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All right, good morning. Everyone. Can everyone hear me? Hi, good morning. Can everyone hear me? Great, thanks. Um OK. Uh Come on and see that presentation now. Bye, good. Um The problem is I can't see the chart, so I'm just gonna stop sharing for a sec and just it. Ok. Correct. Good. Um So I'm gonna be talking about um thyroid disorders. Um This should be actually a pretty uh easy electric cos I think it's quite well taught. Um at Imperial, I also think it's fairly straightforward and I'm a big believer in understanding, er, over wrote knowledge. So, um I, yeah, well, I hope I'll reflect that in my er slide. So here are some of the objectives that I want to get done, so function the thyroid glands and then looking at those disorders and then I'm also talking about calcium later, which I find I found more difficult. Um, so I'll be spending a bit more time on that and so I'm gonna do a refresher on the regulation of calcium to understand the causes of hyper and hypercalcemia. So, in terms of how I like to teach and the timeline of this lecture we'll usually start with anatomy and function because I understand about the anatomy and function help in understanding the next two things, which is the disorder and the pathophysiology. And those two things help understand the features and management is always kind of difficult because um it's not as straightforward as the path of the other four times of the next logical step. But I tell me, well. So let's start with a very simple thing right in the middle of your neck just above the trachea. Um and it's split into two lobes, a left and a right lobe of some people call an h um and the location of it important for future signs in hyperthyroidism. So, how's it work? And I think simple is best for endocrinology and especially for the thyroid gland. So, um we've got the hypothalamus. Uh I'm sure I don't need to repeat all of this for you, but we've got the hypothalamus, um which secretes trh, which er stimulates the anti pituitary gland to release TSH, thyroid stimulating hormone, which stimulates the thyroid to produce thyroxine, which is T four and T three, which is the active form of the thyroid hormone. Both of these have negative feedback loops as you can see uh from the arrows and they inhibit the production of TSH and they also inhibit the production of trh. And that's really simple. Um pretty straightforward and um it's really, really key and once we understand this, uh well, And once we keep remembering this, uh hopefully, things will follow. So that's how the whole uh um axis works. We call this the hypo hypothalamic um pituitary thyroid axis. H PT. Um How does the uh hormone actually works? So, the end product of thyroxine? Well, we've got t three being the active form T four being inactive and T three sensitizers, beta Adreno receptors. Now, this is quite important. It doesn't directly activate them. It just lowers that activation threshold for these receptors. Um And it then activates the sympathetic nervous system, which is our fight or flight um nervous system. And remembering that is actually quite helpful because a lot of the symptoms will be related to the final flight uh symptoms and what the synthetic nervous system does. Um in terms of lowering activation threshold, this just means that basically uh normal levels of adrenaline which activates these beta adrenaline receptors will then um activate them more frequently. Um when there's more thyroxine around. So now that we understand the function of the thyroid gland, what can go wrong with it. And it's really simple, just we can have too little hypothyroidism, hypo being low, less T three and we can have too much of the T three hypothyroidism hypo being more. Um And I've got some causes below. Those are the most common that I've seen. And also in your lectures are the ones that, that have been talked about thyroidism. The lecture didn't really talk about hash mos, but I feel like it does come up quite often and it's important just to know that there is another side that we'll be focusing mainly on high. So we've got graves toxic multinodular goiter and viral and postpartum thyroiditis. So, let's start with a very short answer question. Um, unfortunately, I can't see the chat but uh, I'll just give you like a couple of minutes or something. Uh, 42 year old woman presents with progressively worsening, weight loss, anxiety, heat, intolerance, and dry skin and eyes. So what already when we do Sa Qs, what are we thinking about? From that first sentence? We've got a middle aged woman and we've got some symptoms and they're actually pretty discordant. Um It's not like there's localized pain and everything's going on with one specific organ system. And I feel like this is quite important in terms of your whole endocrinology module. And today is that often because the because hormones affect the whole body in many different organs in different ways when you see these symptoms, which are perhaps a bit peculiar at first, maybe start to think uh about hormones and endocrinology. Anyway, what two further signs or symptoms would you expect for a diagnosis of Graves Disease? Now, this is a specific diagnosis of graves disease, not um a hyperthyroid picture, which is what we get in that first line, that specific. So again, I'll give you 30 seconds or something. Um just think about it because I can't see the chat. Um, ok. All right. So a thalmus pretibial myxedema and in brackets thyroid ACFA. So, these are very specific for Graves disease, which I'll come on to later. Um, I was just putting this in just to, uh, really test, test how much, you know. Um, but, uh, thyroid APAC is not in your exercise, but I feel like it does come up in, um, questions often and it's basically another one that's quite specific to the auto antibody to do with graves. But we'll talk about this later. And then another Graves question. What labs would you expect for a patient with Graves? I've got T three or just T three and T four and TSH. Um and that always indicated with a high, normal or low. So again, I'll give you 1530 seconds or so to um have let three answers. Oh, when I say labs, I mean, like blood tests. Um this is um see, so we're gonna have high T three and, and low TSH. Um So these are some follow up questions to think about uh why do we have this high T three? And the TSH. Well, Graves is a disorder of hyperthyroidism. So anything with hyperthyroidism is gonna have a high um T three. So answers A uh and C are both a hyperthyroid picture. Um And then in terms of TSH, you'd expect that TSH is low because there's a negative feedback um from the T three that causes the TSH to be low. Um However, obviously, it's something still producing the T three. even despite the lack of stimulation. So we know that this is a problem with the thyroid gland and this comes on to my uh next slide. Another follow up question is what might the other signify? But once the slides are released later, I'll let you go through that first off. So, thyrotoxicosis, this is a new word. It's basically hyperthyroidism is what you might see when you search it up. And I thought I'd just include it as a title because often the literature um and the internet use this term as opposed to hyperthyroidism. So you might get more resources this way, but it's basically just hyperthyroidism. And the definition is just symptoms caused by the excessive circulation of thyroid hormones. So this is.