CSI 1B Crashcourse Low Mood Lecture Recording
CSI 1B Crashcourse Low Mood Lecture Recording
Summary
In this in-depth tutorial, Callista offers a thorough overview of the topic Clinical Special Study Index (CSI) on diagnosing and treating depression. She starts with exploring the landscape: what depression is, its symptoms, and typical DSM V diagnostic criterion. She also introduces the Bio-Psycho-Social model, a tool used by GPs to understand the root causes of depression. Callista then ventures into the various risks associated with depression, from self-harm and suicide to harm from or to others. She rounds off the first part of the tutorial with an interactive patient scenario, encouraging participants to use the discussed learning content. The second part focuses on medications, the process of starting antidepressants, and how they function biologically. This blend of theory, practical navigation, and interactive discussion makes the tutorial invaluable for anyone interested in understanding and managing depression in patients.
Description
Learning objectives
- Understand and recognize the DSM V criteria for diagnosing depression.
- Assess and identify risk factors associated with depression, including self-harm, suicide, harm to others and adverse childhood events.
- Gain knowledge on biological management options for depression, including the use of antidepressants.
- Learn and apply the correct advice to patients who are starting antidepressant medication, such as the time it takes for the medication to work, the need for continuous use even after remission and the process of weaning off the medication.
- Cultivate skills in case analysis to identify whether patients meet the clinical diagnosis for depression using a provided case scenario.
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Right ready? Ok. Anyways, hey, hi, you guys. Um my name is Callista. I'm gonna be giving you guys this tutorial today on um your CSI case um for, for a low mood. So in terms of how everything works, I think there'll be a few questions, just put them in the chat um when, when they do happen and I like we'll look over them. Um and if you guys do have any questions that kind of pop up during the tutorial, just put it in the chat and then someone will let me know or like I'll, I'll check the chat like something will happen and we'll make sure the questions get answered. So don't be afraid to do that. Um And also if you are feeling brave and if you want to, you can also just pipe up like unmute yourself and ask the questions more than happy to answer. Um Ultimately, this is you guys' tutorial. So make sure you make the most of it. Ok. So, um basically, what I've done is I've kind of summarized everything to do with your prereading your post, reading your C SS I material is basically summarized onto the slide as much as I can. Um I tried to put m mostly information that's only relevant and stuff that you guys really need to know on there. Um So yeah, do use do do have a look at that anyways. So this tutorial essentially is gonna run. Um There's gonna be three parts of this tutorial. We're gonna start off by, by looking at the diagnosis and so looking at like depression um and kind of everything surrounding that and then we're gonna look at management. So looking more specifically at like the drugs and how they work. Um but also at um social um social management. So kind of like social prescribing and all that. And then lastly look at um date significance. So looking at um like clinical clinical significance and uh stats statistical significance. God, I can't speak. Um So yeah, starting with diagnosis. So this little bit of your prereading, honestly, I think you guys it might be worth to kinda scan over it. It's not really that deep, but essentially, it's just talking about like what depression is. Um it's persistent sadness for a long period of time. It can be triggered by an external um factor. So some event might trigger it or it might be passed down, you might have a family history of it that will also give you a higher chance of having depression. Um And there are lifestyle changes alongside um obviously medication and social prescribing. There's also a lot lifestyle changes that will have an effect on um the level of depression, I guess or like the seriousness of um the patients. So, looking at the DSM V criteria, um this is essentially the criteria that's used to diagnose someone with depression. Um and it is something that I do think you guys should um memorize, it is worth memorizing. And it's most important to know that it's to like in order to diagnose depression, you have to have more than one key symptom and total of five symptoms. Um So looking down the list, key symptoms are um low mood and anodontia, which is essentially um loss of interest or like loss of pleasure. So like if I, for example, really like to play basketball, um sudden loss of that or like loss of joy when I play basketball is, is a form of anodontia. And then in terms of associated symptoms, I kind of like to, I don't like the way I used to memorize it was I'd kind of picture someone who's just like severely depressed and, and sad and kind of like stress eating and all that stuff. That's how, that's the painter, the picture that I sort of painted in my head while I was thinking of associated symptoms. But yeah, um it is, it is something that you guys should memorize cause uh it will be r really relevant for your exams. I won't go through the specific associated symptoms cause I'm sure you guys know it by now and then looking at precipitating factors. So like what causes, like what are different causes of depression, right? Um So this is where we look at the biopsychosocial model, which is essentially a model that kind of encompasses um different factors that can be related to someone having depression. So looking at bi the biob bit, that's, I guess um the metabolic disorders, any like genetics, family history, so on and so forth. Um And, but also looking at, I guess like medications and stuff like that, which might have an effect. And then the psycho bit psycho bit. Um The psychological bit is I guess looking at like self esteem, looking at like beliefs, attitudes and all that stuff, which might also have a play into all of this. And then lastly the social bit which is looking at external um like your work life, your home life, looking at all those different factors and your family and how all of that can support. Um Well, all of that can also lead to depression if, if everything is kind of not in order in a way. Um Yeah, so this is essentially just a model that, that GPS use to look at, um look at different factors that have to do um with people having depression. And I think it's definitely a really important, a really important model because it Acom encompasses a lot of varying things and then looking at risk assessment. This is essentially I'm looking at the different types of um like risks that people may have when they have um when, when they are diagnosed with depression. Um The first one is self-harm, which is most common in females of age 17 to 19. And there are multiple reasons for this. There are three main ones that we touched on. Firstly, is affect regulation, which is essentially people use it as a way to cope with their own feelings. Secondly, communication. So a lot of times when you do self-harm, there are visual signs and you know, it's kind of a way for you to communicate with other people that like, I'm not doing that well, you know, help me. Um and then lastly is control or punishment, essentially what this is is um some people kind of feel like everything around them is crumbling, especially when they're dealing when they have like mental, when dealing with mental health issues. Um and like depression. And so the only way that they feel like they have control over their lives or like control over anything really is um self-harm, which is why it's one of, it's, it's one of the reasons and it's one of the bigger reasons I think. Um And then secondly, suicide that's most common in males um of age 40 to 59 and then thirdly harm to others. So if you're on or if, if you're um if you have like mental health problems you might lash out, you might harm other people, stuff like that. Um, but also harm from others because I feel like a lot of the times when someone is depressed or if someone's in a really, you know, down state, they are more vulnerable and inherently have a higher chance of being harmed by other people and being taken advantage of. So, for example, um, like drugs or, you know, like joining different groups and stuff like that, they are more likely to be affected by, by the environment around them. Um And so average to it adverse child events, I think that's what it stands for or ace. Um essentially is when there are traumatic events that have a negative lasting effect um on Children, especially Children um under the age of 18. Um Children under age, especially Children, people who are under the age of 18. Um and there's a lot of reasons for people um suffering from ac um for example, like depression, like family situations, um verbal abuse so on and so forth. Honestly, I can't lie for the CSI. It's important for you guys to kind of be aware of this and know kind of like what is an ace and what it does. But I don't really think you guys need to remember like remember specific types of um average child effects. Um I think it's more that you guys just need to be aware that this is a thing and that it will affect people, especially Children. OK. So that wraps up the first bit in terms of diagnosis. Um And I have this question for you guys. So patient X A 23 year old female who's who presented with tiredness, she has noticed an increase in weight and is constantly feeling really hungry. Um She gets easily distracted at work more than usual has been feeling like she's not worth being part of this team, although she recently got promoted. Um, I want you guys to take a minute to just think through this patient persona and put in the chat maybe whether you think patient X will be diagnosed with depression and, and also how many symptoms would they have? So this includes both associated and key symptoms. Ok. Getting, uh, not yet. I'll let you know when something comes through. Mhm. Yeah, guys just use the chat feature and try on if you guys need the, um, Bactrol symptoms less. I just put it up. Hopefully, that gives me a few more responses. Maybe good. Ok. It's like we'll just move on. I mean, I'll answer my own question. I'll be like Dora, but, um, essentially no patient X won't be diagnosed with depression because, um, if you look at the different, um, symptoms that she presents with tiredness, increased weight, easily distracted and worthlessness. Um, these aren't any of the two key symptoms. So it's not low mood or anodontia. So it doesn't. Um, so therefore she she's not diagnosed, like clinically diagnosed with depression in terms of the symptoms that are present for? Ok, we move on. Does anyone have any questions for like the first part? Anything that doesn't make sense? Anything they wanna go over? It's pretty straightforward. But like if you have anything, speak now or forever, hold your peace. Ok. Anyways, moving on. So I'm gonna look at um, biological management now. So looking at the different types of drugs, um, and kind of how they work. But first starting off with, um, advice to patients who start antidepressants, I think this is really important, especially cause antidepressants are kind of, there's a lot more that you have to warn patients about, um, when someone does start antidepressants, firstly that the drugs take several weeks to work and actually your symptoms might worsen initially, which is super important because a lot of the times I feel like patients don't know that or they don't expect that if the doctors don't tell them. And so they start either they go back to GP complaining that things have gotten worse or they stop their drugs completely, which obviously doesn't. No, it, it's just not helpful like that's what we wanna do. Um So yeah, really important to warn them that things might get worse, but eventually they'll get better and better than you how, like how they were initially. Um, a second or thirdly that they have to continue it six months after remission so similar to what I was saying before, even if they do get better, they still have to continue it because otherwise again, their symptoms will, will be a cycle will come back whatever. Um, fourthly that the drugs have to be weaned down, um, gradually. So you can't just stop it. Um, you can't do, yeah, you can't just stop it one day. You kinda have to go down dosage. Um, and that there are a lot of drug drug interactions, which is super important, especially with patients who are taking a lot of different medications to just check that there aren't any severe interactions because antidepressants especially tend to um have more side effects and also just um have more interactions with different drugs. Ok. So starting on the different types of antidepressants, we first have um monoamine oxidase inhibitors which OK, basically how they work is um neurotransmitters. Well, usually in a, in a, like in the normal physiological state in the presynaptic neuron, you have um neurotransmitters. Some of them are pack in vesicles and some of them aren't. So the ones that aren't get broken down by an enzyme called um monoamine oxidase inhibitors. No mono monoamine oxidase. Um essentially they break the neurotransmitters down. Um But obviously, this decreases the concentration of neurotransmitters that can be released into the synapse. And so with someone with depression, um this obviously won't, won't be as good because they have fewer um neurotransmitters to depolarize the neuron Um And so essentially what this drug does is it inhibits this enzyme. And so you have a higher concentration of neurotransmitters that can be released into the synapse. Um and cause depolarizations. And so this drug affects oh many different types of neurotransmitters. So, adrenaline, noradrenaline, serotonin and dopamine. Um it does act on the enzyme itself, but monoamine oxidase as an enzyme can break down a lot of different types of neurotransmitters. So it does affect more than one type of neurotransmitter if you know what I mean. Um And then in terms of the types of drugs you guys to see on the screen, um I don't have to read that anyways. Um And then with side effects, the thing about monoamine oxidase inhibitors is essentially the side effects are systemic and there are a lot of them because it's not a very specific drug, which means that it affects a lot of other parts of the body as well. So, for example, inhibits um processes in the liver that prevent um like medications breaking down. So there are a lot of different side effects, which is why it's not very commonly used as a drug. And it's definitely not first line. And then the second type of medication is TCA so tricyclic antidepressants, essentially, um what this does is it inhibits reuptake transporters. So basically, when neuro neurons like presynaptic, um neurons release their neurotransmitters in sa synaptic cleft, it will bind to the receptors and essentially, after that, it gets taken back into the presynaptic cleft through these reuptake transporters to be reused again. Um But essentially, what TCA S do is it blocks these reuptake transporters, which means the concentration of neurotransmitters in the synapse will be higher and therefore, um cause more depolarizations. Um And so these um this um this drug affects both. Oh wait, there's a mistake in my side affects both serotonin and noradrenaline. I'm gonna edit that. Um There you go. So it affects both um noradrenaline and uh serotonin. Um um reuptake transporters and in terms of side effects, it, although not as many as um M AOI S, it does have a few severe side effects. So, because it also acts on other receptors like adrenergic receptors, it can cause dizziness cause it acts on muscarinic receptors as well. It can cause memory impairment and um histamine, it also acts on histaminergic receptors, which means it could also cause drowsiness and it's also really, really toxic at high levels, which is why it's also not um a first line drug and it's also not used um that often. Um And lastly, your SSRI so this is what's typically used first line. Um This the typical first line antidepressant. Um And essentially it works in a very similar way to TCA S. Apart from the fact that it only acts on serotonin reuptake transporters as opposed to both se um serotonin and noradrenaline. It's, it's your like common antidepressant. So like FLUoxetine, sertraline and ci citalopram in terms of side effects. Um it seems like there's a lot more I know like the list looks longer, but if you look at exactly what these side effects are, they, they're not like super serious side effects. Um and apart from like serotonin syndrome, but even that's, but that's, but that's like really, really rare. The most common side effects are kind of like weight gain, sleep disturbances, nausea, sexually functions, like they're not that serious of side effects, which is why they tend to be used more. Um first line. Um but Serotonin syndrome is, is a side effect of SSRI S and it's, although it's rare, it's something that we do have to watch out for. So, Serotonin syndrome is essentially when there's a dangerously high level of serotonin in the synaptic cleft. And this can develop really quickly over hours and can be caused by a lot of different factors. One of which is um medication dosage, especially SSRI S. Um And so yeah, it can cause a range of symptoms like agitation, restlessness, insomnia. Um It can cause like a really high heart rate or really high BP. Um It can cause like autonomous dysregulation as well. Um neuromuscular excitation to cause like twitches and stuff like that. Um It's obvious but it is like the symptoms are obvious, but it is something that we do have to watch out for because when it does happen, it is really dangerous. Um, on the bottom, you can see that there's a high risk of serotonin syndrome if someone has both Ss Ri S and takes tryin, which is a medication used for migraines. So, yeah. All right. So that's about it for the different medications. Um, I just have a quick question for you guys. Please answer this time. Um, so patient, Y is a 40 year old male who presents to his GP with forgetfulness. Um He's worried about Alzheimer's although he doesn't have a family history of it. Um Upon checking his records, you can see that he has been diagnosed with depression two years ago. So my question is what could be the cause of his symptoms and why just put it in the chat if you have an answer or not? OK. Or if you give your guys like a minute or two? Yeah. Fine. Yeah. Yeah. OK. So basically um OK, what could be the cause of his symptoms, the fact that he was diagnosed with depression? Um and he could be on a TCA prescription which means um and one of the side effects is forgetfulness because TCA s also act on muscarinic receptors. So, yeah, I, all right now, moving on to um the social part of management, which is basically your post reading. So you're welcome. Um But essentially um social prescribing is mainly, is, is mainly done by GPS and it's when they kind of refer the patients to a range of nonclinical services in the community. Um And they kind of help the patient with like social socioeconomic environmental support, like in, in their homes or kind of like outside um outside the hospital essentially. Um But it aims mainly to kind of allow the patient to heal themselves in a way um and allows them to like take control of their own health and kind of be responsible for that. Um And the main pipeline that happens is the GPS would refer to a link worker um who would basically coordinate all of this um care in the community for the patient. So refer them to um social prescribing services. Um Yeah, refer them to social groups is what I was gonna say um to social groups and to different um different activities or different um types of help or like therapy that might be out there for them. Um But this is important because, you know, when you deal with the patient, it's not only what happens within the GP setting or like with medications, but it's also how they're gonna support themselves at home, how they're going to go about their day to day lives. Um And just make sure that their quality of life isn't really bad when they leave, when they get discharged or when they leave the GP. Um And so one of the uh main methods of social prescribing or one of the main treatments of social prescribing, um out there is CBT, which is essentially a talking therapy and it focuses on how we, how people think and how that affects the way that they feel and they behave. Um So usually what happens is when someone's prescribed CBT, they go to this therapy session, right? And it's, uh it tends to be a really intense kind of block of therapy. So they go to therapy for maybe like six sessions and then after that, that's, that's kind of it. But throughout these six sessions, um, they're kind of taught how to think and how to, um, get rid of that negative self talk and that feeling of worthlessness and how to think their way through like difficult situations essentially. Um, and so they go home, kind of do their homework. They'd have like, they, they are like sheets of paper and like exercises that they practice at home whenever they do have a trigger or whenever they do have kind of a really hard time, they have something to refer back to. And so an example of the kind of the cycle that CBD tries to bake is, is what is shown here. So essentially you would have someone would have a trigger. So for example, if I'm like cooking right? And I burn my hand on a pan that would be the trigger and then my thoughts would be, oh, like I'm doing everything wrong and then I'd feel like everything sucks. Um, and everything's bad. And then that might cause me to like lash out at someone, right? Or like that might cause me to like say, say bad things to like my friends or family and that would be like the behavior. Um So as you can see, this is, this is a vicious cycle. Um and is, is something that CBT tries to break because this could be really negative to their own mental health and their own wellbeing. If like for example, they already suffer with depression that they have to continue like that. They continue to think these things and feel these things, it could be really dangerous for them in the long term. Um That was really quick anyways. Um So just a summary. Well, so that's, that's everything in terms of like diagnosis and management, um medically on the medical side of, of um low mood and all that. So I just have a quick question for you guys pertaining to everything that we've covered so far. Um So patient a is an eighteen-year-old female who presents to me with excessive vomiting. Um red wee feelings that her heart is racing really fast, shallow breathing. Um She denies ever having consumed alcohol, smoking or taking drugs. She doesn't have any significant travel histories and recalls eating or salad for lunch. Um Toxicology screen was negative your dip had blood. So, hematuria, um neuro exam revealed ankle clonus and her abs are there as well. What do you guys think Yeah. Yeah, we have an answer. Vix, yes, it is Serotonin Syndrome. Um Thank you so much. J I'm gonna shout you out because you're a real one. But anyways, yeah, it is. It is Serotonin Syndrome. Um So yeah. All right. We're nearing the end of the TTO tutorial. We have one more bit left in terms of like data significance and stuff, but ash Office has told me to push the feedback form. so please fill it in. We'll be really grateful. Um If you guys took just a bit of time to fill it in, I'll give you guys some time now. So you guys start to do it after scan the QR code for the N please. So we know what to do for you guys next time. And if you guys like us. Ok? Yes, sir. And I guess in the meantime if anyone's got any questions or anything, they're more like unsure about just please put uh put in the, yeah, low mood is a pretty straightforward case I think personally. Um So which is why we've kind of whizzed through it kinda quickly. So if you guys have any questions, we have time, do pipe up. OK. Okie Dokie. The QR code exists on other sides as well. So I'm just gonna move on. Um ok, so the last bit looking at um significant scientific and clinical significance. So we're gonna start with a question this time actually. Um So a study compared the effectiveness of two inhaled steroids of reducing dyspnea in CO PD patients. Um 80 per, 87% of patients reported that drug A was noticeably better. Um But clinical trials show that the difference is 0.067 and currently the treatment is use, use drug A, use drug B. Um So MS sex basically comes in with CO PD and breathlessness. And the question is, should the drug switch that was not English, should the GP switch to using drug A or stick to drug B? And if so why? Ok. So essentially, um uh obviously, every like GP is different, every GP has their own kind of take on things. But um in this situation, you'd probably switch to drug A because, you know, 87% of patients reported that it was noticeably better. Um Although there isn't a clinical significance, there isn't like a clinical difference. I mean, no, what am I saying? Although there isn't a statistical significance isn't a statistical difference because the P value is 0.067. Um patients have reported that drug A have like they've seen that drug A um is noticeably better and they're having a better effect from it. So most GPS would switch essentially. And so it essentially brings up the idea of clinical significance versus um statistical significance because what is significant in the GP setting with patients might not be what is significant in the labs um with like graphs and P values and all that stuff. Um So just looking at the difference in more detail, stati statistical significance is essentially um looking at the reliable reliability of study through numbers and statistical tests. So looking at the P value essentially, so if it's less than 0.05 then it would be a significant difference. Whereas clinical significance is um the clinician's opinion on whether the findings are appropriate to use in practice. Um So this is a subjective concept that the GPS use essentially. So in this case, in the case that we saw before um the patients reporting back that there is a difference. And so even though it's not statistical, there is a signi uh there is a clinic clinical significance because the patients are seeing a difference. Um So yeah, that wraps up the end of the tutorial. It was a quick one. But if you guys have any questions do ask, do fill out the feedback form. Yeah. Thank you so much for listening. Um Just before we end, do you have any questions or anything you want to be more specifically it to or anything like that? Anything you guys have at all currently, I'm great at teaching. So no, just kidding. Um Yeah, I think that's it off. If anything, if you guys do have questions though, do email me? Ok, then uh I guess we just, we just have a little break, a little few minute break. Um and we'll move on to breathlessness. Um Thank you very much, Lisa. Thank you. Bye.