it was a patient that had bipolar disorder was on lithium for decades. And then they started to get a a nephrogenic diabetes insipidus. The management's actually it can actually be quite irreversible. The management is difficult. Usually you give something like like thiazide like diuretics or you try a low sodium diet or treat the underlying cause. But I say it's quite difficult. Um, the diagnosis for diabetes insipidus is this fluid deprivation, which II would think about like, what would you do? What would happen to you if I stopped drinking water, my urine would get more darker and more dilute. This doesn't happen in diabetes insipidus and, and that's what makes sense. That's what the Rh osmolality is. Um And then you think if you give somebody a DH, does that work and does that do what you're supposed to do? Like does it make it um more darker or more more, I suppose, stronger or more um osmolar that would be a neurogenic. And if that doesn't work, if giving desmopressin has no effect on it and that's nephrogenic. An SAA DH is exactly what it says in the 10. It's the opposite. So it's a syndrome of inappropriate A DH. So you have too much a DH uh the list of causes is about as long as your arm. But the main things for exams would be, again, those like brain injuries, especially subarachnoid hemorrhages. Um, a load of cancers can cause it. Um, carBAMazepine and SSRI S can cause hyponatremia and this is how they cause it. And then some of the atypical pneumonias can as well. Um, it results in the evola hyponatremia, uh, which it, it's part of the, the hyponatremia protocol, which I'll show you and that's just how you treat it is like, well, obviously treat the underlying cause and then you fluid restrict and then stop the medications that are gonna make it worse. Um You could spend an hour talking about this diagram, but it's sort of its own thing like, um, just to show you that um S ID eight is, is on the game guidelines. It down here is one of the causes. Um, and for it, you treat um with fluid restriction then just the underlying cause. Um, so acromegaly is pretty much excess growth hormone. It's acromegaly in adults and then it's like, I don't know what's the, the proper word is, but it's like gigantism in, in kids because they're actually still growing. Um, the features we talk about would be if the classic example for me anyway, would be the great Cali if you watched Smackdown in the, in the mid two thousands. So this would be like a frontal ball things. So you have a big forehead, your hands are spade like hands. Um And classically in exams, you'll get this by hemianopia. So the the sides of your vision are lost because of the mass in the pituitary gland that compresses on the optic chiasm. Um You investigate this with something called instant like growth factors. Uh I II think you do, I can't remember which one you do at first and then the oral glucose tolerance test and then you confirm it with an MRI of the pituitary because this is a pituitary problem. Uh And you manage it. If somebody's suitable for surgery, you do a transphenoidal surgery. This is the one that goes through the nose. Uh or you can give Cabergoline, which is uh I can't remember how it works, but it's just, it's if somebody's not suitable for surgery or you, they can give that like presurgery to, to strength the, to shrink the adenoma and then you can give growth receptor antagonist. It sort of makes sense. I got some MC Qs to go through if you wanna spend a minute reading that everybody was listened to the diabetes and stuff. But the slide. So yeah, the answer for this is e it's the water deprivation test. Um So pretty much, yeah, this is somebody that has, well, it was exactly on my finals paper. It's been on lithium caused nephrogenic diabetes, insipidus. Um So you're urinating out too much, too much and that's the pattern you need to know. And it's also worthwhile looking like that's the um, their serum osmolality uh is high and the urine osmolality is like on the low end of normal question two. Oh somebody's popping in the in the chat. Uh Yeah. So this is uh c so that I'll read out the, the justification is because this is primary because it's common in older females. Um symptoms are mild or absent and this is you have a hypercalcemia in this case and then the kidney function is normal. So remember the prerequisite for like secondary or tertiary is uh an abnormal kidney function. But they really hard questions. Sorry. Uh a few more questions. So this one was uh e so you think in, in the question, it says she's drinking from her water bottle. So her blood glucose is really low, she's conscious and she, so um especially as an outpatient, like you wanna give somebody oral before oral stuff before you give them anything IV or IM a couple more questions. So yeah, the answer here is b so hopefully, you know, by the um the clinical vignette, this is uh hyperthyroidism and as a goiter, your T four T three are way too high. Um And you, you, you, the key word here in the question is the initial treatment. So you wanna treat the symptoms first before you get into anything else. At least I think that it didn't, didn't give a reason for why, but I'm pretty sure that's why it is um last question. So this was the um so I hope if you listen. Um Yes. Well, this is the the the Adison crisis. So remember their, their sodium's low, their potassium's high and their glucose is low. Um And then this is the thing you investigate with that ACTH level and their plasma cortisol. I hope that made sense. Um Thanks for listening. Um II, don't I usually do this for any presentation but ask any questions to, to that's my email or a Campbell's because I usually ask him if you need anything from me. Um And let me see, stop sharing. That was brilliant. Yeah, I'm here. So I just put the uh feedback link in the chat. So if you guys can complete that, that would be great. And thank you so much, Greg. I know endocrine is such a wide topic and they really focus on it. So I think there's an endocrine station like we had it in third year. We had DK. That was my first one. I thought I was gonna pass out just like reading the prompt in front of the station. Um And then for our final year, we had Addison's, which was not really straightforward. So it was like a mini history and then you had to recognize it was Addison's and basically do a mini counseling with the patient and tell them you're going to put them on steroids. Um And then prescribe it. So, yeah, I think, yeah. Yeah. So, yeah, II think it will work Well, and if you have any questions, I'm sure Craig is happy to take them via email. I'm not, I'm more, I'm, I'm sure you're more happy. Thank you. But yeah, no ple please do ask. Yeah. All right then. Ok. All right. Thank you very much. Uh Do you want me, do you want me to send my part one year? How is that gonna work? Um, I think Marie is gonna um chat to you, but they have the feedback link and once they complete it they'll have access to the slides and through the metal app, I think. Oh, that's great. That's ok. Yeah, but you can, you can just send uh, your presentation to Mar, I think she's been in contact with you. Right? Uh, she has been. Yeah, I'll, I'll send an email. That's ok. Yeah. Yeah, just, just send your presentation. Yeah, that's good. Good. Right. Thank you. See you later. Bye bye. Thank you very much. Bye bye.