Mental Health & Psychiatry - PreClinEazy
Summary
This digital teaching session is designed specifically for medical professionals and will discuss the basic physiology of pregenital psychiatry, current hypotheses of depression and how it can be treated, and drugs of abuse. We will discuss conditions such as anxiety, depression, bipolar disorder, and schizophrenia, and look at how neurotransmitters like serotonin and dopamine are implicated in pathological disorders. Attendees can benefit from an open Q&A session, and access to slides for further review. We will also provide a discount of 20%. Don't miss out on this opportunity to increase your knowledge and confidence in the medical field.
Learning objectives
Learning Objectives:
- Explain the basic physiology of neurotransmitters in regard to synaptic synthesis and signaling.
- Analyze how neurotransmitters and their deficit may be implicated in mental health conditions such as depression and psychosis.
- Identify toxins that may interfere with neurotransmitter receptor action.
- Understand the pharmacological mechanism of action behind different classes of antidepressant drugs.
- Apply learned knowledge to be able to answer related questions on medical exams and assessment.
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The following transcript was generated automatically from the content and has not been checked or corrected manually.
that offer questions really good questions and good explanations. Do these questions also use a rescue 20 for 20% off everything you put three, clinical and clinical, mainly clinical. So it might be really useful for your up going progress test in February. We have a community, we post questions, although we have been slightly inactive. But if you if you guys have any questions, feel free to join on, um, who gives it to us and we'll try to answer them are guide you in the correct direction. Now, here are a few set of rules. I'm sure you guys know I'm not gonna go through them again. But if you if you want to contact us, please contact us on skis. The gym A don't come on skis yet outlook dot com or if you want, for if you want really quick replies, contact us on messenger. We usually reply within an hour there, uh, or even on instagram so on. Please follow us were free platform. So we work with sports ones is to find out some a card and stuff. So please, please follow us. I think the the links have been put on the chat at least follows. That helps us a lot of recession is case the case from mental health. The session discusses many different conditions, such as mental health conditions such as anxiety, depression, BBT, bipolar disorder, schizophrenia. So the information presented today are based on the UK guidelines for these conditions and individuals diagnosed with this condition conditions would all have different experiences, which we do not represent through the session itself. We're medical student again. We're not experts in the field, so if you do experience any of these conditions, we do apologize in advance. If we have stereotype in anyway, we're just trying to present with the most common diagnosis and in a way that is really, really convenient for medical education. If you if you do with any of these conditions, please please seek out a professional medical health care health care professional a doctor so that you can get help. Our information. Please please contact the experts in the field. If any coincidences with any questions, any names, they're they're they're purely coincidental. Any stereotypes are common conditions based on common presentation, but you don't mean to stereotype these conditions, but hopefully it doesn't come across as offensive, just which is trying to portray them in a way that you most likely see them. But at the same time, the way that you might see to the examination. So, without further ado, we have to present us today we have Savannah. Megan, who's been be presenting the mental health case. Uh, I'll be there for a bit if you have any questions. Toby, Is that on time? Also that answer. So feel free. I will hand it over to San nose representing it first. Great. Thank you. Okay. Okay. He's e this. Yes. Hi, everyone. The names on a on. But I'm gonna be going over the first bit of this session. Um, like a run said, I just like to give you a quick warning that we will be discussing themes in today's stock. That may be sensitive. Some of you on Greeley saw in advance. And if I, um stereotyping anyway, conditions to do it until health or anything, anything that might be insensitive but accident. I'm going to try to be a spatula. Spots a ble tribe is unbiased. It's possible when I explain things, but I will put like a trigger warning sign on the slides that my home potentially be triggering to you s apologies, Invanz. Please correct me. If I say anything, that's an insensitivity all. Um, yeah. So I will be covering it. Essentially, the basic physiology behind pregenital psychiatry. Things like no transmitters sign ups is how they work, where things can go wrong on Do, um, how this is implicated in psychiatry. Diagnosis like depression and psychosis would be real to go over sleep. Um, well, as drugs of abuse, um, if you feel if you back home at the end, you'll get the slides, and you can see some extra slides on appetite regulation on. But I won't be going over that today. The dog of your time constraints. Great. So if we begin with basic physiology and we talk about very basis off how your transmitters work, which is the bread and butter off like psychiatry, we're looking at chemical synapses. So what is a sign ups? So a sign ups where your transmitters are implicated essentially looks like this. So you have three main things. You have the presynaptic you're on. You have the postsynaptic neuron, and you have a space in between these neurons where they communicate. So this forms your skeleton of psychiatry. Okay, if you know this structure, you can basically apply it most conditions and how they work. Onda help. Things can change. So the's little green, um, structures in the portion out on your own are receptors for new transmitters that are released from the prison after you're on. So what exactly happens when a new transmitters released well, when an action potential hits the presynaptic neuron? This triggers calcium channels to release calcium interests annually into the prison afternoon. The's calcium channels are these calcium I owns our then going to bind to different proteins. You might have heard them snap proteins like, um, Syntagma night and get a cold snap proteins on day bind to the testicles on because the vesicles to then move to the out of membrane off the prisoner in your own on day two. Then release the new transmitter. So, for example, serotonin or North Lynn, these example? Two new transmitters that we'll talk about today more detail, Um, and then what happened when the new transmitters released into the clot sciatic left is that it kind of swims across subject left on reaches the postsynaptic new on membrane where you have these receptors, and usually these receptors are specific to a specific neurotransmitters. If you have serotonin in the Celebrex left, you have serotonin specific receptors on the both. Another neuron is well, and that's going to trigger an action potential in the person out of New York. However, a common misconception is that this always leads to a neck Citatah action potential at it's false, Essentially, in every sign ups. When you have a knack shin potential trigger in a person afternoon, it can either lead to inhibit tree. I'm an individual response or an exciting age response, so that's what he PS. Your PST is. It's excitation inhibitory, so it's not necessarily always an exciting every effect. This is important to note in the context of like GABA, for example, which is which is an inhibitory your transmitter. This is the basic, the psychiatry. So I spent some time explaining this just cause it's kind of the basics of everything. So we then want to apply this to the basics of come psychiatry, Um, less, for example, take a toxin that exists in the environment that can potentially act on these receptors on have an effect on them. Can anyone name any toxins? The Japs, Um, that you can think off That may act here. Can you think of any toxins in the chaps? Let me ask you No says uric cocaine Hold. Yeah. Um, yeah, Someone says Botox perfectly. So bottle, urine toxin axe here on basically inhibited. So it kind of inhibits action potentials. And therefore you get this inhibitory effect that happens. Um, support after Botox works. Essentially, um great. So neurotransmitters the stuff and moves in between these faces. So the main your renter's units know about listed on the screen. So dopamine or adrenaline, serotonin and GABA lose weight and glycine, and many of these implicated in common psychotic disorders they talk about today the's are the new transmitters, synthesis pathways for their transmitters. I've just listed I would learn the intermediate products that are listed here. And I would also learn the names of the enzymes. Um, in terms of the most high yield information, I would remember that the rate limiting step in the synthesis of serotonin is this over here, which is when I tripped. If in is converted to five ht but tryptophan hydroxylase, And this is the rate limiting step, which is important. But also remember that GABA is ultimately synthesized from blue tomate. It's synthesized from glucose on. I would old learn that the census of glycine is a fully dependent reaction, so folate deficiency can lead to problems with, um, placing. Great. So let's talk about how these your transmitters are implicated in psychotic disorders. So if we take depression first, there are many hypotheses about depression out there, and no one actually really knows the truth cause of it all. We have, ah, hypotheses that seem to be true, and that seemed to respond to medication. So the main one, I'm the most widely accepted one. Today is the morning I have a me model of depression on this model kind of states that if you have a deficiency in motor, a means more know a means being serotonin and dopamine in order online that's could lead to a reduction in your moods. So if you have less serotonin, your sign ups, for example, that means you're getting less excitation off the portion that you're on and therefore you having less excitation in your brain, Uh, or in your stimulator in parts of your brain and there for a little mood. So this would then make you think, um, sorry. Megan's gonna talk more detail about depression on about psychiatry disorders. I'm just going to talk about the physiological basis of them. Um, so if we don't consider that a low amount of morning a means means a low moods, then from a pharmacological perspective, when you're trying to treat somebody, you're like Okay, if I can increase the amount of money a means maybe I can better their mood and therefore the hypothesis of pharmacology is that if you can find a way to increase the morning a means you would increase the mood and this is the basis of antidepressants, and this leads me onto talking about the different classes of antidepressants. So we have three main classes that we talk about. The first is the Mona Aiming optic re inhibitors. On these, you may have heard of them. They include tricyclic so selective serotonin reuptake inhibitor. And that's our eyes. Nordgren injury of taking a bit Ear's and serotonin origin. Odjick, your particular baiters. I'll talk about these more detail in the next few slides on. But the second time is inhibition of an enzyme that breaks down these your transmitters in the sign APs. So the more I mean oxygen averages because more normal oxidase breaks down serotonin on go. Also, the third kind is innovation of presynaptic order receptions. All of these just sound like big words. I'm going to break it down for you using some diagrams. So we look at the first one, Mona. I mean reuptake inhibitors. What does that mean? So let's say you have a sign ups here and you've got a bit of serotonin floating around in the cleft. Okay, those think cause that's a return it usually what happens is that at the end of the cycle, most are not. All of this serotonin is going to be re uptaking back into the police. And after you're on okay, and you've got these motor in France borders, that going to transport them back into the term, it's not on your own. Onda in people who already are deficient in these motor a means you kind of want to inhibit this process because if you keep serotonin in the synaptic left for longer periods of time, or you increase the concentration. That means you're going to be able to excite the poor synaptic near on more on for longer, which means you're going to get a net excited tree effect that going to last longer and hopefully improve moods if that makes sense and therefore one way off keeping serotonin longer in the surgical eft is by inhibiting is reuptake and therefore you have SSRI zar. Try and try cycling's, for example that will inhibit these transporters over here. Okay, so tricyclic so actually a non specific. They were actually the original ones. They were discovered first on be a non specific in that they will really take any kind of a mean They're real technology and land on serotonin on, but they're really cared a nonselective. However, SSRI was and and arise, for example, are specific to serotonin and norepinephrine. That's the difference between both of those. So that's how these work the second class we want to talk about, right? Uh huh. Those that can inhibit the enzymatic breakdown. So again, the end goal here is to maximize the amount of serotonin in the synaptic left for the longest possible amount of time. Another way of doing this is preventing its natural breakdown. So the natural, like lifecycle of serotonin in the left. Not only is it taken up back, but before it can be reuptake, it has to be broken down into a digestible form. On more know, aiming oxidation is an enzyme that breaks down serotonin on bear. Four. If you can inhibit to this process, you're going to leave more serotonin, the cleft, and therefore cause more excitation in the Boston you're on. That's how that works. Then. If we move on to the third type, which inhibition of presynaptic order receptors, so what does that mean? Well, this actually has to do with the receptors that exist on the presynaptic nearer to these purple little structures here are called order receptors. Now, usually what they do is that they restrict the release of neurotransmitter. They prevent too much off on your transmitted from being released now in people who are deficient in your these years. John's meters. Obviously, that's not a very good thing, because you want it to be non restrictive. You wanted to release as much serotonin. It's possible, and therefore you design a drug like Mirtazapine. That's going to block. These are two receptors to allow a less restrictive you transmitter release. That's what's gonna happen. And finally, you have more thorough Tony to float around on, because excitation. So that is the basis of the physiology behind how, um, antidepressants work different classes. So what Drugs fall under these different classes, so under tricyclic. So the one you'll see the most often and questions is amitryptaline. And this is, um, the one that's used medically as well. When I press like aches are used. Like I said before, it's non specific. So it's not specific. Suggest serotonin or just no adrenaline and acts and all of the different kinds of receptors. So alpha one receptor, those histamine muscular neck On shortly, we'll talk about the fact that tricyclics have lots of side effects, and that's very much to do with the fact that it is non specific because it has an affect on so many different types of receptors. It can cause many side effects. Um, names. If SSRI eyes, um, citalopram, sertraline, fluoxetine, fluoxetine, Prozac sitting there, all names you will see and names do. You should familiarize yourself with and be able to identifies Yeah, that's that's all right. Um, the main thing I would note about these names is that fluoxetine when it's used clinically, the main clinic a lot about it is that it does have a longer half life than others, says our eyes. So, for example, if you're switching from prescribing someone from one SSRI or not as it's all right, Onda like, from fluoxetine to a tricyclic, for example, we were switching them because fluoxetine has a longer half life you would make make someone stop the fluoxetine completely. First, make sure that their bodies completely devoid of it on Ben start tricyclic. So because it has a longer half life where, as if you were switching from another is, is all right, you wouldn't re you wouldn't really stop it abruptly. You would kind of wean off slowly. That makes sense. It doesn't matter, either. A boxer seen an SNRI Dirac city, and it's just named weeks. Know and identify. Watch us a drug the, uh, in terms of monoamine oxidase inhibitor as you've got isocarboxazid it. To be honest, my ways on actually used very often these days that kind of like the third or fourth line drug eso at your level, You probably never see in the question use clinically. But I would just be familiar with the mechanism of action on this drug name, but clinically, you probably wouldn't see it being prescribed very much. Um, so, like I said earlier, tricyclic so in terms of side effects because it has effects on, like alpha one receptors and histamine receptors and things you have side effects like and you must communicate effects. Um, um and post your hypertension and, um, and even sedation. Um, and it can be very toxic, an overdose. And because of all these random, unwanted side effects, you know, over the years people have come up with a better class of Republican or bitters that are assets are eyes which associated with much less, much less side effects away milder even when they do Come on the notice at the door and start with the orders like that is sedation or like toxicity I. Instead, you get things like G I upset. Um, insomnia. Special dysfunction there are otherwise usually treatable more easily. You can also get syndrome of inappropriate ADH secretion as well, which is quite rare, but it can happen. Um, in terms of side effects of MRI's, um, you can get hypertension acutely as well as sweating. All right, so that's that's important than the others I just mentioned in terms of specific side effects specific to drugs. Citalopram can lead to a prolonged QT interval specifically, and you should know that fluoxetine is a site of crime people 50 inhibitor, Which means that in terms of interactions with other drugs, because it's going to inhibit the liver metabolism, it's gonna mean that other drugs in circulation are going to last longer in your blood stream. It's just something to think nose off. It's not usually a problem, but it's something to note. Um, and as our eyes, as you can see, are generally safe own overdose, whereas tricyclic can be quite toxic quite easily and therefore exercise are the first line treatment first line, pharmacological treatment off moderate depression these days, and then tricyclic so like, quite down the list. Yeah, that makes sense. Um, and the border things, you know, in terms of antidepressants is because you're trying to increase the amount of serotonin I know. It's I know it's I never thought I'd be possible but it's possible to have too much serotonin, and that's when you get serotonin syndrome on. Serotonin syndrome is not side effect. It's more of a disease. It occurs when you have one or two drugs that both act to increase serotonin, and therefore you have too much serotonin being built up, and you can kind of get acute disease from this, and I'll talk about that in a minute. But that's quite important. Um, drug interaction to note serotonin syndrome? Um, an important side effect of Maui. So note is this thing called the cheese crisis. You might have heard of it. It basically, when you have more know mean oxidants, emitters, what's gonna happen as a result off their physiology is you're gonna get accumulation off. This protein called tyramine and Tyramine, is a protein that is actually a sympathomimetic, which means that it's going to act in a way to stimulate your sympathetic nervous system. And that can lead to things like acute hypertensive reactions, which can, which can be fatal. I'm it can be quite bad in emergency, Um, and it's called cheese. Crisis goes up. The cheeses are quite high, entire mean on their four people who are on Maui's A usually discouraged against eating foods containing timing to avoid the side effect. And then finally, we have mirtazapine, which is the auto receptor inhibitor in terms of side effects, the millions of effects of fact that made has been, actually, although not kind of non specific, it acts. Why did acts on the surgeon or two receptors? It also acts in another class off five HT receptors. 5 83 on bees are involved in appetite regulation, so I was. As a result, you can get increased appetite and weight gain over a couple months. Also acts and a similar substance calls drowsiness on the most. A very important side effect of Matassa mean that you should note is I can cause a grand a granulocytosis on. This is basically when you get a acute reduction in a white blood cell count, and therefore that obviously makes your immune immune suppressed, which is dangerous, which means more susceptible to infections. And I could be fatal. That's a bit of a high yield fact for you in terms of mood, has a p great. So no, I'm going to move on from talking about serotonin and norepinephrine to talking more about dopamine. So dopamines, another new, newer transmitter on do It has a very specific pathways in which it works in your central nervous system that we're going to talk about that you should know. So it has certain pathways that it follows in each of the pathways that follows, have a specific function and are involved in specific disease. For example, if you follow the red arrow over here, that's called your measles limbic pathway, and that starts in your ventral tag mental area, which is what VT A s and it goes to your nucleus and Cubans and amygdala and this pathway is involved in things like rewards. Um, on day, feeling good on day, just general like euphoria on my things like that. So this is actually been implicated in schizophrenia. So posted symptoms of schizophrenia like Megan will tell you shot if things like hallucinations, hearing voices, um, things like that on. But this has been associated with over activation or too much dopamine in this means Olympic pathway. We then have these these blue lines. These blue arrow is that is your meter cortical pathway on that starts in your venture, Take mental area over here, over here, Right, And it kind of goes all the way under course. X on it goes to your prefrontal cortex on. And that's always kind of, as you can imagine, involved in things like planning and prioritize. I proteinaceous and like, thinking and logistics and things like that, Um, and negative symptoms of schizophrenia, as making will tell you, are more cognitive symptoms on their four under activation or a lack of dopamine in the music art. The pathway has been associated with negative symptoms of schizophrenia. Okay, And then you have the green pathway over here star substantia nigra and which is in your midbrain and then goes all the way to your basal ganglia. And this is implicated and movement. So this is quite important in, like, Parkinson's disease, for example, And then finally, you have the tumor and fundamental pathway that starting the hypothalamus and travels to your pituitary. And this is important in the secretion of production. Basically, dopamine inhibits prolactin secretion. Therefore, if you have a lack of dopamine, so if you have too much dopamine, you're going to inhibit production. Um, yeah, and if you have to less dopamine. That's going to cause excess prolactin, which can cause things like gynecomastia or like a menorrhea. So, doctor, my dopamine pathways this'll eat to be on two talking about the dopamine model of psychosis. So we just talked about depression, and when I'm going to talk about a bit about psychosis, um, and psychotic symptoms like I said, Megan will go much more into detail about what these diseases, where these disorders are in terms off. You kind of describe them that I'm just going to talk about how your transmitters are involved in them, so it does the psychosis. The main hypothesis is that an increase in dopamine or too much of too much dopamine can lead to psychotic symptoms, for example, like hallucinations. And that was important to note that this would be your measles limbic pathway rather than your meals, a cortical pathway. So on excess of dopamine in your knees. A little bit pathway could lead to psychotic symptoms, and therefore, for pharmacological perspective, you're thinking right. If too much dopamine mean psychotic symptoms, then potentially a little, little less dopamine. It would mean potentially less psychosis. That is the basis in a very very extremely Generally simplified way is the basis of your anti psychotics and how they were, um on this is how the antipsychotics works against your positives on the positive symptoms of schizophrenia. And not you're negative symptoms because you're negative symptoms associated with your music cortical pathway, like I mentioned earlier. So antipsychotic drugs. How do you classify them? So you got me two main classes. Okay, you've got a typical I need got typical. So typical ones are old called first generation antipsychotics because they were the ones that kind of discovered initially on. That includes things like haloperidol, which is still very much used today. Um, on the our first generation of the first ones to be found on, they basically were dopamine receptor antagonists, and therefore they inhibit dopamine transmission in your new trumpet of pathways, especially in your muscle in big pathway. And this helps to reduce our improve your positive symptoms of schizophrenia. However, your second generation antipsychotics, which have come more recently, our results off people realizing that psychosis is more than just to do with the prostate symptoms. Lots of people. Sorry. Lots of people are more affected by the negative symptoms as well, and how the parador doesn't necessarily help with the negative symptoms, and therefore they found that negative symptoms can be helped by antagonizing serotonin receptors. And therefore, second generation antipsychotics target dopamine, two receptors as well as serotonin to receptors. So that's how they're more. They're like the new, that new and better version off antipsychotic drugs. And these second generation antipsychotics include clozapine, olanzapine, risperidone, people's all, Um, and I would become familiar with these names. Like I said before, these are really good, and they're new improved because they can target both positive on the next symptoms off six kids. So when are these indicators? While your first generation antipsychotics you would think they'd be outdated right now and you'd think that our know what, actually is that anymore? Because they're old and the only target D two. Well, actually, they are still use today, although, as you can see, they have a much larger list of indications as compared to the second generation antipsychotics. But you would prescribe how the paradise I'm in episodes of a to delirium, for example, or if you have an adult that is acutely delusional or agitated. Um, where a second generation antipsychotics, um, are used for acute psychosis and schizophrenia. Um, as well as people of Parkinson's who are experiencing psychotic symptoms as a result off their Parkinson's medication. I have a quick sp a few guys if we carry on, Um, then we just launched the pole. I've got it. Oh, thank you. Who did that? Go to 34 year old male who was started on clozapine for a factory schizophrenia month ago. Who presents to hit the emergency department with some fever terms. He thinks he's sweaty and complains of feeling ill. What is the most likely complication caused by the drug he was started on? It's I can't I'm gonna end up there. Yeah, this is perfect. Yeah, majority 66% of you got it, right. The answer is be, um, basically all use. Oh, yeah. It's just a high use fact that Plaza peen, the second generation antipsychotic, is associate it with a kind of fatal side effect of a cannula cytosis also like mirtazapine, which has the same side effect. Um, and like I said again with a granulocyte doses means you're immuno suppressed and therefore wonderful the infection on. But it's just bad news. Basically, uh and that's the high you fact. I would just remember. Um cool. So let's talk about the adverse effects are 1st and 2nd reason you're Asian antipsychotics. So first generation antipsychotics like haloperidol, for example, are involved with things like extrapyramidal symptoms that basically means that can cause your movement disorders. They can cause problems with movement. You're depriving the person off dopamine, and they're nigrostriatal pathway, Um, from earlier than I go straight to the pathway to recap is involved in movement. I can park in this disease if you have. Therefore, if you're describing if you're depriving somebody off this off dopamine in that pathway, you are department off some extent of movement. Um, and the symptoms can be summarized with the pneumonic adapt A for acute Andy's for acute dystonia aids For a cath Easy. A piece of parkinsonism and tea's for irreversible tardive dyskinesia. Um, Onda. Yeah, Like I said, this these results off a lack of dopamine and I go straight to pathway a side effect of drugs Like how the paddle, Um right. This can also cause hypo production in you. Can someone tell me in the chat Why drugs like haloperidol would cause hypoprolactinemia Anybody have any ideas at all? Why would first generation antipsychotics cause hypo? Relax. Anemia. Someone says dopamine in his production. Yeah, exactly. So you know, you've got your timber or in front here below halfway where it connects your help with elements that your pituitary gland and what happens is if you have, um, usually dopamine inhibits production secretion. But if you have on antipsychotics that are inhibiting dopamine release, then these Then a lack of dopamine is going to encourage production release, and therefore you're going to end up with too much production or abnormal amount of production. And this can cause hypoprolactinemia. And like, imagine, earlier side effects of this look like gynecomastia in males. Onda also amenorrhea in females. These are going to psychotics at all to cause prolonged QT interval because they happen to block the the report, or is a shin of potassium channels in your myocardium? Well, um oh, we'll talk about the last one in the second. Um, second generation antipsychotics, like clozapine used more often. I'm not only because they can target both serotonin and of the receptors, but also because they're associated with fewer side effects like the So you get less the extrapyramidal side effects and you get less than half a prolactinemia production. Amia All right, um but you do get some hide effects that are specific to second generation and his psychotics. And this is because the absence there were told in receptors. Well, example of this is the increased risk of metabolic syndrome. So five ht three receptors are involved in appetite regulation like we discussed earlier. And therefore, if you're getting activity, abnormal activity and the receptors, this can lead to increased appetite and weight gain on dyslipidemia and basically metabolic syndrome. Other common side effects are using. Second generation antipsychotics are prompted the interval sedation because of the effects of histamine receptors on postural hypertension as well Duty effect on our for one receptors now with antipsychotics. Sorry, I will see you before that. That again the you should know that closet, being specifically has a high risk has increased risk off developing a green, you know, cytosis, myocarditis and cardiomyopathy. Therefore, it's cardio toxic. It can be cardio toxic. I will say that if you remember how we talked about with antidepressants that you can get a risk off serotonin syndrome. If you have some drug interactions here, you can have a risk off your elastic malignant syndrome. So that's talk about what that is and how they're different. I used to get confused between these all the time because they both have similar categories of symptoms. But the symptoms are quite different if you actually look at it. So I'm going to try to break it down today, and hopefully it'll make sense. Um, Andi, I feel like I've made this slide very bullet point, he said. Kind of get straight to the point. So, like we said earlier, um, you can get serotonin syndrome when you have interactions between antidepressants. So if someone is taking one or two, if someone's taking two or more serotonin increasing drugs at the same time, this can cause too much serotonin. He decided to run syndrome apologies. It's not really a side effect. Calling your side effect is wrong. It's more of a disease as a result of drug interaction. So that's how I would say it. I'll change that provides some it out. Um, whereas neuroleptic malignant syndrome is due to too much dopamine antagonism in the central nervous system. So this is more to do with implicated with antipsychotic drugs. So in serotonin syndrome and in Europe to Milligan Syndrome, your symptoms can be classified into three main categories. You're a very simple trying to remember. The first ever symptoms is autonomic instability, which means they be like So I saying or problems with urination or constipation or tachycardia or things like that. Okay, they will have problems with mental status, like depression or anxiety or restlessness or, um, psychosis, things like that. And then the third category is a mural muscular symptoms. In the case of serotonin syndrome, you have neuromuscular hyperactivity, whereas in the case, neuropathy, malignant syndrome, you have your muscular hypo activity. So let's see how this manifests since they returning syndrome. Like I said, you can get autonomic instability, um, which is like autonomic symptoms. And in terms of newer, muscular symptoms, you get hyper activity. So, like hyper reflexia hyper rigidity, things about where you're quite stiff, very actually, have you very reflexive that social and syndrome is, whereas with neuroleptic malignant syndrome, you have hypo activity. Your muscular least you get a muscle rigidity, akinesia like slow movement or a tremor or symptoms of having to less still coming in your nigrostriatal pathway. Ah, very, um, key points to note in the difference between thesis symptoms of the onset is very different. So where is the serotonin? The onset is well within 24 hours. It's very acute in an m s. It's over days or weeks. It takes time to develop, um, said Jonas syndrome. When someone comes in to any, there's no specific blood test that you can do to kind of corroborates or confirm the diagnosis. Unfortunately, whereas Neuroleptic malignant syndrome usually get a very raise creating kind of enzyme in your blood tests, it's on diagnostic. But it does help with the diagnosis, and that makes sense along with everything else. It's primarily clinical diagnosis for in a mess for both of these, actually, Um, see, I hope that kind of gives you like the main differences between serotonin syndrome and your doctor malignant syndrome. So let's talk about how to treat these. Um, the main things you have to remember is that both of these kind of are emergencies they are need to be treated, need to be able to do immediately, acutely, and therefore the first thing. The right answer always is 80 assessment. You want to make sure that it's an emergency scenario and their primary airway breeding circulation all that sorted. And then finally, it's important to note the mainstay for treatment is like supportive care. So then I see you. They need the board of care. And that is really the most important thing in these patients for both of these diseases. Okay, in terms of pharmacology, in terms of exam questions for serotonin syndrome, you would prescribe super happy. This is definitive serotonin syndrome treatment because it is a serotonin antagonised. So the problem is, you have to much serotonin, and they're so therefore, cyproheptadine is going to antagonize this and you have less serotonin. So the definitive treatment when you're muscular neuroleptic malignant syndrome, you have drugs like Dantrolene and bromocriptine. Um, bromocriptine is a dopamine to and agonist on. Is that going to increase dopamine and help solve the problem? So I hope that make sense, Great moving lots of drugs of abuse. Um, I'm gonna waste past the rest of the stuff because I think I've covered the main stuff. Um, the rest of this is just mostly factual things. You kind of just have to learn. Just going to list them out when you came Drugs of abuse. The best way to learn it is if you get a guy's the interstim. Yellen's on depressants. Okay, So stimulant drugs of abuse include cocaine, and that means like, MDMA on Dick. A teen tobacco. Okay, um, and this is how it works. So cocaine. And that means they work by inhibiting the reuptake off mano a means and dopamine, which means you're getting an excess off certain an excess of dope. Me. And as we just discussed, the's can be problematic. Um, it can be extremely excited tree on do. Yeah, very excited. And that's how you get this stimulant effect. As a result, um, you should note that cocaine is also use clinically sometimes in the hospital. You might see it very, very rarely on that because it helps in vasoconstriction. So if you got nosebleeds, actually access a local basic constriction. Can I stop? Stop bleeding. Um, but this is no reason Teo take advantage of, I guess, um but that's an important point to remember in terms of nicotine, Nexium, tobacco, they work by increasing dopamine, your Ms Olympic pathway and, as we discussed earlier, that's implicated and things like positive symptoms kids, a friend, A a. So like hallucinations and things like that, um, also increases serotonin by reducing monoamine oxidase activity in terms of depressant drugs. Were looking at cannabis a weed marijuana on these, the main. This is a very high you'd fact the main active substance in cannabis is tetrahydrocannabinol DHC, um, which acts via C B one and see we do receptors in the brain, and this indirectly through a series of pathways, causes the release of dopamine, and therefore you get, um, mean release so you can get psychotic symptoms. However, because it binds opioid receptors, you can get a depressant effect as well. Um, in terms of clinical features, um, it's stuff that I just listed so for cocaine, it's like you get euphoria, um, on because it and stuff because of the dopamine, there's only release. You can also get sympathomimetic effects so, like you can get my dry cysts where your people become really large. You can get a doc a cardio. Take your with meals and chest pain. Hypertension with nicotine again, you can get these sympathomimetic effects. Um, I think you guys have attention with cannabis. Um, you could also get the some autonomic effects. Um, but mainly, it's more this slow down CNs, where you're kind of socially detached to your judgment is impaired. You very euphoric. Um, and your perception is just generally off in terms of castle mean, Um, the Catalina is acting on the NMDA receptors, so this isn't an MD receptor over here. Okay, The way NMDA receptors normally works is that it requires glutamate and glycine to bind to it. Okay, It requires both of these things to buy into it too. Then open I'm to allow I owns to flow through it. No, what's gonna happen is that if you know, if you remember, um, you've got GABA allergic neurons. GABA is in inhibitory your transmitter and therefore GABA allergic neurons are inhibitory neurons to inhibit bacteria. See, what catamenia going to do is it's going to inhibit the enemy receptors on the inhibiting you're on. It's inhibiting the inhibitor and therefore you get a net excite a tree effect, you get in big glutamate release, which gives you a nets like excited, very feeling and Therefore, I have until here, but ketamine is a stimulant drug. That's what you talk about sleep and sleep disorders as well. Main points about sleep, you need to know are these could summarize them? First of all, sleep is a lot more important. You think you actually do so much more work in your brain when you're sleeping when you're awake? Memory consolidation. Um, just like, um, like consolidating things, making sure your process of working things that everything happens at night, especially when you're asleep. And that's why I sleep is so important. Um, the main anatomical structures should be aware of in terms of sleep is the suprachiasmatic nucleus or the SC end. This is called the so Kadian pacemaker because it's in charge of kind of setting your sleep cycle. The main your translator's implicated in your sleep cycle and regulation of your sleep Rx in melatonin GABA on a damn is een while your heart rate is measured, what your heart rhythm and rate is measured with HCG. Your brain rhythm is measured with an e G. Um, and easy waves are very useful in that they can kind of tell you what your brain is doing when I was very active, worried whether it's asleep, whether it's working hard, I'm in there for that really useful in diagnosis, sleep disorders and kind of seeing how people are doing. Um, and they want to know each sleep cycle last about 19 minutes and you get about seven hours of sleep a night. You're getting about like 3 to 4 sleep cycles. Maybe on D at 10 is een makes you sleepy. So throughout the day when you're going about your day when you wake up in the morning, your dentist mean is really low. And as you go about with your day, your dentist and increases throughout the day and therefore when it reaches a peak in the evening, if you really sleepy, you're going to want to go to bed. And this is where coffee works. So coffee, even adenosine inhibitor. Therefore, when you wake up oh, it sometime during the day when you have coffee, you're inhibiting identity and therefore you inhibiting the feeling of being sleepy. Uh, which is why you shouldn't have copy too late, because it kind of messes with this whole making you sleepy thing. So that's not quite sleep stages. The three main types of seepage is one is when you're awake. Like right now, uh, before you're just going to bed on you have two types of stages in sleep. So non rem sleep and dream sleep. REM, the full term of ram is rapid eye movement. Um, sleep on. Don't talk about that, Is this I can't. So non rem sleep specifically can be divided into three sub stages. You have non rem one non rem to and Nandan three. So let's talk about what those look like on the EKG. So when you consider your screen here different stages of sleeping with different different squiggles, different waves, so can somebody tell me, um actually, I just really on somebody. Sorry. Um, did the next one, Um so when you're when you're just falling asleep when you just fall asleep, you just enter the first stage of a non rem sleep, and you spend about 5% of your sleeping time here. You get away. Just these detail waves. This is associated with the end. One stage off sleep, So n one wave test eater and two stage of sleep. You get these very specific diagnostic um, signs of a sleep spindles, which looks like this. She's bit of like a It's a bit of ah, crescendo decrescendo kind of kind of squiggle. And you get a complexes will look like this. This tells you you're in the end stage of non rem sleep, and then the enthused age of on ropes sleep is you get delta waves, which is this you don't necessarily need to look. Need to know what each of these waves look like, except for the end to stage of sleep for your exams. So I would learn would learn what this looks like. Your exam. Um And then finally your REM sleep Really rapid eye movement. Sleep uses beater waves and you spend about 30% of your sleep time in REM sleep. Um, sleep. Actually. As you can see, it's very chaotic If you compare from sleep to your other sleep. States like here, you can see that Delta is actually really slow, like it's really slow and steady. Where did you see from? Sleep over here is really chaotic and actually ah, common misconception is that you should get more reps leave to have a more rest fall asleep when Actually, it's the opposite. Brems sleep is not breast. Full gram. Sleep is when your brain is working the hardest. Um and therefore you can see the EKG waging chaotic and you call rapid eye movement because you can like, you'll see people moving their eyeballs under their eyes when they're asleep, and therefore to have a rest a little speak any more time in your non REM. See, that's why you can see you spend about 70% of your sleep in non room and where you are 30% in REM sleep because it's not exactly very rest fall. But it's very important for consolidation of brain matter on for cognitive processes. Okay, cool. Um, this is a pneumonic that waas put together by Toby. Um, thank you to be on, but this helps you memorize what stage is asleep is associated with what kind of sleep ways. So bats drink blood. Um, so beat a wave and bats is, um, beater. If you just remember the order on the left side, and then you can, like, say, the auto off the pneumonic on the right side. So, um, beat up bats Alpha for a be 70 seeds. Spindles for s Delta for drink and beat of a blood have helps you remember what is what is going, Porton. Great. Well, the SBA, um, somebody be able to launch the pole. Please. I could do yourself, actually. Um Oh, great. Thank you. Patients have complaint that a partner has been snoring very loudly. He noticed that the patient is quite overweight and is very sleepy throughout the day. Which of the following scoring systems is used? A screen. Excessive daytime sleepiness. Okay. Okay. Good. Into that. Um, yeah, Amazing again. Most of you got it, right? Well done through the answer is, in fact, the airport score the upward sleeping. A school is basically a measure off someone. How sleepy Someone feels during the day on gets used to help, um, like, diagnose sleep disorders and kind of see how bad someone's insomnia is. Basically, um, so we talked about sleep disorders. I'm not gonna go over them in much detail for the sake of time, but I've listed all the key fax on the screen here. I think my given that has the information on this as well. But, um, the main thing I will say for this is that these are the treatment. These are the diagnostic criteria for insomnia in these bullet points over here, um, I would memorize the, um, diagnostic criteria for climb 11 syndrome. Narcolepsy on behind of Know the difference between Remeron non non rem sleeping disorders over here. Well, also no obstructive sleep apnea. What kind of populations? Effects, For example, obese people on bowel. It's treated basically the CPAP and no one C pap is It's continuous positive airway pressure. It's on the sides later that you get so finally a very short and quick bit about newer development. So the main crux, the main two key words you need to know when your development in adolescence is external violation and santic pruning. These are the two main cognitive processes that happen in adolescence. Okay, during puberty or even actually all throughout, like whenever you're going up happens. Probably happening right now. What? I'm teaching you this, which is pretty good thing about, um, so doing adolescence. You have changes separately. That happens your white matter and your great matter. Okay, if people are so confused because I was confused, the longest time about this gray matter involves cell bodies, New Orleans cell bodies, whereas white matter involves neuron like they're like the axons, not the cell bodies. Okay, so in adolescence, what happens? Your white matter is you got a linear change, as you can see here. Okay, Alina, increase. There's there's a difference with the mayor of female. I'm not really sure why That is that Much of anyone knows why, but I just know that they increase the different rates. They're both leaner and when when they increase Onda This is a drug ated mile a nation off your axon. As you go up, more, more and more of your axon is getting violated with the protein mile in chief, The phospholipid sorry. And therefore, this kind of increases number, amount of white matter And this is a lien. You just know that it's Lena and there was a gray matter changes. This is a non linear change on this is actually a bit different, so it doesn't exactly just increase straight up is quite different. So basically, when you're first born, you're suddenly exposed and overwhelmed with all those new cognitive simulacra getting You got all this new information, you have no idea how to filter it. You don't know what's useful. You don't know what use useless. You don't know what information you going to use in the future. It's your brain. Courreges, like acts like a sponge and collects everything. And actually, a lot of the information is not actually very useful. And you realize you're really care what the color off off like Joe's wall is in his house. You know, I mean, so your brain during puberty is going to feel to the information out and be more efficient. So it's going to undergo a possible sign optic pruning, where you will actually lose some gray matter. So at birth you have very less grey matter on. Then we'll go. But older, you get lots more lot or not. A. Not a. Not a great matter, because you got all that information. Also use our bodies and then we got a puberty. Your brain's like bright. I need to be more efficient about this. I don't actually need all this stuff. I'm just holding for no reason. It's kind of there's a bit of a cleanse called synaptic pruning, where it gets rid of the unnecessary connections and the necessary cell bodies, and it's called a reorganization process, and this is called started pruning. So the end result is, um, this equation which describes total grey matter volume after adolescence, which is the pre pubertal increase, which is over here, plus the post puberty loss. And that would make up you totally gray matter volume. So I hope that's a quick summary of my talk today. These are the appetite. Regulation slides. Um, I put them up on medal, and if you feel in the feedback form, you can have access to these. Uh, but thank you so much for listening to me for any questions. I'm gonna be other calls. I can answer them on the chaps. Gonna handle over to Magan now. Thanks, Hana. That was a really great talkers. Always and such a good introduction to hopefully what I'm going to be going into now. Thank you so much for sticking around. I'm going to try on D was through this topic as quickly as I can, but I know this is quite a big part of the mental health on this case, so I'm just gonna share my screen. Can you see that? Okay. Sauna. Yeah, of it. Brilliant. Thank you. So how everyone? I'm sure you will know me by now. I'm Megan. As Avants said at the top of the session, just to say, my talk is going to be talking about all of the mental health conditions that you're probably need to know in your pre clinical years. So just a heads out. We're going to be talking about anxiety, depression, bipolar, schizophrenia, A said. We're just medical students where using this platform or for medical education. So as a van said, I'm going to be talking what's really high yield for you to know in your exams? Um, I'm definitely not an expert in mental health. Mental health is such complex and sensitive topic, and I definitely don't know every everything. So I will do my best to tackle. This is sensitively is possible, but just a heads up it will be. All of these conditions will be talked about throughout my slides. So the trigger warning if he like, starts from now. So let's say we're going to be going through anxiety and mood disorders, psychotic disorders, disorders a little bit about the mental state exam. Um, if you're in Cardiff, I've just included your lending objectives that I'm going to be covering today. So let's begin. So let's say I'm going to be talking about the three main categories of mental health conditions that we have, which could be brought be categorized into anxiety disorders, mood disorders on psychotic disorders, which I've listed here for your future reference. So let's start off with mood disorders. So mood disorders are also known as effective disorders, and they're basically just illnesses that affect the way that you think in the way that you feel, um, so the main ones that you guys these know, our depression mania and hypo mania on bipolar disorder Tax one and two. So before we get into it, I just wanna get some definitions straight before we start with. So I want to start by talking about effect on mood. So affect is the current observable features of a person's emotions, or how they're feeling so that could be their facial expressions. There gestures, their tone of voice. So it's how they look from your perspective, basically said. Do they look sad that they look angry? Do they look hostile? Do they you looking happy and new for IC. This is really key to differentiate from mood, which is a patient, subjective internal feelings of how they describe themselves as feeding at that time. So the only way that you can determine somebody's mood is by asking the patient how they're feeling. So do they feel that they have a low mood? Do they feel anxious? If you're angry, do the feel euphoric, etcetera. So I just want to emphasize affect is what you see as somebody looking at somebody. So I kind of think this is like the emojis that you see on your mood is how you personally feel you as the person being asked how you feel or how the patient feels. So can anyone pop in the chapter? Me. Does anyone know different types of affect? Does anyone know different disorders that people can have with their effort? Can you just drop some names in the trap for May borderline personality? Well, that's great. Is it Blunted? Yep, running. I think you guys have got the right idea, which is really good. So I'm going to try and explain these with some graphs to hopefully make everything nice and clear. So to start off with is blunted effect. So this is when somebody showing a lowered intensity off their emotional expression, basically. So if someone's got blunted affect, it means that they're showing little emotion even in really emotional situations. So, for example, someone might be describing a car crash or a fatal incident, and they'll be speaking a really monitoring voice with no no emotion whatsoever. Even though this horrible thing has just happened on day might have little face like facial expressions and things like that. So when someone has a bunch of level of affect, as you can see from these blue lines, here basically means that they have a lowered level of intensity of their emotions, either positive emotions or negative. When someone has a restricted affect. This is slightly different. This is when they have a reduction in their expressive range, so they're able to show feeling, and they're able to show emotion. But it's not as much as you would expect based on the situation that's happening at that time. So I've just illustrated that with these little kind of brackets, so they're able to show emotion, but they're only showing a small range of it that might be in the middle kind of no, not much emotion. Or it might be. They only really share a limited range of negative or positive emotions. It's two more to do with the range that they're able to show then if someone has a flat affect, this does what it says on the 10. Basically, they have no feeling or emotion that they're displaying, regardless of the circumstances that they're in. Um, and this is basically a more severe version of Blunted affect. Then we have a label effect on. This is basically a rapid, onda repeated shifts in somebody's emotions. It's once again unrelated to the outside situation, so it kind of looks like they don't really have much control of their emotions. It's just going up and down, up and down, no matter what's happening in the outside world, and then shallow effect is basically the same as bonded affect. But this is when this is used to describe this pattern of affect when when you have someone who's got psychopathic tendencies, so once again they're showing little emotion, really, Andi say. For example, they received a life sentence or they get convicted of something they might respond really in differently and not so much emotion to that. So carrying on, we're gonna talk to a nurse. A harness briefly touched on this the model of depression as a Honda said, they don't People collectively don't really understand fully what causes depression. There are different models, such a zoo Monterey Me model, which are showing here the information model. There's lots of different models for it, but the Monterey mean one is the most important one that you guys need to know because it's the main accepted model for depression. It's the basis of our treatment. So it's a Honda said. The idea of this model is that you have serotonin, which I looked like to think of this happy hormone. It's a type of mono aiming on in depression that's low in the sign Actiq left. So it's a Honda said there's two main ways to treat that we can use SSRI zar, selective serotonin reuptake inhibitors. They reduce the serotonin reuptake into the presynaptic you're on. So therefore there's more serotonin left in the presynaptic left, and therefore the person is more happy or you have our monoamine oxidase inhibitor is so, Azzam said, are moderate. Mean upstate is the enzymes that usually break down serotonin into a monocle called five Hate A, um, when you have these inhibitors that inhibit Monterey, me not stays, is they prevent the breakdown, the serotonin. So you've got more happy hormone in the side Optic left. So how does this all relate to depression? Well, at your stage, you you guys need to know a little bit about how depression is diagnosed. So I'm gonna go through that now, based on the I CD 10 criteria. So for those of you that don't know the I CD 10 is an international classification of diseases. It's basically a book with lots of information on how to diagnose lots of conditions on with our mental health conditions. A lot of them either come from the D. S, m five or for depression, most commonly the I CD 10. So I've mainly got everything you need to know on this side, so I won't just read from it. But the cool things that you need to know is that the core symptoms of depression are depressed, more depressed, mood, sorry and had only a which is an inability to feel pleasure from normally pleasurable activities who someone might have previously enjoyed a certain sport or a second hobby. And now they just started Enjoy it anymore on Energia, which is basically a lack of energy. There's lots of other symptoms which I've listed here, such as changes to your sleep pattern changes to your weight, your concentration, things like that. Um, but for a diagnosis of depression, you must have had a symptom. These symptoms here present for most days for more than two weeks. If it's been less than that, you don't qualify as a clinically died diagnosable depression. Um, these can. Then, uh, these people that have depression can then have their depression categorized by its severity, which have included in the in this little tree map. But the bottom, um, I think the main ones that you guys need to know, uh, the middle three. So mold moderate and severe, um, mild is probably the one that is easiest to remember, and I like to remember is the rule of twos. So you need to course symptoms to symptoms from my list of other symptoms, and it needs to be non intense in that it's not markedly impacting their day activities. Whereas if you take a multi aerate severity depression that has to call symptoms 3 to 4 other symptoms, it needs to have marked intensity. So are they struggling to function? Are they struggling at work? And he's struggling with relationships except, uh, on emphasis. There you need three core symptoms. Four others or more. It needs to be severe intensities. It's really impacting their day to day lives on. They may or may not have psychosis, and when they do have psychosis, it's automatically a severe depression. And it's automatically called a site, a psychotic depression. Um, and these individuals with the psychotic depression really have a disconnect. With reality. They might experience delusions on hallucinations, which I'll be going more into later. Um, but that's just a really tough diagnosis to have just because it really doesn't packed in the day to day lives. There's other, also the different types of depressions I've mentioned here about seasonal effective disorder, so that is a disorder in which you have annual village relapsing episodes of depression, usually in winter, but can be at any time of the year on day, usually go away after a certain period is well, usually in the spring time. You can also get a typical depression, which is a when somebody has a depressed mood. But if they have something really positive happen in their lives, that can make them feel better. But they still have a depressed mood for the majority of the time and typical symptoms of a typical depression. Our weight game on increased sleep. You can also get depressive symptoms with pregnancy so you can get a postpartum kind of baby. Blues is what it's often nicknamed, which is where new mothers are characteristically quite tearful, quite irritable, anxious on gets really common. About 70% of new mothers experience that, so it's not something to be dismissed it all, and it usually occurs about 3 to 7 days postpartum, and it's most common in the lady who's a primigravid, Uh, so where she's having her first birth and her first pregnancy? Um, the more severe version off the baby blues is postpartum depression, which is basically very similar symptoms to the depressed. The symptoms of depression have listed here. On that occurs a later stage, usually about 1 to 3 months post pregnancy. So now I'm going to quickly talk about mania. So the main symptom of mania is this abnormal, persistent, persistent, elevated mood. These people can be quite aggressive. They can be irritable. It depends on the individual. They may also feel that other people are slowing them down or that other people getting in their way and stopping them from doing things that they want to do. Um, on my favorite way to remember, the symptoms of mania is thie ammonic big fast. So, um, the D stands for distractibility, so they're easily distracted. Low concentration levels, irresponsibility So they might have. They might should disinhibition. They have really extravagant plans and behaviors, A quite common and SPS. They might have business schemes, and Mike own spending sprees might have increased libido and sex sexual drive. Um, you might also hear patients saying that they have special talents. They found, uh, cure for cancer. They might say, say that they're sleeping around a bit more, a swell which could put him at risk of STD. So you do need to really lessen toe what behaviors they're exhibiting. Um is kind of related to that. They might have grandiosity, so that's where they have high esteem. They think really highly of themselves to say they might. They might think, Oh, I've got a cure for cancer is quite a common exam type presentation. They also have flight of ideas on. So this is when they're moving between. Different ideas really quickly on Diovan also have quite pressurized pressurized speech. So that's where they're talking to you. And they just need to get the words out because if they don't get them out quick enough, then they just they just implode. And they're speaking really, really quickly and just trying to get all those words out quickly as they come. They can also have activity increase sleep decrease on can just generally be quite talkative. And so in terms of diagnosing someone without the mania or hypo mania. So mania is when someone has these symptoms some of these symptoms for over a week and they need it. Least three of those symptoms have listed. It often begins, quite abruptly all of a sudden on, but for a diagnosis of mania, it must affect their functional capacity. So in my struggle work or in their day to day lives, they might not be looking after themselves as well. So eating, sleeping, drinking a Z should to stay healthy on do if someone has psychotic features, which some people with mania can do. Such a delusions commonly like grandiosity, style delusions where they really think highly themselves or hallucinations, hallucinations commonly kind of vocal hallucinations. When I hear somebody talking to them more about them, then that is immediately a diagnosis of mania and no hypo mania. Hypo Mania is basically just a less intense or severe version off mania. Um, the symptoms that they do have tend to be milder on no impact, their day to day life. Um, really it all, if anything, can improve it. So to say, people have many often have, like energy increases and increasing activity, so these people might find that their performance and work actually goes up rather than down. But it's still really important thing to pick up, because these people, as they say to do, still need, um, support with what they're struggling with. So then we have bipolar disorder, so bipolar disorder is defined as a combination of low moods, so depression on elevated mood. So these manic symptoms that I've just spoken about for a diagnosis. Patients must experience two or more episodes of these ordered moods on either end of the spectrum so they can have to manage to depressive one of each. Or they can have something called a mixed episode, where they have both elevated and depressed mood without a gap in the middle. So they're not separate episodes bit in the same period. They're having really high or really low moods. And Teo define an episode as they you need to have a complete recovery in your mood. So going back to kind of a normal, normal move state. You know my neck, you know, depressed, um, and say, That's what keep the episode separate and defines whether or not you've had two or more episodes. What you guys may need to know is that there are two types of bipolar disorder. Type one and type two. Type one is a combination of mania and depressive symptoms. Their mania should have psychotic features on their depression should be very, very low in terms of their mood will be very low, and it will be very, um, intense depression. Where is bipolar? Type two is categorized by hypo mania on depression that is still enough to warrant a diagnosis of depression. Buts isn't as low as you would find in bipolar type one. Um, you may also hear about another diagnosis relating to bipolar, which is psychothymia. This is a mood disorder where an individual experiences those lows and highs and moods very similar bipolar disorder. But it's generally less severe, and it doesn't affect their work relationships and so therefore, often goes undiagnosed. But it's really important to pick up on this. It's often underdiagnosed and goes, goes, Missed, but it's really important to pick up on these individuals because they're at a very high risk of developing bipolar disorder. So I won't go over this now. But just to explain the difference between the three of my problem by problem to on Cyclothymia here is a little diagram for your future reference. So I'm going to a quick quiz. I've joined you guys three diagrams. Can anyone type in the chapped for me? What am I trying to symbolize by the first graph? What, um what condition is it? It's one of the ones I've spoken about. Is it a, um Oh, yeah. You guys have got a brilliant Yep. well done. Yep. So the first one is depression, so it's a persistently low mood. Can anyone type in the chat with the second one is yet mania. Depression, bipolar one. Brilliant. Yep. So once again, this is by prototype one mania. So you might have psychotic features on a very low depression. And you guys can probably guess what's graphed number three. Yep. You guys have got it yet. Well done. Yes, this is bipolar type two. So just emphasize this is Hypo Mania. So many other isn't as high on depression that isn't as low. So I hope that summarize the mood disorders is clearly as I can. Now, we're gonna go into the psychotic that disorders. Um, these are defined as having features of psychosis on psychosis is defined as having thoughts, ideas or beliefs that, not based in reality ondas to psychotic disorders that you really need to know which are schizophrenia and delusional disorder. So once again, want to start off with some definitions. So a delusion is a fixed force belief that persists even though that there is evidence that the belief is folks or the subject of a delusion does not exist. These are also know explained by racial cultural beliefs. So you can't say, for example, that beliefs in God's are delusions, because that's a religious belief some people would regard. I suppose certain religious things is not as evidence that something doesn't doesn't exist, but you cannot base a delusion, um, kind of diagnosis off anything that's a racial cultural based on racial cultural beliefs, whereas a hallucination is a sensory perception that occurs in the absence of a real stimulus. Eso sensory perception beings that visuals are in order tree and these feel really, really to the person. And it often means that they can get quite distressed. Especially. They're aware that this is abnormal because they really can't separate reality in these hallucinations. They just do feel very real. So, for example, to separate the two a nation will be something like seeing and hearing ago speak to you and, you know, seeing this goes and it looks just a zip. It's really, really life. A delusion would be something along the lines of maybe seeing something hanging up like a towel or, I don't know, jacket or something, thinking it's a ghost on, but somebody turns the light on, there's no no, it's it's It's a towel. It's a jacket. It's not a ghost look. But you persistently believe No, no I. But even though you can see it's a jacket or you can see it's a towel, you still believe it's a ghost. So I hope that makes sense. Um, in terms of the auditory hallucinations, as I say, hallucinations can. There's different types of the main ones that say a visual or auditory. Does anyone know the the different types of order? Three hallucinations We don't want be able to strike. Describing the chapped very briefly. Um, well, a first. A second or third? Um, corded person. Auditory hallucination is like, Don't worry. If no, I can explain them. That's probably what I'll do. So a first person hallucination is when a patient here's their own thoughts. Being spoken out loud, um on it is, it is, basically is if their thoughts are just been spoken out loud, they can hear their own thoughts. Basically, um, a second person hallucination is when a voice or group of voices is talking directly to the patient, using the pronouns like you. So there's different types of second person auditory hallucinations. They can be really persecute arri. So they might be saying, You know, you're going to die, you are going to be targeted. They might be really, really scary things like that. They can be highly critical. Z and you're awful. You know, things like that. It could be really complimentary. A swell they, you know, be grandiosity. You're amazing. Or they can be instructing people to do something, something you need to do this, um, on they the second president Award it. Three hallucinations often mirror somebody's mood. So if they're feeling really what really good in themselves, they might have some of those complimentary hallucinations where they're not feeling a skid. They might have those critical those persecute arri hallucinations and then the third person hallucinations are when the patient hears somebody talking about them but referring to them in the third person. So it's often describing examples. Maybe two voices are agreeing are discussing the patient, saying, Oh, you know, she chews a horrible person person or she she or he is doing this into the so it's it's when somebody is being referred to a shell, he or they, rather than addressing the patient kind of saying you, if that makes sense on those third person hallucinations are often seen in schizophrenia, so I'm going to move onto schizophrenia now. Schizophrenia is a very severe mental health disorder on diets, one that it's really hard to live a typical life if you have schizophrenia. Um, it's very hard to live a life as you would have done if you didn't have that diagnosis. Um, thankfully, it's one of the less common mental health disorders. Is Is this a It's It is a really hard diagnosis to have, um, but I think the main thing that's on a has touched upon, but I will go into more detail here is knowing the difference for you guys between positive and negative symptoms. So basically a positive symptom is when someone has symptoms, changes in their thoughts or their feelings that added on to their normal experience. So these can be things I've listed them here so, like thought disorders. So I thought echo where you're hearing you're in thoughts and say you think something and then you hear it almost a snacker, the insertion. So when you feel like a third party is putting a thought in your head thought broadcast where you feel like your thoughts are being broadcast out to the world. You feel like you think something, and everyone else can tell what you're thinking. All thought withdrawal where somebody feels like they're having these thoughts. But then somebody is just taking them out of their head as they happen. Um, you can also have delusions of control, which is where you feel like your behaviors and your thoughts aren't your own there being controlled by somebody else. You can also have delusional perception, which is a complex thing to describe it. It's basically when you have, um, a true perception or two events to which somebody, um attributes like a a non existent meaning between them are non existent. Connection between them, for example, someone might say, Oh, okay, they might be walking down the street. They say all the traffic lights turned green. Therefore, there's going to be an alien invasion. It's it's It's two very different events. There aren't related, but they say, Oh yes, traffic has gone green. Therefore, this will happen, even though there's no reason to think that would happen. Things like that And as I said, as as a Honda said, and I've said hallucinations is a very common positive symptom. Um, azelas, uh, say the delusions that we just spoke about. And then you can also get some ankle catatonic behavior, which is either an exaggerated or decreased a rate of motor movements. So if someone's having exaggerated motor movements, that's cost is a positive symptom. Where, as as you're saying a minute, if they've got decreased motor movements, that's cost is a negative symptom. So negative symptoms are the opposite positive in that they feel like their thoughts or their feelings of their actions. They're being taken away or they're being reduced. Basically, eso sahan A. Said. You can have cognitive symptoms that just reduced concentration breaks. In that thought, they can have some that blunting that we talked about that you feel really socially withdrawn, know, enjoying things that they proves the enjoyed reduce the picks up there and a lack of personal hygiene. So I believe this level you guys to reading your own time about exactly how you were diagnosed gets a friend a A. But what I really want you to know is that the symptoms need to have been happening for a yeast one month on the strongest risk factor for developing schizophrenia, Um, or any any psychotic disorder is a family history. This was actually something that came up in our final exams last year. So I've written here the percentage risk of developing schizophrenia, depending on if you and your family also has it, so I wouldn't worry too much about memorizing them. But if you if you feel that you can, it would be the thing to know. And just in terms of the management of schizophrenia, it's mainly managed using those second generation atypical antipsychotics. That's a hard talked about. It's hopefully they have less side effects, as well as cognitive behavioral therapy, which should be given to all patients, which is really important for schizophrenia. Then, as I said, the second psychotic disorder that you need to know is delusional disorder. So we talked about what the definition of a delusion ist. The features of delusion disorder is that somebody has numbers are divisions, so these air delusions that aren't true, but they could theoretically happen on they involve situations that could occur in realize, for example, a friend trying to harm you and Maybe trying to poison you is quite a common one that comes up in exams. So theoretically they could happen. A friend could be trying to harm somebody. Or, you know, a neighbor could poison someone. It theoretically could happen in the in the laws of the world, but it isn't actually happening. Um, they also don't have any hallucinations. And he thought disorders that I listed on a couple of sides ago, um, they don't have any mood disorders or any flattening of that affect on what's again. This needs to be present for a least one month. So that was all the psychotic disorders that you need to know. I'm not gonna be moving onto anxiety. So anxiety is, as I'm sure you know, defined is an excessive worry, which could be about a number of different events on it's associated with the heightened tensions. And someone feels quite tense all the time. Um, it's really important to emphasize that in anxiety disorders, the anxiety doesn't go away, and it often does get worse over time, especially if it doesn't receive treatment on what's really important to know is that anxiety experiences with these disorders are much more than the anxious feelings that we all get day today in our stressful situations. Um, their symptoms committee interfere with their daily activities that school work, their relationships, their work. So is something that requires treatment and isn't just this anxious feeling that well, get my stress too. So I've listed here the five types that we're gonna run through. Quick, please. We got generalized anxiety disorder panic disorder. OCD specific phobia on agora phobia. So starting off with generalized anxiety disorder. So as the name suggests, it's a generalized, persistent, excessive anxiety that's really difficult to control. Um is often described as a free floating anxiety, which is basically a general sense of uneasiness. That's importantly, and this is very Heidi old. It's not tied to any particular object or event or situation. So people with this diagnosis of J. J D will worry about a lot of things in their everyday situations. It's not. It's not one specific thing, so they worry about what's where. What's cook situations coming up at school and work, and they just consciously anxious about all of those things. Eso can anyone taking the chocolate deforming any symptoms that you you know, that might come up in a generalized anxiety disorder thinking, maybe physical that symptoms any that you can think off. Kadia populations brilliant for speech took me a tremor yet palpitation, sweating. Yet you guys are doing really well. That's pretty. And so I've listed a few here haven't listed lows, one that come commonly comes up in examples. Muscle tension. They can have fatigue, difficulty sleeping, impaired concentration, irritability. All of the ones you put in the chart as well are very common as well. Um, as I said, it causes significant distress on be functional impairment. So it's much. It's a much more than the the general anxiety that we might get with certain situations in our own lives. Um, it usually comes in episodes lasting more than a week. And for a diagnosis, the person needs to have happy symptoms occurring for greater than six months on. Do something. That's also quite how you to know is that GI idea is a diagnosis of exclusion, which basically means you need to have excluded every other cause of anxiety or every other cause of these symptoms that they might have presented to you with, like fatigue and difficulty sleeping before you can lay with somebody is having a generalized anxiety disorder diagnosis. In terms of managing these people, you don't need to know a lot of this stage, but I think it's good for you to know a little bit about it. So the first stage would be patient education about generalized anxiety disorder. So what it is, what their symptoms are on. Help him understand what they're being diagnosed with. A Z was active monitoring. That's basically just checking up on the patient on. But if things get worse, then you can escalate the treatment. The next step is, uh, I'm helping them himself. Help on differing them on to psycho educational groups, which is basically a type of group therapy where people with the similar diagnosis of the same diagnosis come together on they receive information on their condition is a great on. It really helps because they're able to share their own experiences of what they're experiencing, their tips and tricks of how to manage the condition and that can really benefit a lot of patients. If that's not working, then you, um, escalate further up to CBT and you can also often set off for certain drugs, drug treatment as well. So the first line drug is that SSRI, which is often sexually, which is the heart has talked about really well on. If not, you can use an SNRI as well. It's also very important to know that for patients under 30 years old, and these drugs can increase the risk of suicidal thoughts on self harm. So it's important that you want patients of this. Um, I'm following them up is really recommended on if it's still not being controlled. If their anxiety things just aren't being controlled, it's really having a big impact on their lives. Then you definitely want to get a specialist input from an MD take a multi disciplinary team to help manage these patients. So then we have panic disorders. So this is characterized by recurrent panic attacks specifically, and what's really high yield for this condition is they are primary panic attacks, which means that they're no secondary to any other mental health condition or any other physical condition on the symptoms here. I think you guys may be smashed it on the charts and really well done some of the symptoms of a panic attack so It's all those autonomic sympathetic fight or flight response type symptoms that hyperventilation, palpitations, tremors, sweating, etcetera. And also they get some psychological symptoms as well so they can get the realization where they just They just don't feel like life is really anymore on D. The deep personalization where they don't kill themselves, they don't feel like they belong in themselves. They don't feel like they don't really have a good sense of their own identity. They can also feel that they're losing control when sometimes it could be very severe and they can feel like they're dying. Um, and another thing is that these patients can have a really persistent worry about having an anxiety attack. Um, just because they are so scary to go through that they just will often avoid situations that they know might precipitate an attack. Because it does is such terrifying thing to go through in terms of management once again, get CBT is amazing. It's a it's a great thing to give to these patients. You can also start him on SSRI such a sexually nortripyline drugs that they don't work on once again if it doesn't if it's not benefiting them keep referring them up and involves pressure is mental health services for their care. So now I'm gonna go into OCD or obsessive compulsive disorder before I talk about the condition. I think it's really important. We understand what obsessions and compulsions are so in. Obsession is defined as a repetitive, unwanted, intrusive, thought idea image. Impose on urge. So it's basically where somebody thinks about something on it just keeps they won't leave their head. They just keep thinking about this. So the example I've got here is someone thinking, Did I lock the door? And I know some people will have that, you know, just naturally, I think, did I lock the door? But this is just repetitive, just keeps going and going Ideal. Did I lock the door? Did I lock the door? And it'll just be all they can think about. A compulsion is a repetitive behavior or mental activity that people with OCD feel really driven to perform so they could be really obvious and observable by others. So in my example, somebody might go and check the door they might locket and unlock it. It's obvious that they've got this kind of repetitive behavior on, but it's not always that sometimes it's a mental or none observable act, so repeating a certain phrase in their mind. But yes, I did. But the door, Yes, I did the little like it's It can be something that's obvious to see, but it's important to realize that it might not be obvious to see um, and it's also important to know that these compulsions they're often unnecessary there often purposeless onda many much. Most of the time, patients hate that they feel compelled to do them because they realize how unnecessary and uses they are. But the performing the compulsion helps to get rid of the obsession so much in the short term that it relieves. It relieves their mind of that obsession that they still feel compelled to do it. How is Ah, in the long term, it it helps to make their condition worse. Sadly so, the key to this condition has ever talked about in the second is breaking this link between the obsession and the compulsion. So what is OCD? OCD is that as a it's a type of anxiety disorder, and it's categorized by the presence of obsessions or compulsions. But most commonly both of present, and it's must be causing a functional impairment to their lives on distress. So they say, it's not just the old for a long Did I lock the door? Oh, I have OCD a note. It's It must be really having a big impact on their lives. I mean, causing them a lot of distress and upset. Um, as I say, most people we can rationalize. Yes. Okay, I don't think I looked the door, but I know I did. We can rationalize it and we'll get on with our day. But these patients cannot, and it's say it's all about breaking this link. The cause of C. D is it has lots of causes, basically both genetic on D psychological on, but it's highly associated with other mental health conditions such as depression, schizophrenia on anorexia nervosa as well. In terms of management is, say, CBT is really good for OCD symptoms as well as drugs such as SSRI eyes. But a really important thing that OCD is something called exposure and response prevention or your pee. And this is basically a psychological method where patient is exposed to at a normally anxiety provoking situation, So, for example, maybe someone that doesn't like dirty things may be having dirty hands that would normally cause anxiety. And then in this therapy, they make sure that they stopped the patient, engaging in what would normally be there compulsion or their safety behavior. So in this case, like washing their hands, for example, and say that confront the anxiety it helps to break the think, make the person realize that they don't have to perform the compulsion when they have the obsession, the obsessional cool. So then quickly, just around up our exact anxiety disorders. We have specific phobias, an Agora phobia. So specific phobias are the current excessive on unreasonable symptoms of anxiety related to a specific stimulus. And that's what's really high yield. With these phobias you can pinpoint. This is what's triggering this person's feelings of anxiety. It could be. Is there putz and pictures there? It might be a spider. It might be a snake. It might be blood on. So you have your different probe years like arachnophobia having but taking his hemoglobin. Uh, you have acrophobia uh, which is a fair of high. It's eccentric cetera. You've got a specific trigger to this anxiety Once again you get all those typical anxiety symptoms that you guys amazingly listed out earlier, such as your hyperventilation, palpitations and things like that. Um, these people is well, once again might show avoidance behavior where, if it is, say, say they've got a racket, a phobia and they go somewhere where they think there's gonna be a spider. They know there's gonna be a spider. They're going to do whatever they can to avoid that. Agora phobia is a type of fiber, and it's defined as an extreme or an irrational fear of entering open or crowded places, leaving someone's home alone, traveling alone social situations or being in places where escape is really difficult, really embarrassing. Once again, it provokes all those sympathetic and psychological symptoms. Um, and once again, these patients can show avoidance behavior as well. That's just a specific Probi that you guys should be aware off. So our final section for the day I'm not gonna go into too much detail, cause a lot is on the slides. But is the mental state example the MSE. So the MSE, basically what it is, is it's a structured way of observing on comprehensively describing on reporting a patient's current mental state. Um, and when when you do this is part of your kind of psychiatric history. Taking an examination when you do that for work up alongside the exam, the observations that you pick up from the patient, it allows you to most accurately former diagnosis, because you know that you've covered everything that you need to know. It's really important to know this provides a snapshot of the patient's condition, so it doesn't reflect this. Say how they're all of the time. But it can be useful in seeing how their condition improves or deteriorates over time, based on how they rank in each of these sections, Does anyone know and just quickly pop in the chat any of the domains there in the MSE? So what? The different categories that we mark or not marked. But judge patients on in the M. S. E. And does anyone know, just pop them in the chart. If you don't parents behavior, that's the kind of thing I'm looking for. Yep, great guys. Appearance, memory, attention, speech, speech affected that yet you guys have got the right idea really well done, because in nailing it. So these the main ones you need to know for the domains. Three. Chemo, Emory A. That you need to know is accepted. So appearance and behavior speech, emotions or moved Perceptions, thoughts inside and cognition. Now I'm not gonna go into these in a lot of detail, cause most the information is on the slides. But firstly, for appearance and behavior, you just want to look at how the patient is overall. What's that weight light? Is there any evidence of self harm? What's that, Bill? Does it look like they look after themselves? Their personal hygiene? What's that? Clothing, right? What's what's their facial expressions like? How are they acting towards you? Do they look like they want to engage with you? Or do they look like they just want to be left alone in your speech? There's a lot of things that you can say about some speech. Is it fast? Is it slow they talking a lot or no. Uh, do they have that, um, blunted kind of monitoring nature to their voice? Are they struggling with what they're saying? They having preservation with the speech in that matter what you ask them, they always give you the same answer or they repeating themselves quite a lot. Then you have moved says to say we talked about about what time effect is and how that differs from moved to. Hopefully you guys remember that on gets really important to assess bios. Um, both how you see the patients emotions and also how they feel that they are at that current point in time on. But it's also important to see if the mood and the affect much so you might look at a patient. They look really sad or they look really just down. Then you might constipation how they feel in there. But yeah, I you know, I feel euphoric and I feel amazing and it doesn't quite add up. So that's quite important thing to note down. And you also want to look how their emotions and the mood change over time. So we've spoken about about bipolar disorder on mania and hyper mania and depression anxiety. You want to see how their mood changes over time so you can almost put it on one of those graphs in your head. Then we have perceptions. So these air talk about things that the hallucinations. Are they experiencing any of those? Do they feel that they have depersonalization where they feel like their thoughts and their actions? Their feelings aren't really, um, really aren't really really. And they don't belong to themselves. What do they have? The realization where they feel like their surroundings in the world around them is, um, really? And then the other three catch reasons they have thought So. What's that stream of? Are they really struggling with that thought? They starting to show that they're thinking of anything. They have a thought block. What is the form of their thoughts? Are they? They quit cause a cricket processing things or they flight of ideas moving from place to place like this or mania? Are they having like, a loosening of their associations when they speak? So are they jumping from unrelated topics with no Lincoln between? They're just talking about really different things all the time. Are they being over inclusive and what they're telling you? So are they telling you things? They're telling you about something that all? Yeah, I'm my my captain this this morning, and it's nothing to do with what you were talking about. they're adding really unnecessary and irrelevant details doesn't know, um and also are they going on tangents on then, um versus are they coming back to the topic? So there's an important principle there of circumstantial itty and ton gyn tangentiality. So if someone's going on a tangent, they have a topic, and then they just go. They go off the topic in, and they keep going off the topic where someone has circumstantial itty, they will kind of go on a tangent, But then they will come back to the original topics. That's an important thing to different sheet. Um, the biggest thing with thoughts, I would say it's content. So if someone has delusions, obsessions or compulsions, that's really important to know. Um, but a major thing is assessing for self home or any suicidal thoughts or any violent behaviors. Sometimes these can be quite subtle. I know I've had patients where the only thing that alerted a medical professional to potentially something like self harm was the fact that she mentioned a time on just the fact that she mentioned the time was like, Okay, what's happening at this time? We need to We need to dig more into that. So sometimes it's not obvious. But if the patient gives you any clues, definitely it's important to assess for that. And I've spoken a bit about what do they feel about the possession of their thoughts? They feel like they own their own thoughts. Are they being inserted? Withdrawn? A ball cost it elsewhere. Then we have insight. So does the patient understand that they have a mental health problem on that? Their experiences are numb. Abnormal? Or do they think that, Yeah, this is normal. There's there, Are there are ghosts or there are aliens invading this room right now. Like you know, everyone can see it when they can't. It's It's often the severe mental health conditions, particularly schizophrenia, where patients often lose in sight on do. They don't necessarily realize that they need treatment from a doctor or a medical professional. And that's a really important thing to assess and finally, cognition. So you won't see if somebody's orientated to time to place the person. Do they know where they are? Do they know roughly what year were in what they is? They know who they are. Are they able to concentrate? What's their memory, like it Septra. And you can If you want to further assess their cognition, you can look into a formative assessment, buy a, like a marker or the mini mental state exam or anything like that just to formally assessed for their confessions. Like so, thank you guys for listening and staying on. I know it's getting late, so thank you very much. I've got some SBA is if we could quickly launch the pole. Okay, so I'm ready quickly. I think I think I just realized it from the Navy. 50 more seconds living are nice and quick. Several going enjoy a little bit of their evening. If you don't know, just give it a guess. Okay? Five seconds. Get those ounces in. Okay. Brilliant. So it looks like the majority of you got this right. Although there was a bit of a split. So the correct answer here was D. So the correct answer was specific phobia. And that's because this patient is displays that called Astra phobia, which I wouldn't expect you to know. But that's basically a fear of thunder and lightening. So we've got a specific stimulus. Um, and this patient is kind of showing symptoms of the psychological symptoms of a panic attacks. The fear of losing control and wanting to take control is there's the sympathetic symptoms as well, such as it's things sweating and flushed. Um, the light Kyle's that I was referring to. The end of the question is basically showing that sometimes these patients who have a specific phobia can anticipate the trigger in daily life. So even though I like I'll cover wouldn't necessarily mean that there's gonna be thunder and lightening she she's. I'm implying that she's getting kind of overly worried, kind of out of proportion of what somebody without a specific program would feel in terms of something like thunder and lightening. So your key learning point is that specific phobias haven't attributable identifiable stimulus, whereas generalized anxiety disorder and panicked. It'll just don't So next question if we could really launch the pole. Okay, So 55 54 year old man presents the GP, complaining of difficulty sleeping and eating low for three weeks, explains he's been performing poorly. It work. She feels guilty about, as he is finding, he's easily distracted. You also mentioned that he has no attended his local gardening great for two weeks, despite having the energy to go as it's not enjoyable. And he has not seen the point in going. If he doesn't feel like eating the food there growing this summer, you suspect this moment could be suffering with depression. What is the most likely severity level of this presentation? A five more seconds. Okay, I'm gonna in the pool there. So we were quite split between answers B and C. So don't worry about that world unto every one of you that puts. See, that is the correct answer. So I know I didn't focus on this too much in the presentation, so make sure to look back over it when you get the slides in the recording. Um, so the main thing that I want you guys remember is for mild depression is the rule of two. So it's two core symptoms to others. For two weeks, this gentleman has had depressed mood and and had only a which is the inability to find pleasure in something previously pleasurable. It's in this case, his gardening, but it says here that he does have the energy to go. So that is to course, symptoms on He's also mentioned a difficulty sleeping, excessive deal, poor concentration and decreased appetite, which is four other symptoms. So therefore he fits into the category of moderate depression. I hope that makes it a say. I would remember what the the the rule of twos for mild depression. And if it looks like they have considerably more other symptoms, it's more likely to be a moderate depression. And finally, one last SBA or re launch the pole. There we go. So you asked assessments. Is Cevallos, a 34 year old female who has been within psychiatry Ward for three months because she has not been speaking to anyone on the ward for the past month? Midway and explaining her thought, she begins looking around the expansion, his ghosts saying that they're going to kill her. Initially, she looks very scared of them, but quickly speaks in a joyful tone. Happy to see them, she asked to speak to the doctor to help get rid of the ghosts. Which of the following is the patient most likely not displaying. Um, says I'm not displaying. Okay, I'm going to end the pole there. So the majority of you went for a unfortunate. That's not correct, I'm afraid On the correct answer is a, which is delusional disorder. Um, the reason why it's not a is because it's quite subtle, so I can understand why you guys have chosen a is because she asked to speak to the doctor, had to help get rid of the ghosts. That is a common way that questions will imply that a patient has insight because they're not going to say the patient has insight, because that's too obvious. The fact that she's requesting medical help is a good idea that even though subtle, she does realize that something's going on. Um, the fact that her emotions are changing, so the fact that she was very scared of them, but then quickly species and joyful tone that suggests the label affect that we spoke about with the Pink line on the graph, she's having hallucinations and sacred. He's hearing those ghosts, and she likely has schizophrenia as well. So the correct answer is there for a and that's because you, the key learning point, is that collusion of disorder presents with numbers are delusions, so things that could theoretically happen. This isn't a delusion. This is a hallucination. Um, Andi, even though some people believe in ghosts, I'd like to say that it is a bizarre delusions rather than and, um Brazoban. So thank you so much for listening on. Thank you so much for sticking around. We really hope it's been useful on do. Yeah. If you could fill in that free back form, that would be amazing. Um, we hope you have a lovely rest of your evening and you're weak. And, um, in answer to your question potentially, yes, you could argue that she doesn't have full insight. However, the fact that she's requesting medical help suggests that she she does have some insight. People that are hallucinating. They might not be explicit in the way that they say that they know there hallucinating. Hopefully, questions would be maybe more clear. But the fact that she's requesting medical help is quite common way that they ask, or that they in SPAC imply that a patient has insight. Um hum, That's okay. Thank you. I'll post thief you back link in the chat again. Thanks. Hun has done it. I'll do another one. Thank you so much for coming. Thank you so much.