Computer generated transcript

Warning!
The following transcript was generated automatically from the content and has not been checked or corrected manually.

this part of the osteo bi teaching? Yes, I've been given a lot of lectures. This part of the osteo bi teaching program, uh, generally enjoy teaching. It's one of my questions, and I'm very excited to be presenting today session on today's session, as you know, will be on endocrinology. Okay, so it's a continuation off our finals. Easy, Siris. Tell folks is gonna be on endocrine. Okay, very high. Your specialty. Ah, it's one of those specialties that most of the content is is within the scope of knowledge that's required for another graduate. Okay, there's not much in under crime that is sort of outside the scope of knowledge. You need to know as an undergraduate. Okay, it's all very rare relevant to clinical medicine, clinicals clinical examinations and things. So the super important specialty, which hopefully try and cover as comprehensively as I can, uh, also could notice. I had a bit of a long day. I get if I seem a bit sleepy. Tried the lecture. Herpes. Excuse me. It's been a bit of a long day, but I'll do my best to, uh, make this section engaging for you guys and hopefully Ah, really, make it a useful learning experience for you guys as well. So before we start just some quick fax about studying endocrinology, so endocrinology as a specialty, it focuses on hormonal imbalances. Okay, it's all about the hormones, okay? And the key thing is that endocrinology is primarily it's an investigation based specialty. Okay, there's no much in terms of sort of procedures and surgery that you see an endocrine. It's primarily a very medical speciality, heavily focused around investigations and working up patients for all these different hormone imbalances on D managing them accordingly, as with all specialties having a good foundation off, Um, foundation knowledge is important, okay, particularly anatomy and physiology. But endocrine in particular is crucial to have a good understanding of physiology because all the different ENDOCRINOPATHY is we'll talk about is directly relevant to the underlying physiology. Okay. And the way of structure today's session is that for each different and a crime condition will talk about the relevant physiology before. Okay, so we'll talk about all the different access, Okay. All the different hypothalamic pituitary and organ access. Okay. And then the relevant apology it is Well, okay, so hopefully you guys will have a strong conceptual understanding of all of these different conditions. And also just to keep principle to remember in endocrine. Okay, whenever you're investigating any condition in endocrinology is that the first step to investigating patient is to work out if ah hormone is in a deficit or access. Okay, before you start searching for lesions, Okay, before you start trying to localize where a lesion ist first need to confirm ever hormone is in deficit or access. Okay, that's a very important principle for all of these conditions in underground. Okay. So gently a suggest rule for under crime scans and radiological investigations are never really the first line investigation. Okay? It's usually the blood test, the test for, um, investigating hormone levels and working out the IT balances. Those are usually the first line investigations. Okay, so you want to screen for the hormone imbalance initially, But also remember basic concepts here if you have a disease, often endocrine gland. Okay. The end big target. Underground gland as a primary disease. Okay, so if you have a primary hypothyroidism and means that you have a problem with the thyroid gland, disease is about to be the trick land is a secondary disease. Okay, so if you think about the access, you have a lesion at the level off the the two gland. That's a secondary disease. Finally, you have disorders off the hypothalamus, which is generally quite right. You call it a tertiary disease. Okay, Just basic principles. We're getting out the way. So it's it's got a few SPS today, Okay? But a lot of them will be quite challenging. But here's our first one. And if one of the team members can load the polls, I'll give you guys about, um, I'll give you guys enough time to, uh, have a cover. Think about the answer and, uh, hopefully answer, answer with good thinking as well. So Sunday. Is the polls active? Yeah. I'm just launching to do all right. Yeah. If you don't know what's happening with these any of these SPS, don't worry. We'll talk through all of these conditions from first principles. But we do. We'll do some SPS just this sort of test. How much you already know when some identify some importantly bites. Okay, It's so he's on now. Sorry, guys. Thanks. Yeah. Okay. All of that. Getting you guys right. Okay. So pretty tricky question to start up with. Most of you went forward. D on the correct answer here is actually be because of decreased episode travels. Okay, so And as I said, the key reason for that is because high levels of prolactin will call suppression of gonna drippings. Okay, so let's break down this SBA. Okay? So what is the diagnosis? That what is the cause of the symptoms in this patient's? What is the underlying diagnosis? They can be done in the chat adenoma yet. So specifically, you call you calling it a prolactinoma. Right? I guess it was definitely this This patient has a prolactinoma. Why? So we'll we'll talk about this, but plastic clinical features off prolactinemia is glacto really and amenorrhea. Okay, very common clinical features. Okay, the colectomy isn't that common, but it menorrhea is definitely a common feature in, uh, hyperprolactinemia. Okay, I've told you that there's that four millimeter mass in the pituitary gland. Okay? And classically hyper prolactinemia is commonly caused by a prolactinoma. Okay, so on adenoma and the the two line on D can you tell me is this a small? I don't know. Is it a large adenomas and microadenoma. Or is it a macroadenoma? Yeah, it's a small one. Okay. For minimum forming, which is is small. Okay, so it's a microadenoma. Okay. And to 40. So it's above 200. So it's very likely that this patient has a prolactinoma. Okay, so So we've confirmed that the patient has a problem to normal. Okay. And basically clinical pictures and on the MRI now, in terms of the option. So why do you get decreased episodes? Levels in prolactinomas are specifically hyper prolactinemia. What is the cause of the decreased appetite levels? Was the physical physical article mechanism increase dopamine? So increase dopamine. Well, um decreased prolactin secretion. So yes. So suppressions. Oh, yeah. I've said I've told you so. High high prolactin will inhibit. Release off accusation. LH. Okay, well, inhibit cannot. Atrovent's on the Logan. Other truck through pens is one of the key causes off most of the clinical features you see in a prolactinoma. Okay, so that's why you get decreased FSH. Okay, that's a key thing to remember. You have low gonadotropins and a prolactinoma. Okay, uh, so if you talk about to some of the other options are increased estradiol level. So estradiol was basically a because to Easter gym. So you'd expect a lower estrogen levels with a product, a number decrease Colazal and free t four. So with it, if an adenoma it's compressing other structures within 2 to 3 gland, you could get max effect leading to reduce secretion off the pituitary hormones. But this is this is a small adenoma. Okay, for me to the small, you're unlikely to have a mass effect. Okay? Same thing with abnormal visual fields. So if you have a particularly large to tree adenoma back in potentially compress chosen structures in the visual, papa. Okay, but this is again. It's a microadenoma unlikely to be causing any kind of visual field defects and increased libido. So you have low gonadotropins. So you have a decreased libido. Okay, so that's hopefully that that question is clear. Uh, this second part to that question as well if you fall again so we'll talk. We'll talk through all the different, uh, distinction between my credit. Almost. Microbelover, sir. Just have a go downstream. PSP is for now. That Okay, So most of you went for a a couple of you went for C and B as well. So mostly you got the correct answer on that is eight back down to here is a stock, um individual in on follow up with an obstetrician. Okay, so this is a patient, same patient who's had a diagnosis. Prolactinoma. Okay, remember, it's a small prolactin on that, a microadenoma on. But we'll talk about management. But the mainstay of management or prolactinoma is where the medical therapy. Okay with dopamine agonists. Okay, Onda, can you guys tell me why? Why would you give a dopamine agonist in prolactinomas? What's the why is dopamine agonist going to be effective in lowering productive levels? Yeah, very good. Okay, we'll talk about the physiology, but don't mean inhibits and don't means one of the main inhibitors of productive, please. Okay, so that's why I don't mean agonists are the main stay off managing prolactinomas. Okay. And conversions, the very common commonly describe dopamine agonist. Okay, but the key thing is, I've told you this SP that this patient has had a proposed plenty test. So as I said here, So generally you have to stop dopamine agonists in pregnancy, okay? And obviously, and follow up with a specialist. Okay, So generally, for dopamine agonist, you stop in in pregnancy, particularly because this is a very small adenoma. Okay, you don't need to worry too much about it. You know, in pregnancy, productive levels can rise anyway. And you might think that might cause the adenoma to grow even more. But generally, because it's a very small prolactin normal. It's not going to grow too much. So you can stop the Augmentin, Agnes, and follow up with a specialist. Okay, if it's a very large adenoma than you know, it's some particular special cases. They might continue it again with extensive monitoring. But generally, dopamine agonist should be stopped in pregnancy. Okay, Terms of the other option. So switch to bromocriptine. So there's there would be no reason to switch. Okay, continue vigilant and check prolactin level. So there's no point checking prolactin levels and pregnancy. Okay, because prolactin is going to go up anyway. Okay, if anything is just gonna make you make you more scared. That patient having a high prolactin levels and you're gonna make a patient scared of you keep checking prolactin levels. Okay, So remember in pull it, remember in pregnancy prolactin levels is going to go up anyway. You know, you're not gonna add in another dopamine agonists, okay? And you don't need to do visual field testing because it's a very small abnormal so that it's unlike it's be causing and mass effect. Okay. And I got another SBA here, and then we'll start talking through some key clinical principles regarding prolactin on this. Yes, Um, said it's a broken in that it's safe in pregnancy, but generally used to stop the dopamine agonists. Okay, because generally they have some associative association 50 fax, and I was in pregnancy. Prolactin levels. They're going to go up anyway to General. You don't want to interfere with that physiological processes. Well, do it productive. Just go up to helping breast tissue development as well got call it that. Okay, So most of us for B and that is definitely the correct answer here. So risperidone. Okay. So if getting to remember is that not all causes off a high prolactin level is going to be caused by a prolactinoma. Okay. And no, all causes us to do too high prolactin levels. Okay. There are many other causes. Okay. Particularly many medications can cause high prolactin levels. Okay. And risperidone is one of them. Okay, so, Gemzar, the SBA. So this patient has features off prolactinemia on. But I've told you that the pituitary MRI has showed no lesion, and, um, in terms of a lot, these options risperidone the most likely want to cause hyperactive levels. Okay, so, risperidone, it's ah, in a typical antipsychotic. Okay. And I've told you, this patient has history. Mental health problems, like probably what? I'm trying to get out with the responses on risperidone on drospirenone is one of the causes off hyper black tenia Okay. Ah, Can you tell me what? What about any of the medications that can cause high prolactin levels? You guys know what other commonly prescribed medications can cause high prolactin levels? That's low for my very good. And psychotics, particularly the typical antipsychotics, like haloperidol. Very good. Good. Yes. It it doesn't mean doesn't mean with the student very good. So people on the pill people taking the combined or contraceptive poke, you can also get a prolactin as well. Good. So we're gonna start off by talking to some pituitary disorders. Okay? Particularly prolactinomas on the major pituitary disorder you remember that we're going to talk about is the pituitary adenoma. Okay, so and when we're classifying pituitary adenoma is the main way we can fight is by its size. So classify it as either a marker, a microadenoma or a macroadenoma. Okay. And the key sort of size this thing, the the size difference is that is 10 millimeters. Okay, It's less than or equal to 10 millimeters. You call it my garage enema waited. And 10 millimeters. You call it Macrodantin. Okay. As a general size differentiating back. Okay, so you classified by size, but you can also classify it functionally. Okay, You can ask the get to try out new ones which are functional opportunity adenomas, which are non functional. Okay, of what I mean by functional is that is the abnormal producing hormones. Okay, so that's another way you can differentiate. You can pacify Ademas, Okay. And another key thing is that most I did almost effectively. Pituitary gland are sporadic. Okay, so they just occur. Now I say that. Can you guys tell me any any hereditary cancer syndromes which might predispose patients to developing the to jab? Enormous. We'll talk about it later. But you guys know men. Which type when you do a specific as you can't men one. Very good. Okay, So multiple endocrine neoplasia type one is associate it with the two Children of us. Okay, we'll talk. We'll talk about men later, but very good knowledge. And so physiology in a Okay, so it's key to understanding physiology to understand endocrinology. Okay, so let's talk about the access, okay? And when you talk about prolactin that we should talk about the another trip, it's a swell. So how is prolactin produced? So generally it's produced is produced from the anterior pituitary gland on the main thing that's going to stimulate it. Release is low dopamine levels. Okay. So dopamine will normally inhibit prolactin Release from the answered the tutor gone. So when you have reduced openly levels, you get increased secretion off productive. Okay? Prolactin, and it's physiological function. It's mainly responsible for increased using breast issue. Okay, to prepare the mother to prepare mom for lactation. Okay. And also, it's going to inhibit ovulation because it has a suppressive effect on, um, you're not a drop in releasing hormone. Okay. G N R h. Okay. And so because as this suppressive it back, it'll actually decrease, cannot drop ins. Okay, so this is why, in a prolactinoma when you have loads of prolactin, you get low gonad a trip. It's okay. Very important. Um, physiological mechanism to remember. Okay, so some reflect on prolactinoma. Okay, We've already talked through most of this stuff, but a prolactinoma is the most common functional pituitary adenoma. Okay, awful. The hormone producing adenomas prolactinomas on the most common functional ones. I've talked to some of the drugs that can cause high prolactin levels. Okay, particularly but closed minded and psychotics are very common ones. Uh, prolactinomas. Generally very small. Okay. So generally you don't get mass effect, okay? You don't get features off the adenoma compressing other structures. Uh, but if it's Radley can be very big and might need to hypopituitarism okay, the clinical features. So most of these clinical features are mainly going to relate to the low gonadotropin. So you get it, uh, get galactorrhea because of the high prolactin levels. But actually, it's actually quite uncommon to get bacteria, and all the other features are going to relate to the low gonadotropins. Okay, so amenorrhea reduced libido. Gynecomastia and man reduced fertility. These are all common clinical beaches. Okay, now I've told you that I told you the clinical features. Now, can you guys tell me who is going to present earlier with a prolactinoma man or woman who is more likely to present earlier? Generally speaking, if you think practically who was more likely going to present earlier, where they prolactinoma we're getting a bit of a next. Yeah, Bit of a mix, I'd say. Well, I see a woman to have a stroke. A woman? Uh, probably more likely to be present earlier with a peaches of hyper black anemia. Okay, because of irregular period because of amenorrhea. Okay, generally woman combat two men. Okay. You know, men, the erectile dysfunction. Initially, you know, then I'm not going to initially strep present straight away to the GP because they skipping erection or something. Okay. Being amenorrhea, a lot of women will presents initially, because off about pregnancy and things. Okay, amongst other differential for amenorrhea men, generally speaking, epidemiologically, they're going to present later. Okay, Now, if I tell you that men generally present later, who who's who's more likely to present with features off mass effects. Okay, Who present most Who's going to present more likely with features or mass effect with a big adenoma man. Very good. Okay, cause man presenting later, so it's more likely at the adenomas mean to grow a bit bigger and more likely to compress other structures. Okay, very good. Uh, in terms of the, uh, investigation. So you obviously you're gonna measure prolactin levels. If it's more than 200 it means it's likely if it's greater than 500 you'd be worried with. It's actually a very big adenoma. Okay, Onda, uh, scan the cuticle and obviously and obviously for any woman presenting with changing periods and amenorrhea and I prolactin level of you, You what you you want to do you want exclude pregnancy? Okay, cause pregnancy one is one of the most common causes of high prolactin levels. Okay, treatment. So this is very important. Okay. Prolactinoma is pretty much the only functional under crying functional patootie. Add adenoma, which you treat initially with medical therapy. Okay. For the other functional adenomas you generally, first line is to do surgery okay to remove the abnormal. But prolactinoma is specifically the main other number where you treat industry with medical therapy specifically dopamine agonists. Okay. Oh, Janey, it's generally first line. Okay, on be something you might think. Why? Why? Why can't you just remove it? But surgery has complications, and prolactinoma is in general of very responsive to medical therapy. Okay, If you can treat them with medications, then you do that. Okay? So dopamine agonists are generally very effective in in reducing besides off the prolactinoma. Okay, Okay. Next question is we talked about prolactinomas that Let's keep going on. So some of that's why you get osteoporosis. So yeah, you're right. It's because of the lower Eastern levels. Get I will, uh, to be a bit more time. Oh, okay. I'll call it that. Okay, so you got big split between a and be okay. It's an understandable split, but this is a question highlighting the important principles off investigating, um, investigating this condition. So let's talk about it. So correct. Answer here is See a case, a measure insulin like growth factor. And that's because the first step invest in investigating acromegaly is to measure the insulin like growth factor one levels. Okay, so this is a patient who has many clinical peaches that are characteristic off acromegaly. Okay, acromegaly is a condition characterized by excessive levels off on growth hormone levels. Okay, so I spoke to some of these features. So this patient has so with the growth hormone, obviously, the big thing is things are going to grow. Okay, so we got finger swelling because of that. Patients having difficulty with integrate gripping objects. Hypertension is very common with acromegaly because of excessive growth hormone levels. Ah, possibly because you're getting a change in change in size of structures. You get changing facial features. A specialty. Just gonna be a much more course. I have also do a common way people can notice. This is that they noticed that that driving license driving license picture is different from, um, from what they look like right now. Okay. On what? Also also, I told you that tapping the back of the right wrist produces shooting pain on the lateral side of the right time. Uh, can you guys tell me what am I trying to get up with that specific feature? Couple times under a Very good. Okay, So a couple of acromegaly is in the differential for couple times syndrome. and centuries because you're getting on increase growth off soft tissues around in that area that can compressed a couple tunnel. I can't leave Tol tunnel syndrome and also said that, sadly, is wedding wedding ring no longer fits him a swell. Okay, this is all related to the increased growth off soft tissues. Okay, No. When you investigating acromegaly? Why why? Why do you not measure the growth hormone levels? Why did why is the first step to measure I, Jeff one rather than growth hormone levels? Can you tell me in the chart what's what's the problem with measure in growth hormone levels, you know, and tell me why is it better to measure the I GF one also the Advair against the growth hormone? It's released in a positive fashion, okay, and go to him and has a short half life. And it's it's one of these stress hormones. Okay, so it can be very variable Congar up in if a patient, if a patient is stress and things I just want is is produced by liver, it's a very it's very it has very stable levels, has a very long half. Life is well competitive. Common so first step in investigating acromegaly is to measure I g f one. Okay, because growth hormone will stimulate the reduction of I g f one. Okay, just look what acromegaly now. So we'll talk about acromegaly. We need to think about the access, which is relevance for acromegaly, which is the, um, access related to growth hormone production. Okay, so how is growth hormone producer growth hormones least from the anterior pituitary gland on? People often get confused about the differences in function off growth hormone. And I GF one. Okay, no growth hormone. The actual direct functions that growth hormone has is that it's mainly an anti insulin. Okay, it has anti incident effects, so it will reduce glucose uptake into south. So increasing blood glucose levels and also increased, like policies are increased fat breakdown. So that's deed FX directly. And that's directly done by growth hormone. Okay, how indirectly growth hormone conduce, um, functions as well, and that's mainly by causing the production off insulin like growth factor. I g f one. Okay, so growth hormone will stimulate the production of IVF one, and this is this is being brought home on doesn't actually really cause it broke. Okay. Growth hormone is not the one that does the growing in acromegaly. Okay? It's actually the idea of one which is actually causing things to get bigger. Okay, It's going to stimulate the cartilage formation, but increased Kalita growth. Okay. And increase protein census. Okay, so it's going to cause all the talked issues too and large. Okay, so that's very important. Okay, so so see, I just one that's mainly causing the growing growth. Hormone itself is mainly involved in the blue coz metabolism and the fat metabolism. Okay. And in terms of other things that don't mean will also inhibit anterior pituitary gland and that can also reduce secretion of growth hormone. Yeah, So we talked about acromegaly and also we talked about in excess levels off growth hormone. Okay. And the major cause of acromegaly is pituitary adenomas. Okay. And more than 90% of cases of acromegaly will be caused by 2 to 3 adenoma. And unlike prolactinomas, acromegaly is usually because of a macroadenoma. Okay, So usually with acromegaly be actual adenoma is actually quite big. Okay? Because they're quite big. You have risk off complications such as mass effect, okay? And also because of the I've been over compressing other structures within the pituitary gland. Okay, Now, you might you might hear of another condition called gigantism. Okay, So, Jack and is, um is it's it's similar to acromegaly. Just means that you're getting the excess growth hormones before the infusion off the fifties. Your plates. Okay, so it happens in Children and because it's occurring before the plates actually fuse. That's why Children with gigantism actually grow much more compared to patients with acromegaly. Okay, because they that bones and soft tissue just enlarge much more before because the state's having actually fused together. Okay, clinical features are you. You guys can probably figure out most different features. Okay? Things are getting bigger things. I signed hypertrophy get this figured mint. Okay, you get changing body habits, changing facial features, a lot of different things. Okay, correctly you get you get excessive sweating because off Patricia of sweat glands get features related to the soft tissue swelling. So, whitespace teeth from the busing. Okay. Spayed like hands. Okay. A couple tunnel syndrome we talked about because of compression of the couple tunnel and in the history patients might say that things like shoes and rings are not fitting them. Okay? And we talked about mass effect. Okay, So because of the large adenoma, you can get headaches and get problems with vision. Will talk about the visual field defects in a bit. Treatment of acromegaly is different to prolactinomas. Okay, so first line in acromegaly is surgery. Okay, unlike in prolactinoma is where you can you put medical therapy is usually sufficient. Okay. With acromegaly, patients need to have the adenoma removed. Okay? And the reason is that because of the confirmation, the complications are much higher in acromegaly. Okay. And off. See, the the typical features are much more dangerous with an acromegaly, so it's important to get rid of the adenoma as quickly as possible. Okay, Uh, if the patient is on suitable for surgery off, the patient has symptoms after surgery. Then you can try some of the medical therapy slight, create tight and things. But generally, surgery is that the key thing is that surgery is first line. Okay, Many complications associated with acromegaly. Okay. And they're all going to be related to the excess growth hormone levels causing proliferation off difference organs. And you can um, ugly and things. And so that's why it's very important. That condition is that patients get treatment as soon as possible again that it's identified it as soon as possible. Okay, No. So can you tell me what is the classic visual field defect you get with a prolactinoma over it with me? But it's over the acromegaly. What's the what's the most common? What's a classic visual field defect you get with a It's huge adenoma causing mass spect bitemporal hemianopia. Okay, let's talk through some visual field defects now. So go little picture here. So we have the toujeo gland here. On on top of it, we got the optic chiasm, but they were both The optic nerves are meeting on, So if you have a Makharadze know, my case of the gland is getting really, really big. Then that pituitary tumor can compress on the optic chiasm on. You tacitly get a visual field defect known as a bitemporal hemianopia. So I made this little schematic representation off the visual pathway. Okay, top. Everyone understands some of these defects. So, with a with a pituitary, I don't know, but the lesions going to happen here. Okay, at the off the chiasm. So if you follow the visual pathways, So if you have a lesion affected the optic chiasm, you're gonna lose the visual information coming from the nasal hemiretina off the left eye and the nasal honey right now, the right eye. So you're going to lose the left visual fields off the left eye. So the temporal visual fields off the left eye and the poor a visual fields off the right eye. Okay, So in terms of what the actual defect will look like, this is what the defect will look like. Okay, so you're losing your temporal visual fields, and that's what a bitemporal hemianopia is. Okay. Very important. Very high yield point to remember with the toujeo adenomas. Not okay. So it might be useful for two. Just revise some visual field defects with you guys while I've got this diagram. So it's a hopefully be a useful revision as well, but be quite fast. Can you tell me what kind of visual field defects are you going to get if you have a lesion? Are that I've drawn here? What's the visual field defect you get? Yeah. Monocular vision loss. Okay, So this is a lesion of the optic nerve. So you're going to lose vision in that left eye. Okay, so you get left monocular vision loss, Okay. Ah, let's go. Let's go. Here. You have a lesion. At this point, what's the visual field defect you're going to get? So I want you to be as specific as you can when you're when you're giving the answers. Very good, right? Homonymous hemianopia. Okay, So this is a lesion affecting the left optic track. Classically lesions affecting the optic trucked. You'll get a contralateral homonymous him. You know, Pia. Okay. Without macular sparing. Okay. And, uh, so I classically that caused by middle cerebral artery occlusions. And so this is the station would have a right, uh, monocytes hemianopia. Okay, now, okay. These wonder a bit tricky. Yes. So let's talk about a lesion at this point here. Water is the lesion. What type of visual field defect that you're going to get? Whatever visual field defect, would you get it with the lesion? I just from there, I'm getting a bit of a mix, so it's so it's a right. It's Ah, right. Um um, on a muscle superior quadrantanopia. Okay, so you get a superior quadrantanopia, you lose the right visual fields, but specifically the superior quadrants. Okay, because we're the lower bundle off the optic, Grady. A shin that carry special information from the lower right now. So you lose your superior visual fields. Okay? On day, just a complete. So if you get a lesion affecting this point, you will get an inferior quadrantanopia. Okay, well, I hope you talk about this more in your Oh, you're up in your old gym thing. I'm just trying to revise quickly with you guys. Finally, if you get a lesion affecting the left primary visual cortex, what's the visual field defect? You're going to get very good, right? Homonymous hemianopia with macular sparing okay, so classically with a lesion affected the primary visual cortex. You get macular sparing. Okay. And obviously, because if you get a contralateral Oh, mama's hemianopia as well. Okay, Okay. That was a bit of useful revision for you guys about side the scope of under crime. But I made this diagram. I thought my swelling kind revise some stuff with you guys is well, so the main back to acromegaly. So investigating acromegaly PSA The first step Measure idea if one levels. Okay, if it's normal, that basically rules out acromegaly. Okay, If it's high, that means acromegaly is likely on. The first step is going to be discounted. Pituitary gland. Okay, so do the MRI. Okay. And confirm that. Confirmed the adenoma. Okay. Confirmed the functional to Chattanooga. Okay, um, if the eye Jeff one is unequivocal. Okay, I eat. You can't You can't tell if it's like you if the patient has acromegaly and not use your insurance. So then you do you do an oral glucose tolerance test. Okay, So, essentially going to give a glucose load to the patient's okay and room that remember, I told you that growth hormone is directly involved with increasing glucose levels. So if you give a Blucas load normally, if a patient had a normal growth hormone levels, you'd expect growth hormone to be suppressed. Okay, because of negative feedback. But if someone has excessive levels of growth hormone levels, then then it won't be suppressed following an oral glucose tolerance test. Okay? Again. All because Stolen says if growth hormone is failure to suppress growth hormone means like acromegaly, it's likely and then you should do the I'm all right, but your gland. Okay, so I was a quick run through of acromegaly. Okay. Ah, Got another recipe, if you guess just what I just wanted to special session. Probably last the full hour and a half. Okay. Potentially. Even longer than that. This endocrine is one of those massive content field specialties, but, uh, hopefully will have a really comprehensive uh, revision. So, actually, you guys Yeah, this is a dust. So you want to explain or glucose tolerance test. So So remember that with the growth hormone is normally going to increase both hormone levels, right, so it goes home and normally will increase group glucose levels. So if you give loads of glucose to the patient, you expect from told them to be suppressed because of negative feedback, Right. Okay. If someone has normal glucose, normal growth hormone levels, you'd expect growth hormone to be suppressed by giving a glucose load. But if a patient has acromegaly where you have excessive on both hormone levels at the glucose load will not suppress the growth hormone levels. Okay. And that indicates the patient cards acromegaly. Okay, get under there. Most of you have got this. So mostly you got the correct dance here. So for tutorials Kenya. Okay, so, basically, still on the topic of pituitary disorders, they're gonna move on to talk about sort of hypopituitarism, but Ah, so this is a patient post partum. Okay, so this a patient to has, uh, delivered recently on be complicated by post partum hemorrhage. Okay. And one of the complications off most severe postpartum hemorrhage. Is she on syndrome? Okay, So, essentially, because of the massive hemorrhage and massive ischemic events to the pituitary gland, you can get symptoms off hypopituitarism. Okay, so you get 2 to 3 a skin here because of that massive hemorrhagic events, and that can lead to these symptoms off of the toujeo. Is, um okay. And that's known as she hadn't syndrome. Now there's a couple things that points towards, um, low pituitary function. Okay, so, uh, blood glucose levels are low because she's not producing ACTH. So not able to produce quarters are levels are not able to increased glucose levels. Okay, so you get low glucose levels, and also TSH is low. A swell. Okay, so these are all features off low pituitary hormones on day. She and syndrome is is one of the acute causes off hypopituitarism quick slide summarizing hypopituitarism. Okay, So usually usually most commonly would be caused by macroadenoma is compressing the to compressing the future gland. Okay. And I've sort of listed the key symptoms regarding deficiencies and this hormones and the classic order in which you get get these deficiencies. Okay, Um, so this is this is when you have, um, type of the toujeo. Is, um, because off mass effect. Okay, because you're having a normal compressing the, um, compressing structures in the pituitary gland that this is the classic order in which the hormones get deficient. Okay, but there's other causes as well. Such a she hunts syndrome what you talked about. Okay, now we're gonna talk about thyroid gland. Okay? I was a quick run through off the pituitary gland and some of the key relevant disorders. Okay, there are some other ones, and I've put them as post lecture notes for you guys to revise from in your own time. Uh, but let's not move onto paragraph, which generally they're students are pretty solid on thyroid. Thyroid is one of those glands which students usually study pretty well and, uh, smashed those SPX past ESPs find the SBA is a bit easier to access compared to the other ones. I say that, but I've tried to make me tired experience a bit harder. Okay? Yes, sir. The yes, the unconsciousness was due to the hypoglycemia. Sorry, didn't go through that. So because of the low ACTH causing hypoglycemia on, that's probably why she had an episode of loss of consciousness. Yeah, I call it, uh, roof. This is a big split I gave you. Got a genuine split between a, B, C and D. Here. Okay, So took ESP A, but ah, it's funny because of the way it is. Yes. Try to trick is a tricky sk. Correct. And the hair is non pitting edema. Okay, so let's let's go through. Ah, this SPS. So this is a patient who has speech is of anxiety, insomnia, heat intolerance, weight loss. These are all features off thyrotoxicosis. Okay, Hypothyroidism. Okay. And I've said this stuff about her friend studies medicine says the symptoms might be due to autonomous functioning of tired and audios. Okay, so that's a feature off. Um, that's a description off a condition called toxic multinodular Goiter. Okay, where you have multiple auto autonomous thyroid nodules producing thyroid hormone. Okay. And on on examination, there's a mass in the parotid gland. Um, So I've asked you which of these things points away from the diagnosis being toxic multinodular goiter. Basically. Okay. And the other thing other main, most common cause off. Uh, hyperthyroidism is obviously grave's disease. Okay, so this question is basically asking which of these which of these clinical features is specific to Grave's disease? Okay. And out of all of these features, non pitting edema is the one that's most specific to grave's disease. Okay, Can you guys tell me why do you get non pitting edema in, uh, graves' disease was the cause of non pitting edema and graves. Disease? Yeah. Myxedema. Okay, you get pre tibial myxedema again. That's a specific feature off grave's disease. Okay, we talked. We talked about this in hepatology. Okay, remember this. There's only two main causes off non pitting edema. This myxedema. And there's, um, lymphedema. Okay, those are two main causes off non teaching a demon. Okay. Onda pretibial myxedema is a specific feature off grave's disease. Okay, as someone's told me that little like suggest graves eye disease. Okay, I see what you mean. But like specifically, it's not specific to groups. Okay, you can get little, like with, with with any course off by a toxic OSIs. Okay, there's other specific features of graves eye disease like except almost proptosis the detraction, but, like, in specifically is not a specific feature of graves. Eye disease. Okay, So let like it's where you get you get the vision to follow the finger and swing your finger down in Austin to follow it on. Like specifically, you can get that with other causes off. Diarrhea toxicosis. Okay, Approximate muscle weakness. Or you can get that. And it's not. It's not specific to Grave's disease s V t. So super ventricular tachycardia. See thyroid hormone. It says if you have high diet woman that can lead to tachycardia, So okay, it's not specific to grave's disease and diarrhea, so tired hormone will stimulate g i motility. So you get diarrhea. Okay, if you have increased your motility. So that's why the correct answer here is non pitting edema. Okay, tricky. Get tricky Question about important learning points. Okay, so quick recap of thyroid physiology. So you guys all know this, Okay, so from the hypothalamus, Yeah. Hates which stimulates the anti opportunity gland to produce TSH on. That's going to stay like the thyroid to produce t four and t three. Okay, so, thyroxin, and, um, it's just remember, t four t three. You don't need to remember. The actual and word for it on D 43 will cause negative feedback. Okay, so remember, we talked about the different levels of the lesion, so it's a primary primary cause off hypothyroidism, or if it's a primary cause of hyperthyroidism, it means there lesion is at the level off the para gland. And but and, Ah, and if it's a secretary means it's solution effect in the anterior pituitary and the hypothalamus. You have all of these different blood tests values for thyroid function test, depending on where the level off the lesion is. Okay, I'm not gonna go through all this, but just talk about how primary hypothyroidism. So if you have a primary hypothyroidism, it means that your paragard is not functioning to produce enough thyroid hormones. Okay, so doctor gland is basically under active. Then you're gonna have low t four and t three and you have high TSH because off. Ah, lack of negative feedback. Okay. And if it's primary hyperthyroidism have high t four and t three, but you'll have low TSH because of negative feedback. Okay, Have a read of some of the other investigations. Okay, but that's the That's a key recap of physiology. You guys know what the generals features are off hyper and hypothyroidism, Okay, I don't need to go through. You know, generally hyperthyroidism is going to speed things up. Hypothyroidism is going to slow things down, okay? And these are all the classic clinical features you get depending on if you have high or low diet Homans. Uh, what I will mention quickly is that there's something funky peaches that are specific to grave's disease. Okay. And the key ones are, uh, graves eye disease, which I basically except almost periorbital edema Does a speech is specific to Grave's disease. Critical myxedema as well in hypothyroidism is specific to grave's disease. Okay. And also the things like Barry Acropachy is well, we get sort of digital clubbing. That's also a specific feature off Grave's disease. Well, there's many different causes of hypothyroidism. Okay, I'm not gonna go through this, Okay? But essentially have a read. Most common cause, which you guys know is Hashimoto's thyroiditis. Okay, which is more these days. People tend to call it chronic autoimmune thyroiditis, but that's the most most common one. Probably the most important one to know for finals. Okay, make sure you know how she motors, but have a read of some of these other important cause is gonna talk about Ah, still on the topic of hyperthyroidism. So I would go This s p A. Yeah. Yeah. Okay. Course it's a most. There's a bit of split between be on day the Indy. Okay. And go down to here is D. Okay, so very soft tablets. Okay, so this is Ah, we talked about management of hypothyroidism now. Okay, So you guys you guys know mainstay of managing hypothyroidism is to replace style home. Okay, are giving levothyroxine. Okay, Uh, key thing to remember is that ferrous sulfate tablets, so ferrous sulfate use to treat I'm deficiency anemia is is going to interact with the VA thyroxin. Okay. And beer. So first off, it will reduce absorption of levothroxin on that can lead to patients not being treated, not receiving adequate treatment for the hypothyroidism. Okay, Because for herself, people essentially reduce the efficacy off. Believe that the rocks and by reducing the absorption of levothroxin. Okay, um, so what? Why I told you that the patients fatigue has low MCB on that that, uh, hyperthyroidism undertreated, and that's most likely because she was taking first started to treat her iron deficiency anemia. Okay, it's only that made sense that it's just it. That's just an important back to remember about levothyroxine. You advise patients who are taking levothyroxine and I'm tablets to generally take it about four hours apart. Okay, Because because there's an interaction that so appetite is a management, just basic things to remember. Levothyroxine first line. Okay, just to replace, replace diet hormones, uh, for pregnancy, there's an increased demand for tired. Homer. Okay, So generally you increase the dose in pregnancy, okay? And you have, ah, lower TSH target. And and there's also some things to remember for subclinical hyperthyroidism. So have a read of that. And also, like, we talked about one of the major major interactions to remember with the va the rocks in is that it can interact with iron tablets. Okay. Barrasso. Bates. And so they should be taken at least sort of four hours apart. Okay. You know, a lot of patients won't actually be compliant with this. This is just general advice to ensure that levothyroxine is having its normal efficacy. Okay, um, some dust does. One of the other drugs can cause interaction, so drugs, like stones accounts incompetent. I think calcium carbonate can do it. PT eyes condone it. Um, the oral contraceptive pills. Another important cause off, uh, another drug that contract with levothyroxine this. Well, okay, but first, I'll take tablets is a really important one to remember. Okay, uh, this has ago this question. Okay? Yeah, I call it, uh okay. So most of you want for D on Dallas? The correct answer. So, yeah. TSH receptor antibodies on. The reason is that I've described it. Basically, this clinical vignette is describing a scenario off the patient presented with grapes disease. Okay, this is a classic history of a patient presented with graves' disease and the sort of part of physiological the pathophysiology behind grave's disease is that patients produce antibodies against the TSH receptor, and that's causing the hypothyroidism. Okay, so I've described classic symptoms of hypothyroidism, and also, I remember, remember I told you that. So some features are specific to grave's disease and that certain features of graves, eye disease and that speed proptosis and sort of peri orbital edema as well. Okay, so this is a description of graves eye disease. And so that's why correct answer here is be okay. Okay, Have a good this one. This is another question regarding hyperthyroidism. This is, uh this is probably one of my favorite SPS up today. Uh, I did this is that this is a tricky question. Is that testing your knowledge of some different specialties as well can call it that. Okay. Okay. I got a bit of a split again. I'm sorry of these STDs. Every hard did that. I made them hard just to sort of emphasized importance turning points. But don't worry if you're getting them wrong, okay? They're all I made them hard on purpose just to sort of emphasize key learning points and really trying to test you guys for finals. Uh, we'll go through this. So right down to here. Is he positive? pregnancy test. Okay, so you guys might be really confused because I've told you this is a man, but the patient would actually, like we have a positive pregnancy test in this case. Okay? And the reason is that the patient likely has a choriocarcinoma. Okay. Can you tell me why? Why I wanted this. SBA suggests that the patient has it choriocarcinoma the car carcinoma. It's one of the testicular cancer test. Okay, one of this SP a suggests that the patient has a choriocarcinoma non tender mass in the scrotum. Very good. Okay, so the description has a classic description for testicular cancer, right? So it's a non tender firm mass. That doesn't transilluminate. Okay, Can you tell me if they're ignoring the hyperthyroid symptoms? Can you guys tell me if the if the mask did trans illuminate What? What diagnosis would you be thinking about? Okay, there's a fluctuation mass, Which transilluminated. Very good hydrocele. Okay, but this is definitely not a hydrocele in this instance on. So the key thing to remember a very interesting thing to remember about Korea cost normal. Okay, It's one of the non seminoma testicular cancers is like choriocarcinoma is produced loads off be to hate CG. Okay, so you guys know be taking the the pregnancy hormone choriocarcinoma is produced loads of pizza hcg okay. And interestingly, beat a hasty GI has a similar structure. Do TSH Okay, so thyroid stimulating hormone. So if you have low to beat a hasty G diabetes, it HCG can mimic the function of TSH and cause hyperthyroidism. Okay, so that's why this patient has a choriocarcinoma on Because it's a bit of a TG producing tumor. The patient would likely have a positive pregnancy test. Okay, because obviously practices detecting the levels off pita hate cg. Okay, so let's go to someone's house. Do they also produce a f p? So can you tell me which testicle it cancers produce a f p alpha fetoprotein which testicular cancers typically will produce FP Yeah, yolk sac Tumors in particular will produce loads of FP. Okay, teratoma scan. Okay, produce low, but classically yolk sac tumors. One of the germ cell tumor is can produce loads of FP. Okay, but yolks activist themselves, they're not associated with producing beat hcg and closing hyperthyroidism. Okay, so that's why these patient more likely has a choriocarcinoma. Okay, on over. That's clear. The end. The house, Some of us. Who do you spend? What I hydrocele is the hydrocele. It's essentially it's referring to a a flexion mass that trans illuminates. Okay, so if you shine a Shaina torched, I'm kind of, like, so straight, you'll be able to see the light source on the other side of the scrotum. Okay, that's essentially the description of the hydrocele. Okay, way. Probably cover this in urology someday. I gave a little better revision on testicular cancers, but it's just an interesting thing how specialties can relates. Okay, so choriocarcinoma she can cause hypothyroidism. Okay, so, again, I'm not gonna go through all this, But there's a lot of different differentials for hyperthyroidism. Okay, In terms of the causes of hypothyroidism, obviously the most common one is is grave's disease. Okay, but other other ones, we have other ones that you can have a read about. Okay. Onda. Very important thing to remember that I wanted to make a separate side about is the actual diagnosis of these conditions. Okay, particularly Grave's disease. And Hashimoto's both autoimmune diseases. Okay. And they both have, um, lose the different antibodies, associate it with them. Okay, now important thing to realize with these antibodies is that it's not that one condition has antibodies and the other condition better. Okay, there's a lot of overlap in these antibodies, Okay? It's just that one condition has a stronger association with these antibodies, and another condition doesn't have as from an association. Okay, so the two main ones is Grave's disease, and Hashimoto's thyroiditis okay, the graves' disease. Most patients will have anti TSH receptor antibodies. Okay, Most patients will have that, and most patients will have anti TPO antibodies as well. Okay, more than 70% of patients will have onto TPO antibodies. Okay, uh, you can get antiviral goblin antibodies. Um, but yes. So the main ones with graves' disease is the entity of state Aricept antibodies and anti thyroid. Peroxidase antibody is okay. Hashimoto's on the had other hand is not as strongly associate it with anti TSH receptor antibodies. Okay, they're much more common in Grave's disease in an SBA. If they have anti TSH receptor antibodies, you be thinking more about grave's disease. Okay? Anti TB or antibodies, on the other hand, is much, much more strongly associated with Hashimoto's thyroiditis okay, As well as anti thyroglobulin antibodies. Okay, So anti TB on antiviral globulin are more commonly seen in Hashimoto's started like this. Okay, But again, just to emphasize these antibodies, uh, there's a lot of overlap, as you can see, and often they're not. The diagnosis can be unclear. Just basing. Just based on the antibodies. Okay, so you should put the antibodies in contact with the patient's clinical features. Okay, Now I want to talk a little bit about graves. Eye disease. Okay, cause it's ah particularly important feature in patients with graves' disease. Okay. And holding teachers are graves. Eye disease is except almost. Okay, So you see the orbit, the eyeball protruding out forward. Get ocular motility motility disturbances. Okay, so you get problems with my bowel movement. Literature action. Is this teacher seen in grave's disease? Okay, so you can see the century. You can see the top of the square above the pupil, and the big worry would graves. Eye disease is optic nerve damage. Okay, because you're getting, um, production off very different proteins and accumulation of protein snack and cause pressure on the back of the eye. You worried about patients developing compression off the optic nerve. Okay. And the big risk of that is visual loss, actually. Can you guys tell me what are the different symptoms you'd expect to see in patients presenting in patients with optic nerve damage where they're different clinical features, off optic nerve damage? What kind of things would you be asking about and looking for? If a patient has started as features off optic nerve compression, what kind of different things would you be? Uh, would you see on examination, or ask this all but the pain with a patient tell you on in history Very good. Reduced color vision. Okay. Color vision is very important. Feature. Okay. Reduction in color vision reduce visual acuity. Excellent. Okay. Um, if you have optic nerve compression, classically patients can develop with juice visual acuity, and also patient can get a script. Oma a zoo. Well, okay. Just got, um, essentially sort of blind spot in the visual fields. Okay, these are all peaches off. Um, optic nerve damage. Actually, there's another one can yet on examination. What else could you see if you have optic nerve damage? Yeah, Someone's got r a p d. Okay, so a relative afferent pupillary defect. Okay, these are all important features to look for, uh, with patients with graves eye disease because you're worried about them getting, um, optic nerve compression. Okay. Very important. Most of the most important things to say to a patient with graves' disease is to stop smoking. Okay, because smoking is one of the is the key risk factor for patients going on to develop graves eye disease. Okay, so we're the most important bits of lifestyle advice to give to patients with graves' is to tell them to stop smoking. Okay, if patients have severe disease, Okay, so if they're starting to get symptoms off optic nerve compression, for example, then you need to get started into them. Okay? You typically you're going to give intravenous methylprednisolone because you're worried about them getting vision, loss and things. Okay, Good. Now, quickly. In terms of management of hyperthyroidism. Okay, uh, there's no sort of order. Two things. This there's a various different therapies available to patients. Okay, but there's no specific order, okay? It's usually just like the actual choice of therapy is usually decided on a sort of patient case by case basis, and depending on patient preference is okay. Generally, to manage these sort of symptoms off hyperthyroidism you can give propanolol. Okay. Remember, giving carbimazole combine those old takes time? Okay. Usually takes a couple of weeks to actually at so managing their those initial initial symptoms off hypothyroidism, you can give a pizza blocker like propranolol. Uh, copy result is the first line anti tired drug you give. Okay. Very, very commonly prescribed. Five thyroidism, uh, proprietary yourself is an alternative drug, but it's generally only used in the first trimester of pregnancy. Because problem is all has associated Toronto Genesis teratogenic necessity. So of the first trimester pregnancy. You can prescribe profile, though, you know? So okay, and then switch them back to carbimazole. Okay? Radioactive IDing can be given. Okay. It's generally curative. Okay. Although there's a risk of patients going on to develop hypothyroidism because of over treatment. Essentially, uh, keeping to remember, radioactive idea is contraindicated if they're pregnant. Okay. On For patients who are refractory to pharmacological or pharmacologic therapy or two major active idea. Uh, then you can do surgery. Okay. So removed the paragard. Okay. And they sort of really high yields complications to remember with thyroidectomy xyz hypocalcemia Okay, Yeah, can I said, why do you get hypocalcemia? Where the thyroidectomy Why would you get Why would you get low calcium? Why would you get low calcium with a directly very good So damage to the parathyroid glands there. So you know, parathyroid glands sit very close to there to the barrel, and so his risk of hypocalcemia on. But you can also every current lounge on the 40. Okay. So you can get hoarseness of voice. Good. Okay, so now we're gonna talk about adrenal disorders. Okay, This is the last topic, okay? But it's quite a chunky topicals. Well, but a dream adrenal is one of those things which it's important to gain a conceptual understanding because it can be quite tricky to understand. A lot of the investigations with the adrenal disorders have a good this question. Okay. Yeah, some of that's what's the difference between acceptable Mohs on proper Tosis eso into my knowledge? They're actually they basically mean the same thing. It's okay. They're they're interchangeable. They basically they both based both basically referring to the patrician and the forward protrusion off the eyeball. Okay. I wouldn't worry too. much I do my knowledge. I'm not I don't think there's a difference in your a one. C correct. In the chat. Feel free to, but to my knowledge, except almost and proptosis mean the same thing care. Call it, uh, tricky. Okay, so most of you went for a, uh, most of you went for a 40. 60 of you went for a bit of a split on the other ones. Correct? Answer here is See. Okay, so this is tricky. A tricky, tricky SBA. Okay, but let's talk about this. So this is a patient who has cocoa features off Cushing's syndrome. Okay, I'm sure most of you would have been able to get that. Okay, So Cushing's syndrome, the high levels are cortisol on the body, and it's a lot of things are going towards this. This patient has a weight gain. Obesity, reduced libido, acne strike a thin, easily bruisable skin approximately lost muscle weakness. Okay, So difficulty standing up after sitting high glucose levels is a liters off high cortisol levels. Okay, Hyper quotas. Old. Any a. Okay, So pushing syndrome. Okay. No, we're gonna talk. We'll talk through the different causes of Cushing's syndrome. on down. To be honest, you're in Concord practice. You're not going to diagnose someone based on based on this feature. But can you tell me why is the answer most likely to achieve? What? So the reason the patient has pituitary microadenoma is because off the this thing about darkening of mucous membranes, So And I've told you that the hyperpigmentation occurs in high. Shh. Little. So why would this patient have increased melanocyte stimulating hormone? What? Is that what? I'm trying to get out here? Yeah, so? So the patient has high ACTH. Okay, so with So if you think about the cause of the high cortisol level said if you think about, um, high cortisol caused by pituitary, my accurate microadenoma as you get high cortisol levels because you're having high ACTH levels. Okay, so you're getting high ACTH ACTH levels, which is driving more cortisol be to be produced. Okay, so on the thing with if you have states of high ACTH travels, the important thing to realize is that you also get high levels off M S H levels. Okay, So Milan, a monogamous sites stimulating hormone. Okay. The reason is that melanocytes stimulating hormone FSH and ACTH that both derived from the same precursor molecule precursor. And that's known as pump. See. Okay. Eh, So you don't Don't worry too much about remembering the names, but essentially, if you have loads of a CT if you have whenever ACTH is being produced, you have, um, a teacher being produced. Okay, so if you have loads of ACTH, you have high a message. Okay? So if you have high MSA age melanocytes stimulating hormone, my mom in sex and the hormone will basically cause hyperpigmentation of skin. Okay, you get skin hyperpigmentation. That's why the patient has darkening off mucous membranes. Okay, so that's why that's why the patient has a tooth problem here. Because the stent and hyperpigmentation here suggests that the patient has high ACTH levels. And if the patient has high ACTH levels causing Cushing's syndrome, that means that the patient likely has a pituitary problem. Okay, So can you tell me what do you call? What would you call the What would you call the syndrome here? What would you call call the cause of the Cushing's syndrome here if it's caused by pituitary disease? Yeah, Cushing's disease. Okay, so if you have Cushing's syndrome caused by a pituitary problem. You call it Cushing's disease. Okay, It's quite confusing terminology, but that's essentially what you're where you say it is. What you're what you mean by staying. A patient has cushings disease. Okay, so this is a problem. But if is a urology out, so I'll try and explain that stuff again. But essentially, this is the access that's related to predict production off cortisol on production, off androgens and melon and as well. Okay, so the it's the adrenal access, as well as the and less each access as well. Okay, So ACTH is released from the anterior pituitary gland, and ACTH will stimulate the adrenal cortex to produce cortisol as well as androgens. Okay, if that is produced by different layers of the adrenal cortex, But essentially, ACTH will stimulate cortisol production and androgen production as well. Okay. And remember, this is from the adrenal cortex. Adrenal, middle of it is is essentially an extension off the sympathetic nervous system. Okay, Real cortex is the one that's producing cortisol and 100. It's okay. So Oh, Okay. So, essentially. And if you have high ACTH, you're going to get high MSA. Okay. And the reason is ACTH and M s H are produced from the same, um, precursor palm. See? So if you have high ACTH levels, you can get high M S H levels. Okay, so that's what I'm trying to get out with that s k there. So to talk about Cushing's syndrome. So we know Cushing's syndrome. Its course is referring to high cortisol levels. And when we're thinking about the causes of Cushing's syndrome, we can divide them into either ACTH independent causes causes of Cushing's or ACTH dependent course of Cushing's. Okay, so let's think about the terminology here if it's ACTH independence. That means that the patient is having high cortisol levels independent off the being high ACTH levels. Okay, so common causes are patients taking steroids. Okay, so patients taking exhaustion a steroid. That's the most common cause of Cushing's syndrome. Um, and also patients who have adrenal lesion. So a functional adrenal gyma causing hyper secretion off cortisol that can also cause that cushions. Okay, but again, because it's ACTH independent, that means that be easy and teach will be low. Okay, because if it's dependent it will be, it means it would be high because it means that the high levels of cortisol is being produced because off high levels off ACTH. Okay, so it's independent. It means that the high levels of cortisol is happening. Independence off ACTH. Okay, in terms of ACTH dependent causes, there's mainly to to cause is there's two treat pituitary problems. Okay, which we talked about. So if you having a pituitary adenoma producing too much ACTH second course, Cushing's and that's known as conditions disease, Or you could get ectopic a CTX secretion. So from a small cell lung cancer. Okay, so small cell lung cancers, it can cause a paraneoplastic syndrome, and that can produce excessive levels off ACTH. Okay, terms of features of Cushing's syndrome. So there's many locate a not going to go through all of this, but I common once remember things like mood disturbances, acne, her citizen been easy. Bruisability skin. Um, fat redistribution. Okay, central obesity. Little bit fat accumulation in the back of the neck. Okay, buffalo homes and things hyperglycemia. Amenorrhea is old various different clinical features that you can get rid Cushing's syndrome. Okay, It's a very hard condition to actually pick up. Okay, cause because the presentation can be very northern specific again, and the feet symptoms can can resemble many other differentials. But these essentially the collection of symptoms which patients can present with. Okay, so we're gonna talk about investigating Cushing's syndrome. Now, uh, so have ago, this SP Yeah, yeah, yeah, yeah. Someone send us as a blanket rule in endocrine, but whether it's hyper pigmentation, there's involvement the pituitary of the pituitary. Um, so I I'd rephrase that saying, if there's hyperpigmentation, it means that there's a high FSH levels, okay? And commonly, if there's high FSH levels, if because patients are how they have high a CT troubles, okay, because if you have high ACTH levels will also get high. Um, initiation was Sorry, I'm not loaded. The port story. You can call it that. Okay, so again, I think I've done most of you this one. But most of you were going for D. Okay, Low dose Dex medicines, depression test. Uh, company went for ee and a couple of one for a correct answer here is actually a a a ct adrenals. Okay, so this is it. So investigations for Cushing's syndrome is one of those. It's a very complex topic for students. Understand? Okay. And I'll try to go through it properly, but it can be quite. It's a lot of different tests. Okay to understand. Okay, But to bring this down So there's a patient was classic local features of Cushing's syndrome. Okay, in terms of the key things. So this patient has a elevate 24 hour urinary, three quarters, all okay. On also has a low 18 ACTH. Okay, So keeping the first step to investigate in Cushing's syndrome is the first confirm high quarters of levels. Okay, I remember other started. I said that the first step in endocrinology for investigating is the first confirm if there's an access or a deficit off off the home. Okay. Now, I told you that the 24 hour urine, a free quote result is elevated. Okay, so that you've done the first step. You've confirmed high cortisol levels. Okay? Next step is that the ACTH has been measured. Okay, Now, ACTH a low ACTH means that because off the Cushing's is that it is an ACTH independent cause of Cushing's. Okay, remember I told you that two main causes of a seat independent Cushing's is exogenous steroids and adrenal cancer. Adrenal tumor. Okay, so because the infection has a low ACTH, it means that it's an ACTH independent course of Cushing's. It's means either adrenal it's an adrenal lesion or because of exception of steroids. Okay, and there's nothing about steroids in this in the answer, so it's most likely it's an adrenal tumor. The next step is going to be a CT. The adrenal glands. Okay, so get a scan of the adrenal glands and localized a lesion. Okay, because you've done the initial test to confirm high cortisol levels, and now you can do test, too. Localized disease. Okay, so that's why you can go straight for CT adrenals. Um, so the other other options so shorts and at contests, that's for adrenal insufficiency. MRI, pituitary gland. So this is a patient who has a c t. H independent Cushing's. Okay, if the patient had the two a tree out of pituitary adenoma calls and Cushing's, you'd expect the ACTH to be high. Okay, so that's why uh, you don't need to MRI. Okay. Low dose dexamethasone suppression test. So this is a test you can do to confirm high cortisol levels But you've already confirmed high cortisol levels by doing the urinary cortisol. Okay, so you don't need to do the low dose dexamethasone suppression test. Okay? Now, the high dose dexamethasone suppression test is a test you do to investigate patients who have an ACTH dependent cause of Cushing's. Okay, so you do it essentially to differentiate Cushing's caused by a pituitary problem. And Cushing's caused by, um, ectopic ACTH. Okay. Caused by small cell lung cancer. So because the patient has low a c t h. Do we know that it's an ACTH independent cause of Cushing's? So that's why we can just we know the problems in the adrenal gland so we can do a CT scan of the adrenals. Okay, so again, the learning point, a low morning ACTH indicated a stage independent cause of Cushing's syndrome. Okay, so it's all about investigations. Okay, this is big. Okay? This is super important to get a conceptual understanding off because it's confuses people all the time. But let's try and go through this systematically. Okay, So remember, most of the most common causes of Cushing's syndrome is people taking exogenous steroids. Okay, so first you want to exclude that you want to take a comprehensive history, evaluate the drug charges, check that they just not being taking steroids exogenously for a long period of time. Next step is to confirm high calls, our levels. Okay, So, again, screen for the high cortisol levels. There's three main ways you can do it. You can check urinary cortisol. You checked midnight salivary cortisol levels, or you can do a low dose dexamethasone suppression test. Okay, so essentially, dexamethasone is it's essentially glucocorticoid. Okay, so if you give, uh, I think they've dexamethasone you. You'd expect cortisol level state drop, Okay, because of next feedback. But if someone has high loves a cortisol, you won't suppress the cortisol levels. Okay, But out of all of these things, the most commonly, you get a low dose X medicine suppression test because it's just easier to do. Practically okay. It's quite cumbersome to do 24 hour urine cortisol. So most commonly, patients these days just get a low dose dexamethasone suppression test too. Confirmed. The high loves the Colazal. Okay, eso once you've confirmed high loves of cortisol, then the next step is to measure the morning ACTH. Okay, so if the morning ACTH is low. That means that it's an ACTH independent course of cushions. Cushing's such as an adrenal Juma. Okay, so if it's a service and if the estate is low, it means the problems in the adrenal glands. But if it's normal over, it's of it's high, that is, that the cause off the Cushing's is directly relevant to They're being high levels off ACTH. Okay, so we know that this ACTH being produced from somewhere in the body okay, And remember, it's either because of a pituitary problem, okay? Or because of ectopic ACTH from a small cell lung cancer usually okay. And the way you can differentiate that is by doing an a high dose dexamethasone suppression test. If you do a high dose dexamethasone suppression test and the A C E T. H is suppressed, uh, that will cause the um that means that it's pituitary problem. Okay, because high dose dexamethasone will suppress sthe that pituitary disease. It's not suppressed. That means that it's ectopic a stitch. Okay, that's basically what you're trying to get up with. The high dose Dex medicine. So it's basically helping you differentiate if it's a pituitary problem or if it's an ectopic problem, okay? And that's how you investigate Cushing's syndrome. Okay, Hopefully, that's really clear. Okay, that's very important. Okay, But you guys were I can go to that again at the end if you want, but those are the sort of key principles to understand. Okay. And just to make sure you really understood that I've got another question for you on investigating Cushing's syndrome, and hopefully this you guys will be able to make extensive this one on be able to answer it. Yeah. Yeah. So it's probably gonna rub on over by another 15 minutes. Guys, I got a couple of more dream of the soldiers to go through. It's all recorded. Don't worry. So if you ah need to get a head off, that's fine. You can review the recording, but yeah, if you want to stick around and keep interactive with me and I'll be good to smoke. Oh, so you mostly you got it. Uh, so yeah, but hopefully I to me that tells me you guys I explained that well enough for you guys. The most of you got the answer here. So Kirkenes here. Small cell lung cancer. Okay, So again, we got a patient with features with features Are Cushing's syndrome. Okay, Um, and in terms of the investigation, So morning ACTH is elevated. So that means it's an ACTH dependent cause off Cushing's. Okay. On down. Oh, sorry. Uh, it's the You're checking it. Cortisol levels are suppressed. Sorry. Okay, so the cortisol levels is not suppressed after low dose dex, a matter and the high dose dexamethasone suppression test on day. So that means that it's likely means And it's an ectopic east teach, um, production. And that's out of all these cause it's usually small cell lung cancer. Okay. Just all right. I should go back. I I forgot to change in this light. I remember. I made them say this should say cortisol. Okay, so with the Dex noticed impression that you're checking it cortisol levels, it's suppressed. Okay, Sorry. Sorry about that. But you checking if the cortisone was suppressed after the dexa minutes. Um, okay. Quickly in terms of management. So I just go to for patients who are taking excessive story short, they got If they have Cushing's syndrome because they're taking steroids excessively long term, then the key thing is that you don't just abruptly stop steroids, okay? You don't just suddenly just take started away from the prescriptions, okay? Because we'll talk about this. But if you just suddenly stop is if they've been taking steroids long term and you just studying, you asked him to stop taking them and that there's a risk of patients going into an Addisonion crisis where essentially that their adrenal guns just shut down completely. Okay, so you just you start a gradual taping regime. Okay, so you gradually reduce the steroids in the patient's prescription, and you always safety netting. Okay, so tell them to keep following up and keep monitoring the patient. Okay? I have a refill for some of the causes off some of the other cause cause of pushing center. Oh, that's interesting one. So if you have, if you have high levels, the cortisol cortisol has mineralocorticoid activity so we can act in a similar way to aldosterone and cause, um, excessive potassium excretion. Okay. And you can get hypokalemia because of that, so spironolactone can be given because it's going. It's a mineralocorticoid antagonise, so it can essentially block the effects of cortisol. Okay, so if they have to be a hypocalcemia because of high cortisol levels, you can get spironolactone. Okay, Next question. I think we have, Ah, Two more SKs left. We'll talk about this disease, and there's two marginal We sort of we will talk about and then I'll be it. Uh huh. Those some of those can explain why you get metabolic alkalosis in Cushing's syndrome. Yeah, it's a good question. So essentially, Because if you have, um, said remember, the function's off aldosterone aldosterone will cause excretion off hydrogen ion. Right. Okay, so my mineralocorticoid is cause excretion off. Um, tasi Um okay. And cortisol. Well, as mineralocorticoid activity. Okay, Increasing. Sorry, it'll cost increase it Increase excretion off hydrogen irons. Okay, So if you get increased excretion of hydrogen lines, you get and get a metabolic alkalosis. Okay, so that's why you can get a metabolic alkalosis in Cushing's syndrome. It must have got it so often, you know, adrenal isis, adrenal like this. Okay, so this is this is pretty obvious, but this is a classic description off adrenal insufficiency. Okay, so why so fatigue? Weight loss classic for adrenal insufficiency. Hypotensive. So adrenal insufficiency means you're not produced. Many of the adrenal hormones such as mineralocorticoid such as aldosterone is if you know, producing enough testosterone you can get hypertension on because you're not producing aldosterone get hyponatremia and hyperkalemic because remember, aldosterone will normally cause potassium excretion and sodium retention. So if you have low aldosterone levels, that's a classic electrolyte disturbance you can get. And remember, don't forget this. Okay, so the palm increase talking. It means that you have high levels of a message. So this patient likely has high levels off ACTH. Okay? And why would this patient about hae levels of ACTH? Because because the adrenal glands are not producing anything because the adrenal glands are damaged, the pituitary is producing high levels off ACTH to try and try and compensate. Okay, but the adrenal glands are just not functioning. Okay? And again, if he had high levels off, ACTH will have high levels off em. Shh. And that can lead to skin hyperpigmentation. Okay, now, because this is a problem in the adrenal glands, it means that it's a primary adrenal insufficiency. Okay. More commonly known as Addison's disease ondas many causes off Addison's disease. Most commonly, it's autoimmune related on. This is emphasized by the fact that this patient has been till I go a swell. Okay, Another autoimmune disease. And so this patient likely has autoimmune, um, autoimmune, Addison's disease. Okay, so in terms of the relevant physiology here, So we're talking about We're talking about adrenal insufficiency where you have low production of adrenal hormones. So if you think about the access primary, adrenal insufficiency means that you have a problem in the adrenal cortex. Okay, that's Addison's disease. So if you're dream of bands or not working, you're gonna get loads of ACTH being produced to try and stimulate cortisol levels. So that's why you get high ACTH. Okay? And if you get high ACTH you're going to get high FSH as well. Okay. And also, if you have so you because you're not producing any of this cortisol and androgens, you lose that negative feedback. So again, you get that high levels off ACTH. Okay, secondary renal insufficiencies. A problem in the pituitary gland. Okay. And tertiary adrenal insufficiency is gonna be a problem in the hypothalamus. Okay, So tissue adrenal insufficiency is actually very common. Okay? It's one of the It's one of those end of crime diseases where a social disease is actually common. Can you have? Certainly. What is the main cause off? Tertiary adrenal insufficiency. When would patients get, uh, lesion? Well, it's not technically a lesion, but when a patient's going to get 23 adrenal insufficiency, someone's had TB is not TB. So Yeah, you guys are thinking too hard about this, Not not my serious. The tissue adrenal insufficiency means that you have a shot down off the entire access. Okay, So you having nothing being produced in the hypothalamus? Nothing being produced from the anti your pituitary. Nothing being produced by the adrenal cortex. And so this is because when patients are taking steroids long term, and then they suddenly withdraw, you get completely shut that off the access, Okay. And so that's that's going to cause a tube. That's essentially it's a 23 adrenal insufficiency because the whole access is shut down. Okay, so, actually, totally adrenal insufficiency is actually comin. Okay, because patients, it happens in patients who suddenly stopped taking steroids. Okay, Okay. Sometimes the adrenal activation. See, I'm not going to go through all of this, okay? But the main complaint features are going to relate to the low adrenal hormones. So because of the low cortisol or low aldosterone low androgens and high ACTH Okay, so I'm I'm just gonna go about some of the different she eating factors. Okay? If they have a primary adrenal insufficiency, all of these things will happen. Okay, They'll get low cortisol, low aldosterone, low androgens and high ACTH. Okay, because the adrenal glands are not working. However, if they have a secondary or tertiary adrenal insufficiency where the adrenal glands are still working, they won't have low aldosterone levels Because of doctor, um, levels is dependent is not dependent on ACTH. Okay, aldosterone levels is dependent on I'm tense in too. Okay, so if you have so because that access is separate as aspirin levels should be fine in, try it. It's a zoster. Levels were low in primary adrenal insufficiency. Okay, because, um, because it's dependent on that being because it's dependent on angiotensin two. And because the adrenal gland is damaged in primary journalists efficiency, you'll get low off the estrone in prime your drill insufficiency, where, as with the other causes, uh, aldosterone because it's not related to a C. T. H. The aldosterone levels will be actually be fine. And the other causes and hopefully the a city. It should make sense if you have a problem. In the adrenal gland, you have high ACTH levels. Okay. Whereas of the other ones, you get low ACTH levels. Okay. And you can have a read of some of the clinical peaches you get because of these because of these deficiencies. Okay, Now, when you're investigating, adrenal insufficiency have some important points to remember is that at the first step is generally to measure the morning cortisol. Okay, so cortisol is generally highest in the morning. Okay, so I like to think of cortisol as a sort of double expresses shots. Okay, so I have it. It's highest in the morning because it helps you wake up as lowest in the night when you're about to sleep. Okay. So morning. Cortisol. So if the morning cortisol is low, Okay, so remember, normally, morning cortisol should be very high. Okay? So if it's low, it means that the patient likely has adrenal insufficiency. Okay? It's sort of in the normal range, which then it could Sorry, if it's between 100 to 500 then it could be a drill insufficiency, but you need to check by doing a a city stimulation test, okay? And we'll talk about that. If it's high, okay, and normally hide, then it means that insufficiency is unlikely. Okay, So a city of stimulation test basically means you're giving a C T h to the patient's Okay, a synthetic form of a C T h. On. If the adrenal glands are not functioning, then I mean, is that because the levels is not gonna rice? Okay, so if you have primary drills insufficiency when you give a c T h d adrenal glands will not produce will not be producing more cortisol. Okay. Whereas with the secondary and tertiary a drill insufficiencies. Um, because, you know, guns are fine. It's it can be sure. Typically rice. Okay. Often even with secondary and tertiary adrenal insufficiency, uh, the drug that will actually atrophy. And you might and in mind that you might actually get that rice. Okay. So, essentially, the key thing to remember is that if you have a normal ACTH stimulation test that basically rules out primary adrenal insufficiency, Okay, So you mainly looking for primary adrenal insufficiency. Okay, Quickly on Addison's disease, so we talked about some of the most commonly. It's autoimmune related. Okay, TB is most common worldwide for crime disease. We talked about you get conquered features depending on because of the low cortisol. Lower cost run low under Jen's, patients can develop an Addisonion crisis if they have a sudden and severe drop in adrenal hormones. Again, patients get hypertensive on, get be very unwell. Okay, because of because of the severely low calls or lower testosterone levels, Okay, they can go into shock and develop many different complications. Okay, so so for chronic disease, Okay, generally for normal crime like Addison disease, you want to replace the Lyrica Corticoid? Okay. And you can give hydrocortisone if they're low and mineralocorticoid like aldosterone that you could get fludrocortisone importantly patients. I should carry a Medi alert. I d. Again a step steroid card because, um, if they get on well, it's important that people are aware that they're on long term steroids because, um, you don't want them to. There's a risk of them going into an Addisonion crisis, okay? And also because if they get a an inter current illness, okay, so if they have a short time illness, and it's very important to advise them to actually double that dose off steroids. Okay, because, uh, you don't want them to go into an Addisonion crisis. Okay? So if they have an interferon alone issue, don't tell them to stop steroids were actually tell them to increase that dose of steroids. Okay, this is very important. Sick day rules for Addison's disease. For the in terms of the acute management of Addisonian prices. You want to get intravenous hydrocortisone and into them, and you also want a fluid resuscitate a zoo. Well, okay. Okay. You got two more SPS and then we will be done. Uh, so it's dry. Sorry. This is quite happy. Uh, endocrine is one of those huge, content filled spectrum of these which is difficult to cover in the entire day. One session, but, uh, trying to be as comprehensive as I can to you guys. Uh huh. Okay, this is covering some pretty, Uh, this is a question covering some pretty niche and adrenal stuff, but have ago. Yeah, Yeah, they probably think I'm gonna probably take this to the full nine o'clock. I said, but stick with me if you can. That's called, Uh Okay, So this is a difficult question. Okay, We got, you know, split between B and C. Uh, correct answer here is actually a a a 11 beats hydroxylase deficiency. Okay, you might get This is one of those topics. Whether you might you probably get one sp on this in your actual final exams, but it's it's useful to know it is a useful topic to know. Okay, so it's they said so this is basically talking about congenital adrenal hyperplasia. Get a group of, um, metabolic adrenal conditions. So let's talk about this. So we have a newborn baby here. Okay. Recently delivered on this baby is hypertensive. Okay, go high BP on. And what also can Typically, this patient has a 46 excess xx karyotype. Okay, so this is means that the baby is born genetically female on important things is that there's evidence of total enlargements. Okay, that's a feature off. That's a classic thing that happens in females, but also this patient. This baby has labioscrotal fusion gets a labioscrotal fusion. That's what happens in boys. Okay, so this this baby has features off female and male genitalia okay. Even though this baby is a genetically female. Okay, so there's evidence of genital and ambiguity here. Okay? No. So this patient has classic as features off high mineralocorticoid. Okay, so high sodium levels and low potassium levels. So this is all referring, Teo a condition off congenital adrenal hyperplasia. Okay, we'll talk about what these are but essentially 11 beats. Doctors deficiency will need to hypertension as well as a realization. Okay, So realization basically means male genitalia and a female. So 11 beats hydroxylase. We can't ask you cause a combination of both these features. Okay, so there's another diagram I made to try to basically show what I'm talking about here. So this is ah, diagram representing all the steroid hormone pathways that's happening in the adrenal cortex. Okay, um, so basically, what we're talking about these enzyme deficiency is we're talking about specific enzymes in these pathway, which is deficient. Okay, On the three main enzyme deficiencies are 21 beats hydroxylase deficiency, which is deficiency of this enzyme. 11 be tied rocks. Those deficiency, it is here on also 17 hydroxyl eight off their doc's place deficiency. Okay, we're just here. Okay. Now, uh, because the time I'm not gonna go go through the detail off what's happening here. But I'm gonna give you a little way to remember the main things to remember about this disease. Okay, so it's referring to a group of autosomal recessive conditions. Okay. And essentially common features for all of them is that you get high ACTH okay, because you're having an enzyme deficiency on because the pathways blocked some way you have. You have high ACTH, okay? And I will lead to adrenal hyperplasia. Remember? Keep talking about it. You have high a citate. So you also get high M s H O U get skin hyperpigmentation. And because of the deficiency and enzymes, you can also get low cortisol levels. Okay, Now, doing the way to differentiate these conditions is either if it causes hypertension or if it causes high androgens. Okay, so if it causes high androgens, you're classically get symptoms like realization. Um, acne on bigger scheme on big was genitalia and things. Okay, so the way the best way to remember this is to think about where the number one is. Okay. If the number one is is coming second, I'm inside. It's going to cause hyperandrogenism If the number one is coming first, that means it's going to cause hypertension. Okay, so 21. So the number one is coming second. So it's only going to cause hyperandrogenism with 11 beats hydroxide efficiency. So they both have one. So it's going to cause both hypertension on high androgens, okay. And with 17 alpha hydroxy deficiency. So the one is happening at the start, so it's only going to cause hypertension okay and not know hyperandrogenism. Okay, so you don't get the realization with a 17 hour find rocks, lays deficiency. Okay, so that's probably the easiest way to remember it. Just remember, if the one comes second, it's going to cause high androgens. If the one comes first, it'll cause hypertension. Okay. Okay. This is this is the last SP Okay, we have it. We're almost there. Yeah. Okay. A call. It, uh said tricky question for the last one. But we'll go this mix off. C and e on guard down the hair is C is a check. Plasma. Freeman at a difference. Okay. Ah. So the reason is that we talked about this other start, So this patient has speech is off a hereditary cancer syndrome known as multiple endocrine neoplasia. Okay. Specifically, men to be okay. Um, so multiple endocrine neoplasia to be is associated with various different things, particularly medullary thyroid cancer. Marfanoid happen test on day deoproce I told us. Okay, so we'll talk about the Ocrevus I tumors in a bit. But middle retired cancers that suggested by the history of the neck lump history, family history of thyroid cancer Well, as elevated calcitonin. Okay, So moderate thyroid cancer classically will cause increased calcitonin because it's essentially, it's a cancer affecting the see salads, which will need to I constitutive. Okay, um marfanoid habits without suggested by the patient. Having erection back actually gets a really long fingers. Okay, uh, biopsy really very malignant cells that feature off the debris. Thyroid cancer as well. Okay. As well as the nausea. Okay, So because men to be is associated with If you promise I Thomas, the most appropriate step here is to check the plasma feeding that metanephrines. Okay, so that's one of the biochemical investigations for a pheochromocytoma. Okay, so it's ah, adrenal. It's a tumor affecting the adrenal medulla, but you're getting mask it. Production off Catacholamines. Okay, So can you tell me why is it particularly important to check if the patient has a few crackles? Cytomel right now. Well, what's the reason? Very important to immediately check if the patient has ah, has a few chromosome time has adrenal gland. Adrenal medulla tumor. Why is it important? Is yes. So? So yeah, so the red if you're falling out for that. So what's the problem? If the patient has a hypertensive crisis in this patient, why is it important for the patients who have good control of BP in this patient? Why is it particularly important to make sure the patient has good BP control? Yes. Someone's got it. So patient, is it likely need to have surgery for the thyroid cancer? Okay, so if the patient's going to have a thyroid back to me for the thyroid cancer, it's important that the patient has good BP control beforehand. Okay, so that's why you want to check in. The patient has a few crumbs, Saitama, because obviously, with a few more, um, Cytomel, there's a risk off a hypertensive crisis. So you want to make sure that the patient's BP control is under control before the going to have surgery for both retired cancer as well as for the pheochromocytoma. If they need to have that removed this well, okay. So quickly on men syndrome, so is a little cheat slide to understand, multiple and neoplasia. Okay, So, essentially, there's three different syndromes as men. One which is associated with the three piece so can suspect in the pituitary gland. Uh, pancreatic new new underground tumors. And our direct line, I meant to say, is associated with the two peas as well as one m. Okay, so it's associated with cancer is affecting the artery glands. Do you promise? I tomer as well as medullary. Thyroid cancer is okay. And finally, men to be is associated with only one p. But, uh, to ems. Okay. It's actually three m's, but it's only one p. Okay, So do you promise I Tomax medullary thyroid cancer marfanoid habits. And because on your, um, ms Okay, that's about the basic things you need to remember about men syndromes. Okay. Just remember which cancers are more common on with any different types. Okay, Last light. There's a few chromosome tumor. So you're close eye tumors like we talked about. It's a tumor off the adrenal mass dollar. Okay, And remember the adrenal medulla. Any producing catacholamines like adrenaline. Okay, so if you have a tumor in the adrenal medulla that can lead to massive production of catacholamines and actually two problems, okay, if you talk about associated with men to a swat other newer, cutaneous, hereditary syndromes like, you know, for going toast is type one bone hip, a lindau syndrome. Okay, uh, what's the classic sign was the classic clinical picture you get in neurofibromatosis type one cafe au lait spots. Very good. Okay. And with bone, hip, bone, hip, a lindau syndrome water, the other cancers, you classically get withdrawn. Hippel in down syndrome. We don't know. I can't sit very good on day. You can also get things like hemangioblastoma is a swell. Okay, uh, toxic clinical features. So hypertension is obviously a big thing with your chromosome, Thomas. Okay. And the key thing that's different about the hypertension and tear chromosome toma compared to other causes of hypertension is that the hypertension is typically episodic. Okay, so, between the episodes of hypertension, patients can actually go. I have a normal or even low BP. Okay, so that's here. And episodic hypertension. Okay, but the big concern this side of patients get a hypertensive crisis. Okay, Terms of investigating pheochromocytoma. So it could be It's very variable, depending on the hospital, Board of and hospital centers. Okay. Generally, the things you're measuring is thematic difference. Okay, so the breakdown products of the catecholamine so plasma free matter nephrons and urinary metanephrines are the main ones. Okay, um, if they have, if you have high chemical suspicion, generally you go for plasma from metanephrines. Okay, so they have some kind of hereditary cancer syndrome, or if they have believed in, if they have, ah, hypertensive crisis and you suspect it's because of abuse from his automa. Generally you can go for the husband for you metanephrines. Because it's quicker, uh, treatment. So this is very important. Okay, So surgical resection is the mainstay. Okay, so you want to remove the tumor? Um, very important is that you want to make sure that the patient has good BP control before you do the resection. Okay. On the main thing to remember is that to get good BP control, you give alpha blockers okay. And you you can get you have to give alpha blockers before you give any pizza blockers. Okay, so alpha blocker, is it? This is a crucial safety thing to remember. Okay, you have to get out there because before beats blockers. Because the problem is, if you can't beat the block, its first you're going to cause you're gonna block all of the pizza receptors. And that means that there's only going to be off the receptors available for the had a cold means to bind to, and that can lead to a massive hypertensive crisis. Okay, so you you give alpha blockers first. Okay? Such as phenoxybenzamine on such a spent olamine. So you want to make sure you've got good control of the BP first before you start considering if you need to give a beat the blocker as well. Okay. On adrenalectomy is the surgery of choice to remove be cancer. Okay, Very important. That's it for me today. Okay. Sorry we dragged on, but I've got some post lecture notes to you guys, so we have some notes on diabetes insipidus the notes on polyuria notes on SIADH. Note. Some parathyroid physiology notes on hypoparathyroidism No cheat table on different bone profiles. Little cheat slight on thyroid cancer, little bit on primary hyperaldosteronism and a little bit on polycystic ovarian syndrome as well. Okay, all important conditions.