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Post high heels drugs um that you should know about, it might also be useful for six years, um and potentially for fourth years as well. Um If you want to get a bit of a head start. Um But yeah, so today we're gonna be talking about probably the most important classes of drugs in terms of high yield knowledge. So we're gonna first talk about SSRI S which are used to treat depression and various other um um mental disorders. And then we'll talk about antipsychotics and we'll talk a bit more about um the side effects of antipsychotics um and the side effects of Ssris as well. So that's kind of our aim for the next 60 minutes or so. Um And if you wanna drop messages in the chat, um then please do and hopefully we'll, we'll get to them at the end. Ok. So if we start with SSRI S then, so SSRI S um hopefully you guys know the indications but if not, um SSRI S are indicated as first line for a whole host of sort of a whole host of disorders including depression, including anxiety, including, you know, postpartum depression. Um Some kind of mild eating disorders, but the main indication is depression and anxiety. Um There's some research that they are actually better anxiolytics than antidepressants. But yeah, and the mechanism mechanism of action is in the name. So, serotonin, serotonergic, sorry serotonergic reuptake inhibitors. Um So you can see the diagram that it's literally just blocking the reuptake of serotonin. So the serotonin lingers around in the in the brain longer causing more of an effect. Um But there's a bit of, well, there, there is more to it than that, but that's kind of all you need to know really. Um because this is very much oversimplified. OK. So this is kind of SSRI s on one slide in terms of what the high yield content is. Um the four main ones that you should know about are there are on the left. Um But there's also a bunch of others and ones that are like being researched and stuff, but they're all functionally very similar. Um They will act in very similar ways whether or not you're put on one or the other depends on like very minor kind of indications. Um Like you might get better side effects on one than with another, but in terms of mechanism of action, it's all the same. Um So sertraline, so some points to pick out with regards to each of them, sertraline is the best um post M I um don't ask me why, but that's just something that comes up on pla me now and again. Um Citalopram and escitalopram, there is a risk of QT prolongation. Um and the other things that come along with that like Torsade, um et cetera, et cetera. FLUoxetine is the most used one in Children and adolescents and with paroxetine, you shouldn't give it in pregnancy. Um All right. Um And then we've got a whole list of um side effects in the orange box on the right there. Um If we just go through them. So the main ones to know about are gastrointestinal um sexual dysfunction. And I think probably the hyponatremia and we'll talk about serotonin syndrome in the next slide as well. So with um gi effects, you can, the main things are like diarrhea, nausea, having a dry mouth and you can also get gi bleeding as well, especially in older patients. Um There are some CNS side effects. Um but they're not s they're not super characteristic, um except anxiety actually. So anxiety is much more common in the first few weeks um of taking an SSRI um someone raise their hand if you wanna type in the chat. Um What your question is, I'll get to it at some point. Um OK. And there is also a lower seizure threshold, which is something that you can see as well in some antipsychotics which will come on to you later. Um, suicidal thinking mostly in young people. Uh It's, it's one of those ones which it's very uncommon to happen, but you just need um you need to follow up with young people more um often just to check that that is not a side effect that's happening. Um Yeah, sexual dysfunction is probably one of the most common side effects and I think it's the commonest reason why people stop their SSRI s. Um and it can range from like um erectile dysfunction to not being able to orgasm or like having orgasms which aren't like pleasurable. Um And even when people stop the SSRI, there can sometimes be this period where they still experience those side effects um which is obviously not fun. Um And a a huge ra huge reason why people start SSRI S um and obviously something that's quite difficult to talk about for the patient. Um Yeah, and then platelets, yeah, increased bleeding risk, hyponatremia. Um These are ones which are kind of niche ones which you should just remember or try and drill into yourself. Um But yeah, main ones, like I said, like gi side effects sexual dysfunction. Um Yeah. OK. Um They will also interact with other things. So I mentioned the bleeding risk before. So that's why nsaids and aspirin are on there because obviously they will increase your gi bleeding risk as well. Um And with the Serotonin Syndrome, we'll talk about that in a second. But um other drugs which will increase um the chance of serotonin syndrome will interact with SSRI S to give you a bigger chance of having serotonin syndrome. So, SSRI S should not be prescribed with any Triptans or any monoamine monoamine ox monoamine oxidases. Um, because those two classes can also cause serotonin syndrome. Ok. Um And then the final point at the bottom is that if you give SSRI S, um, and someone gets better and wants to come off them, uh, you shouldn't take them off the SSRI until six months after they've stopped taking it. Um because that increases the chance that they won't relapse after they come off it and when you do take them off it, it should be withdrawn over a period of four weeks. Ideally or even longer, there's actually been more research into this recently, which has shown that um usually our withdrawal um regimens are too short and people get withdrawal symptoms. Um So ideally, it should actually be for even longer than a month, like possibly three months um with a very, very gradual down titration. Um because the pharmacokinetics of it are actually like exponential. So sorry, II don't wanna go into it too much, but basically, withdrawal, withdrawal um symptoms are a huge concern. Um And they basically just as, as I kind of mentioned here, um they, it's better for some um SSRI s than others, but for um things like escitalopram, sorry for things like um paroxetine, um which has the worst discontinuation sym symptoms of SSRI S, you can get stuff like again, gi side effects, again, anxiety. Um again, like I guess relapses of, of the original thing that it was meant to be treating for. Um So yeah, discontinuation symptoms will overlap a lot with the actual side effects of the SSRI if that makes sense. Um OK, so let's have a quick talk about SSRI S uh sorry about um names. OK. So this is a case study. Um and I've probably given it away a bit earlier, but does anyone know what's going on here? Yeah, Serotonin syndrome. So this guy is flushed, tachycardic, Tachy Nick, he has clonus hyperreflexia and dilated pedals and that cluster of symptoms after you've taken an an SSRI uh or anything else that increases your serotonin is basically serotonin syndrome um until proven otherwise. So, uh this is Serotonin syndrome on one slide. Um Main features are obviously altered mental state, autonomic dysfunction. So the flushing like potentially diarrhea, that kind of thing, anything where there's sero serotonin receptors, um neuromuscular hyperactivity. So, myoclonus tremor hyperreflexia. Um So hyperreflexia is an important one to remember when you differentiate between this and neuroleptic malignant syndrome, which again, we'll talk about later. Um But yeah, so in terms of causes, obviously, SSRI S is the main one. monoamine oxidases TCA S. So tricyclic antidepressants um and then recreational drugs like ecstasy and am fes. Yeah. So in terms of treatment, it's mostly supportive. Um So, you know, IV fluids don't give any more if what caused it, obviously, and if they're agitated, you can give them benzos. Um And in really severe cases, you could give a serotonin antagonist, like Cipro heptadine or chlorproMAZINE. OK. All right. So that's essentially all I wanted to talk about in terms of antidepressants because there's obviously loads of other classes as well, like SNRI S and TCA S. But given this is a sort of introductory talk, I don't wanna overload you. So we I'm just stuck with like the main class SSRI S. Um So now if we move on to antipsychotics, this is a bit more complicated. Um we generally, so you might remember this from way back in the day in MDA. But there are two main classes of antipsychotics. So typicals and atypicals. The atypical antipsychotics are the ones that were developed like way, way back um in the 19 100s and these all act on D2 uh receptors. So they're D2 antagonists and that's their only mechanism of action to whereas the atypicals um which are being developed more recently act on a whole host of other receptors. So they also act on D2, but they also have an action on five ht and receptors. The main ones being five ht two A and five HT two C, they also act on histamine receptors. So, h one and then some alpha receptors as well. Um Yeah. And, and so, and you know, you don't need to know the mechanism of action for each individual receptor. Like you don't need to know that, you know, block uh stimulating five HT two A like decreases D2 signaling, that kind of thing. Um It's just good to know that there's a, a wide range of, of receptors that these act on. Um And then yeah, the future atypicals might include some of these other receptors, but don't worry about that. Um OK. So here's the kind of general algorithm for schizophrenia management um which is obviously what you use antipsychotics for. So, uh you would generally start on um you would try one antipsychotic one atypical as your first line. And if they fail that you'd go onto a different atypical or atypical actually, and then if they failed that you would go on to cloZAPine. Um So, cloZAPine is an atypical which generally has the best e efficacy um for schizophrenia, all right. Um In terms of what was explained. OK. So in terms of other things as well, I mean, just to mention the facts that, you know, you can't just throw antipsychotics at someone, um you also have to kind of build up the social structure and supportive structure around them. Um So CBT family therapy, social support, you know, education, training, volunteering, opportunities, all of that um to support people to like reintegrate. Um And I'll talk a bit more about that later. Uh after I talked about the like pharmacological stuff. Um So, yeah, so this is the treatment algorithm in terms of uh cloZAPine specifically, um there's a useful mnemonic that I have which for some reason I haven't put on here, but it's scan where s is for sei seizure threshold. So it lowers seizure threshold. C is for constipation. Um A is for agranulocytosis and M is for myocarditis. Um So yeah, the main one to remember in that is probably agranulocytosis because that's the one that tends to be uh asked about all the time on password. Um Yeah, and in terms of monitoring antipsychotics, a lot of things have to be monitored because all antipsychotics can cause quite, quite severe metabolic symptoms. Um You, it can cause a lot of weight gain, hyperprolactinemia. Um So you wanna be checking up on people's weight, the BP, prolactin lipid profiles, HBA1C S, all of that and especially for cloZAPine. Uh You wanna be looking at the FP CS um just to check that they haven't developed again, the agranulocytosis. Um Yeah, so weekly FBC S for the 1st 18 weeks. Ok. And as a side note, abruptly stopping smoking can increase cloZAPine levels. Um which is, I don't, I don't think it will come up, but that's again, just something on past me. Um ok, so if we talk a bit more about the different types. Yeah, so typicals. Um there's a list of them there. So haloperidol chlorproMAZINE, tri fluoperazine, fluPHENAZine, zuclopenthixol and flupenthixole. I literally have never seen any of these in use except for the first two. So haloperidol and chlorproMAZINE. So don't worry about the others. Um Yeah. So in terms of how, how the typicals work and what specific um yeah, what specific things they cause. So the typicals are, you know, most infamous for causing extrapyramidal side effects as you might remember. Um And that's kind of the reason why the atypicals were brought in because they had a much lower chance of causing extrapyramidal side effects because they weren't just acting on D2 receptors, they were acting on loads of other things as well. So, um yeah, so with the typicals, um the main, yeah, the main things to know about with the extrapyramidal side effects, there's kind of a list of a list of different extrapyramidal side effects here. But the most acute one is acute dystonia um which is when basically all their muscles will contract. Um And you can get things like ocular gyrate crises, which is where your eyes kind of roll up. Um And you can treat that with um procyclidine which is an antimuscarinic. Um You also get this thing called a akathisia, which is defined quite subjectively as a quote unquote sense of inner restlessness. Um but apparently it's really like debilitating. Um you also can get pseudo Parkin Parkinsonism um which essentially just presents with the features of Parkinson's, but it's been induced by anti by a typical antipsychotic. Um If you remember, um Parkinsonism and schizophrenia are kind of opposite sides of a spectrum. And if you treat parkinsonism by giving dopamine, you can kind of push someone towards um presenting with a schizophrenic like picture. And if you give someone with schizophrenia dopamine blockers. So, antipsychotics, you kind of push them towards um a Parkinson's like picture. So really useful to conceptualize it as, as two ends of the scale. Um Yeah. And then tardive dyskinesia that's, that comes on a lot later. So it's kind of late onset, months to years. Um and that's like repetitive movements. Um So like lip smacking, pouting that kind of thing. So those are really important ones to know about just to kind of wrap your head around the different names like what aesthesia is, what acute dystonia is, what part of dyskinesia is. Um because those extra primal symptoms are obviously the reason why atypicals actually exist. Um Yeah. And then in terms of the other side effects of typicals, you've got um anticholinergic effects which are much more pronounced than with atypicals. Um anticholinergic effects. You can remember them by just like everything dries up basically. So you get dry eyes, dry mouth and you get constipation because your stools become dry. Um you can get blurry vision because your eyes become dry, that kind of thing. Um Weight gain as well. Um Sedation, you can get QT prolongation specifically with Validol. Um Yeah, but the main things obviously to know are the um are the extra prominal side effects. Ok. Um So then if we move on to the atypicals, so again develops because they don't tend to cause extra pram or side effects. Um they still have side effects that, but the main one this time is actually metabolic syndrome. So putting on weight causing um central obesity, diabetes or glucose intolerance, hyperlipidemia, hypertension and also hyperprolactinemia. So that's the main thing to remember with atypical antipsychotics is that they put on weight much, much, much more easily. Um And you really need to like stay on top of it. Um And you know, make sure that they're not developing diabetes because of it and making sure their lipid profile is all fine because you don't want anything cardiovascular happening um because of these medications. Ok. And then a list of um atypicals that I've put there. So risperiDONE, OLANZapine, QUEtiapine, ARIPiprazole and Cozine as well. Cozine I mentioned on the last slide um has its own kind of um yeah, side effect profile which I talked about. Um So the one that causes the most weight gain is probably OLANZapine and it's why OLANZapine is actually being trialed for use in eating disorders as well where it's shown quite a good effect. Um Yeah, what else was I gonna say? Um All right. So I think we'll just move on to some kind of more severe side effects that can happen. So here's another emergency case study. Um Does anyone know what is happening here? Talked about it briefly in the last slide. So I'm really sorry if you can hear music in the background, there's like a practice room literally next door. It's really awkward. OK. Yes. Acute uh acute dis yeah, exactly. So his head is fixed towards the left, his neck muscle is spasming. Um So, you know, all of his muscles are contracting basically. So this is an acute dystonic reaction. Um Yeah. So I've talked a bit about this but just to go over it again. So ocular gyro spasms. So eyes rolling up neck um twisting. So that's to, that's called torticollis. Um basically only happens with the typical um and because it's obviously it's called acute. So it happens in the early stages of treatment or after an increase in dose. Um And yeah, like I was saying, you can give procyclidine to reverse. Um Right. And what about this one? What do you think is going on here? Yeah. So, neuroleptic I Good syndrome. Is that just? Yeah. Yeah. So, neuroleptic Malignant syndrome, we didn't mention this before, but it's kind of the equivalent of Serotonin syndrome. But for antipsychotics, um although the mechanism of action of how it actually happens is a bit less clear. Um essentially, it happens whenever um you kind of overdose on antipsychotics um or you withdraw from Parkinson's disease medications. So basically, whenever there's like a rapid drop in dopamine, this might happen. So either you give a medication that intentionally drop your dopamine or you go off a medication that was raising your dopamine, you can get neuroleptic malignant syndrome. Um So it can be quite easy to confuse with um Serotonin syndrome. Um because there are some overlaps like pyrexia tachycardia. Um But the main thing to remember in terms of differentiating them clinically is the fact that neuro neuroleptic malignant syndrome presents with decreased reflexes. Whereas serotonin syndrome presents with increased reflexes, that's the main thing I use um to differentiate them because they'll usually have that in the stem of a question. So yeah, an important point to remember. Um it can, so it can lead to like muscle breakdown, so raised creatine kinase and that can lead to um you know, renal failure and multiorgan failure. Um And yeah, the mortality is quite high because of that up to 10%. Um Another way to differentiate between N MS and Serotonin Syndrome is that N MS tends to develop over a longer period of time. So over days to weeks, whereas Serotonin syndrome tends to occur quite quickly. So within hours to days. Ok. And then in terms of treatment, obviously, you stop the antipsychotic um mostly supportive again, but you can give some other things like bromocriptine, which is a dopamine agonist. So basically reversing what initially happened, you can also give Dantrolene um which is a ryanodine receptor antagonist. Uh You can also give him Aine, but the main ones to remember here are Dantrolene and bromocriptine as your options for treating N MS. Um OK, good. So this is just like a little summary of how to differentiate them. And OK, so I mentioned the reflexes. Um men, the course mentioned the onset. Um and then, yeah, you can differentiate cause of people's cause with serotonin syndrome, you've got that like autonomic activation whereas with N MS, you don't um in terms of neuromuscular stuff, yeah, you tend to get more of a myoclonus and a tremor, the serotonin syndrome. Whereas with N MS you get rigidity. Um So this is a usual thing to remember. Ok. And the last thing, yeah, the last thing before we go on to like a few MC Qs that I've got for the end is just talking briefly about lithium. Um just because again, it's one of those things which you need to know about and comes up quite a lot. So lithium is the main drug that we use to treat. Uh bipolar. It's a mood stabilizer. Um There are also other mood stabilizers out there um like anti antiepileptics. Um but lithium is kind of, you know, the wonder drug and you know, that's the reason people think that um lithium is being put in the water or the conspiracy theorists. So if we talk a bit about side effects toxicity and monitoring them. So with the side effects, a useful mnemonic similar to the scam mic for cozine is lit is the, the mic lithium, um which I quite like. So the L is for leuko leukocytosis, the I is for insipidus. So, nephrogenic diabetes, insipidus. Um T is for a fine tremor. Um And remember so, so fine tremor is a side effect of lithium. But when you actually overdose on lithium and you get toxicity that actually causes a course tremor. So important to differentiate between those two. the H stands for hypothyroidism and with long term use, it can cause hyperparathyroidism. Um So hypercalcemia as well. I stands for increased weight. Um The U Well, I think here they've changed it to a be vomiting and diarrhea. Um and the m is just like metallic taste which obviously makes sense cause lithium is the battle. So, um but yeah, so that's a really useful acronym to just commit to memory. Um ok, good. So toxicity then. So lithium is, is excreted by the kidneys. So essentially anything that makes the kidneys sad will cause lithium toxicity because you'll get a build up of lithium because the the kidneys can't excrete it. Um So dehydration, well, renal failure diuretics, um especially thiazides. So all of these things will impact the kidney. So they won't be able to excrete lithium. So you get lithium toxicity, um also febrile illnesses and heart failure. So in terms of how toxicity presents, um you get um the one thing to remember is you get a coarse tremor that differentiates it from the, the fine tremor that you kind of normally get with just a side effect of lithium. Um and you get early gi um effects like nausea, vomiting and diarrhea, and those develop into later neuro effects. So that's when the course tremor comes on the ataxia rigidity, hyperreflexia. Um and you also can get some cardiac features like bradycardia, bradycardia, um and conduction blocks. Ok. So again, kind of difficult to disentangle all these kind of toxicity syndromes. So like lithium toxicity syndromes and um in your la malignant syndrome and serotonin syndrome. But if you kind of just learn very distinctive features of each, for example, the fact that lithium toxicity comes with a coarse tremor and uh and it's hyperreflexia or not hyporeflexia, that kind of thing. It makes things a bit easier. Um because this is yeah, uh overdoses is something that Cambridge likes test on. So yeah, um the main thing again, as with all the others is just supportive treatment. So measuring the lithium levels and doing EC GS to make sure that the heart's not being affected, giving like a load of IV fluids. Thank you. And if that all doesn't work, then you might have to go on the dialysis if it's a really severe um toxicity. Yeah. So very important to be monitoring lithium levels because um it is actually quite a narrow range that you need to keep it in. Um So toxicity can actually be quite easy to fall into. Um it doesn't take much to overdose basically. So um lithium levels should be less than one. You should check, always check lithium 12 hours after the last dose. Um After you start it, you should check it weekly. Um And also when you change the dose, you should check it weekly until the concentration is stable. So basically just titr it until the concentrations stable and then you can check it for every three months for the first year and then every six months thereafter. Um But yeah, really important to keep the lithium levels in that narrow range of less than one. Um Yeah, and then also monitoring a bunch of other things. So yeah, weight and BMI because it can cause you to put on weight um T FT S because it can cause hypothyroidism. Um And yeah, EGFR as well because of um kid. Yeah, just checking the kidneys are OK to excrete it. OK. So that was kind of a whistle whistle stop to through SSRI S and their side effects with Serotonin syndrome as well. Antipsychotics. Um the two different types, their side effects and neuroleptic malignant syndrome. And then I briefly talked about lithium as well. Those are the, yeah, so I basically covered depression and anxiety treatment, psychosis treatment, and bipolar treatment like the first lines for each. Um But there is obviously like uh more to learn beyond this. This is just kind of an introduction to the three, you know, the, the first line treatments of the three main um mental disorders that tend to crop up. Um So yeah, I think we'll do a few Mc Qs and then hopefully that gives us a bit of time for like questions and discussion and stuff. OK. So fairly easy one to start off with. Um you guys can drop what you think the answer is in the chat. Yeah, exactly. Citalopram all done. So yeah, Cital um Citalopram being one of the SSRI s um Sildenafil is actually Viagra. So you would expect it to have the opposite effect. Um OK. The next one. OK. Is prolonged security prolongation. I love how it's like the same three things you um feel free to um guess as well if you want. So, yeah, this is prolongation of the QT interval um which is a characteristic ecg side effect of haloperidol. Um And remember as well, actually, Citalopram can cause prolonged Q QT interval as well. Um OK. How about this one? Yeah, well done. So again, this is the characteristic um agranulocytosis uh side effect. Uh I realize I didn't really define what that means, but you know, it's when you, you don't get as many granulocytes. So neutro your neutrophil uh count drops um and you're much more susceptible to infection. So, yeah, so that's a side effect that she's experienced. OK. What about this one? Yeah, part of this kind. Exactly. Exactly. I think the key here is that um he's been treated for many years. So it's not gonna be the other more acute side effects like oculogyric crisis. That's an acute side effect. A Akathisia would have shown itself before. Um, and so would the others probably. Um, and there hasn't really been any change in Medicat in medication level. It's just kind of happened like after a few years. Um, and that's kind of classic of Todd of dyskinesia. And he's got, yeah, these repetitive movements like grimacing, smacking his lips, protruding his tongue, um smacking lips is probably the most like classic one that they'll put in a a question stone. OK? And then last name. Thank you. Yes, exactly. I think this one was fairly obvious even even though it's a psych talk. But um yeah, so she has had a history of diarrhea, feeling thirsty, passing more urine. Um She has a fine tremor as well. And yeah, these are all classic um signs of lithium side effects. Um It's not um toxicity though because if you know the the tremor is a fine tremor and not a course tremor. Um So she probably just has slightly high that your levels. Um and then yeah, so feeling thirsty passing more urine. So that's, you know, nephrogenic diabetes, insipidus, which lithium causes and then it can also cause diarrhea. Ok? Cool. So there's that ii kind of wanted to put this slide in just as a footnote because I think psych especially as a med student can very easily, just be reduced to like a list of drugs and presentations and symptoms that you have to learn. But obviously, psychiatry is a lot more than that. Um, drugs aren't solutions and they have to go hand in hand with like therapeutic relationships. Um, and all the other, like soft stuff that Cambridge, then students don't really like that much. Um, but so with psychopharmacology, there's like a whole host of other things that will determine whether or not the person gets better beyond the drug. It's also the way that the drug is prescribed, the meaning that the person ascribes to the drug. Um There are patients who can have very strong feelings about medication and if they feel very negatively about a medication, they're being prescribed, they just won't have a good reaction to it. Um Either because, um, you know, uh they won't take it or because they'll kind of somatically induce side effects. Um or they just, they, they will just become treatment resistant, that kind of thing. Um Because the power of the mind is very, very strong and if someone doesn't want to get better on a medication, they generally won't. Um So I think there was a really interesting study actually that the top, so the best prescribers actually get better effects with a placebo drug than the bottom third of prescribers get with an active drug. Um So that just goes to show that it's not just the drugs that's having an effect. It's also the way you talk to patients. Um, and how much your, your patients trust you. Um, ok. So that's just something I wanted to put out there. Oh, what makes you in the top third or bottom third? So, it was stuff like how your tone of voice, like how much time you spent with the patient. Um, like how much of a history you took from them, how much like you got to know them as a person as opposed to just like having like a five minute conversation with them on a ward, that kind of thing. Um And it, they also showed that the top third of prescribers, all their patients tended to get better. Um Whereas with the bottom third of prescribers, not, not so much. Um So yeah, this is just a footnote essentially. Um to remind you guys this psych is a lot more than drugs, ok? That's the end. Sorry. That was very much like rushed.