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Hi guys, there is a bit one second. Let me just try and get rid of that. Ok. Um Right. So, hi guys and welcome to our first um Endo lecture of the series, which is going to be on Pituitary Gland and Pituitary Hormo uh Tumor. Sorry. Um So today will be Charlo who will be giving this lecture and I'll let her introduce herself in a minute. But just to remind you guys, it's really important that you guys attend all of these lectures fill in the feedback form. We have five of these ENDO lectures coming up for you guys and they'll be running on Tuesdays and Thursdays at seven o'clock. Just make sure you fill in the feedback. That's the most important thing for it. Make sure you fill in the feedback form and then you'll receive your own personalized, unseen set of SBA S for Endo at the end of the series, if you do so. So I'll hand over to Charlotte. Hi. Um I'm Charlo. I'm a third year medical student at Brighton Sussex. Um and I'm a grad student. So I've also done a BSE in biochemistry from the University of Leicester. So I will be taking today's lecture. Um That's just a, a little bit about me. Um, but let's move on. So, um, this lecture is gonna be on the hypothalamic pituitary axis and the many axis that come off it as well. So we'll have a look at the anatomy first. Um, what it is, where it, where it is, what it does, um, how it gets its blood supply, we'll then break it down into the two lobes of the pituitary gland, looking at the anterior first and then the posterior and then we'll look at the hormones um that it secretes afterwards. Um And then finally, we'll finish on some pathophysiology as well. So we can understand what should happen and then what happens when nothing works. Um OK. So heading into the first section, we'll look at the anatomy of the pituitary gland. So, where is it? Well, it's obviously located quite deep inside the brain. Um You'll see this sort of structure up here quite often. Um This is the brainstem moving through the middle and then at the top, you have that sort of curve shaped connective tissue, that's your corpus callosum. Um just below your corpus callosum is where you'll find the thalamus that highlighted yellow bulb. Um That's just below your, um that's where you have your hypothalamus. So that's hypo being low and thalamus. So below the thalamus, right. Um There's this connective tissue connecting the hypothalamus to the pituitary gland and there's two lobes of it. So this is called the pituitary stalk or the infundibulum. Um So the infundibulum is located just there in that kind of blue. Um blob if you like um connecting the pituitary gland to um uh hypothalamus. So, the clinical relevance, you just have to remember this for now, I'll come and address it afterwards. Um But the optic chiasm is located really, really close to the pituitary gland. Um So just keep that in mind, we'll come back to it and look at that in a little bit more detail afterwards. Um OK, so the pituitary gland anatomy itself, um you can kind of see again that kind of different view that you essentially see the brain stem heading up through the middle, then your connected tissue and your corpus callosum over the top. What you might immediately notice though is that the pituitary gland is actually enclosed in its own sort of cain of bone. So we have this kind of ability to protect things that are really important to us. So your lungs and your heart are protected in the rib cage. Um Your brain is protected by the skull and your pituitary gland is therefore protected in this little helmet of its own. Um And that means that it's obviously of some important relevance to the body. It's a master gland for a reason. So it's incredibly important and it's involved in a lot of different things. Um So it's the sphenoid bone that encases it located at the ventral surface of your brain. Um The pituitary gland is two functionally and anatomically distinct lobes. It's not one thing. Um They are two very separate lobes and you have your posterior which is your neurohypophysis and your anterior which is your adenohypophysis. Um So if we have a quick look at the blood supply to it, how does it receive its blood supply? Uh it's incredibly well vascularized and compared to other tissues in the body, because it has to produce so many different types of hormones. So, the majority of that blood supply is coming in through the superior and inferior hypophyseal arteries. So that's coming in right at the top for the superior and inferior. Um sorry, it's coming from the top for the superior and a bit lower for the inferior hypophyseal arteries. And they come off the carotid artery. The hypophyseal portal system is the connection between the two plexuses. Um plexuses are capillaries. Um They're just capillary beds, basically, that's your portal system. Um connecting that is your long portal veins. They run down the infundibulum between the primary plexus and the secondary plexus located in the anterior, the adenohypophysis. Um The one really important and interesting thing to take away from this as well is the sinusoidal nature of those capillaries and the capillary beds. So, capillaries are kind of found everywhere in your body and there's different types. Um but these ones are quite unique, they're sinusoidal. So what that means is they really have fewer type junctions between the cells in those capillaries. And that means that there's bigger gaps that literally just makes it easier for larger molecules to pass through the capillaries, which is perfect for a system which is producing hormones um to get in and out of that blood supply. Um So, yeah, the capillaries found in the pituitary are sinusoidal in terms of nervous innervation is located deep within the brain and is connected directly to the hypothalamus. Um This is a part of the brain and there are several important nuclei coming from it. So, the important distinction between the two is that you have a paraventricular and supraoptic nuclei that are projecting all the way down into your posterior lobe, your posterior lobe, your neurohypophysis really is just a bundle of nerve terminals. That's all it is. There's nothing really glandular there at all. Um There's not many different types of cells. Um So your hormones are secreted directly from the nuclei up there because your nerve terminals um are there and then they come down into the posterior lobe a little bit different. On the other side, your arcuate nucleus is what projects to the primary plexus at the top of your anterior lobe. Um So, hormones are released there, moved down um through the long portal veins and down into the lobe. So, here's a quick question just to get started. Um long portal veins are present in which region of the hypothalamic pituitary axis. So I'll give us a couple of minutes to just think about that and then we'll move on. Uh You can put your answers in the chat by the way. That's fine. OK. I'll get one more minute. I've had one answer come through. Ok. Um So here's the answer. Um It's, I can see why it would be easy to put down the anterior lobe, but it's actually found in the infundibulum. It kind of, it's the connection between the hypothalamus and the pituitary. So it comes down and then it goes into the plexuses in the lobes. Um And so that's why it's the infundibulum and not the anterior lobe if that makes sense. Um So yeah, if we move now on to section two, which is going to look more closely at the anterior pituitary gland, um some of the hormones and the pathways and some of the cells as well the other. So we have releasing stimulating nontropic or tropic hormones. Um typically in this order and they work quite nicely in your anterior lobe generally. Um That's just the way it works. So, releasing hormones, stimulating hormones, nontropic or tropic hormones. And if you're thinking about it, it's not how it works in the neurohypophysis and we'll come to that um later on. So the arcuate nucleus produces these hormones into the primary plexus that travels down the long veins, they head down into the lobes where they all have different cell types, those hormones will bind to the cell types, produce the hormones and then will immediately go into the blood supply there in the secondary plexus and enter circulation via the normal endocrine pathway. Um Let me change the slide. Yeah. Um So now we're going to move through each of those hormones and look at them in a little bit more detail. So we'll have a slide, that kind of looks at what it does and what the hormone is and then we'll have a slide as well that matches its regulation. Um So for growth hormone, it's secreted in response to growth hormone releasing hormone. Um So you've got a releasing hormone right at the start and you've got a stimulating hormone, which is your growth hormone that's produced by somatotrope. These are cells of the like in the anterior lobe. Um and there is, and you'll see a diagram in a minute somatostatin and that acts as a sort of negative controller for it, but this really comes into the pathway a little bit later and you'll see it pop up and why it might be relevant. Um It does have several effects, one of which is in the liver to produce IGF one, which is an example of a nontropic hormone. Um So the net effect is to increase the amount of energy from glucose. Um you get more glycolysis and then more energy so that energy is then being used in your bone and muscles to increase growth. It's a growth hormone. So it does what it says on the tin, right? Um its effect is on your adipose tissues as well. So um it tries and gets again more energy. Um So yeah, the net effect of growth hormone is more energy for growth. So if you try and perturb this, then you're going to end up with things like um acromegaly or gigantism. And we'll look at those in a little in more detail later. So this is kind of an illustration of growth hormone regulation in response to things like sleep or fasting or exercise. Generally, the hypothalamus is stimulated to produce growth hormone, releasing hormone, um growth hormone releasing hormone moves down into your pituitary and at your pituitary, it binds to those somatotrope and that produces growth hormone and that heads down to your liver, bone muscle and your adipose in out there. Um There, it's then producing IGF one which has that kind of sort of synergistic effect. It works in the same way growth hormone does. Um And they sort of work up to amp each other up if you like. Um And obviously you've got your kind of negative feedback. So you've got a classical short loop inhibition and A L loop inhibition as well as well. And that comes from um growth hormone preventing its own production both at the level of the pituitary, but also at the level of the hypothalamus as well. So there's another layer to this, which is that we don't have all have growth hormone being produced all of the time. Otherwise we would be quite big. Um I DF one is also acting negatively to kind of regulate the expression of growth hormone as well as preventing the growth hormone and growth hormone releasing hormone. So that's kind of where somatostatin comes in. Um IGF one leads to the production of somatostatin which dampens down the system even further. So you get the effect of growth hormone producing that sugar, you get that boost, you start to get your insulin growth factor one and that amps up the whole kind of system and then calms it down again. So it's not dysregulation. Um Somatostatin is just like a negative equivalent of the growth hormone. It does the opposite by antagonizing the effects. And yeah, that's so that's basically kind of a summary of growth hormone regulation there. Um So next, we have uh adrenocorticotropin hormone. Um this is produced in response to corticotropin releasing hormone and the net effect here is to eventually go and produce cortisol from corticotrope. Um And the idea here again is to increase the amount of glucose available and several other effects by degrading proteins. Um And again, we don't need energy going to make proteins, right. So we need it in different places at times of heightened stress and it also dampens down your immune system and preventing energy kind of being used up in your immune system when you're under attack or you've got heightened stress, you need the energy where you need the energy, basically. Um So a pathology associated with this if you've got too much is Cushing's syndrome. Um and there's this pathway and you can see there are some environmental stimuli again. So exercise stressors, some neuronal signals that can all lead to the production of corticotropin releasing hormone. That's crh from the hypothalamus, uh heading down to the anterior lobe and the pituitary um of the pituitary. Sorry. Uh it produces a th this then goes to your adrenal glands and then produces cortisol. And you see those kind of negative effects of bone muscle and in the immune system, but you get that positive effect to produce more glucose in your liver. Um Again, obviously, you have that classical negative feedback, it's preventing its own inhibition. So we should really have homeostasis and a relatively stable level of that pretty much all the time unless there's periods of heightened stress and then things kind of go AWOL and a bit mad. So the next one is thyroid stimulating hormone. Um The P is really well defined and very, very well studied here. So, your thyrotropin releasing hormone is what leads to the release of thyroid stimulating hormone and the production of it. Um And again, it's again, releasing hormone stimulating hormone. Um and these are produced by thyroid drugs, those are particular specialized cells in the lobes of the pituitary. So it heads down and produces T three and T four, T three and T four are your thyroid hormones. Um, and they largely exist as T four for the majority of the time and it's secreted as well, largely as T four. Um, there is some T three and it is converted from T four to T three to become active. So T four is metabolically in art, it doesn't really do much. Um but as T three, the net effect is really to amp up metabolism. So it acts as a massive amount of cells in the body and a lot of places in the body has thyroid hormone receptors as well. So, yeah, pretty important. So, um this is what I was describing, just kind of in more of a diagram form. Um Thyroid releasing hormone gives you thyroid stimulating hormone. And then you've got that thyroid hormones T three and T four and they're acting to increase that metabolic rate there. Um And obviously you've got your negative feedback loops, so your short loop and your long loop inhibition as well. So we also have luteinizing hormone and follicle stimulating hormone being produced by your anterior lobe of the pituitary. This is in response to gonadotropin releasing hormone binding to those gonadotrope. So that's what produces these hormones basically. Um again, these apps through very classical negative feedback loops and the effect is in both males and females are kind of different, but they do act in both males and females. So, in biological males, when it heads to the testes, you get that production of testosterone and mature sperm. Whereas when it heads to ovaries, uh you tend to get things like follicular growth and things like that. So these pathways are very, very similar except you change the target organ um at the bottom. So there's ovaries in the testes. There is obviously that again, classic negative feedback loop that we've seen before. Your short loop, your long loop. Um So the short loop acting at the level of the pituitary and your longer loop acting at the level of the hypothalamus. So dampening its own secretion, essentially, there is some positive feedback here um occasionally and that leads to ovulation. Uh So prolactin, uh it's one of those ones that are a little bit different from the others and it doesn't really act in the same way um as that like releasing hormone stimulating hormone. But I guess you can kind of consider dopamine to be its releasing agent. Um but it actually works a little bit differently. So it works to inhibit lactotrope. So the predominant control of prolactin expression is actually through its own disinhibition. Um you have to take away the inhibition before you get prolactin being produced. Otherwise, it's not really producing, it's circulating normally every day, every week. Um at very low levels in the body and you have to take something away um to take away that inhibition for you to get prolactin being expressed. So, one example is suckling behavior from a newborn baby. Um This activates Makana receptors and then leads to the inhibition being taken away. So you get that prolactin being expressed. Um So the primary function of this is generally in milk production in the breast alveoli and that's why it's kind of related to the suckling behavior. So if we have a look at that kind of sort of pathway, again, um you can consider dopamine as your releasing hormone um but it does act a little bit differently. So what you have here is actually a really nice example of positive feedback, suckling behavior. So the dopamine inhibition is being released. So you get milk produced. If there's milk found in the breast, a baby is more likely to suffer again. So you get more and more positive feedback and the system continues to go until breastfeeding stops and then that inhibition comes back, prolactin stops being expressed and the milk isn't produced anymore. So that's an example of positive feedback. You have that background environmental change that is promoting it. So in the background, environmental change here is the presence of sling behavior. Um when that suckling is taken away, it goes away again and regulates back down to low levels. And obviously, there is some short loop inhibition, but there really isn't much longer loop inhibition here. So everything on this slide is what we've seen before. We've pretty much covered it. Um But what I've done is kind of put it in a table form to make it maybe hopefully a little bit easier to summarize. Um So you have the different types of cells and I've included the relevant um like the prevalence of each type of cell as well. Um And then what they're stimulated by and what they produce as well. So, if you want a summary, hopefully that should help. So I have another question again. Um So I'll give you a couple of minutes. Please feel free to use the chat as well. So, the secretion of IGF one is promoted by which hormone. OK. So another minute, hopefully and then we'll find out the answer. OK. So the answer is growth hormone and that leads to IGF one. OK. Moving on. Um let's now look at the posterior pituitary gland. So um there are loads of nerve fibers here and they're just projections of the paraventricular and the supraoptic nuclei that then head down into the posterior lobe. Um They are just nerve terminals, a bundle of nerve terminals and not much else wrapped up in an incredible amount of blood supply. Um There aren't really a whole load of cells here. It's literally just nerve terminals that then lead to the secretion of hormones that goes directly into the blood supply. Um And you can see it traveling down the paraventricular and supraoptic n those black arrows kind of help show you the direction in which things move. Um So one example of a hormone that is secreted from this lobe, um Your neurohypophysis is oxytocin. Um So it's called neurohypophysis if it wasn't clear already because there's just nerve terminals there. Um But yeah, coming back to Oxytocin. So it's secreted from the nerve terminals of the supraoptic and paraventricular nuclei. These are both triggered by mechano receptor activation. So some behavioral environmental stimuli that leads to the production of Oxytocin. These then spike which produce a positive feedback loop. And this is one of those kind of slightly odd positive feedback loops. The targeted tissues are either breast alveolar epithelial cells or in the uterus. And what they're doing is targeting muscle contractions. So in the breast, you might get milk ejection. Um You've had your product in producing the milk and Oxytocin works to eject it if you like. Um and down in the uterus, what you have is the muscular contractions that are needed for childbirth and labor. So, Oxytocin being produced by that lobe heads down to your target tissues and it's suckling behavior that activates those Makana receptors that create that positive feedback loop. So more milk, more suckling um and so on. So, similarly, it's pressure on the cervix that activates Makana receptors um down in the uterus activating these afferent multi neural pathways. Um the long pathways heading up to your hypothalamus which triggers those nuclei to produce oxytocin. And the example, again of childbirth there. So the presence of that developing fetus or kind of newborn um and that moving around activates the Makana receptors and you get more muscular contractions. Um And yeah, for, for better want of a better word like you get ejection of the baby basically um rather than ejection of milk. So targeting muscle contractions, but it's in a positive feedback loop. Um You don't get muscle contractions all the time. It's only when there's a background environmental change and when that goes away, the positive feedback loop disappears and it's just negatively regulated again. Um So one of the other ones that we probably should cover is um the antidiuretic hormone that comes from the neurohypophysis. So, diuresis is a kind of sort of filtering of fluids by your body. Um more particularly your kidneys. So what ADH does is it starts to prevent diuresis. So the main aim of it is to try and increase the amount of water that your body is retaining. Um So when the body realizes there's not enough water, it kind of starts to panic and uh ADH comes in, pulls the water back into the system. Um So this works by detecting the amount of osmolality, osmo osmolality in the um blood. So, um now I've written down at the bottom there because I always get confused by what that means. So, osmolarity is the amount of solute, the thing that is dissolved in the solution. So if a solution is particularly dilute, you will have a low osmolarity. You have a lot of water relative to one particle or salt. So if you have a high osmolarity, you might have lots and lots of that salt and um or you might have kind of still only one, but you have hardly any water. So it's a ratio between the salt and water basically. Um So it's more concentrated if you have a high osmolarity, less um in the other way around, it mostly works on your kidneys and on your sweat glands as well. And again, it's water retention and sweat reduction there. Ok. So what you tend to see that higher osmotic pressures um means that less water is in the blood is more concentrated, um whatever is in it. So that could be kind of a drug. It could be sugar or it could be whatever that activates ADH to be produced. This then leads to the kidneys to hold more water in and your sweat to stop. Um When what, what this then does is your osmotic pressure suddenly drops and your osmo receptors aren't being activated anymore. So you don't get a eight being produced. So what I've shown really so far is that the two lobes are very functionally and anatomically distinct, but there is some interplay between them. Um So the hormones can interact with each other to produce different biological effects. So we've seen the example already of prolactin and Oxytocin, they obviously act quite similarly and in a cooperative manner. Um you have Oxytocin that's leading to the muscle contractions at the breast alveolar epithelial cells. But this is happening through suffering behavior. Um It's also leading to dopamine being taken away because you have those afferent multi neural pathways leading to the inhibition of dopamine. So therefore, you get prolactin which induces lactation and those two pathways synergize and you get this kind of massive amplification of this behavior. So, milk is being produced and ejected because there's a baby that's suffering. Um There is therefore an off target effect of prolactin as well. So, prolactin also acts to inhibit the production of gonadotropin releasing hormone. So, during periods where there is elevated prolactin expression, basically, you've just had a baby and there's suffering behavior going on. You have that dampening down of some of those hormonal pathways that are controlling fertility. So it's almost like nature's contraception. Um Basically saying you've got one baby right now, give all your energy to that one baby and just make it survive and develop and grow and let's not put energy into making another baby right now. Um So this is basically like a classical defined interplay between the two anterior and posterior lobes. Um But I really just wanted to highlight that really and make sure you understand that there is an interplay between them even though they are quite distinct lobes and anatomically and functionally. So the last section is going to be the pituitary pathophysiology. Um We're going to try and kind of wrap up all the loose ends that I've kind of thrown out there. Um But if we've hopefully understood how some of those pathways work, they should be quite straightforward. So, yeah. So as we mentioned, first of all, um the pituitary is located very deep in the brain and it's enclosed by that sphenoid bone. And you can actually see here there is a little bit of space around it. So it's not wrapped right up against it. Um There is some space for it to enlarge within that enclosure. Um And typically, we can see it on CT scans and that's kind of the image on the top left. Um It's really hard though to define where the pituitary gland is on a CT scan, but then came along an MRI and it's really, really clear on an MRI to see it. Um It's very well defined through the middle. You can see that brain stem the curve structure at the top, which is your corpus callosum. Um And then the lobe of the pituitary gland as well. So the MRI coming along has made it a lot easier to visualize and assess the pituitary gland um which otherwise with CT is quite difficult. Um And you can also see then when you have an enlargement of it. So you have any kind of swelling. Um And abnormal pathology is very visible on an MRI. Um OK. So we briefly talked about this kind of idea of adenomas. Um You can have adenomas that are related to any of those cell types that we looked at earlier. So, thyrotrope, somatotrope, lactotrope, gonadotrope, and corticotrope. Um There are different pathologies that are associated with each of them. And if you have an adenoma in your thyrotrope, they're called TSA. Um that's incredibly rare and you kind of hardly ever see them. Um And you get this rare condition called thyrotoxicosis. Um You have too much of your thyroid hormone being produced at massively regulated levels. Um This is different to hypo or hyperthyroidism because the dysfunction is at the level of the thyroid. Whereas in this, the dysfunction is at the level of the pituitary. Um if it's in your somatotrope, you might have a growth hormone secreting tumor and we've seen kind of a little bit, we've spoken about acromegaly and gigantism so effectively you have too much growth hormone. Um So yeah, if it's in your lactotrope, um you might get prolactinemia, prolactinoma, sorry. Um And if you get too much prolactin, you can get galactaria, which is essentially can become quite toxic and you'll get reduced gonadal function because it's inhibiting that gonadotropic tropin releasing hormone as well. Um Down there. So, yeah, your gonadotrope um gonadotrope then. So these generally like that's quite rare to find. Um you generally get too much FSH and LH and these are hypersecretion syndromes. Um again, quite rare. Um And then if you've got it in your corticotrope, you might get Cushing Syndrome. Um That's basically, you essentially have too much ACTH being produced. So these are not always functional, you can have an adenoma or a tumor occurring at the level of pituitary but not being functional. So when I say functional, I mean, secretory, um it's secreting excess levels of it. If it's nonfunctional, it's just a mass um that's causing a problem, but you don't have too much of the hormone. So the problems might develop, the problems that you might develop can be related to an adenoma on the pituitary, but they might not be related to the um hormone being produced too much or too little. Um So, yeah. Yes. Yeah. Um So looking at one of those functional adenomas, the secretory type is producing too much of a hormone. So the one I'm going to talk about a little bit first is pituitary Cushing's syndrome. And I've emphasized pituitary Cushing syndrome because it is possible to have Cushing's Syndrome if it's an adrenal Cushing syndrome. Um as well, essentially, you still have too much cortisol being produced. So what you can see on the far, right. I don't know how clear it is, but um there is the mechanism that of kind of a normal feedback loop there. Um Sorry, hang on and yeah. So there's a mechanism of the normal feedback loop. You have your negative feedback coming from cortisol, which is leading to less expression of ACTH and crh respectively. So yeah, um if and like kind of as illustrated by that like yellow dot uh I know it's not very good, but that's like an adenoma. You have too much ACTH being produced. So your adrenocorticotropic hormone um as a result, your adrenal gland kind of ramps up that production of cortisol and you have a ton of cortisol being secreted. What that means is that you hardly have any crh produced. Um So the adrenal glands are going to kind of realize that they're not getting much A CDH and you might have an adenoma there because it's not responding to the classical feedback loop because you've got an adenoma producing too much ACTH. You get too much cortisol. This is why it would be pituitary crushing syndrome. So when you have too much cortisol, you can get kind of a lot of symptoms associated with that kind of disruptive um physiology, normal physiology of cortisol. Um So you can get very high BP and you might notice in like the pictures that the girl on the left, um she has quite red cheeks. So elevated BP can cause that and it's actually one of the things that is most lethal in Cushing Syndrome, that kind of high BP. Um and if it's left too chronic, it can get really high and you can get aneurysms and things like that. So it's not very good. Um, you also get excessive weight gain. So it's rather unkindly called moon face in Cushing's where you get that fatty deposition on the face. Um, and it makes the face look a lot rounder than it should be, which is where the kind of term comes from. You also then get truncal obesity as well. So that fat deposition is very much located in the trunk and you end up getting very thin extremities. So your calves, um your legs, they all get very thin as do your arms. Um So yeah, even novel fatty deposition, if left unchecked might go into the back and between your shoulder blades and you can get a characteristic hump. Um Yeah. Um So the treatments for it are either removing the tumor that's via a transphenoidal surgery. Um going past that sp sphenoid bone and then they enter through the nose or a radiation therapy as well to kind of get rid of it. Um We then obviously have acromegaly and gigantism. Um This is too much growth hormone being produced, whether you develop gigantism or acromegaly is dependent on what point you have that. So if it happens after bones are fused, the bone plates at the very top of your bones, you don't get those bones growing anymore. Um But the growth hormone still has an effect. So it increases the size of your features. So on the left, uh this patient is 10 years apart before the onset and after the onset megaly. Um Whereas on the other side, you have Silton Cosin um and his bone plates hadn't fused yet. So he's got excessive growth of the bones and muscles and you get an enormous height as a result. So you can look at the level of IGF one or growth hormone to diagnose it or to confirm it if you've got suspicions through your kind of clinical observations and presentation. Um The treatment then again is surgical removal or radiation therapy. Um And I think this is my last slide. So hopefully, I haven't rambled on too long. Um So when we look at nonfunctional adenomas, um at the beginning, I kind of mentioned that I wanted everyone to keep in the back of their mind that the optic chiasm is very close to the pituitary. So what happens if you perturb any of the kind of points of the visual pathway? Um you get very different features in your vision. So you can have some sort of lesion or occlusion right at the top. Um uh in the left optic nerve, for example, maybe that's compressed and you lose all vision in the left side. Essentially, it's like wearing an eye patch. Um If however, you say have it at the optic chiasm where the optic nerves are crossing and diverging right at the optic chiasm next to your pituitary, what you get is something called bitemporal hemianopia and the outer hemispheres of your vision are completely blocked. And then if you end up kind of tracing those nerves back all the way, you'll notice that the nerves um that are compressed on the other side. So this is because as light hits the retina, it's flipped over. Um So the vision on the outside, so it's the vision on the outside that's perturbed. Um Whereas if you had it at the right at the back of the eye, um you might find that the vision on the outside um is what's kind of being expressed. So when looking through the diagram, always remember that light coming into the retina flips the vision. Um So think of it as the opposite of the nerve if that makes sense, hopefully it does. Um Just to finish off. I have one last question. Um So pituitary crushing syndrome is initially caused by an excessive secretion of what? So I'll give a couple of minutes before we go through that one. So I'm gonna go through it now. Um I've seen one answer in the chat, which is really good. So yeah, um it's your adrenocorticotropic hormone. Um And the emphasis there is basically just that it's the pituitary cushings and not necessarily the adrenal cushings that we're talking about. Um So, yeah, thank you very much. I hope that that was helpful. Um And yeah, back to I think if she's here. Um So yeah, I guess thank you guys for coming. Um If you've got any questions then just hit me up. Um But yeah, that's fine. Um Yeah, there's gonna be a feedback form I think at the end. So yeah, just hold on tight for that. Um But yeah, otherwise thank you very much for attending. Thanks guys, I'm gonna end the call now. Um but yeah, thank you so much for coming. Lovely, lovely to see you guys. Ok, cool. Have a great evening.