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Hi. Hello. Hi, I'm Shruti. And today we're gonna be going through the dreams to begin with and then you'll be having some lectures um on lower gi um and him as well. Um So let's just get started. So, um starting with adrenals, as I said, so session structure is kind of like normal. So we're going to go through etiology, history, presentation investigations and management, which is generally what's asked in the exam. This is kind of the different sessions that we're going to go over today. Um So let's just get started. So to begin with, let's go through the adrenal structure and function. So, um this is kind of like nice and easy marks and the main thing you need to know is the different parts of the adrenal gland and what each um part produces. So from our adrenal, we've got sort of two main um layers, we've got the cortex and uh we've got the medulla and then you can break down the cortex into the zona glomerulosa, zona fasciculata and zona reticularis and the me mela is just like one layer on its own. So you really need to know what um hormones are produced by each one. So the zona glomerulosa, which is the outermost layer produces aldosterone. So, um this is what helps uh regulate your BP. So, if we've got a lot of aldosterone, then um we can have a high BP, zona fasciculata. So that produces glucocorticoids like cortisol, which um you know, as the name suggests um is involved with uh glucose regulation. Um and actually at very, very high levels, it can have um aldosterone like effects, which is kind of important to know because if someone has something called Cushing's where we've got excess cortisol, um they can have a high BP and then finally, your zona reticularis. So that's kind of like the innermost layer within the cortex. So the outer layer here, which is the cortex is broken down into sort of three smaller layers and within those three smaller layers, the innermost one is called the reticularis and that produces androgen. So your sex hormones um like testosterone. And then finally, we've got the medulla which is uh right on the inside. Um and that produces catecholamines like norepinephrine or epinephrine. So these are just um other words for, for adrenaline and noradrenaline. So, but they're ba basically the same thing. So we're gonna start off by going through Cushing's syndrome, um which kind of has a lot of different causes. Um And it's important to know uh all of the different types because um the investigation results are gonna be different depending on what is causing the Cushing's syndrome. So Cushing's syndrome itself basically means high levels of cortisol. So if we say Cushing's syndrome, we can't tell what the cause is. We just know that there's excess cortisol, we then want to decide what the cause of that excess cortisol is. So we've got two types, we've got ACTH dependent, we've got ac ACTH in independent. So ACTH dependent means that there's a high ACTH and that's what's driving the high cortisol. So this makes sense if we think about it from the basics again. So the adrenal gland is what produces cortisol and it produces this because our pituitary is producing ACTH. That's, that's the driving hormone that in normal people will drive the production of cortisol. But we, so we can have ACTH Dependent um Cushings where we've got too much of this ACTH and that's driving too much of the cortisone. However, we can also have ACTH Independent. Um Cushing's syndrome where actually the amount of ACTH is quite low because what's happening is there's something wrong with the adrenal gland itself and it's just churning out a lot of cortisol and this is going to have negative feedback. So when we have too much cortisol that feeds back onto the pituitary and tells it to stop producing a, so the problem with ACTH independent um uh Cushing's is something that's not the pituitary gland. Whereas ACTH dependent Cushing's, that's a problem with the pituitary gland or something else that's producing ACTH, so we can break that down further. So, if we start off by looking at ACTH Dependent Cushing's, we've got two types. Well, we know that there's excess ACTH and that's what's causing the excess cortisol, but there, where is the ACTH coming from? So one option is something that we call Cushing's disease, which is where the pituitary gland itself is producing too much ACTH. Now, this is the commonest um endogenous cause. So it's the commonest um like cause within the body. So um I'll come on to it in a minute but actually in ACTH independent, um Cushing's, we can have exogenous steroids. So for example, a patient might be on steroids for another like long term condition like SL E or something. Um And actually that can cause Cushing's Syndrome. Um because, you know, um you, you're kind of artificially giving the body too, too much steroids. Um And then, so that's the commonest cause overall. But if steroids or if artificial involvement isn't a problem, then the commonest cause is a Cushing's Cushing's disease where the pituitary is producing too much ACTH. The other option is that you could have a paraneoplastic syndrome. So like a cancer, um usually lung cancer which can produce ACTH. So it's not from the pituitary, it's from elsewhere in the body. Um And that's producing too much ac which is going to have the same effect, it's going to cause too much cortisol from our ACTH independent causes. So here there's no issue with the pituitary gland. Um So we already went through one option, which is where we're artificially giving the patient steroids. And then the second option is where there's something wrong with the adrenal gland itself. So either there's an adenoma, so like a small tumor or um a hyperplasia where the adrenal glands get bigger or a cancer and all of these can just churn out loads of cortisol and the cortisol is going to then have negative feedback and it will, it will suppress the ACTH. Now, the reason why all of this is so important is because as you can see, ACTH can be both high or low in Cushing's syndrome so that you can't like the purpose of measuring the ACTH is to try and work out the cause rather than to diagnose Cushing's itself. It's to work out which subtype we've got um just a little bit of epidemiology. So it's, it's more common in females as with a lot of um conditions. Overall, most common cause is ex exogenous steroids. So this one here ACTH independent exogenous steroids um and the most common endogenous cause is Cushing's disease. So the pituitary cause. So it's not the adrenal tumors, it's the pituitary tumors. Um That's the commonest cause. Uh if steroids isn't the issue. No, I think you've probably come across this a lot before like the classic signs and symptoms of Cushing's syndrome. You would have covered it in like 1st and 2nd year as well. And it is worth like knowing just because they, you know, very common questions just to like throw in a few of these like buzzwords and then you need to work out that it's Cushing's disease, Cushing syndrome that they're talking about. Um So things like moon face and Buffalo Hump, Trbe. So that just means like central obesity. So, um usually they have a lot more fat accumulation in their, in their tummy compared to the rest of the body, they'll have muscle wasting, um also called proximal myopathy. Um They can get easy bruising, they get diabetes, um they get hirsutism which is like excess um hair growth, um and, and so on. So these are the kind of main symptoms that tend to t out and the investigations you want to do. So firstly, you want to do something called an overnight one mg dexamethasone suppression test. Um And so this is also called low dose dexamethasone suppression test. So, basically what happens is you give the patient dexamethasone, which is a steroid and if your body is working normally. So if you don't have Cushing's, um you would expect the cortisol to be suppressed 48 hours later because it makes sense. If you're giving someone exogenous steroids, the body's gonna be like, ok, let me switch off ACTH production. Um And let me switch off my own uh cortisol production because I've got too much. But if you've got Cushing's syndrome, then obviously, your body's not gonna respond in that way, you, you're gonna have lost that negative feedback. And so you won't have suppression of cortisol. So you, you do this test and if they don't have a suppression of cortisol, then that's positive. That makes you think, OK, this is Cushing's syndrome. The other thing you can test is 24 hour urinary free cortisol. It's quite difficult to practically do because you have to collect like urine over 24 hour period, which is obviously not that easy. Um And then you can also do a late night salivary cortisol, which is again, probably not ideal cos it's in the night. Um then moving on. So once you kind of know that it's Cushing's Syndrome, you then need to work out here. What's the cause? Whereas the primary issue because obviously your treatment is going to differ based on that. So firstly, you want to measure the ACTH if it's low. Um That means it's our ACTH independent causes. So remember, we said there's two potential options. One is a um exa exogenous steroids. And you'd know that because it'd be in their history, they'd help for some condition or, or they'll tell you that they were on steroids for a particular reason. Um And if they haven't said that, then the other option is it's probably a adrenal tumor or cancer or something like that. Um And so you'd wanna do an adrenal CT to, to confirm that if it's high. Um So that's our ACTH dependent causes. So this is either a pituitary tumor or like an ectopic a from somewhere else. You want to do something called um inferior pits sinus sampling. Um So IPSS and this is basically where it, you're checking ACTH level kind of close to the pituitary. Um So if it's high, then.