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Okay, perfect. So, hi, everybody. Um, welcome to our first session of our revision series. My name's Jess. I'm the Vicepresidente of Welsh Foundation Trainees Surgical Society. Um We've got quite a number of sessions between now and the next exam date in May. So keep an eye are on medal for our events, but also on Facebook as well as any changes will be updated on there. Um And now I will hand over to Ben who is going to be doing our talk for the day. Any questions, if you pop them in the chat or any queries, then we can keep an eye on it if you can't hear or see anything. Let me know. This is the first time we've used this system. Um And yeah, hopefully, hopefully you'll learn a lot. So enjoy. I'll hand over to Ben. All right, thanks dot So, let's see how well this works. All right. Seema slides there, Jess. Yeah, we can see them. Yeah. Uh That's perfect. All right. So, yeah, just said my name's Ben. I'm the corps trainee working the heath at the moment and I've been asked to teach you about some endocrine conditions for the mrcs. So I, I had a little trawl through the syllabus. Um So, um it can come up is, it probably represents about between five and 10% of marks that are available from your part. A these on screen now are guaranteed areas, guaranteed numbers of questions should I say? And then there's some variable inclusion of it across anatomy. The and I hate this phrase so called high yields topics uh there on the left, but it's also fairly well described in a part of syllabus that it took me absolutely ages to find. So hopefully, this matches up with your expectations as well. But we're going to go through some topics on the thyroid, parathyroid adrenal and hopefully we'll have time for all of that. And then we can mention multiple under crime neoplasia, right at the end. So, kick things off with some thyroid anatomy. So it's a butterfly shaped organ. It sits around vertebral level C 52 T one. It's enclosed with its own connected tissue, uh like fibrous connective tissue called the thyroid capsule. And it resides within the visceral compartment of the neck, surrounded by the pretracheal level of uh cervical fascia. Uh This lovely diagram is a actual section through the neck and just shows some of the relations to the thyroid gland. So the thyroid gland is in pink here. Um The red outline here is the pretracheal fascia that I mentioned and it sits deep to the strap muscles. So the infrahyoid muscles, they're also known around the trachea, uh anterior essentially to the esophagus. And it's a bit difficult. I don't know if you can see my cursor but just sort of posturing area to each lobar. The thyroid, there's a little nerve there, which is the recurrent laryngeal nerve. Uh and I'll come back to some relevance later on the blood supplies. The thyroid is pretty straightforward. So you've got the uh the arterial side, the superior thyroid artery that comes off the external carotids, doing the superior portion of the gland and then inferior thyroid's coming off the thyrocervical trunks bilaterally. Um about 10% of people as well. You get this thyroid's Emma if that's how you say, I've never heard anyone say out loud because it's only present in about 10% of people. And the venous drainage is pretty similar. Although you've got a middle thyroid vein that also drains into the internal jugular along with the superior thyroid vein and then both inferior thyroid veins drain into the left breaker catholic. Now, everyone's favorite. We'll do a bit pathology as well. So, the thyroid parenchyma is made up of thyroid follicles, which essentially simple epithelium is either cuboidal look, eliminate. It varies um with a central lumen containing uh keloids. So, which is mostly thyroglobulin, which is the precursor to the thyroid hormone secreted. It's also where the eye ordination of the thyroid globulin occurs before it is secreted. Now, there's another type of cell that, that is present in the thyroid parenchyma as well called the parafollicular cells. And these haven't have a secretary function as well. They secrete something called calcitonin which um is suppresses bone resort shin. And that's, but they're also known as C cells. You may have seen that written somewhere potentially as well. Um And I've written there that the neural crest cells that come back into relevance later when we talk about multiple endocrine neoplasia. So as far as physiology goes, the function of the thyroid gland is to store and synthesize thyroid hormone and calcitonin. As I mentioned, um the thyroxine that it secretes as mostly as T four ratio of about 20 to 1 A T four to T three T three being the more active version of thyroid hormone. And it kind of just turns everything up like it increases your basal metabolic rate. It promotes gluco neogenesis present Insys either stimulating them to occur more frequently or or faster. The it is governed as a lot of endocrine organs are by sort of hypothalamus. Pituitary access the negative feedback in this loop as well is just circulating amounts of thyroid hormones. It's meant to try and keep it in a fairly constant state ticking over um but it can respond to temperature. So if you've got a cold body temperature, your hypothalamus detects that and through this cascade can increase the amount of thyroid hormone produce. So this is just a cartoon. Now on, on a cellular level of what happens when the thyroid stimulating hormone attaches to receptors on the thyroid follicles is that it will stimulate the uptake of iodine into the keloids. And the by ordination I organization, I think thyroglobulin super Poritz exa types exocytosis that it's active in its active form. Oh, that was a mouthful. So that was just a whip through there with some of the basic science related to the thyroid glands. Any questions in the chat before I press on. Probably not. That is fairly basic stuff. I appreciate barbarous. All right. So let's get more bit into the media stuff that um you may well get examine them as well. So, one of the principal um tests of the thyroid function, so called thyroid function test involves measuring TSH and free T three and T four in the blood. Um So you might get in the exam like a question of a bit like this potentially. So, um it's a 19 year old woman attends clinic with symptoms of lethargy and constipation on examination. A lump is palpable, the midline but neck and it doesn't move on, throw on, on tongue protrusion and you have these blood tests here. So high A TSH, low T four. And so what does this clinical picture indicate if someone would mind saying in the chat? Just to make sure you're all awake, what's going on with this patient? Perfect. Yeah, exactly. I know. So ask the question on the second page. But yeah, you're absolutely right. The hypothyroidism so, can't get any easier, can it? So you've got low, low amounts of T three and T four and consequential, high amounts of TSH due to the reduced, well, the HPT access breaking down. So, primary hypothyroidism, um, is when the gland itself fails to produce enough thyroid hormone. Um, the, the most common cause in the UK or in the western world, at least is autoimmune thyroiditis. So, something like hashimoto's uh and the developing world however, is, in fact higher d deficiency that can cause this the drugs at the bottom there as well, obviously consider thyroidectomy. But the drugs, amiodarone, a lithium are the most important iatrogenic causes of hypothyroidism. Of course, secondary hypothyroidism describes when there's a low amount of TSH is much less common. Um can be caused by nonfunctional pituitary adenomas or iatrogenic causes like removal of the pituitary gland itself for cancer surgery, let's say on the flip side of that. Of course, we've got primary hyperparathyroidism. Now, that's um just the opposite. So it's high T four T three um in the primary in primary hyperparathyroidism, that's when the thyroid gland is producing too much. Um Grave's disease is by far and away, the most common cause of primary hyperthyroidism. Um and it is, it's interesting. So you get antibodies that bind to the tear ch receptors in the gland which act in a stimulatory fashion and causes the gland to produce more thyroid hormone as a result. You can also get toxic goiters. Um which uh yeah, just to make up the latter 25%. And these again, rare as hen's teeth, never heard or seen of them, but they just need to know that they're possible. So, secondary hypothyroidism being caused by like a TSH psa creating tumor in the pituitary, for example, uh never, never seen it. And these are some other goods vignettes for the exam is that, that's like a kind of really important thing about your vision is to kind of pick up on key stems that, that come up and pair them with, with answers rather than having to learn all of the stuff from scratch. So if anyone have sick, you thyroid's, that's when you can get some abnormal thyroid function tests in the context of a non thyroid royal illness. So the really typical one is, oh, your patient's been admitted to ICU for recent X Y ZED and they found out some routine bloods to have deranged thyroid function that it's um they're not recommended to be done in the critical care setting for that reason. And, but that's what they call it a sickie, you thyroids. The other ones that I found a bit more confusing when I was doing this the first time around. So you can have an acute infectious thyroid itis, um which is like everything under the sun except for viral pathogens can, can cause this though, though itself happens pretty and frequently you almost, almost always have a normal thyroid function test. Um uh For that the one below that, the so called subacute or de Quervain's thyroid itis is, is almost always thyrotoxic. Um It's so it follows an acute period of thyroid toxicity followed by transient hypothyroidism as you, as you recover from it. And, and that is um the viral cause or post viral. And um it is tested for usually what? By measuring inflammatory markers and your thyroid function. Mhm Yeah. Publix. So yeah, in in summary conditions that cause hyperthyroidism just kind of turn all your body processes up and hypothyroidism, it's the opposite. Couldn't be so easier, could it. But it's just about knowing which the most common cause is because you might get asked a question about like, oh look at this scenario, what is the most likely cause of this clinical picture? So like graves for hypothyroidism. Hashimoto's for hypothyroidism. And then knowing all those other little rounded ones that I mentioned on the last slide where as well. So moving on to some benign thyroid lumps, there's not, not a lot to say here other than kind of to know that they exist. If you're given like a vignette about a patient that is having a neck lump exam. Uh These are some of the causes of benign lumps that affect your thyroid's um there's a classic one at the bottom there, thyroglossal cysts that comes out basically all the time and it's the one that moves up in your throat when you stick your tongue out. Um, but yeah, I think we've covered the others already really the main meat of this bit of the presentations to do with thyroid cancer. Now, this comes up every year. Um, I've done part a twice and obviously unsuccessfully the first time and this has come up multiple times in each exam that I've sat. And you just kind of need to know some key differences between the different types of thyroid cancer. So, papillary, most common, um they're all more common in women across the board. Um Histology is that it goes, goes with the title, it, there's a papillary cellular picture under the microscope. Um And these ones, it's important to remember spread via the lymph system. So be in the stem like a painless lump in the midline of the neck with palpable deep cervical lymph nodes or something cause it's spread via the lymphatic route. This is the second most common follicular uh pelicula, thyroid cancers again, like I said, the small common in women a as this produces like a microscopic invasion of the capsule on under the microscope and this one spreads fire blood. So it normally metastasizes to bone all the lungs and these that round out the list as well. So they're much rarer than the other two thankfully because they all have pretty poor prognoses. Um anaplastic is the one that is locally invasive. That's the bit that one needs to remember for this. And then a medullary thyroid cancer is, is a cancer that arises from those parafollicular cells that I mentioned very briefly earlier. The ones that secrete calcitonin and these are often associated with multiple endocrine neoplasia is because they're neuroectodermal cells from, from the m buren or four gap. And then here is another little one as well. Like it's the rarest of all of them. But they often ask questions that relate to this fact. At the bottom. Here is the fact that that this is the type of cancer that if you have hashimoto's, you're at greater risk of essentially. But that that's kind of the thing to look out for it in your stems. So to briefly summarize the thorough cancers there in terms of useful facts, you've got the prognosis are worse from an A plus anaplastic down that list to papillary incidents. Papillary and molecular. The most common by far, papillary spreads by the lymph pellicula spreads by the blood and the dollar just both anaplastic is locally invasive. And it's worth noting. So I don't think I mentioned it as well earlier that uh serum thyroid globulin is useful for the surveillance of all of the tumor's except for medullary. In which case, you can use calcitonin right now, getting towards some of the more interesting bits then. So for any sort of thyroid lunk, whether or not it's benign cancerous hyper hypothyroid, there's normally you can, you can think about it in terms of whether you can treat it conservative medically or surgically. Cancer ones always get referred to an MD tea. That's um that's pretty classic. But yeah, broadly speaking, you can say that it depends on the the etiology. So, hypothyroidism you treat with, you just replace easy peasy. So you give the patient levothyroxine. no worries in hyperthyroidism, you have a bit more choice. So you can, you can treat it medically. Um using thyroid was this thyroid peroxidase inhibitors um such as carbimazole, that's the most often use except in pregnancy where you use pro high all thiouracil, you do need to do a block and replace strategy with these. So it's where you give them lots of carbimazole and then you replace it with levothyroxine afterwards. Radioiodine is another medical management. It's it's a good definitive treatment for graves' disease. However, if you do have the eye disease related to grave's, then it can make that worse. So that's something to consider. If that, if that comes up in as part of the question stem, no business end really. So the cancers, this is normally your first line with the exception of sort of adjunctive chemotherapies in certain cases, but it can also be used with medical management fails for uh toxic goiters, for example, um you can do sometimes you can do half thyroid removals, your hemithyroidectomy knees, but it's more common to just go for a total thyroidectomy, which then of course, will require permanent thyroid replacement afterwards. Here we go. This is, this is my favorite bit. Um So I'm going to ask you guys some more questions now. Um So this one is about the complications that can occur from thyroid surgery. So, if your patient returns to the wars after having the thyroid out, uh and several hours later, they developed stride or, or respiratory distress, what is the most appropriate management from that list? I'll give you a couple of minutes for someone to say which option they think is right in the child. Excellent. Yes. So I'll go with the first one because that is right. So, yeah, this is a case describing a expanding hematoma following thyroid surgery. Um, and they can progress to course airway obstruction. Um, so, I mean, you assess these patient's, I'm going to put that in brackets in an eight hour. We fashion, but you get stuck at a because they've got an airway problem and the treatment is to just remove the sutures there and then like, don't laugh around, just get them out and then you would book them into theater after that. So it's, yeah, it's trying to bait you to say, oh, I would book them for a cat one C pod when actually you just do it on the ward because there's no time to back around. So there's another one. Um So if you're asked to see a patient following a total thyroidectomy because they're complaining of some tingling in their fingers. When the nurse takes their BP, the patient's cell have some involuntary, painful carpopedal spasms distilled to the BP cuff. So, what is the most important, most appropriate initial management? Again, if you could put your answer in the chat, that would be great. Any takers? Excellent. Yeah. Yeah. be is IV calcium replacement. So um hypercalcemia, a severe hypercalcemia is is a potential postoperative complication of thyroidectomy. If you remove the parathyroid glands by mistake, um sometimes difficult to see them. So if you uh have a patient who has symptoms or a serum calcium below a certain threshold will be according to local protocols. But yeah, you just need to replace it, to be honest. And most local guidelines that I've seen say it's like 10 mils, 10% IV calcium gluconate. Um in the first instance, followed by ongoing uh slower calcium infusions now. So it's not in the typical style of a of an mrcs question. However, this is something they do ask about as well. I've been tricked by this one before myself. So which nerve has been injured in the following vignettes here. So, so in a they've unable to do slow rising pitch and whereas be in this situation, they just have a horse breathy voice which has changed in pitch. They have noisy breathing when they were cold. So if you wouldn't mind, someone trying to guess which nerve has been injured in a, which nerve has been injured in b and then we'll talk about it. I'll just give you another minute to think about it. But if you don't want to answer, I, I don't blame me. Uh So hopefully I made this clear enough for the purpose of the, of the, at the power point. But, so this is a, it's a really tricky one because the a is meant to be the superior laryngeal nerve. Whereas be is the recurrent laryngeal nerves otherwise known as the inferior laryngeal nerve. So, um they are both protect, they're both quite close approximation to the thyroid gland posteriorly and both potentially injured and the, however, the superior laryngeal nerve, the only supplies the cricothyroid muscle, which is, which is the tensor of the vocal cords. And it's also known as the singer's muscle because it essentially allows us to do slow up like gliding increases in, in vocal pitch, which is called Girl Sando apparently. And if that's injured, yeah, you might have some generically similar symptoms in terms of hoarseness. But if they make any reference to this, either glass ondo or, or slow a sense in pitch, then you've got to be thinking about the superior laryngeal nerve. Whereas the butter classic of this scenario is, of course, the recurrent laryngeal nerve, some, sometimes they call it the inferior laryngeal nerve just to try and mess with you. But the, yeah, it's the same thing. So it supplies all of the other intrinsic large your muscles. And so it's a lateral injury will cause it's um, the what the, it's electoral vocal fold to be paralyzed and in bilateral injury, of course, it will give you Stridor and um, yeah, it's a bit of respiratory compromise. But that's, that's a really tricky one. But you'd be, you got to, you got to watch out for that because they like to make these exams sneaky on purpose. So I'm, I think I've got some, if anyone's got any questions about the thyroid because I think, I think we're leaving that for now. Um It's mostly all straightforward with the exception of that relational anatomy bit at the end. But yet you've got a question has hit it in the chat. I'll give you a minute or 22. Did you say? Okay? All right. So we shall continue. So, next down on the list of things that is always asked about is parathyroid glands and hold on. Do you mind showing the summary slide, your thyroid cancer again, please? Of course, I would, hopefully I'll be able to circulate these slides. Um, but I'll ask just about that afterwards. Um Where was it? The cancer one? Yeah. Here we are best one. So, you know, just, just showing, just worth being aware of which route by which they metastasized because they often build that into questions about the thyroid cancers. So, if you're happy with that, then I will uh crack back on. So, if I'm fine where I was, yeah, I'll see if I can get these slides sent out to all of you at the end. Um Right. Uh Here we go. So, parathyroid glands always asked about because of their role in calcium homeostasis. So there's normally four, I've recently found out there can be between two and six. Um And so they're not always uh cited inferior early on the thyroid gland, but this is where they're most commonly found. It's where you'll find them in the textbooks as well. But the, as I've written down at the bottom of the slide, there, some can be found as far south as the superior mediastinum who knew. But anyway, they're arterial blood supplies is mostly from the inferior thyroid artery. Though the superior parathyroid glands does occasionally take some from the superior uh thyroid artery, but they're both are supplied by the inferior. Uh Yeah, this is a sneaky one. If they ever ask you any questions about embryology, I hate embryology. It's too complicated, but the superior glands are derived from the fourth pharyngeal pouch. And they, during embry a logical development, they kind of switch sides. And so the inferior end up being below the superior in, in once you've been born histology pretty straight forward in the sense that there's a cell type called the chief cells that secrete the parathyroid hormone. And then there are also these oxy fill cells, which, as far as I can tell, no one really knows what they do. They might secrete a bit bit mindy if anyone knows what they actually do, if that'd be great. And to let me know, but I couldn't seem to find any consensus on, on their role. But it, it's the chief cells there at the business sent here. So, yeah, parathyroid hormone, it's very important in the maintaining the balance of calcium in the body. So it acts well, it is released in response to low serum calcium. Um and it has the effects described on this picture here. So it increases uh bone resort option. So too. So it takes calcium from bone into the blood and in the kidney, it increases the resort shin of calcium and excretion of phosphate. It also has some rolls in in vitamin D production in the kidney as well. So it doesn't have any direct effect on the gut itself, but it does indirectly increase the amount of calcium absorbed via vitamin D. It's kind of what I just said a moment ago. Um This is a good one that if I found, I think it's on the mrcs website so that the PT H is a phosphate thrashing hormone in the, it gets rid of it. Um So count phosphate. As I learned when writing these slides, apparently, um lowers the free calcium available in blood. So whilst it does parathyroid hormone that is increase the amount of calcium resort in, in the kidney. That's not its main role. It's it's more to do with getting rid of prostate. So it indirectly stimulates um osteoclasts to resorbed more bone. Again, annoying, never straightforward as you'd like it to be. So it, there are parathyroid hormone receptors on the osteoblasts which in turn, stimulate the osteoclasts to break down more bone and release calcium into the bloodstream. And this are kind of alluded to this already. But yeah, the the effect on calcium in the kidney is a minor effect of parathyroid hormone. Um So urinary calcium is actually increased in in cases of hyperparathyroidism. Um because of the hypercalcemia in the blood, that's a much greater effect on the expression. Hence why you get kidney stones is because you're peeing out loads of calcium. So the going onto some pathology. Well, pathophysiology now. So is hyperparathyroidism, most common cause of hypercalcemia. Um The second most common cause of hypercalcemia is malignancy. But yeah, the it's often found incidentally because you will, we won't often have symptoms of it. But yeah, the these again, just little little bits of information that they can often test you on. So about love, they give you a vignette that's like, oh here's a person with primary hyperparathyroidism. Blood's what is the most likely diagnosis? The answer is pituitary adenoma, for example, um the secondary hyperparathyroidism is what happens when you chronically lose um lose calcium through diseases such as chronic kidney disease. And as a result, your body produces more than it otherwise, normally should of parathyroid hormone. So you won't necessarily see the hypercalcemia in secondary hyperparathyroidism, but you will see an increase in the hormone which then inevitably will lead to, I say inevitably it doesn't have to be inevitable, but it can lead to tertiary hyperparathyroidism which again will have high P T H and high calcium because the parathyroid gland becomes all big and hyperplastic and just kind of autonomously produces uh parathyroid hormone. So another question for you all now. Um So this is this question is seared into my brain. I think it's been in both exams that I've done. So a patient is diagnosed with kidney stones and the test show these below. So they've got high calcium, quite high calcium and high parathyroid hormone. And you can see the X ray and an abdominal film there, which if you can't make it out, there's a left sided renal calculus. Um So what is the most appropriate initial management of this patient? So if you wouldn't mind, just someone answering. Excellent. Yes, someone read the question properly. So, so it's all about, it's what is the most appropriate initial management. So you could argue that these are all appropriate in the management of this case, but there's only one that's the most appropriate initial management, which is IV fluids. That's how you treat any severe hypercalcemia acutely, is you hydrate them. That's the most important thing because the bisphosphonate, apparently it doesn't really drive down the calcium in your blood that much. Which both of the questions of why we, we give them, I've not really got round finding it out, but it is part of every treatment protocol in, in every hospital I've worked in any way. Um, so coming back to talking about how you treat things conservatively, medically or surgically. So, primary and tertiary hyperparathyroidism, you can treat medically. Um It's more common to try that first, especially with, with primary um with all this fascinates and seen a calcium is a drug. I can't remember how it works, but I think it increases your excretion, calcium perhaps into your urine. I might make that up. But who knows? But that is effectively acts to lower the amount of calcium in your blood and then you can treat it surgically. So you can take out the parathyroid glands according to nice in the brackets here. These are the only indications for doing that. So if you have symptoms of your high calcium end organ disease, so like kidney stones, for example, or seizures or if you have a corrected serum calcium of greater than 2.85, that's it. So I think that's it with the parathyroid. It's um so it's the most common cause of hypercalcemia, as I mentioned, the second most being malignancy, it's very important because if you get a patient with hyper calcium here, you need to exclude malignancy as well. Um, often asymptomatic undetected incidentally. So you might get that set up where they ask you a question about a patient who's coming to a preop clinic. It's kind of a giveaway vignette to, to ask you basically anything in medicine. Um And yeah, that it can be contributed quite effectively medically, um, or surgically. I suspect not because it's a bit more straightforward than thyroid. But do you have any questions about the parathyroid before I move on? Oh my God, excellent. So I'm going to change things up a little bit now. So um getting into the 40th minute, which means everyone's going to be switching off. So a themed bit about the adrenal gland around all around questions specifically rather than doing it in the, the more didactic way they've been doing so far. So first up patient of yours develops nausea and vomiting confusion a few hours following the right hemicolectomy, they have low BP and the blood tests show the following. What is the most appropriate management of this patient again? Give you a couple of minutes to answer that. Excellent. Yes, it is. B so this patient is having a adrenal or slash Addisonian crisis. So this can happen to patient's that are on long term steroid therapy. Um They often have something called sick day rules like, well, so when um they've got cold, well, well, maybe they're more severely ill than account where they are meant to double their steroid doses. But surgery provides a significant insult to, to, to the body. So, if it's not noted, let's say that they're on regular steroids and the peri operative plan isn't made accordingly, then this is something that could happen to them. So the symptoms, you normally get like confusion, nausea, vomiting, mild abdominal pain, low grade temperatures. So, so it's all things that could signify. Uh I don't know, symptoms that are of like a intraabdominal sepsis followed like an anastomotic leak, you know, or they've got a bleed or something like that. I don't know, it's it. But so the key things to look for in the investigations that you do is what is their electrolytes. So, so in, in the Addison's patient, you will get or rather a in the quarters of deplete patient, you get a low sodium and high potassium. Now remember that because it's important for the next bit. So, yeah, in Addisonian crisis, you have low sodium and high potassium. The treatment is as described below here. So first thing you do is I'd be hydrocortisone and then IV fluids and then you essentially infused them gently with it over the following 24 hours. So, next question. So we have a patient who has failed to respond to uh three different types of antihypertensive medication and their BP is still high. The blood test show the following. Um So what is the most likely diagnosis out of that list? They answer away? Sure. Uh Any take it is good, good effort. But no, unfortunately, it's, um in this case, it's an adrenal. I've known that otherwise known as consin drome. Um So why, why is it that in this been yet? So, because this again, I'm 99% sure. I was asked this. Um, so patient has failed to respond to multiple different types of anti high BP medication. Um The blood tests show hypernatremia and hypokalemia. That's the most important part of the question here because in primary hyperaldosteronism such as consin drome, you, you lose potassium in your urine and retain salt. Yeah. So exactly meds there. So it's low potassium because you have high amounts of aldosterone. I think that is what differentiates this vignette between pheochromocytoma and adrenal adenoma is because if you have too much aldosterone, you lose potassium. So it's um yeah, this is a case of uh primary hyperaldosteronism. Um Aldosterone is it's a mineral course coins released from the zona glomerulosa in the adrenaline in the adrenal medulla, adrenal cortex. Sorry. And a really neat way of remembering which order the layers are in that I've learned recently is G F R like as in as opposed to glomerular filtration rate. It's a glomerulosa particular to particular is G F R I think that's, that's quite nice a way of remembering it. And yes. So hyperaldosteronism is when more often than not, you get a tumor that causes to secrete aldosterone independently of the rash system. So, you know, the region and your tents in aldosterone system, but you thought you were rid of that when you left medical school. So um the the endpoint uh it's the the last hormone in this cascade and it causes not in in uh you to retain sodium and therefore fluid in an attempt to increase your BP. So, as you can imagine, patient's with hyperaldosteronism, they present with refractory hypertension with low potassium and sometimes high sodium, but it can be normal. But it's um because of this sodium potassium antiport a channel which acts on. So yeah, the most common causes classical cons which is an adrenal adenoma. There's about 80% of primary hyperaldosteronism and then the other 15% is adrenal hyperplasia. So you noticed that was in the question as well, but that's not the most likely because that would be the adrenal adenoma in that case. So just to summarize there cause that was, that was a lot really to take in, to be honest, these two things are almost opposite. Um So you've got your Addisonian in patient who has low sodium and high potassium, they might present in a crisis with low BP and then your cons or hyperaldosteronism has your high sodium and low potassium will present with high BP. So I don't know if I've made things more confusing by lining those up next to each other. But if you can remember what aldosterone does, it makes remembering the difference between those two much easier because if you have too much aldosterone, you lose potassium and you have high BP because that's after all the point of, of aldosterone in healthy physiology. Cool. So I think this is getting towards the end now. So you've got a patient that attends your pre op clinic, like I said, classic way of asking about basically anything patient attends a preop clinic. They've been treated by their GP for hypertension with Ramipril have been told that they are prediabetic, their routine bloods at the clinic show this what is the, so BM is local ecos if you weren't sure and the rest are all self explanatory. What is the most likely diagnosis? Yes, it is Cushing's disease. Absolutely. So, um now this is a similar, you could argue um a kind of a kind of vague similarity, at least to the con syndrome vignette from before. So you've got patient that's being treated for high BP. Um their routine blood show low potassium liking cons. However, they've helpfully added in the fact that they are sort of pre diabetic or have impaired fasting glucose tolerance, which basically leaves you with Cushings to be perfectly honest, because in Cushing's disease, classical Cushing's disease, you, you have high amounts of ACTH which stimulates your uh what you call it adrenal glands to produce cortisol and eldest it. So yeah, I'm sorry, I'm IBM is blood glucose is um, yeah, so it's called the capillary blood glucose tests on the wards. Um, so yeah, your ACTH actually does increase aldosterone production as well. Um, so you get the same loss of potassium and high BP as a result of that. But then you also get the glue, the impaired glucose tolerance that you would get from having too much cortisol investigations a described here. They, they're often blood test related. Um You need to decide whether or not this is a primary or secondary hyper quartile salty mia through testing the serum ACTH because that cool guide your ongoing imaging investigations. So like a classic um pushing disease is caused by a pituitary adenoma. That's the most common type that's um of, of uh what you call it A C T H dependent. Uh Cushing's Pushing syndrome overall, however, is most commonly caused by uh exogenous steroids. So like a patient on lifelong prednisoLONE, for example, and then an honorable mention for incidentaloma because I didn't know when I was sitting the exam. But I do now that this is actually the most hospitals have guidelines and nice even may have a guideline about how, what to do with when you find an incidental adrenal mass. So let's see what you guys think. So if you have a patient who has an incidental finding a three centimeter adrenal mass which has no worrying radiological features. What is the most appropriate next step in their management? Yes, it is. B you're smashing it whoever you are. Yeah. The um uh one of this size you would refer for further tests. So this is a common occurrence which is why I guess so many hospitals and nice of guidance on it. Um So if the incidentaloma so called is um less than one centimeter, you can just discharge him. No follow up. Um It is between 14 centimeters. You investigate with the listed endocrinological tests there. And then this one is a bit less clear, but normally if it's above four centimeters, some people say you should just operate because great and even if it doesn't look sinister on the scan because it has a greater malignant potential that the bigger it is, I'm almost finished and I'm under time. So does any, does anyone have any questions before I, before I go on to the last little bit? Excellent. So there's the last little bit. So for the MRCS, you have to know loads of annoying things that almost you'll never come across in your whole life. Is a practicing surgeon and this is probably one of them. I reckon it's so it's a, it's a cancer syndrome of sorts called multiple endocrine neoplasia is they are, they are very rare there in heritage um There so they have specific associated tumor suppressors or proto-oncogene and subdivided based on what kind of tumor is you get with each of them. If you've been doing, ask questions on the MRCS, you might have come across this already, but I've certainly not come across this in real life. Um These are the different types of men's syndromes. So men one easiest to remember because it, well, the gene is the easiest to remember because it's just the same as the syndrome. Um You'll get pituitary adenomas. So these can be functional or nonfunctional annoyingly, never, never, always the same, a variety of different pancreatic tumors, most commonly gastronome Azaz um or an insulinoma. Then the other two, they're apparently involved, both involved the reps proto-oncogene how and they're the same with the exception of the marfanoid body habit tous and make you mucosal neuromas. So, so they both involve this. So it's not a parathyroid adenoma like with hyperthyroid hyperparathyroidism is parathyroid hyperplasia specifically, they often try and trick you with that in the exam and then medullary thyroid cancer. So you remember to all these, these are all neuroectodermal tissues. Um So that's the power of follicular cells and the thyroids and theo chromosome time is as well. Everyone, everyone's favorite. I put a little footnote there because this is a question that does get asked about and I didn't mention it anywhere else in this talk, but the seems a bit random to tack it on here as well. But theo Chromos automa as the investigation of choice is urinary VM. A don't ask me to pronounce it because I can't. But it's um it, that is the urinary assay that they used to detect pheochromocytoma. So if you think the patient has that and that's an option in the question, that's what, that's the answer. Fine. So, yeah, that seems a little bit a little bit pointless to know about. But because it's a classification system and there's these similarities to one another, They often ask you questions about it. So sorry, it's just one worth being, being aware of. So that's it for the, for the talk. Thanks very much for listening. So I've just compiled a few little tips in general for it. I mean, if it's not your first time sitting, I apologize because you probably already know these. But personally, I would try and advise avoiding getting bogged down in detail. Like um your time is probably best spent, ironically given that I'm delivering a lecture about about mrcs stuff is just doing loads of past questions. E mrcs is the one I use. The time that I passed. It's, it's relatively cost effective and is more similar to the exam than, than the other one. What's that one called? Past past test? I think, I think the mrcs is more similar personally and just do as many as you can like I am to do something basically every night. Um If you can, but then around the exam time, just try and get some rest. Like there's no point in cramming. Like you just want to be well rested for the exam itself and, and make sure you take your study leave. It's, it's, you're entitled to 55 days before the exam. So get it. It's because you're entitled to. Would I recommend time tests on the msds over class test? Um Well, it depends, it depends if you feel like you are, how, how quick you are at doing the questions. So, um if it's something you need to work on then, then yes, but I personally, in terms of the platforms, I prefer D mrcs. So I did a sample time thing on past test and then use the friend's account for a bit as well. I just didn't find that the questions were that similar to the real thing like and they just make you feel like you're more stupid than you are, whereas the mrcs seems more fair in my personal experience. Cool. Well, thanks very much for listening. What is the best Q bank part? Yeah. Hmrc estimate. That's the one I would recommend is E I'll just so it was clear E mrcs, it's the, it's the, it's the most cost effective. It's the most similar to the real thing like past test is really expensive. Didn't find it that worthwhile. Cool. Uh Thank you so much, Ben. I hope everybody who found it really, really helpful. I'm just going to send a feedback form. In the group chat now, hopefully everyone can see it. Um If you get a chance, we'd really appreciate it. Obviously, we can send them to Ben as well. But just in terms of how this has worked, like, say, this is the first time we've used this platform. So we just want to know, has it been helpful? Um Is there anything else that you, you'd like to see? And we've got to talks next week um off the top of my head, we've got low G I and we've also got a T L s and shock. Um So at a different time, so just keep an eye out on medal and on Facebook for those times in which one comes first. I can't remember which order is at the moment. Sorry. Um And yeah, like I say, hopefully you find it really, really useful. Thank you again, Ben. Um Also, once you provide your feedback, there should be certificates that automatically get sent out if not give it a couple of days and I'll resend them out. So hopefully you'll get a certificate from, from this session. Um So yeah, thank you so much for attending. Thank you everybody.