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OK, so I think we should be live now. Um Hi guys, welcome to um Osi's Case 10 revision session. OK. Um So we'll be releasing the slides at the end, er, using the feedback form. Um I'll be managing the polls while Marriam presents um and then vice versa when I'm presenting. Um so Marriam is gonna be touching on kind of all the um the neuropsych er, the neurophysiology um and the, the um scientific element of Case 10 and then afterwards I'll touch on the psychiatry elements. Ok. So without further ado Marian, um you take over. Yeah. So can you see my slides? Yeah. Yep. OK. And like they flicking through. Yeah. Brilliant. Ok. OK, cool. So OK, welcome guys to Case 10. So as mentioned, I'll just be going through the first bit in terms of the antidepressants, anti psychotics and the side effects of them and then the personality theories and um things like that. So should we get started? So the topics that we're gonna go through neurophysiology, pharmacology of antidepressants, pharmacology of antipsychotics, drugs of abuse and the personality theories. So the content of this presentation is for educational purposes only. Um there are many references to mental health and mental health disorders. There is no intent to cause any harm and we apologize if any of this uh content is triggering. And um so to start off with physiology. So this is the neuron which is um found within the nervous system and it's a network of neurons that make up this nervous system. And so we've got the dendrites at the end um which connect to the cell body, which then have an axon which have these um rolls of myelin sheath around them, which then make these little gaps called the nodes of nodes of Rviia. And then you've got the synapses at the end. And the way each neuron connects to each other is that a synapse would be next to a dendrite at the end. And then that would be your synaptic cleft, which will be our next slide. So this is our synapses. So what first happens is an electrical signal reaches the presynaptic terminal causing depolarization. Then the voltage gated calcium channels open and calcium enters into the presynaptic terminal. So now calcium is filling up within the presynaptic terminal. The calcium triggers the vesicles which contain the neurotransmitters to fuse with the presynaptic membrane in order to release the contents of the vesicle, which are the neurotransmitters with into the synaptic cleft by exocytosis. And then the neurotransmitters diffuse across the cleft and bind to the receptors on the post synaptic terminal and the the neuro transmitters are then cleared up by reuptake and by um enzymes that break the er neurotransmitters down or just by simple diffusion, the er synaptic vesicles are then revived and refilled with new neurotransmitters and then reused for the next signal. So, it's a reuse process and the contents that are broken down by the enzymes as well that are present within the synaptic cleft. So once they break the neurotransmitters down, the, the substances that are formed are then also taken up by the presynaptic terminal in order to be reused um for the next signal as a neurotransmitter. Um Then you've got the uh four main types of new transmitters. You've got your dopamine gaba serotonin and your glycine. So this is just a diagram to show how each of them are made. So in terms of like with tyrosine, um with dopamine, it's tyrosine, then l dopa dopamine, then it becomes noradrenaline and the enzymes that are involved within each of the processes. And then with Gabaa, it starts with glucose, glutamate and then Gaba and then serotonin, it's um l um tropfen, then five HTP and then serotonin and then five H IAA and then you got your um serine and your glycine, which are interchangeable. So you can go either way and that's how each of these neurotransmitters are made. So you just really need to know the, the enzymes that are involved in each of the processes and how, what comes before and um the new, the enzymes that are involved have the name of the um substance before. So, like, for example, if you look at the dopamine one, it's the um triazine, uh hydroxylase. So the triazine is the thing that's comes before. So just if you remember that, then it's easier to remember which enzyme comes in order to break it down into L dopa and then dopa decarboxylase, you've got the dopa from the substrate above goes down. Let's get the gist. So that's a good way to remember the enzymes and the substances. And then you've got the function and where they, where each of them are made. So dopamine is made within the substantia nigra mainly and um the uh VTA and the hypothalamus, it's involved in regulating uh reward, motivation, mood, motor control and the prolactin secretion. And if you guys remember with uh Parkinson's, for example, if you one issue, like it's the degeneration of the substantia nigra, so lower um amount of dopamine which causes these motor symptoms such as that clog wheel rigidity and the shuffle gait. So that's also a good uh way to remember. Dopamines um role in terms of the disease of Parkinson and how Parkinson's has that motor effect. And with Gaba Gaba is um made within the gabaergic neurons which are found in the cerebral cortex, um hyper hippocampus and the basal ganglia and the spinal cord. And it's a primary inhibitory um neurotransmitter and it just reduces neural excitability. So that's mainly what you need to know about Gaba, it's just an inhibitory neurotransmitter. Then you've got your er serotonin which is made in the rough eye nuclei and this is involved in your mood, sleep, appetite, gut motility, blood flow and platelet aggregation. Glycine is really your glycinergic uh neurons and the liver for metabolic functions and its main role, it's an inhibitory neurotransmitter, but it's a co agonist to uh glutamate in the NMD receptors. And it's involved in collagen synthesis, detoxification and energy metabolism. Then you've got the theoretical models of depression. So, um the mona ay model is that uh a neurotransmitter deficiency can lead to depressive symptoms. So a mono, so if you've got less um monoamine, it would mean that you've got a lower mood. So a monoamine would be that dopamine and that serotonin that we were talking about. So if you've got less dopamine, you'll have a lower mood. Therefore, a depressive, you show depressive symptoms. And then it's a, the chronic deficiency can result in hypersensitivity to the monoamine receptors. So it can also exacerbate mood regulations. So, rather than your mood, having small fluctuations, you'll have larger fluctuations within your mood. So you'll have be really happy, really sad because of the increased sensitivity and then the impair uh synthesis release and reuptake of monoamines can also contribute to the symptoms. So if you're getting, if your monoamines are getting reuptake, if the monoamines are getting reuptake at a larger volume and a larger frequency, there's not enough getting through. So it would also as a result, mean you lost less monoamine as a result, less mood. So in the terms of just the presence of the neurotransmitter, the less of it, you have, the lower your mood is. So that's basically the overall of the monoamine model and then you will your dopa dopaminergic pathways. So there are four main types. So the first one being mesolimbic. So this one begins within the VTA and then goes to your nucleus er Uman and then this is uh central to uh feelings of pleasure, reinforcement and goal directed behavior. It influences um emotional learning and memory and it is associated with the positive uh symptoms of schizophrenia. Whereas the mesocortical is involved with the negative symptoms and the cognitive defects within schizophrenia. So when we say positive symptoms is the things that are added on, so you'll get or hallucinations with schizophrenia, for example, whereas the negative symptoms within schizophrenia would be that low mood loss of energy. So it's a loss within our function and it the mesocortical starts within the VTA as does the mesolimbic, but this one goes to the cortex, not the nucleus iban and it's involved with attention decision making er working memory and it balances your Emmo er emotional responses and your social behavior. Then you've got your Niagra striatal pathway which comes from your substantia nigra and it goes to your striatum. So if you remember, I don't know if you guys think it was last year and year one for you guys, maybe the striatum is involved in motor movement. So the substantia Nigra would create the dopamine and then it would go to the er striatum which would then cause that motor movement to occur. So it regulates the voluntary movement and coordination by moderating the basal ganglia activity and degeneration within this. You're seeing Parkinson's disease. Um So it leads to that, that slow movement, the rigidity, the tremors that you see within Parkinson's is due to that degeneration of the substantia nigra, which we were discussing before with the dopamine. And then you've got your tuber um in the in infra ibular uh pathway. So that comes from your hypothalamus to your pituitary. So this is mainly with um it inhibits prolactin uh secretion by acting on the D2 receptors in the pituitary gland. And the doping. Um blockage can cause hyper prolactinemia which can lead to like issues with um loss of periods, sexual dysfunction and issues with producing milk within breastfeeding women. So it's the inhibition of the prolactin. Then you've got your antipsychotics. So there are two main types. You've got your first gen, which is your, also known as typical and you got your second gen, which is also known as atypical. So your first gen, they just involved in with the D2 receptor antagonist. So they lower the dopamine in the mesolimbic pathway and reduce the positive symptoms. And some examples of them are like hyperdol and then for your second gen. So second, meaning like think of it as in like 22 receptors. So it um affects your serotonin and your dopamine receptors and they're antagonists. So this works on the mesolimbic um both mesolimbic pathways and the mesocortical pathway. I've, I've read mesolimbic twice but it's mesocortical. I'll fix that when I send that slides over to you guys. So, mesolimbic and mesocortical pathways and they reduce both negative and positive symptoms. So, um an example of this would be OLANZapine. And so the first SBA is a 50 year old man with schizophrenia is started on OLANZapine and the FBC S and the UN ES and LFT S lipids, weight, fasting glucose and prolactin BP were all monitored. He also had an ECG done. What are the posi uh possible side effects of this medication? Is it metabolic syndrome? Is it depression? Is it psychosis renal failure or hyper um thyroidism? So if er so if you could just let me know in like 30 seconds what everyone says, so that I could just move on guys, give it a go. So I ca I literally can't see anything other than the actual slides. So, yes, just give it a go. And if you guys do have any questions, please do put in the chat and I'll try my best to answer them at the end. OK. So I think, I think the majority are saying uh option a, option A and the majority would be right. It is metabolic syndrome. So we'll go through that in the next slide. So first, so the first gen the typical um antipsychotics, they have um the main side effects that they have are is the adapt um acronym. I don't know if you guys seen that yet, but it's the acute dysonia, dystonia, the um Akinesia, the Parkinson's and the um travel dyskinesia. I can never say these, but I can always like you'll know by word. So these are just motor issues. So all of these have some sort of uh motor issue or a tremor or a spasm. So if you, if you see that uh antipsychotic is causing a motor issue, think like first gen it's a typical antipsychotic and it also causes um hyper hyper prolactinemia and it also prolongs your QT interval and it there is a risk of uh neol malignant syndrome. Whereas the second generation it has uh fewer extrapyramidal side effects. And it, it's less significant in terms of the hyper prolactin, it's more high risk in the metabolic syndrome, which as we said before, OLANZapine, which is an example of the second gen has a side effect of metabolic syndrome and it also increases the QT interval and causes sedation. And this, this also has a risk of neuroleptic malignant syndrome and cozine can have issue. There are significant issues with um the white blood cells and the cardiac stuff. So be aware of cozine in terms of the uh white blood cells and the the cardiac side of it in terms of the side effects. So that's that. So all in all neuroleptic malignant syndrome is just associated with antipsychotics, there is another syndrome that's thrown around in case 10, which is serotonin syndrome, which we'll cover later, which is just for antidepressants. So when you think neuroleptic malignant syndrome antipsychotics. So next question, um a 35 year old male with schizophrenia has been on Harper for six months. Uh He has now presented with restlessness, um repetitive leg movements and he, he has an inability to sit still. What is the most likely diagnosis? Is there a tremor, acute dystonia, a akinesia um ch dyskinesia or is it the Parkinson like syndrome? The Parkinson like symptoms. So if you could please have the pull up and just let me know in like 30 seconds that, ok. So you've got kind of a, a split between option C akathisia and option D which is tardive dyskinesia. But option D is, is starting to pull away now. Oh, ok. Yeah, it is the option C. So that's related to leg movements and I believe correct me if I'm wrong. The um disc um disc is related to, is it the jaw movement, repetitive jaw movement? But misery. Yes. Hello. Yeah. Yeah, I just wanted to ask, is it the is it related to the jaw in terms of like lip smacking and sticking your tongue out? Tr uh dyskinesia just to confirm. Uh Yeah. Yeah. So you have like different, you have like different types. So yeah, you can have like orofacial and like orobuccal lingual um which basically means like which, which area are you getting the like the, the movements that you're talking about? Yeah, but it will be mainly within the jaw area with um travi whereas the uh Akinesia is mainly with like restlessness and leg movements. So that's question two Serotonin syndrome, which we mentioned with antidepressants. And then you've got neuroleptic malignant syndrome. So, the causes of serotonin syndrome is that um SSRI S uh ma S traMADol and ecstasy and amphetamines, they can all cause serotonin syndrome. Um It, there's neuromuscular effects. So it causes hyperreflexia rigidity and it can cause you to sweat and um become very warm and you become get confused and it doesn't show up on blood. But you can tell by asking about the history in terms of what medication that they have taken that you can find out that like, oh, that due to the maybe an increased dosage or an increased intake of SSRI S that they have got Serotonin syndrome. And then the management for that would be the IV um uh cyproheptadine. And if it's severe, then you also give IV fluids and the onset is normally within 12 hour, 24 hours. Then you've got the neuroleptic malignant syndrome, which is related with your antipsychotics, your levodopa, your doping uh blockage um drugs and they can, they increase within the glutamate release can lead to uh neurotoxicity as well. And this can cause rigidity, tachycardia, um hypertension confusion raised um creatinine and leukocytosis. So that's the difference uh that you can see between neuroleptic malignant syndrome and Serotonin syndrome is in bloods as well. So you will see the raised creatinine within kinase within neuroleptic malignant syndrome. Whereas Serotonin syndrome, the bloods are nonspecific. The management for neuroleptic syndrome, the three Ds. So discontinue the antipsychotics, stop the root cause of the neuroleptic malignant syndrome, then give them Dantrolene and then give them a dopamine agonist. So to counteract the effect that the um antipsychotics had then antidepressants, you've got uh these are the monoamines. So the monoamine inhibitors. So you've got your SSRI S. So an ex um the examples of those is citalopram, which um prolongs your QT interval. You've got FLUoxetine, which is normally given to Children and adolescents and have a longer half life. So you have to keep that in mind, especially in terms of when you're stopping FLUoxetine because you would slowly start to reduce the dose and then give them one week of just no medication at all, just so that they can cleanse their system in terms of just washing out the FLUoxetine due to that longer half life. And then you've got sertraline, which is the most common first line SSRI that you'll hear and it's er suggested for individuals post M I and the interactions with SSRI S are Warfarin and Heparin. So you wouldn't give an SSRI, then you would give uh Mirtazapine and with NSAIDS, you need to be careful. So you would give um PPI S because of um gastric issues and side effects. Then you've got your tricyclics, you've got your amitriptyline, which is a neuropathic um is normally used for neuropathic pain. And the side effects of those mainly are that it's the antimuscarinic effects. So, you've got that dry mouth, constipation, urinary retention and you've got a long qt interval. So, in terms of when we say long qt interval, you need to be careful whether or not your patient's got a cardiac history. So if they do, you don't want to give them a drug that would complicate their cardiac situation. So, in that sense, you need to be careful when you read these questions on whether or not this patient or this individual has uh a cardiac history and whether or not it would be suitable to give them this medication. And then you've got your uh SNRI S um which is uh D DULoxetine and uh Venlafaxine, Venlafaxine um with the duo bit, it sounds like dual. So it's a good way to remember that it's both nor serotonin and noradrenaline um inhibitors, whereas the SSRI S are just uh serotonin and then you've got your NRI S which um is uh Rubox Rubox. And then sa number three, an 18 year old patient with a major depressive uh disorder has started on SSRI S and after one week after one week, they complain of insomnia and nausea. Which of the following SSRI S are they most likely to be uh prescribed? Is it mirtazapine, sertraline, um paroxetine, paroxetine, um citalopram or FLUoxetine. Mr Do you have any answers? Yep. So about 50 to 60% of people are going for option E FLUoxetine, option E OK. So and FLUoxetine would be right? Because FLUoxetine is used for your adolescents for your younger patients who have depressive symptoms then um discontinuation of SSRI S. Um this is a good acronym that I found uh finish. So the symptoms that you'll experience when you stop SSRI S, you'll first experience flu like symptoms, insomnia, nausea, imbalance. So you'll have like vertigo and dizziness, sensory disturbance and headaches. So that's a good way to just summarize what discon attenuation syndrome is like uh with SSRI S and for reviews with them, uh normally you would review them after two weeks, but if your patient is under 25 review within a week and continue the SSRI S for six months, um If you're getting a good response to reduce the relapse risk and if you are stopping an SSRI um stop it gradually over four weeks and give them um paroxetine in order to red, reduce that risk of getting the discontinuation sym symptoms. And then you've got um the fourth SBA which is a 65 year old man with hypercholesterolemia takes um statins for his um lipid modification and citalopram for depression. He has recently suffered an M I and the register in charge is considering changing the citalopram for another drug. What is the name of this drug? So, is it um mirtazapine uh Rubox FLUoxetine, sertraline or um Mo Moloi moclobemide. Moclobemide. Oh drug names Moclobemide. Yeah. So I think we have gone through this. So hopefully you guys do remember. So he's getting depressive symptoms and it's post M I Yeah, so about majority is going with option D sertraline and certainly will be correct. Yup. So um monoamine oxidase inhibitors. So these were the, wait, let me go back. These are, well, I want antipsychotics too far this bit. This is your monoamine inhibitors. So we're gonna go through that bit now. So, um they're used to treat atypical depression and no, they're not. I'm sorry, they're different. Just ignore what I just said. These are different to what I just showed you now. They're different, they're different, they're different. I just confuse myself. They're different. So those are a different class. These are a different class. So, um, so these are the ones that um you're not allowed to eat um Tyramine rich foods in. So you can't have your chocolates, your cheese when you're taking these monoamine inhibitors. It's because that um tyramine displaces other neurotransmitters within the cleft and causes uh sympathetic stimulation. So, if you're already having foods rich in the thymine and you're already um increasing that through the inhibitors, it would lead to like overdrive. So you'll, so you don't want that to happen. So that flushing and that headache. So that's what your hypertensive crisis would look like. So to avoid that you tell them, don't take these foods when you're on these medications. But if this does happen, the treatment for it would be um uh phenol amines because that's what you would give in order to treat the hypertensive crisis and drugs of abuse. So this is a summary of all the drugs of abuse that you need to know. So you've got your ketamine, your cocaine, your n your MDMA S, your cannabis, your fentaNYL and your nicotine. So your ketamine are um there are two functions of it. So you've got the analgesia side of it where it antagonizes the NMDA receptors which prevents the sensitization of the dorsal horn of the neurons and the antidepressive side of it which stimulates the ap uh receptors and then the cocaine which blocks the dopamine reuptake transporters. So it increases the dopamines half life within the cleft and blocks the um voltage gated sodium channels. Um M MDMA. So, ecstasy um blocks uh serotonin dopamine and noradrenaline reuptake. So, it causes an increase of those um cannabis. Um It gives the feeling of relaxation, euphoria and the THC causes dopamine release by antagonizing the um C B1 uh psychoactive uh effects. So the antagonizing the CB ones and the CB twos. So the CB ones are involved in the psychoactive effects of the cannabis. And the C B2 is of the analgesia, the pain relief, the relaxation side of it. Um the fentaNYL, um it activates the uh m the mu opioid receptors which causes hyperpolarization and suppresses the, the Gaba by activating anti uh neurotic um pathways. And to treat this, you would give uh the, the count, the counteract drug for opioid overdoses, which is uh nalox which uh prevents the respiratory depression that occurs if you are on an overdose with opioids, the nicotine which is psychoactive, increases the mesolimbic dopamine levels and reduces the mono um amine oxidase activities as a result increases the serotonin. Then you've got your personality traits. So they're summarized within the word ocean. So you got openness, conscientiousness, extraversion, agreeableness and uh and uh um neuroticism, neurism. OK. So, openness is when you are creative and insightful and you have a vivid imagination. So you have a wide range of hobbies and the the activity of this was it is within the dorsal lateral prefrontal cortex. Then you've got the conscientiousness side of things, which is the organization, thoughtfulness, the self discipline, getting the tasks done on time and being very on and focused. Um This is also done in the dor uh dorsal lateral prefrontal cortex and is associated with positive health behaviors. So people who have the conscientiousness, um personality trait are more likely to reduce smoking and reduce the alcohol intake when they're told to because they're very organized and self disciplined within their actions. You've got extroversion which is like the extrovert. So like sociable, excited, um just the life of the party kind of vibes and the activity within this is within the prefrontal cortex and the amygdala. So this is more associated with harmful and dangerous behaviors because they're more than likely to be involved in risk taking behaviors. Um The a of ocean is um a part of the, the compliant, the trustee, the empathetic, sympathetic, the, the individual that would be like, I'll compromise in this situation. I'm not gonna, I'm not gonna cause any friction. I'll just agree to whatever happens within the group. And this uh mainly the activity of this happens within the posterior singular cortex. And these people like this adhere well to treatment. So they're like the yes men kind of vibe. So like they'll just be like, yeah, I'll do whatever you say or yeah, like I'll just do that or like, yeah, whatever I'll do it. So, so that's why they're more likely to adhere to treatments that you would suggest to them. The end of ocean is involved in anxiety, emotional instability, easily get upset or moody. So they get stressed out very easily. And it's found that the serotonin activity uh is high within the thalamus and the insular cortex and is associated with anxiety and depressive disorders. So a good way to like, remember this would be if you had to associate someone within your life with each of these traits. And uh if you just had to imagine that person, you could imagine the traits um that you would see. So it would be a good way to like, organize each of these traits. Um just for like memory purposes. So if you could just think of someone within your life who has like, oh you have like the openness, personality trait or you have the conscientious. So it would be a good way to split uh things off like that ready for S two. And then you've got your personality theories. So you've got your behavioral theory, which is based on the environmental and response to stimulus, which shapes your behavior. You've got your biological theory, which is your inheritable traits. So this is like your genes and your phenotypes and genotypes. You've got psychodynamic theory, which is the unconscious mind and uh childhood experiences which shape ideas such as for sex, aggression and conflict. So this is why um adverse childhood um events are very significant in terms of um psychiatry because a person's childhood can really shape the way they see things and the way they interact with people in the future. So that comes under the psychodynamic theory. The social learning theory is the uh cognitive expectations of the world, shaping your personality. The humanistic theory is free will and individual experience um impacting personality. And the another question. So I think this is the last question I have. Yeah. So this is the last question that I'll be doing. Question number five. So this is a 40 year old woman comes into clinic, complaining of weakness within her legs and difficulty talking and swallowing. She says her symptoms are getting worse near the end of the day. And she notices that her eyelids are drooping, the production of an antibodies with the production of an an of the antibodies against which receptors can cause this condition. Is it the dopamine receptors, the gaba receptors, serotonin receptors, the um the uh iconic the nicotinic um uh acetylcholine receptors or the glutamate receptors. So, if you could let me know this question is very high yield, I believe on PT S because I feel like this con condition comes up a lot within it. But it's so I think it's a good brownie point to just know that which receptor causes um the weakness within the legs, difficulty talking, worsening throughout the day, the eyelids drooping. These are all signs of a specific condition which affect a specific receptor. So if you guys could just answer this question, this is the last one for me and then we'll have a break and then will go through the the disorders and the other conditions. Yeah. So most people are going with d nicotinic acetylcholine receptors. Yeah, nicotinic acetylcholine receptors is correct. So this is my senior gravis. So that's just an issue with the acetylcholine not going through. And it literally you just need to remember weakness throughout the day, drooping of the eyelids. If you see that, just mycena gravis, just nicotinic acetylcholine receptors, it will be a quick way to sort out PT points er, in that sense. So weakness, difficulty talking, just general mu muscle issues throughout the day and it worsens and eyelids drooping. So that's it for me. These are my references and please do feedback, the feedback form which will be given after ros half and yeah, thank you for listening and partaking within these SBA S. So I think we'll go for a break now and then we'll come back for. Yeah. How long should we say? Like um it's up to you though. Five minutes, five minutes. Yeah, five, let's say let's say 10 minutes. Ok. 10 minutes. Ok. So we just come back to it. Um we'll, we'll start, we'll start the part two at 5 to 5 to 7. Ok, guys. So welcome back for part two. Ok. Um let's make a start. Ok. So um I'm gonna go going through kind of the, the psych um stuff that's in case 10 talking about um kind of mood disorders, um anxiety disorders, psychotic disorders. Um and I'll go through kind of, um, the main aspect of the mental state exam. And then also I'll take a deep dive into not a deep dive, but explain a little bit about sleep physiology. Um, as that's something that's very, um, you know, tied in with a lot of these psychiatric disorders. Ok, cool. So, again, as a disclaimer, um, a lot of these um disorders um are gonna be, um, it could be pertinent in your own lives and you might have experience of that. So um just a, just a, just a disclaimer. Um is that so mood disorders? Ok. So depression, um this is one of the main mood disorders um globally. OK. And the pathophysiology, so, Marian went a little bit into this as well. Um The pathophysiology is not fully understood yet. So there are a couple of models um to explain what could be going on. So the monoamine model, as Marian mentioned, um mainly the thinking is that the reduction of monoamines in the central nervous system might be leading to depression. Ok. If you reduce your monoamines, you're gonna be reducing your mood. Ok. Simple as that. Um And the reason why this could be is because of increased monoamine oxidase activity. Ok. So reducing the amount of serotonin er monoamines that are in the actual synaptic cleft that can actually then go on and have its effects. Ok. The other two models are quite interesting. So the neurogenic model is um kind of explains that perhaps there's a trigger event that then leads to the suppression of this thing called adult hippocampal neurogenesis. All this is is that in your hippocampus, you know, it's um hippocampal neurogenesis is talking about the creation of new kind of brain material, right? So it's about um delaying atrophy. Ok. And what they found is that in patients with depression, they tend to have smaller hippocampi. Ok. Um And so, you know, a possible theory is that a trigger event such as, you know, trauma, um childhood events that can lead to hippocampal atrophy or suppression of this neurogenesis, which can then lead to depression. Ok. Another thing is the inflammatory model. So again, it's kind of like an immune trigger that then leads to inflammation within the um you know, the body and then this can affect um some central nervous system neurotransmitters, ok? And particularly the the balance. OK. And again, like Marian mentioned, overall, it's about serotonin, OK? And your monoamines, right? Hence why the treatments for depression heavily revolve around increasing the amount of serotonin and other monoamines in your brain? Ok. Cool. So let's start off with an SBA. OK. So do replacement. You see a 27 year old patient presenting to his GP as he has been feeling generally unwell for the past few weeks, his mother has accompanied him and reports that he has not been himself recently, which of the following symptoms would be the most suggestive of depression. Ok. So, auditory hallucinations, palpitations, flashbacks of childhood trauma, early morning waking or nightmares. Ok. I'll give you a, a few seconds to answer this again. Marian, if you could let me know um what people are saying, that would be great. Yeah, everyone went for d brilliant, brilliant. So, yeah, early morning waking is one of the, one of the um the biological symptoms of depression, ok? And it very often manifests earlier than your general insomnia. Um And this is thought to be a function of the cortisol imbalance or disruption that happens in the body. So when, when a person, when a patient gets depression, ok. Um So you have your hypothalamic uh pituitary um axis. So that basically and your adrenal axis, sorry. So, h pa axis and this gets disturbed, ok? And so therefore your cortisol, your stress hormone can um that can fluctuate and that changes the normal circadian rhythm of your cortisol. And that's why you can get early morning waking sometimes. Ok. Now, it's also an important point to mention at this in this SBA that, you know, if, if we weren't thinking of depression, you could also be thinking, you know, feeling generally unwell, not being himself. There's a lot of other mood disorders that it could be ok. And we'll kind of touch on some differentials apart from psych ones that you should always be on, on the lookout for when a patient presented some of these symptoms. So, symptoms of depression. Ok. So you've got your core symptoms. Ok. Now, these are the ones that the nice guidelines and the ICD 10 and 11, these kind of state that these are the core symptoms. So a diagnosis kind of revolves around these uh these symptoms. So in the consultation, when a patient presents to you, these are the questions that you wanna be asking to make sure that you know you're on the right lines for a diagnosis of depression. Ok. So you've got to ask about their mood. Ok. Have you been experiencing a low mood recently? Ok. Um That again, that's obviously right? Very in line with depression. And also the other one is anhedonia. So this is loss of pleasure, ok? Um or loss of interest in things that you once found or that you found pleasurable. Ok. Um And these two questions are really a important to ask patients in order to screen for depression. Ok. Now, if they do say yes to one of these, now you then want to ask about any associated symptoms such as your biological and your psychological symptoms. Ok. Biological things like anergia, which basically means a lack of energy. Ok. Anergia. Um oh sorry, uh disturbed sleep. Ok. Again, um insomnia is a big part of depression and something that a lot of patients with depression um deal with and then poor appetite or overeating. Ok. Um and then also psychomotor agitation or retardation. So, agitation, they kind of get very fidgety retardation. They get very, kind of slow, their, their movements become sluggish. Their speech becomes sluggish. Ok. Um, that's, that's another biological manifestation of depression. Some psychological symptoms are irritability, low self esteem, hopelessness. Ok. Poor memory, slow thoughts and, and, um, one that should not be missed, which is suicidal ideation. Ok. Um, and the picture of eo there, um, is just a little bit of, you know, fun trivia. So it's thought that all the characters in the Winnie the Pooh, you know, cartoon series is um thought to relate to a certain mental health condition. Um And this was, this theory is actually proposed by the Canadian Medical Association or something. Um And so you can actually, you know, with an adult brain on, you can kind of see how e or would present with not present but you know, show certain features of depression. Cool. So what about making a diagnosis then? So I kind of talked about it. Ok. Um Mainly it's the fact that one of these core symptoms, ok, the anhedonia or the um the low mood, those have to be one of those has to be occurring most of the day, almost every day for at least two weeks. Ok. Because remember it's very, very, very normal for all of us to experience low mood, ok? From time to time, it becomes clinically um clinically, it becomes depression when it fits these, these categories. Ok. When the symptoms cause an impairment in your daily functioning when one of these symptoms is, you know, the, the anhedonia or the um low mood and when it's been occurring most of the day, almost every day for at least two weeks. Ok. And at that point, you then ask about your associated symptoms and you need to have, I think maybe uh, three of those symptoms as well. So how do we classify depression then? So, because obviously depression is, is a big, um, spectrum. Um, well, we base it mainly on the number of symptoms that you could have and the severity. Ok, and how much impacts your daily life? Um, and so nice have come up with this little patient health questionnaire. Ok. Um, and this can help break down the patient's symptoms and help you, um, kind of determine how severe their depression is. Ok. So question two. Um, an 18 year old patient presents to the GP with persistent low mood for the past three weeks. She's stopped playing sport as a hobby as she reports. She is not enjoying it anymore. She also says she doesn't w er, think as highly of herself anymore and says her grades at school have been slipping as she's been finding it hard to concentrate. Ok. The GP suspects diagnosis of depression. What is the most likely severity level of her presentation? Ok. Give that a go guys and mar just let me know when we've got about a decent number of responses. Um So most people want for B B OK. Interesting. So actually the answer is a OK. And the reason for this is because mild depression is classified as having two core symptoms and two other. Ok. So we can see we've got the low mood and you've got the anhedonia and then we've also got um two other symptoms which are um the low self esteem. So she's not thinking of herself highly anymore and also the heart difficulty concentrating. Ok. So this kind of slide shows you how that's kind of thought about. And this was using the ICD um kind of guidelines. So mild is having two core symptoms, two other symptoms, er, biological and, or p psychological and at least two weeks, moderate is having two core symptoms but having more associated symptoms. Ok. So for example, the hopelessness, the, the er insomnia, the differ disturbances in appetite. Ok. And then severe is having kind of three coys. So sometimes anergia can be considered a, a core symptom as well. Um And obviously four other symptoms, more intense symptoms. So this can be affecting their daily life a lot more. And the key thing is for severe depression, it could be with psychotic features or without. Ok. And then if they do have psychotic features, then that would be classed as psychotic depression. Ok. Cool. So how do we manage depression then? Ok. So the main thing is that with depression, it's all based on patient preference, their situation and also the severity of their condition. Ok. So for less severe cases, first line management will always, always start at the very um you know, the least invasive kind of thing. Um So this is kind of self help, but this is guided. So you will guide them through this process of helping their situation through things that they can modify themselves. Ok. So you can see that this, this, um, this set of management guidelines from nice, they talk about guided self help, they talk about CBT. So CBT is great because um, CBT targets closer towards the root cause of depression and it, and it tackles the issues from your environment to your thinking, whereas drugs tackle from your thinking to your actual symptoms, right? So CBT is great. Um, and you know, it's very, very effective as effective as medication. Ok. Um, however, not all patients want to have talking therapies and counseling and, and you know, go to these CBT therapies because, you know, they might not have the time, they might not think that's useful for them. So they might request medication if they do so, then it's SSRI s first line, ok. For um, low, less severe cases as Marriam was talking about, ok. Um, classic ones are sertraline citalopram, ok. FLUoxetine. Um, as Mary mentioned. So then for more s for more severe cases, you know, it's more about a conversation with you and the patient um talking about what are your needs? Um, what are your wishes? Um, but you know, with severe cases you kind of want to start initiating medication. Um and so SSRI S and SNRI S tend to be first with those um more severe cases. Ok. But these guys can, you know, for less, more severe cases, sorry, you can combine different therapies. Ok, cool. So let's talk a little bit about another mood disorder which is bipolar affective disorder. OK? Now there are two types actually type one bipolar and type two bipolar. And the difference is that um a patient will a type one bipolar patient will experience something called mania. OK? A a manic episode alongside depression. So it's go they go through a manic episode and then maybe a depressive episode and then a manic and depressive. So they can fluctuate really, you know, massively between their, their their mood states. OK? Now mania is very, very high elevated mood. OK? The reason why there's a type two bipolar is because you can get something called hypomania hypomania is where you get mania, but it's not as elevated. Ok? So if you think of you know mood as a spectrum, you've got high mood, low mood, um depression is obviously low mood mania is on the high mood and then hypermania is just a little bit towards the middle as you can see on that side. Ok? So it's not severe enough to require hospital admission and the depressive element is more severe. But with type one bipolar, you've got mania and depression and it's more common. Um and manic episodes may require hospital admission. Ok. Yeah. So distinguishing between mania and hypomania. So both of them have to have three or more symptoms. Ok. Duration with mania it's a little bit longer. Ok. So about more than a week you then you're talking about, ok, they have a manic episode and it impairs functionality in social and work settings. Ok? Um and it may require hospitalization and can potentially harm themselves or others, which again is why you might think about, you know, admitting them to hospital and they may have psychotic symptoms. Ok? And we'll talk about psychotic symptoms in a bit. Um hypomania hypomania. On the other hand, shorter duration does not impair functionality does not require hospitalization, but psychotic symptom may also be present. Ok. Cool. So symptoms, what, what is, what are these episodes actually like then? So they have a really elevated mood, but with that elevated mood, they can have periods of irritability. Ok. Um With their speech and thought, um pressured speech um is kind of a feature of mania hypomania and also flight of ideas. So flight of ideas kind of thing, you know, that you've got a load of ideas at once and you kind of um very easily distracted by your thoughts. Ok. So it's kind of like jumping from one train of thought to another. Um and then also the short attention span, OK. Again, very easily distracted. So with the behavior you get increased appetite cos it's almost like your mind is working on overdrive and you have a reduced need of sleep. Ok. So this is interesting. So they almost when you're undergoing a manic episode, it's like you're experiencing, you know, kind kind of like euphoria and, you know, you feel like you don't need to sleep very much, the opposite of depression, ok? Where, you know, depressive patients can sleep for, you know, throughout the, the day or, you know, um you know, that can be affected in different ways and also you can get lots of inhibitions, ok? Um So overspending risk taking sexual promiscuity. So again, it's about that elevation of mood and certain um ideas and thoughts. Ok? Cool. So let's have a quick go at another SBA. So a 40 year old patient presents to the GP with his wife. He says he doesn't understand why his wife has dragged him in. As he has been feeling great upon observation, the GP notices the man is very talkative, easily distracted and uses extravagant hand gestures. His wife reports that this behavior is completely out of character for him and he has been like this for the past two weeks. So what sign or symptom would be most associated with this gentleman's diagnosis? Give you guys like 30 seconds, Marian just let me know um when you've got like a clear when majority of people have answered. Um Yeah. So most of them went for B B OK. Interesting. OK. So actually the correct answer is um e OK. Now if you go back, that's kind of talking about the reduced need of sleep. Ok. Um And yes, in some, in some cases with manic and hypomanic episodes, you can get psycho psychotic symptoms, which yes would be, you know, a delusional perception but more would be most associated because remember the SBA single best answer. So um the most associated would be this kind of decreased fatiguability. Ok. Um because they're kind of on the go all the time and it almost feels like they don't need to um sleep. Ok? So it's almost like they, they can't get fatigued. Ok? I hope that answers will settle some confusion if you guys pick the wrong answer. Ok. So moving on to psychotic disorders. Ok. We'll start with another SBA. OK. So a 32 year old woman complains of feeling no drive to do anything and a noticeable lack of motivation. She reports that she often hears voices, whispering derogatory comments about her when no, no one is around. She also de describes experiencing moments of intense fear and paranoia believing that someone is constantly watching her. Additionally, she has been neglecting her personal hygiene and withdrawn from the social activities over the past few months. What is the most likely diagnosis for the patient. Hopefully you guys should, should get this cos I know um did a lot of this in case 10 most people went for e Yeah, perfect. So yeah, schizophrenia. Ok. Sounds very much like it, doesn't it? So the presence of both positive and negative symptoms is kind of really what gives it away here. So the um abolition. Ok. Um the which which is the lack of motivation um is and the social withdrawal, the kind of neglecting her personal hygiene. Those are both, you know, negative symptoms, right? It's something that I'll talk about that in a bit. So we've got negative symptoms there and also the positive which is the um paranoia and also the auditory hallucinations. OK? Er about the derogatory comments. Cool. So schizophrenia is, is an interesting disorder. Ok. So the central feature is psychosis. Now what is psychosis? It's essentially where the patient or person has some sort of loss of contact with reality. Ok. Now this can happen in many ways. OK. So hallucinations, er delusions. Ok. There's many different ways in which um a patient can experience this loss of contact. Now, at least one of these core symptoms needs to be present. Ok. Um So for example, delusions, um thought disorder. Now this is a really common one. So sometimes patient can feel that they feel like someone else's thoughts are being inserted into their head. Ok? Um Withdrawals. OK. Um And broadcasting. So their thoughts are being spoken out loud for everyone to hear. OK, which can be really, really disturbing for patients um to, to undergo, you know, to go through this experience and obviously hallucinations. So the most common one is auditory, but patients can also experience visual hallucinations and also tactile hallucinations. So maybe the feeling that, you know, insects are crawling around on, on their body or, you know, um particularly, you know, um they can have some nihilistic delusions thinking that, you know, their body is wasting away and also have hallucinations that then can actually reinforce that. Um So maybe smell, for example, er, olfactory hallucinations can also be sometimes very common. So the symptoms should be present for most of the time during a period of at least one month. Ok. Cool. So talking about the symptoms of schizophrenia. Ok. Again, talks about a lot about the positive versus negative symptoms. So positive symptoms are basically symptoms that people with schizophrenia get on top of what you should normally have. Ok. So it's like an additional bonus, not a bonus. Sorry, it's an additional extra feature um that they're experiencing that a normal person would not have. Therefore, it's like a plus you're adding on symptoms. Ok. Whereas negative symptoms are where you have a loss of something that a normal person would have. Hence, er, the minus. Ok. So negative, um you've got something that's been taken away from you, for example, you're five A S OK. Um quite easy to memorize using this. So, Anhedonia, Alogia, which is poverty of speech. So sometimes they can't um talk properly, OK? Because of all of these, you know, thought echo insertion withdrawal broadcast, sometimes it can be hard for them to organize their, their speech. So that's why you might get Alogia um avolition, which is the lack of motivation, which you talked about in the SBA and apathy as well. So loss of kind of um interest in something, OK? And also the last a is blunted affect. Ok. So lack of emotion. Um and then obviously, we talked about the positive symptoms. So, thought disorder and delusions. Um So, delusion is a fixed false belief that a patient will not let go of even though you might say, well, this is clearly not true because of this. They will still hold on to that belief. OK? Um And this is really, this is a really common psychotic feature, OK? And again, hallucinations which we've talked about. So I think um Maram touched on upon this really well. So positive symptoms occur because of hyper activation in your mesolimbic and your nigrostriatal pathways. OK. Whereas negative symptoms occur due to your, the hypo activation of your mesocortical, ok, dopamine pathways. And you know, this is why atypical antipsychotics. So your second gen antipsychotics are so good is because they can tackle both pathways and resolve both positive and negative symptoms er for schizophrenic patients. Ok. So moving on to um anxiety disorders. Ok. Um Let's have a go at this SBA. So a 24 year old woman with no significant past medical history was grocery shopping when she suddenly felt severe chest pain, shortness of breath, palpitations and her whole body trembling, she was extremely frightened and believed she was going to die. However, after about 10 minutes, her symptoms resolved, which of the phone did the woman most likely experience? Was it a asthma attack? Ba panic attack, c anxiety D adrenal crisis or e fight or flight response? Um Most people have gone for b brilliant. Yeah. So this is really classic of a panic attack. Um you know, uh so it's important that there's no significant past medical history is there, right? Because otherwise it's sounding, you know, very serious, isn't it? Chest pain, shortness of breath palpitations, I believe she's gonna die. Ok. Um You definitely want to be, you know, calling an ambulance at that point. But you know, the fact that she has no past a significant past medical history gives us an indication of, ok, and might not as likely be that, but also because it's the fact that she felt extremely frightened, believed she was going to die and after about 10 minutes, her symptoms resolved. So typically in a panic attack, the symptoms don't have a trigger unlike anxiety. Ok. So in an a in anxiety, you have, you know, these anxious thoughts and this worry and then that brings on the symptoms with um, a panic attack, your kind of sympathetic nervous system, um, kind of goes on overdrive and that's why you get these um, symptoms, ok, like palpitations, shortness of breath, um, muscle, muscle, kind of er, twitching and contractions and um, trembling. You can also get er, sweating as well. So all of this kind of points towards a panic attack. Ok. So some common anxi anxiety disorders are um you know, as follows. So, Gad, which is generalized anxiety disorder, O CD panic disorder and phobias. Ok. So if you go through them one by one, Gad is basically excessive or disproportionate anxiety. Ok? Um that negatively impacts everyday activity. Ok. So this is kind of when most people say, you know, um anxiety, you know, sometimes they fit under this er category of um disorders. So it has to be persistent, ok, occurring most days for at least six months. And quite importantly, you had, it shouldn't, it should not be caused by substance use or another condition. Ok. And again, the symptoms um include, you know, a range of biological to psychological symptoms such as uncontrollable worrying, restlessness, difficulty relaxing, palpitations, headaches, and sleep disturbance. Ok. Um The key thing is that it's excessive disproportional um and that it's negatively im impacting um someone's daily activity. Ok. If we move on to then O CD. So O CD is obsessive compulsive disorder. Ok. Now, it's, there's an interesting cycle in O CD. So you get this cycle of having an obsession, which is an unwanted or uncontrollable thought that just kind of pops up um such as um oh my goodness that if I leave the house, the house is going to burn down. OK. Now that's an uncontrollable thought that a patient might get, that's very, very difficult to ignore, right? Um And then suddenly that drives anxiety. OK? And they, they, they get this compulsion, OK? This compulsion that OK? Um I need to check off, I need to check that all the, you know, electrics and the plug sockets are er empty and I've turned off the stove and everything. OK? Um And they feel that these, this action must be done um to handle the obsession. OK? And this can be normal. OK? So you, you normally do these things like locking the door or whatever when you leave the house or making sure you know, um the the stove or whatever is is switched off. But with O CD patients, they will do this repetitively maybe 10 times, checking and checking and checking because what happens is the obsession comes arises, they get this anxiety if they don't do the compulsion, um their anxiety increases. So they do the compulsion, which is the action, this then provides temporary relief, however, which reinforces the compulsion by the way and then also the obsession reappears. So it's this cycle of obsession, anxiety, compulsion, relief, obsession, anxiety, compulsion Ok. Um, so hopefully that helps with understanding O CDA little bit more. Ok. And then panic disorder. Ok. So panic disorder is when someone experiences these recurrent unpredictable panic attacks. Ok. Um, and panic attacks, as we talked about very sudden symptoms go away, um, very quickly. Um, and also it's important to note that you can have panic attacks, um, without having a panic disorder. Ok. Now, for it to be panic disorder, it has to be, you know, recurrent, unpredictable and there should be at least a month, you know, persistent worry about having another attack. Ok. And now phobias, I feel like there's a very, very common one that, you know, we all have some sort of experience of so or, you know, knowledge about. So which is a phobia is a strong fear or dread of a thing or event. This is the key bit that's out of proportion to the reality. Ok. Um, so, you know, if a venomous snakes only appeared in front of me, of course, I'd be very, very scared but it's to the point where a phobia is when, you know that p that fear and that dread is out of proportion to the reality. Ok. Now, um, yeah, so with phobias, all these kind of anxieties and these un uh, these um, excessive, er, this excessive fear that, that can manifest as physical and psychological symptoms. Ok. Such as avoiding, um, any situation where, you know, something that the where the stimulus might remotely appear. Ok. Um And also physical symptoms such as you know, fainting, um palpitations. Ok. Cool. So move on. Ok. So mental state exam. Oh, sorry, talk about piglet as well. Cos I included um another character which is thought to have, you know, maybe er generalized anxiety disorder just threw that in is a little fun front image. Cool. So the mental state exam. Ok. Um this is, this is quite long and it's a very in depth examination or consultation that you can have with a patient that you think might be going through um you know, a mental health disorder. Ok. No, there's a lot of things. So I'll, I'll try and break it down for you. Ok. So you kind of go through this um process. OK? It's almost like a, an abdominal exam for um a patient coming in with a gastro problem. Ok? You have the, you know, a certain order in which you um go about the examination. Ok. So you start off with the basic appearance and behavior. Ok. So you might um look out for any scars, any evidence that you know, they're self harming themselves, any signs of drug use? Ok. IV. Drug use, things like that. Ok. Um Are there any signs of self neglect? Ok. Um How, how, how are they keeping themselves um are they, you know, are they dressing themselves appropriately? Um are clothes put on properly? Um And also you know other disease as well could that can give you, give you um a sign of what might be going on underneath. Another thing is weight. So weight can give you a good i idea of whether, you know, a patient might be overeating, undereating, et cetera. Ok. Um And also obviously, very importantly, facial expression, eye contact, body language and engagement. These can always give you a really good idea of whether a patient is whether what the effect is like. OK. Now, if we move on to speech, OK, um their, their speech could be um you know, something called pressured, which basically means that um you know, the they're stuttering or kind of um it's, they, they, they ha they it's, they have a tendency to speak rapidly. Um And sorry, yeah, the pressured speech means that they have a tendency to speak very rapidly. Um And it's motivated by an urgency that you can't sometimes understand, OK, if that makes sense, sorry. So pressured is very rapid, urgent speech. Whereas slowed speech is obviously, you know, the the the rate is very slow. OK. Sorry, I hope, I hope I clarified that. Um and then the quantity so minimal or excessive. So patient could be, you know, absolutely, you know, um you know, verbal diarrhea or they could be talking very, very little, very short sentences, long pauses, OK, which will indicate one thing or another. OK? Depending on what it is and also tone, OK? So monotonous, so often patients with depressive disorders will come in and talk in just one tone. Um And you know, that can sometimes give, you know, certain conditions away. Ok, then mood and effect, sorry. Um So yeah, this is quite, you know, self explanatory. Um what is their mood like? What is their effect like? Which is basically another way to say mood um kind of effect is how emotion shows on their, on, on the outside kind of thing. OK. Um If they, if they see you very euphoric, then um you know, you might be thinking about a manic episode, whereas if they're low mood, um you know, you might be thinking of depression. Ok. And then thoughts. So thoughts is really important. Um You know, you can, you can really get an idea of um where a patient is in their mental state by the thoughts they're having. So the speed of thoughts um can be really important as, as we kind of talked about and that will be speech and thought will be, will be tied in with each other quite a bit. OK. Um Flight of ideas as I mentioned before. Um It's kind of when ideas kind of run into one another. Um they might not finish one idea off before they start another kind of like jumping from train of thought to another. Um like if that makes sense and circumstantiality versus tangentiality. Ok. Now, these are just really um like complicated words, just to say circumstantiality is that when the thoughts that they are having seem to be very, very irrelevant and unnecessary, but eventually they come back to the, to the point of conversation. So it's like they will, they will start on a thought, deviate off, talk about loads of unnecessary irrelevant things and come back, tangentiality is basically where, um, they diverge from the main conversation but they don't really, um, come back all, all the, all the things that they're talking about is unrelated, abstract and kind of er irrelevant to the main conversation that you're having. Ok. Um Cool. So, yeah, and then obviously um thought um disorders are really common um especially in schizophrenia, psychotic disorders. OK. Um So yeah, phobias, delusion, obsessions, suicidal thoughts. These are all things that you have to kind of screen for and ask um to elicit what kind of mental health disorder um this patient is having, OK, if we move on to perceptions. OK. So um depersonalization and derealization. So this basically means depersonalization means that um the patient feels that they're no longer their true self. OK. So de personalization, they feel like they're not their true self anymore and they see themselves as you know, someone different or someone strange derealization is a sense that their reality around them is not so true anymore. OK? Um Illusion versus hallucination. OK. Now, this is quite important. So an illusion is where the patient will misinterpret an external stimulus such as like, you know, a shadow, let's say, um And kind of imagine that that's someone there to, you know, um a shadow is so someone there to kill them, for example. OK. Whereas, and hallucination is where their brain um basically produces a re a reality for them. OK. So they believe that that's, you know, that's actually happening and it's real. Um And there's no stimulus. OK? So illusion there is a stimulus which the patient misinterprets. Um Oh Sorry, I think I've accidentally copied over the same slide. Sorry. Um And cognition. OK. So cognition is basically where you have where you test the patient's orientation in time place and person. OK? Where you can test their memory. OK? Um And perhaps form, you know, a cognitive exam like am er like a mocker um an M se OK, mental state exam. Sorry. Um And um you know, your other, you got like a mini ace for example, OK. Um And then inside judgment risk. So this is quite important as well to um to understand um and ascertain whether the patient is actually aware of their condition. Um And then really importantly, their judgment are they able to make considered sensible decisions and you need to check whether they're a risk to themselves or others. And this is a really key part where you can make a decision as to, you know, whether we need to admit this patient to hospital or they're safe to be in society where they are right now. Ok. So it was a very long winded um explanation of the mental state exam. But again, it's very, it's a very useful exam in psychiatry. You can get a lot out of it. Um, again, like, like I said, it's like doing an ABDO exam for a patient coming in with um liver disease, for example. Right? Um It's just, there's a lot of things you need to think about and ascertain from the patient. So, last couple of things now, OK. Um Sleep physiology. So let's have a look at this in t in three different stages. OK. So when the brain is waking, what is happening? Ok? Or when the brain is, you know, awake. So you have neurons um in your upper pons area where acetylcholine is produced. Now, this acetylcholine is gonna go to your thalamus and activate your thalamus. OK? And the thalamus then channels signals to the cerebral cortex. Ok? And cerebral cortex is basically one of the main sites of consciousness, ok? Um And another thing is orexins. So, orexins are a peptide made by the hypothalamus that also reinforce arousal. And we'll have a, we'll have a look at some disorders where actually you do, you might have low erections or low amount of erections, which means that you don't have this, it's very easy for you to um kind of fall asleep because you're not having this reinforcement of arousal and wakefulness. Ok. So that's when it's awake. Now what happens when the brain tires? So the brain is constantly using ATP. OK? And when this ATP breaks down, you obviously form adenosine, OK? Because A AP is adenosine triphosphate. So when this adenosine is broken down, uh sorry, the when this ATP is broken down, adenosine builds up, OK? And this increase in adenosine in the brain triggers activity in an area called the V LPO. OK. The ventrolateral preoptic nucleus, OK. Now, we'll come on to that in, in the, in the, in the next kind of um in the third bit when the brain end asleep, but that's quite important. OK. So adenosine builds up and this triggers the V LPO to, you know, that increase the activity in the V LPO. Now, the SE N is really important. The S CN is kind of like your master clock, right? Stands for your suprachiasmatic nucleus. OK. Now, this is controlled by signals from your retina which you take in from the outside world. OK. Um And what happens is this kind of um fine tunes your circadian clock. OK. So, signals from your retina come in your SE N um kind of er regulates your circadian clock. And then um that is, that also influences the activity in your, in the V LPO. OK. Now, an important um uh sorry chemical here is melatonin, OK? It's an important hormone. So it's your sleep hormone. So when the se N um kind of promotes uh melatonin secretion. Melatonin will increase sleep pressure basically. Ok. Um And so when the brain enters sleep, what happens is the V LPO is getting activated by the adenosine and you know, melatonin and all this circadian control from the SE N and when the, when the V LPO V LPO neurons are activated, they will release um Gabaa and galanin. OK. Now, these two molecules will then bind to receptors in the hypothalamus um to inhibit your arousal system. OK? Thereby kind of um causing your brain to enter er your sleep stages. OK. Now, an interesting point about caffeine here, OK. Caffeine works the way it does is because it blocks your ad adenosine receptors, right? Um and so forth, you know, your identity levels are building up but you, it doesn't trigger the same activity in the V LPO because you're blocking the receptors for it if that makes sense. So you reduce your sleep pressure, thereby increasing your wakefulness. OK? Cool. So, oops going to say so we talk about the sleep stages very quickly. OK? Um You've got a nice mnemonic here, OK. That's drink blood. So, B for beta waves, OK? When you're awake with your eyes open, OK, alpha waves for when you're awake, but when your eyes are closed and you're nearing sleep, OK? You're, you're, you know, approaching rest. Um and then you have t which is for which stands for theta waves, OK? Now the waves are present in the brain, you know, when you're entering N one stage of sleep, which is light sleep. OK. Sorry, it's important to note that there are four stages of sleep. OK. Um Three of which are non rem, which is the N one, N two and three. And then you have rem sleep. OK. Um So theta waves are primarily seen in your first stage of non rem sleep. OK. Then we go into this interesting um phase of sleep, which is N two, right? And in this stage of sleep, you can see these certain features in an on an E eg which is an electroencephalogram. OK? Um called sleep spindles and K complexes. OK. Now, what these are are basically little bursts of neuronal activity that help you stay asleep despite um external stimuli. OK? And, and also it's thought that K complexes may help in retaining memory. Um and you know, keeping, you know, in that sleep stage, OK. Despite, you know, things going on in your environment. Now, the next wave um is your delta wave. So this is your, this is the stage of sleep where um you get your best quality sleep. Basically, what's the most restorative OK. N three, which is deep sleep um is the most restorative stage of sleep. OK. And you can see that this is where your brain waves are kind of the the most, the the most slow, right? It's the slowest um stage of sleep in terms of brain waves and brain activity. OK. And then we have rem sleep. So this is called paradoxical sleep. But a because actually when you look at the E eg waves, your rem sleep mimics the beta waves, right? And it, they are actually beta waves. And so it mimics when you're awake. Um and this makes sense because actually you dream when you're in rem sleep. Ok. So it's almost like you are awake while you're sleeping. Ok? And obviously, rem stands for rapid eye movement sleep. OK? Because they notice that your eye makes these jerky little movements. Ok. Um And it's really important that your whole body is paralyzed in this stage of sleep because otherwise, what happens is you tend to act out your dreams when you don't have sufficient paralysis of your, you know, of your body, which is normal during sleep, obviously, right? Cool. So quick question then OK. Um Testing your immediate recall here. So a 34 year old woman was referred to a sleep clinic by her GP after having trouble sleeping and suffering from nightmares for the past six months. So probably sonography, a sleep study is done to monitor her sleep stages and identify if any sleep patterns are disturbed. The patient is now at the stage where the E EG has picked up sleep spindles and K complexes in her brain waves. What stage of sleep is the patient in? How about 30 seconds to on this and then we'll move on to. I think that, which is the last slide. Are we getting any um majority answer? Mario? Uh Yeah. Uh So see. Brilliant. Yeah. N two. OK. Awesome. Yeah. So overall your brain activity slows but like I said, you get these powerful bursts of neuronal firing um which are your sleep spindles and then also your K complexes OK, which have certain functions um of maintaining sleep. And also some um you know, it's thought that they can be um involved in retaining memory. Cool. So very quickly, last slide guys, um well done for keeping, keeping with us today. Um So sleep disorders. Ok. Now let's go through each one, each one of them, one by one. Insomnia. Ok. So insomnia is difficulty falling asleep. Ok. But when does it actually clinically become insomnia? It's when you get a lack or a reduction in sleep quantity or quality three times a week for three months for more than three months. Ok. So just imagine that, you know that three and three, ok, three times a week, um or sorry, at least three times a week for more than three months. Ok. Um And the treatment for this is, you know, good sleep hygiene. Ok? And also, um you know, short term medication could be the Zopiclone, ok? Um Usually these medications will increase Gaba, ok? They increase Gaba. Um because remember we want um Gaba to act on the hypothalamus and the pons to then inhibit the ascending arousal system. Ok. Sleep apnea is a very, very common condition as well. So this is where your upper airway becomes completely or partially blocked while sleeping. Ok. So, breathing repeatedly starts and stops and the treatment for it is CPAP. OK? Because this makes sure that the upper airway patency is maintained. Um And often patients won't notice this themselves. What they'll come and tell you is that, you know, they're feeling really tired throughout the day. Um, you know, they, they feel really tired, they fall asleep during the day. And that's because they're not getting good quality of sleep during the night because they're not breathing properly. Ok. So often, you know, they'll do some ox oxygen sats monitoring while they're asleep and notice, you know, their oxygen sats are going down dropping to 80 during, you know, sometimes when they're sleeping. Um, and also a lot of the time, um the patient's partners will be telling them will be coming to the doctors with them saying, you know, you know, my partner's um, snoring repetitively and sometimes just stops breathing and then starts breathing again. Ok. So also com also very common with obesity, ok. Um In which case, it'll be called, you know, obstructive sleep apnea because there's something obstructing, you know, um kind of fat pads around your neck. Um, could, you know, put pressure on your airway while you're sleeping. Ok. Cool. So restless leg syndrome. So this is interesting because um Mary mentioned Akathisia. Um and you know, um yeah, Akathisia just earlier. So, restless leg syndrome is an idiopathic condition. Um that occurs mostly at night or during sleep. Whereas Akathisia, you have it, you know, um any times and actually restless leg syndrome is relieved with activity. Ok. Um And it's this constant urge to kind of move legs at rest. Ok? Um The treatment again is good sleep hygiene, dopamine agonists, um like the like how you would treat akathisia as well. And also codeine if the patient is in pain because this can be quite a painful um condition. Um and hypersomnia. Ok. So, hypersomnia is the opposite of insomnia almost. Ok? Um It's this, it's this condition where they need more sleep um than a normal person would. So, you know, it's feeling exhausted even after, you know, a good, you know, 8 to 10 hours of sleep. Um and it's feeling excessively sleeping during the day and treatment is, you know, usually good sleep hygiene or fixing some sort of sleep hygiene. Ok. Narcolepsy is the the one, the condition that I said mentioned earlier about um the lack of orexin. Ok. So you get irregular sleep wake cycles because it's peptide that's driving wake wakefulness might be a little bit deficient or um you know, you might be lacking in it. So the treatment to that is then stimulants such as medda modafinil, uh dexamphetamine or Potala. Ok. Um, and you know, patients often report that, you know, they just suddenly in, at inappropriate times they just suddenly just nod, um, you know, fall asleep and just, you know, um, nod off and then parasomnia. Ok. Parasomnia is basically abnormal or unusual behavior. Ok. So just night terrors, sleepwalking, er, sleep related eating disorder, nightmare disorder and sleep paralysis. Ok. Now, I would just, in terms of S two and PTI wouldn't really worry about knowing these conditions in a lot of detail, just have a broad understanding um of what they are. Ok? Um But mainly for case 10, I would focus on your neurophysiology, the drugs, OK? And brief, you know, understanding of especially depression and schizophrenia and have some II understanding of bipolar disease, um bipolar disorder, sorry and anxiety disorders as well. Ok. So, um I hope that was useful. Um Please do fill out the feedback form and then you can get access to the slides. Um And thank you for engaging with us. Um I know it's been a long one. But yeah, thank you very much guys. I hope that was useful. Um And Marriam I think, have you managed to put the um the feedback form in the, in the, the feedback forms in the chat? So if you guys could just fill it out and then slides would come your way. Perfect. Awesome. Thank you very much guys. Thanks for your attention. Thanks for joining us and I hope that helped. And if you guys have any questions, do you put them in the chat or? Yes? Ok. Well, if there aren't any more questions, um I think we'll end it there. Ok. Thank you, everyone. Have a good night. Um The feedback form is in the chat, so it should be available. But let me see if I can send it again. So hopefully you guys can, yeah, one feedback form for sessions it applies to both of us. We'll both drink his time. So, yeah. Um, in terms of recordings, Rose, do you know anything about recordings? I'm not quite sure. Um I'm not 100% sure either. Sometimes I know, um, you can sometimes maybe only the slide gets the slides get put up. Um So I'm not too sure, but just have a look when you get the feedback form and then, um, obviously if the recording isn't there and you'd like to access that then maybe just message um os easy, um, you know, via email or any of the socials as well and hopefully they might, they might be able to help you a bit more. Yeah, no worries at all. We'll give her two more minutes and, uh, marry him and then end of the, if there are no more questions.