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Okay. Here we go. Okay. All right. Hi, everyone. Welcome to the case. 10 SBA SBA day series. Um, in case you didn't already know who I am, I'm, um And I'm the current method presidente. Um, this session is happening in collaboration with medics Revision Society. Who are specialists in, um, teaching high yield and concise topics. Give them a quick follow for, like, PT and clinical cont sent. Um, that includes the famous topic in 30 minutes. Um, that gives you the high yield stuff in 30 minutes so you can go enjoy the rest of your evening. Rather being stuck in long revision sessions. I'd also like to say that we're joined by Cardiff Uni Psychiatry Society. Um, we're planning many revision sessions around psychiatry. So if you do like this session, do you get them a follow as well? Okay. Um Nope. This is the wrong slides. Give me a second. This is very good, Ms. Sections, as finally is Chris. It's the introduction slide product. All right, we're back on track. Whatever. And this is how not to start a session in a sec. Okay, right. There we go. So this is case nsb a series. As I mentioned, just a quick shout out to our sponsors at the MD you for making this episode possible. Um, and it wouldn't be possible without, So, um, they they do offer medical protection throughout your medical career. So do check them out as well. Um, for this kind of stuff. And don't forget to follow our socials. Um, we do post questions on a weekly basis, and that helps you with quick fire questions, even when you're scrolling through instagram and finally become a member today. You know, uh, during our community of like minded individuals, we can keep up to date on events like this via a mailing list. Um, you do even get access to our SBS earlier than other people. Um, and our committee are more than happy to answer any questions that you might have about the course or medical life in general. Okay. And just a few housekeeping rules. So, due respect your tutors and your peers, um, ask questions and do be curious. Um, active engagement. So do you get engaged with the polls and everything? Um, please do keep your mix and cameras on mute. Um, and do you feel enough your back forms. That really helps us out. Um, to improve our sessions for the future. Don't forget to follow our instagram and you share events with your friends. You know, get that together and join the session. Cool. And just a final note. So this topic is on psychiatry and will roughly be about two hours long. Um, it's going to contain some sensitive information that some of you might find upsetting. And we do apologize for that in advance. Um, if we do so, But we are conducting this session for educational purposes, and we do hope that this knowledge can help others in the future. Now, if you do feel like you might be relating to some of these cases and you are worried about it, please do consult a medical expert as we are just students, um, teaching about these conditions. So we are unable to provide any expert clinical advice. Um, however, that's enough of me talking, so I'll hand over to Chris now, who will take the session away. So, uh, do I share the screen or Yeah, if you share screens. Yeah. If you share screen and I'll yeah, can everyone see this side. Yeah, uh, So I'm gonna be teaching about the New York physi physiology part of the, um, case 10. And this is the first learning outcome. Yeah. So, um, you are a second year medical student in the neurology ward, and you see a patient with multiple sclerosis, which results in stiffness and weakness. You learn that this occurs due to damage of wonder component, which is necessary for faster transmission. You're on. What is that component? Does anyone wanna answer? Yeah. Uh, so the there's still more hands is coming up. Okay, I will show you the answers now, uh, so the correct answer is Yeah, the which is what everyone answered. Uh, that's great. Um, so we will move on to the next question. Just, uh, you're in the middle of s one exam, and you come across a question about neuro transmitter determination. What is the, uh, mechanism of neuro transmitter determination which allows for neuro transmitter to be recycled without any additional process? So, um, half of you answered a and another half answered. Be, um the correct answer is A. And that's because, um, the question asked for, uh, the neuro how the neurotransmitter can be, uh, like, directly recycled into the, uh, and then released via synaptic physical. And that's only via the transport, er, because if if it's b, then it has it will be broken broken down and then have to be reconstituted back into the original neuro transmitter to be released. So, yeah. Uh, the, uh, third question is you're currently revising content in the first year. Uh, you remember that there is three channels involved in deep polarization and report realization. What is the state of channels and re politization? Uh, there seems to be a mix of different answers, but the correct answer is e Oh, sorry. Yeah, the correct answer is e uh, that's because, uh, the sodium potassium pump, uh, is closed during RuPaul ization and, uh, two. During RuPaul ization, there'll be influx of potassium ions, but there's no movement of, uh, sodium. Mine's So the, uh, sodium channel channel is closed. But the, uh, potassium island channels open. Uh, neurology ward one of the patient ask you about memory and learning. You look back to see how the connection between the synapses are strengthened. What results from that from that process in the synapse. I think this might be a bit more tricky question, but okay, the correct answer is B, which is what majority of you guys answered. Um, yeah, and we will get onto why? That's the case. Uh, so we're just gonna, uh, best question is your second year medical student learning about different hyper hypothesis regarding schizophrenia, You learn that there is a relationship between the symptoms and your transmittal receptors. What is the receptor responsible for negative and cognitive symptoms of schizophrenia? Uh, so the correct answer is B, which is the one receptor, Um, uh, so the two receptors involved in positive symptoms of schizophrenia D one receptor is involved with, um uh involved with, uh, negative, including the symptoms. Gover receptors are, um, also involved, but it's not a symptom specific. Um, yeah, so they're now we're gonna quickly review the year €1 size. So this is a structure in neuron, And you have then rights, uh, axons and, um synaptic, um, axon terminals and synaptic terminals in between. And you have depolarizations going all the way from then rights and then passing through the Axion Axon, which is myelinate, which will be covered by myelin sheath and reaching the axon terminals. Uh, so this is sodium, potassium pump. It pumps. Um, so you put test him out of the cell and to protest him into the cell, and it allows for maintain resting membrane potential. Uh, so this is the state of channels during depressurization, uh, sodium. Potassium pump is closed, but sodium, uh, sodium channels open, but potassium my own channel is closed, and then vice versa. For repeal ization. I also, uh, first thought that the sodium potassium pump would be, um, open. But during reposition depressurization, the sodium potassium pump is closed. So there is a different rea uptick channel. Uh, there's, um, different methods of neurotransmitter determination, Which your curse, Uh, you know how neurotransmitter gets released from the synaptic vehicle. And after that, they have either three options. They can be, uh, re uptake by a transporter on this, uh, pre synaptic membrane. Or they can be, uh, degradated by enzymes. And third option is that they can, uh, defuse out of the synaptic cleft and then later will be broken down by enzymes outside of the synaptic cleft, um, sites that Oh, uh, So there is various enzymes and re uptake channels. That would be that's important to know, and we will come onto them later. But the main ones are showing the screen. Uh, we need to know about certain and transporters deployment transporters or under and transporters and enzymes including, you know, I mean oxides. Uh, COMT, which is Cata Kal, or missile transfers and P m m t. I don't know how to pronounce that. And a seat I'll causing esterase is why do you guys think, uh, do you guys know why? Uh, closing X rays is quite important to know. The reason is that, uh, acetylcholinesterase, um, inhibitors are used in Alzheimer's disease, Uh, and slowing down the progression of Alzheimer's disease as well as, uh, it's useful. Uh, something, uh, I can't remember now, but it's useful. Um, two most certain conditions. So yeah. So? Well, come on. Too long term potentiating and depression, which is related to that question that was talking about memory and learning. Uh, and long term potentiation is, um how is how, uh, synapses of strengthen. So, basically, when there is sufficient, uh, glutamate binding to the emperor receptors, uh, there is influx of, uh, ions, which allows for put, uh, postsynaptic, uh, neuron too deep or allies. Uh, and this movie removes the, uh, mg uh, museum iron blockage, which is found the NMDA receptor. And then which allows for the costume, uh, to influx through the NMDA receptor. And this triggers a, uh, allow for more receptive to be inserted into the pre synaptic membrane and allows allows the channels receptors to be more sensitive to glutamate. Uh, there is long term depression as well, which is kind of the opposite of long term, potentially a shin when there's insufficient glutamate binding. Basically, the magnesium iron is not removed, but some of the the NMDA receptors allow for small influx of customize. Uh, but But if the, um, signals insufficient amper receptors removed instead of inserted, and this causes the link between the synapse to become weaker and they become less likely to be activated and basically long term, potentially a shin is how we can consolidate our memories and how, um, how we can learn something. Um, so we would So we will come out to your neurophysiology depression. Um, so there is Do does that, uh, I think everyone knows what There's Mona Amy Theory and depression. Basically, which suggests that serotonin deficiency dopamine deficiency in order deficiency is linked with depression and certain in deficiencies particularly linked with depressed mood and feeling or guilt. And dopamine deficiency is linked with anhedonia, which is lack of interest. Uh, neurophysiology in schizophrenia. Basically, there is dopamine theory, and, uh, increased the to receptive trying neuro transmission. And the subcortical region, uh, is what's contributing to the positive symptoms, and positive symptoms are includes something like delusions, hallucinations. Do you want receptor in your transmission in the prefrontal cortex are attributed to negative and cognitive symptoms of schizophrenia. Uh, and you can see the what the positive symptoms and negative symptoms are. Uh, I think it will be covered later in the and, uh, and the other learning outcome as well. But this is just a heads up. Okay, Next. Uh, so this is the second learning outcome. Um, relating the neuro anatomy of C. N s to its function and how that relates to change in mood. So you are a second year medical student learning about various dopaminergic pathway and how it relates to schizophrenia. Which pathway can cause the positive symptoms when their activities increased. Um, I can't see the pole. Oh, thank you. So the answer is there more people answering the question, um, doesn't seem like it, so I'll go into the answer. Uh, so the answer is Ms Olympic, uh, pathway, Yeah, which is what majority of you guys answered, answered. And I'll just, um we'll get onto what the pathways each of the pathways do. Sorry. Later on, uh, the next question is, uh, one of the, uh, one of the lectures just talked about the dopaminergic pathway. And you know that there's two pathway music cortical and muse Olympic, which starts, uh, from a group of neurons in the brain. What is the area of the brain, uh, referred to as so Yeah, The correct answer is ventral tech mental area just D. And, um, this is where the music cortical and media limit pathway connects from. And, yeah, and, uh, the next question is, uh, 62 year old female patient presents to the g p, complaining that she has multi discharge from her nipples. She has already had her menopause, but she has been diagnosed with hypertension, diabetes, schizophrenia, gold and has been taking ramipril metformin glipizide um, Tele Parodontal and omeprazole. What, uh, drug has caused her to experience, uh, discharge from her nipple. So the correct answer is higher haloperidol, which is, um, antipsychotic, Typical antipsychotic. And it causes, um, virus, things like gynecomastia, uh, oligomenorrhea. And And it was called Galactorrhea. And yeah, So this is the door Open surgical pathway. And as you can see, there is a music cortical pathway and muse, Olympic pathway. And that's the tibia infundibular pathway and nigrostriatal pathway. I'll cover, uh, So there's meta cortical pathway, which connects from the from the venture tech mentor area all the way to the cerebral cortex. And it's, um, decreased activity is associated with it's negative symptoms, which is, like, uh, nerve via, uh, lack of empathy. Lack of spontaneity and pathway show in red, uh, mesolimbic pathway, which connects the ventral tech mental area to the nucleus accumbens. Uh, and, uh, increased activity in that, uh, in that pathway is associated with the positive symptoms, which is delusions, hallucinations. And that's the that was the what the previous question was asking about. And, uh, past Asian yellow is nigrostriatal pathway, which connects the substantia nigra to stratum and which decreased activity is, um, associated with the extra Pimental symptoms. So, like basically generally affects your movement and causes tremors and twitches When when there's decreased activity, um, past Asia in green is to burrow infundibular pathway, which connects the opportunity gun to the hypothalamus. And, uh, and antipsychotics, which decreases the activity of this pathway, uh, causes prolactin secretion, which causes, uh, the symptoms I just mentioned before. And yeah, next, you see a 20 year old pensioner which, who comes into the emergency unit after being hit by a hammer by a group of gangs, he loses a consciousness, but then regained consciousness and then walked into the emergency unit where he's being seen. He seems to have had five bags of press and 20 cookies while he was waiting to be seen. And while taking history, he made he makes an appropriate comment, uh, inappropriate sexual comments. What is the most likely, um, area that has been damaged and to make it actually a bit more easier. Um, he's also bleeding from, uh, from the form of his skull pop. So yeah, the correct answer is prefrontal cortex. Uh, yeah. Uh, your, uh sorry I probably should explain the question. Sorry. Uh, so there is, um, amygdala. When it's damaged as well, it also causes similar symptoms. But, uh, why it's not? The answer is because, uh, it's less likely to be damaged physically. And, uh, it's, um, you see these symptoms for medulla and when there's bilateral region caused by a, uh, Coover Busie syndrome, which is typically seen in, uh, HSV one encephalitis and prefrontal cortex. Um, when it's damaged, you get these inappropriate, uh, impulsive, uh things. And you get personality changes as well, which fits in with the oval presentation of this patient with, uh And that's why that's the answer. And all the other ones, um, have such as hypothalamus and memory bodies. Would you get a memory damage instead of these, um, inappropriate, Um, or in, uh, like people, the patient making inappropriate sexual comments. You couldn't see that. So that's why B and C is not the answer next. So you are a first year medical student, and you're learning about the pain perception. You read that the pain perception changes with the emotional state of the person. What is the area of the brain which is involved in the modulation of pain. So the correct answer is deep Paradox. Aqueductal Gray, um, one of the person answered lateral portion of the ventral, um, posterior nucleus. That's where all the information, the pain touch, Um, and, uh, pressure all goes into there. But it's not actually, uh, where it's modulated. So D is a better answer than a So that's why. Okay, next question. Hippocampus is one in the area with of the brain, which is involved in the consolidation of information for short term and long term memory. But within the structure, there is another structure where the neurogenesis is affected during depression. What is the structure referred to as? I think this is a bit hard. I would not be I wouldn't be able to answer this question. So So the answer is denta Jarosz and, um, well done to people who got it right. Um, so denta jars and hippocampus proper is what's contained within the hippocampus, so all the other answers will not be right. And you get the choice between hippocampus proper and dentate gyrus. But, uh, the neurogenesis is actually affected during depression during, uh, dental jars, not in the hippocampus proper and patient was patient with depression often, um, have damaged. And then, uh, sorry often have, uh, decreased neurogenesis and dental jars. Uh, next. So now let's quickly review a year one and ask me your anatomy. And as you got as you guys all know, prefrontal cortex is involved in the planning execution. Uh, pre multi cortex is involved in, you know, modulating movement. Hippocampus, which is found in the median temporal lobe, is, uh, what's where the There's a consolidation of short term long term memory as well as, uh, storage of special memory memorably bodies, which is involved in the storage of episodic memory basal ganglia, which is involved in an initiation initiation of voluntary movements and adjusting posture amygdala, which regulates emotion. Uh, such as fear and aggression. Yeah. So let's go on to the last learning outcome. Dalby cover, which is, uh, describing the neurotransmitters, uh, system physiology and how this might be influenced by psychotropic medication and the drug abuse next slide. Uh, amino acids are converted into neurotransmitters, which, uh which amino acid is certain and drived derived from. So the correct answer is B tryptophan tryptophan, um, turns into serotonin and uh, explaining the other answers fee. Now, Alunan is, um, converted into duberman, uh, into Sorry, Uh, his city, Uh, his city is converted to test a me glutamine glutamine is converted to Gaza. Arginine is converted to urea and nitric oxide. Um, uh, address the oxide and yeah, we're researching about the different recreational. Uh, let's skip that one. Um, you're writing about, uh, your case. 10. It's for the next CBL session. Uh, you hear that? You should not eat cheese and m o a m a o inhibitors together, which best describes the reason behind why you cannot take both Harriman and M A O inhibitors. So the correct answer is B. Oh, yeah. So the correct answer is B uh, Manoa inhibitors inhibit monoamine oxidase, which breaks down tire men and basically basically, um, which result in a retirement accumulating and displacing other neuro transmitters and the synaptic cleft. And they bind onto the receptors, causing a what's called a hypertensive crisis so you can never eat uh, tire mint rich food along with mayo inhibitors. Tyrant rich food includes, like chocolate wine, cured meat, cheese and stuff like that, uh, 52 year old female comes into the g p uh, complaining that her depressive symptoms have not improved and she's continuing to have really low mood. She has been taking sertraline in over six months. She wants a different medication and gets prescribed Venna flaxen. What is the mechanism of Axion for this new medication that she's been prescribed? So the correct answer is see which which is what everyone got. Uh, basically, Venna flaxen is a certain in order, uh, reuptake inhibitors. So it inhibits both certain in order and re uptake. And next so but not working, um, to just to summarize, uh, tryptophan is converted into serotonin, and it's broken down by M a monoamine oxidase and 25 h i A. And then female island in uh is converted into tyrosine and which is converted into el dopa, which is converted to dopamine and dopamine Can be, uh, converted by converting to homo homo. You've been Ellick acid by M A o and uh, C o m t, which is the enzyme that we I mentioned previously. Or it can be converted to know adrenaline and then can be then convert to Admiral in, um, good, mean can be converted the good mate, which can be converted in the GABA. Sure, I think the presentation. Uh, sorry. This one was meant to come up before before, but I think the presentation is it, Uh, can I stop worry about that? Next? Um, so what is the logic behind antidepressant? Um, if you can remember back to mono aiming theory of depression, uh, decreased, Mona, I mean, which is like serotonin, dopamine, or Axiron is associated with low mood. So they thought if you increase the mono, I mean, you can also increase the person's mood. And so the way they, um, do that is using re uptake inhibitors, which prevents the re uptake of, you know, transmitters. And the examples are S S r I N r I s and SNRI. Yes. Um, as you guys all know, SSRI contains the tile plan sertraline for oxygen, which are notable medication, which prevents re uptake of serotonin NRS, which is less used. But the example's ARV, oxytocin and SNRI includes, um, Ben Affleck's and your oxytocin, uh, which prevents the re uptake of both your adrenaline and serotonin. Um, tricyclics are, um, for example, I'm a trip thrilling are nonspecific reuptake inhibitors, and they just prevent the re uptake of, um, certain, uh, territory Narada run and other Monet means as well as history. And, uh, this is you only typically used for a patient with severe depression because of how bad the side effects usually are. Um, and the last medication is one of the I mean, um, oxidate inhibitors. Which increases I So Kobach, uh, boxes did. And this basically inhibits the Mona. I mean, oxidate it's from converting, um, certain into five h i A a which allows for, uh, increasing amount of, um, uh, serotonin and, uh, dopamine, which allows for increased mood. Uh, so what is the logic behind antipsychotics? Um, if you can, guys can remember back to the deployment theory for schizophrenia. Increased duberman is associated with increased psychotic symptoms. So they thought that if you decrease the duberman, you decrease the psychotic symptoms. Um, So there's 22 types of two categories of antipsychotics. One, which is the first generation, uh, which is called the typical antipsychotics, which includes something like Howard parallel. And these are D two receptor antagonists, and they're usually not as used as a typical, and they're useful things like, uh, the Ribhi, um, and their second generation, which is also called the atypical antipsychotics, which are more useful. Um uh, schizophrenia. And they they include clozapine, olanzapine, risperidone on. And they are both a serotonin antagonist and, uh, dopamine receptor antagonist. Uh, they are used for a que psychology assists and psychotic symptoms caused by Parkinson's medication like al dopa and, um there also used in schizophrenia as well. Close the pains are really good for treatment resistant psychotic disorders. And, uh, they're usually prescribed for patient with persistent, persistent, suicidal, uh, suicidality next. So this is a lengthy one about, uh, 28 year old female patient presents the emergency in it in the midnight with her friends, she appears to be agitated, and she is sweating profusely. One examination. She appears to have flushed skin and daily people's and her reflexes. Her brisk from history is revealed that she had a seizure just one hours ago and she has been having diarrhea for several hours. Observations revealed that temperature. She has a temperature of 38.3 degrees, her rate of 110 degree 100 bpm. Respiratory rate of 24 breaths a minute. BP of 145 over 95 a G and oxygen saturation. 97%. Um, her friend tells that she has taken m d m a r earlier in the evening. Her friend also tells that she's also know where, uh, also aware that the patient has been recently diagnosed with depression and it's been taking, uh, new medication recently, what is the most likely diagnosis? So the correct answer for this is B, which is what everyone answered. And I would what most of most of people answered. And why is it not in your, uh, a, uh, neuroleptic malignant syndrome happens when you take antipsychotic. So is not, uh, um, option. Serotonin syndrome is the correct one. Because this patient took ecstasy and probably been taking, um, SSRI s or SNRI. Yes. So which would cause increase serotonin and that causes serotonin syndrome. Lithium toxicity would also be another differential because she has a seizure and hyperreflexia. Uh, but But because of the fact that she's been taking MDMA and she's being prescribed, it's more likely that she had serotonin syndrome. Next, uh, so going through the side effects of antidepressant, uh, she SSRI called the GI Distress, uh, situation, uh, of inappropriate ADH release SIADH And sexually, uh, dysfunction, Uh, like erectile erectile dysfunction, low libido anorgasmia. And for particular things settle plum is, um, involved in prolonging QT intervals for Eckstine is see wai be 450 inhibit inhibitors. SNRI s are on top of this. They also increase BP and increased sweating MAOI eyes. Um, as explained for, um when you take, uh, paramount rich food with, uh, using the medication or if you have less than two week washout period from when you're switching from M A o I to another depressant, uh, antidepressant or from antidepressant, too. MAOI you get risk of hyper and hypertensive crisis, which is when you have high BP. Um, Price, I clicks, uh, they have a lot of effects in the sense that they can call sedation. Uh, anticholinergic effects like tachycardia, urinary retention and dry mouth. Uh, they also have, uh, alpha genetic, uh, blocking effect. And they called postural hypertension. And they can also cause cardiotoxicity the coma and arrhythmias all, uh, so the side effects of anti psychotics, uh, typically the 1st, 1st generation, the typical antipsychotics have much worse, uh, side effects compared to the second generation atypical antipsychotics, The first generation presents with extra Pimental symptoms such as acute dystonia, which is what you see on the patient moving their head and you see anesthesia, which is when you have, like, movement in your leg parkinsonism. Um and, uh, after a long time, you can develop tardive dyskinesia, which is when you like, move your mouth when you hit your lips. Uh, when you move your arm and almond face and, like, uncontrollably uncontrollably, uh, it can also cause hyper poking You anemia was just, you know, galactorrhea ligament area. Gynecomastia is because it blocks the 22 receptor, which, um, which calls, uh, the receptor in Toubro and fund the biller pathway, which causes, uh, increased prolactin and then therefore you get these symptoms. It also prolongs to the interval. Uh, second generation atypical like cause, uh, clozapine and olanzapine, uh, have less few, uh, less symptoms. And they also have less hyperprolactinemia. Um uh. Let's also cover psychiatric emergencies, which includes serotonin syndrome. And these certain in syndromes are caused by, um, any drugs that increases S s, um, serotonin, such as SSRI, SNRI S T C A s MAOI s and tramadol, which is like a pain killer, and ondansetron, which is antiemetics and they can also called, um it can also be increased by triptans, which is used for migraines and headaches. Um, the symptoms include hyperreflexia Curtis, Hypertonia, Hypotonia and Tremor. Um, uh, they can also cause economic dysfunction, like hypothermia, excessive sweating, and they can also cause altered mental status. And this occurs within around the day. And it's usually managed by, uh, stopping all the certain drugs and giving some something called cyproheptadine, which is a certain antagonist. Uh, and you also get, um, you can also have neuroleptic malignant syndrome as well. This is usually caused by taking anti psychotics. Uh, it's usually occurs with tip taking power paradigm, which is a typical antipsychotics. Uh, and the symptoms include fever, muscle rigidity, akinesia hammer opted mental status. Uh, Sergeant and Syndrome and neuroleptic malignant syndrome have very similar, uh, symptoms, but they don't typically have autonomic dysfunction like hypothermic uh, excessive sweating in neuroleptic malignant syndrome and neuroleptic malignant syndrome. You also see creatinine kidneys being increased. Uh, and also it occurs around it takes around a few days. Two weeks. So it's a much longer time period, Um, for it to occur. Uh, it's managed by stopping all the, uh, antipsychotic drug and giving supportive care. Uh, giving, uh, Dantrolene and Roma clipped a t Clifton, which is a deeply antagonist hypertensive. Um, there's also a hypertensive crisis as well, which was explained before. So I'm not gonna explain again for you guys with detailed, um, it's also managed with Pantelimon. Um, there's also a tricyclic overdose, which is which occurs by taking excessive tricyclics like I'm triptolin and it closes respiratory depression hyperreflexia and prolonged QT interval. And it can sometimes put a patient into coma state. It's quite dangerous. Um, it's usually managed by looking at the e c g to see if the QT intervals, uh, prolonged and um, uh, sodium, uh, sodium carbonate, uh, is, um, provided to counteract the metabolic acidosis. And you can also give activated charcoal if you took it around 2 to 4 hours of consumption. Uh, T T c A. So last question, uh, 19 year old male comes into the emergency department after having fallen from the stairs while trying to take history. He gives nonsensical answers on top of, uh, and he seems to be frightened by the doctors examining him and tries to punch them whenever he's being examined. After taking collateral history, they're both in a house party. Uh, just few hours ago and his friends decided to take him to the E D. After he fell from the stairs thinking that he can fly, his friends mentioned that he had too much drink from his medical record. It is clear that he has been diagnosed with, um uh, he has not been diagnosed with any medical condition. And he has no, uh, significant family history of any medical conditions was the most likely cause of the patient's behavior. So the answer is, B uh, some of you guys answer, See, which would also present with similar symptoms. Uh, but the reason I it's not C is because, um, the patient was in the house body and they she, uh he has no, uh, other medical conditions. And he's not been, um, he has no family history of the psychiatric conditions. So more likely it was be compared to see, um uh, alcohol withdrawal. You also get the really, um, and you also get delusions and hallucinations. But because the patient we were drinking and didn't stop drinking alcohol withdrawal is less likely. Um, and schizophrenia is also not likely because it's very much tied to, uh, family history. So So I'm just gonna quickly go over the substance abuse. Um, uh, things like cocaine, amphetamine, MDMA a are all monoamine reuptake inhibitors. And they also release storing mono a means and MDM a, uh uh, inhibits, um, serotonin reuptake transporter. More potently, um, nicotine, um, access agonist for nicotinic acetylcholine receptors, um, which and also can increase the mesolimbic dopamine level, which is which is what contributes to the addictive quality of nicotine cannabis. Uh, T T C h ax fear. Uh, C b one and C V two receptor in the brain, which can indirectly increases dippers release. Um, yeah. This is the end of my, uh, k stand and all right, perfect. Thank you. We'll hand over to, uh, head. Now, we will focus through some psychotic disorders. Um, and this is probably quite important for your case. 10 exams. So, um, you stay tuned for this one? Yeah. Thank you, Chris, for that one, right. Hi, guys. I'm ho hen. Yeah. Three. Doing L4 and five. Can you see my screen? Yep. Nice. Is the pole in the way of the foundation? No, it's fine. No worries. Okay, right. So the so the first L0 L4 is, um, prevail INS and clinical presentation of common psychiatric conditions. Mhm socks. So 25 year old male rugby player presents a GP clinic with fatigue and insomnia. On further questioning, he reports that he has been down as he lost motivation to continue with his career. Although he has not had suicidal thoughts, he has not talked to his teammates in a while. Was the best option for the management of this patient. You start the pool, please. All right, that's it. Close to pull note. Mm. Let's jump to slide. So, um, the indications would show God itself help for this patient, and most of you have picked be. And this is because he does not qualify for severe major depressive episode, which I will, um, explaining an X slide. So depressive episode is defined by I c. D 10. And you find that that's the case for the size. Keep jumping to remember uh, depressive episode is defined by the I c D 10 with the presence of history or, um, period of depressed, depressed mood or diminished interest in activities occurring most of the day nearly every day for at least two weeks. And the time span is important because that's how you qualify. And it's a company about other symptoms, which I'll explain in the next few slides as well and prevail ins. You can look at that later. Um, it's not so important for your exams, but it's good to have a look that's defined by sex, age and gender and race, race and next slide. So this is a depressive depression Episodes, um, classifications and the relevant treatments will be in the next slide. Um, so this is again defined by CD 10. A mild depressive episode is at least one of the one of the core symptoms. Depressed mood, loss of interest. And another name you might hear is anhedonia, which is, um, depressed. Mood lost of the ability to feel joy and abolition. I believe it's loss of interest or motivation, and that's mild. You also have the pick. You have to get at least two of the secondary symptoms two or three and a moderate depressive episode. You have to have two of the core symptoms and four of the secondary symptoms. Severe depressed episode is special. You have to include suicidal thoughts and somatic symptoms, and these are the dramatic symptoms and also this recurrent depressive disorder, which is the what people normally refer to as depression as long standing depression, where you have two or more episodes of this without a history of Manya, which we will talk about later and in terms of, um, classification we talked about. And this is the again, the nice, nice government guideline for what kind of treatment you would initiate for patient's based on the severity. And you kind of go down a wheel if you're in primary care. But if you're in secondary care specialist psychiatry wards, that might be different. I've included a link in the presentation and just to quickly explain what each of these are because I'll be talking about these later on so I'll do the explanation. First, guided self help is focused on how thoughts and beliefs, um, interact and teachers coping skills with to deal with things in life differently. is goal orientated suits. People who don't like talking about the Depression in the group, uh, is mainly indicated in mild depressive episodes, not when it's not severe enough to, um, not severe enough for you to give antidepressants because those come with lost of side effects. And then there's group cognitive therapy, which is delivered by at least two part practitioners, which you don't need to know. Actually, I just wondered about that is usually eight people is mainly helpful people who need to recognize negative thoughts or unhelpful, unhelpful patterns they wish to change and especially people who need peer support. And in this group, behavior activation, Um, which is more useful people who has, um, social withdrawal. So they stopped talking to people, and they've stopped going to work, stop interacting. And that's also the same as, um, roughly the same as Group Act cognitive therapy. But the activity is a little different when you're in. The group is also a group of eight. And then there's interpersonal psychotherapy, which is more useful with people that has depression associated with interpersonal difficulties such as relationships, lost loss or changing interpersonal rolls. Something like postpartum depression, Um, for example, and then the psychodynamic therapy for people that have emotional development difficulties in relationship and that has contributed to their depression and the therapy focus on painful experiences, especially in families, are mostly in families, and it can be initially distressing. And you do need to do need to remember that in practice the last two, uh, interpersonal psychotherapy and psychodynamic therapy it's going to be quite difficult to get your patient these therapies because, for example, in Wells is 11 psychiatrist to 12,000 patient's. So yeah, that's just in practice. Next question 70 year old woman presents at E. D with low B m I hypertension bradycardia. Her bio chemistry results include low white cell counts, hypokalemia low sex hormone levels and raised growth hormone and cortisol. What is the best initial management for this patient? This might be a bit difficult, all right. Only two of you have answered. He's got three more answers in, and then we'll close to the pool. Yeah, we've got a bit more now, so most of you answered D. Unfortunately, that's not the right answer. Um, the correct answer is E. T. G. And I'll go into that later Actually, I'll go through option where each of them mean actually first. So level thyroxin is for primary hypothyroidism, which is the long term treatment for people with hypothyroidism, Um, which is not applicable here, Um, and then IV 520% glucose plus insulin. That's, um, treatment for hypoglycemia, type one diabetes and the next one, the saline, um, is Option D is the maintenance dose of maintenance dose of, um saline, which people normally use when they're on the ward and they can't And the patient's aren't really taking in fluid properly. And fluoxetine is the recommended antipsychotic SSR for depression. That's, um, and it's particularly effective in young adults. So what this patient has now what she's presented with is, um, anorexia. A severe exacerbation of, um, acute exacerbation of anorexia nervosa is characterized by deliberate weight loss induced and sustained by the patient and epidemiology. Wise is more common in young woman and less common in young men, but does occur, and then it sort of pre predisposing factors. You can have a read go through all of these, uh, presentations, investigations and management, so patient will present with extreme weight loss. Then the parents uh, abnormal blood counts, fatigue, insomnia and absence of menstruation in women. You won't get that in men. Um, and then also constipation and diagnostic criteria. I've included the D S M five criteria this time because I thought that would be more useful. Uh, you can kind of swap between r c D and D. S M that kind of up to the same standards. But sometimes the wording is just a bit different. So in terms of in in investigations, um, the main thing is, um, looking at the energy intake relative to requirements whether that leads to a significantly low body weight in the context in the context of their age, development trajectory and physical health as well as sex and another. Another criteria is intense fear of gaining weight or becoming fat, even though they're underweight disturbance in a disturbance in a way in which one's bodies, weight or shape is experienced. Um, this is the undue influence of weight or shape on self evaluation. Um, or sometimes they can be in denial of the seriousness of the, um, low, unhealthy, low body weight and sometimes, um, patient's don't meet the criteria of DS ds m five. But that doesn't mean they're fine. That means they might have other severe eating disorders, which we won't go into now. Um, there's also you need to bear in mind this atypical anorexia individual who meets the criteria for anorexia but aren't but are not underweight. But research studies that the clinical presentations and morbidity as well as treatment is basically the same for the two. So think of it as anorexia and in in terms of management. First one, you start with the cycle education, and you want to monitor their weight, mental and physical health. That's most mostly done through primary care, and you want to help them reach a healthy body weight level through the nutritionist input. And in terms of definitive treatment, there is mantra. That's one of the examples, which is a CBD program designed specifically for anorexia has 20 sessions with with mental health practitioner. Um yeah, that's really all you need to know. Um, and then there's individual eating disorder focused cognitive behavioral therapy, which is, I explained earlier, it's just focused on eating and in this family therapy for young people, which is, um um, which is the most likely treatment uh, doctor will prescribe younger patient's. And then if I go back to the options in the side, this is a bit of a trick question, to be honest, um, we you do e c g because patient who presents at the emergency departments with anorexia, they usually have this disturbed, um, electrolytes level because they haven't been eating. And you and things goes wrong when you have the not, um, you Stasis was the verb. The electrolytes level aren't right. And the one you're particularly worried about is hypochelemia low blood potassium, and that can cause long QT syndrome, which can develop into ventricular fibrillation, which is pretty much the same as your heart. Stopping your heart won't be pumping out a new blood, and you would do an e c g to rule that out to start with when they present in the e d. And then you would proceed to give them to give them new nutrients, as as advised by the nutritionists. And so our the underlying problems. Okay, third question. Now 65 year old man presents at the GP clinic, complaining of depressed mood, weight gain, appetite, decrease sleep disturbance and cold intolerance on further investigations. The patient also has radio cardia and delayed reflexes. What's his diagnosis? Okay, go off your answers in and you're all currently correct. So, yeah, most people have picked option C, which is the correct answer is hypo Hypothyroidism. Sorry, and I'll come. I'll go on to explain why so hyper hypothyroidism is underactive. Thyroid can be several causes which we won't go into now because that's endocrinology. Um, basically, you don't get enough thorough hormones. That can be t four t three. Many T four t four causes the somatic symptoms, and then these patient will present with Oita, which is enlarged thyroid glands. You see, like center of the neck. Something will swell up and can be due to, um, inflammation or autoimmune like this can be infection or could be autoimmune. And also there can be metastases, and then the second symptom is fatigue, increased sensitivity to code depression, hyperreflexia, constipation, dry skin weight gain, high cholesterol and muscle eggs. And you can see that a lot of symptoms are the same as, um, depression, such as fatigue, constipation, weight gain and muscle eggs, which sometimes happen in depression. But when you get a sign when you get these other signs going to, uh, increase sensitivity to code. And the main thing is, high poll reflects CIA and dry skin. You you wanna you wanna rollout hypothyroidism? Yeah. And in terms of investigations, you have thorough function tests. Uh, and then you have Ardan levels. Ardan level is important because thyroid hormones are made from Aberdeen, and if they don't have a nobody in in the body, this can be a cause of primary hypothyroidism. And then you want to do, um, thorough biopsies if you suspect metastasis or neoplasia. So that's benign tumors and meta metaplasia is, um, malignant chambers and then MRI it is metastatic, and then you need to do we need to bear in mind is actually quite important. Quite a few drugs such as lithium, amiodarone and our died 13 can cause drug induced high hypothyroidism. Uh, 13 131, 13. Sorry. That was type one. A slide out of 13. And I've just put in the table to compare the main Hallmark symptoms, uh, between depression and hypothyroidism. You guys can have a look at that later. Fourth question. Now 30 year old woman presents to the emergency department with a five minute history of palpitations. She also has breathlessness, chest pain and diaphoresis. That's, um, sweating a lot. She's afraid that she might be having a heart attack. Her symptoms may improve after 10 minutes. Initial investigations, including includes E, C, G and troponin, which are normal. She has had two similar episodes of this month, both of which also had a normal e, c, G and proponent. She said the symptoms are usually sudden and unpredictable, but she suspect that they may be related to crowding space, which it was the context of the tax and has started, uh, started, uh, type of, uh, she started to avoid crowds. She denies alcohol and substance use. She asked if there is a medication available, which may help. And can we get pulls? Thank you. That's pretty good. Most people have selected a B. C. D. Unfortunately, those are not the right answer. The correct answer is S citalopram, and I'm going to explain why. So this patient is likely to be suffering from generalized anxiety disorder again, you want to use ICT 10 criteria to diagnosis, which is generalizing persistent anxiety symptoms, including apprehension, motor tension, and autonomic activity. And that's the palpitation she's getting. And motor tension. You can read on an explanation and in terms of prevail ins 1.6% of the whole population. Um uh, suffering from generalized anxiety disorder at any point. So it's quite common and thing to bear in mind that this is very rarely begins. Like the first presentation. We will very rarely begin after 35. The reason why, I don't know. I suspect that's because if they do suffer from, it will present early and then in terms of treatment again, you want to follow the nice guideline, which is most things in medicine unless you're consultant, um, so initial education about that's for mild general anxiety disorders, and they don't have any mood disorders. And you wanna give them education about generalized anxiety, how they can deal with it and monitor the symptoms so that will be done in primary care. And then, in terms of active treatment, that's, um, G P prescribed non facilitated self help. So that's that means secondary Cat still won't be still won't get involved yet, And that's for patient. Who has clinical significant distress or impairment in social activities left outward. Uh, sorry. And then high intensity, psychological intervention or pharmacological intervention. You you always try to delay pharmacological intervention as much as possible. Um, because that comes with side effects, which I wish people follow more. More Clinicians follow that rule in real life, but they don't. Um, so yeah, this is when the patient's have severe symptoms and they're not responding to the initial low intensity interventions. Then you would refer them to secondary care at all at a pharmacological intervention, which is as as, uh, Escitalopram escitalopram. Yeah, that's how you pronounce it. Um And then you want to refer him to specialist management If they have very severe functional impairment, persistent suicidal thoughts, that's important. And then when? Especially when they have multiple psychiatric comorbidities. So such as depression, bipolar schizophrenia. Okay, Next question. 37 year old metal box er admitted to a psychiatric ward after reckless behavior and insomnia, questioning his relatives on questioning his writers. Uh, it has found that he has previously had episodes like this and also has a history of depression. Which blood test should be performed when starting Long term pharma pharmacological treatment in this patient. Okay, so most people like to see. But the correct answer. Oh, sorry. The order is messed up, but the correct answer is a thorough function test. Because if you remember, um, lithium is, um, causes, um, hypothyroidism. And you want to check if they have hypothyroidism before you start lithium and lithium is the gold standard treatment for this patient's condition, which is, um, bipolar effective disorder. And I'll explain the components of this disorder first. So mania, uh, CD 10 is elevated mood out of context. Carefree joviality, basically recklessness. And they have increased energy. They don't sleep, they speak really fast, and they kind of don't have much concentration on any certain things. They move from one task to another, um, impulsively. And another key thing is grandiose ideas and overconfidence and also loss of normal social inhib inhibitions, which is what you see in this patient and then hyper mania, which is less severe form of, uh, mania, Uh, the symptoms actually quite appealing, uh, to have so you have elevation of mood, increased energy and activities. You I feel really good, and you feel that your mind is working very efficiently. You have increased sociability over familiarity, increase sexual energy and decreased need to sleep, and you still be quite alert during the day. And it shouldn't lead to any severe disruption or function or resulting in social ejection. Uh, and one thing I put in is, um, the management. You would do as, um, clinician in a clinical setting. If you see someone with a severe manic episode, if they post danger, you want to give them back to the IPIC. That's the penal neuroleptics to basically knock them out and then take them to a secure unit with the security. And also you want to stop any antidepressants they're on because one of the side effects for antidepressants is manic episodes. Um, if the prescription is not monitored well and you want to offer an antipsychotics, which Chris has explained, and I won't go through that and each of them have different strengths and, um, adverse drug reactions. So you want to look into that. If they're already taking mood stabilizer, consider increase the dose according to be N F. And I'll talk about the mood stabilizers later. So that's a definitive treatment for bipolar. And so I was talking about manic and hypomanic up. So these are components of bipolar disorder. You have bipolar, effective disorder. If you have two or more episodes in of man two or more manic episodes, plus depressive episodes in between and between each of those episodes, there has been more than, uh, the episodes must be distinct. So they're depressed and the manic and in depressed, it can't be a mix of both. And if they have hyper mania, um, they're only classified as bipolar type two, which is like, um sorry, my bad. Uh, if they present with hypomania or mania without symptoms of depression, they're classified as bipolar type two and then, in terms of prevail ins of bipolar, um, effective disorder. Uh, it's lifetime prevalence of 1% in everyone, and bipolar type one is more common. So the more severe form of bipolar is more common, and the mean age of answer is 20 years old. Diagnosis, um, long term management diagnosis is made based on clinical decisions. So you see the presentations and you decide and whether they match the I CD 10 or D. S. M five here. Yes, and five criteria. And then long term management. Like we said, the gold standard. First line drug is lithium, and the second line alternative, if they don't respond well to lithium, is Val Crate. You need to bear in mind that you cannot prescribe evaporate in primary care. It can only be prescribed by, um, under advice of, um, specialist secondary input. And you want to want to get them access to psychological therapy as well, such as CBT interpersonal therapy and family therapy. Depending on the age and severity. The age of patient and severity of the presentation. 23 year old female presents at G. P at the G P reporting low period where they are tearful and feel hopeless. They say that they don't socialize and preferred to work from home. The depressive periods are followed by periods of that ablation and have have lots of energy for 2 to 3 days. Between the highs and lows, they don't experience any symptoms. So this is just a quick test on whether you remembered the last two last few slides. Can we start the pool piece? Okay, so most people selected see, which is by prototype, too, which is incorrect because the patient does have distinct episodes of, um, eyeball mania and depression as we see here. And yep, it's bipolar type one, which is like, which is more, more severe if they have, If they don't have symptoms of depression that be bipolar, type two slightly confusing. But it's okay. Next question. A young male with with I'm not sure why type there. It's type of, uh, young now during the ward, round said. Oh, a young male says that during the ward round, aliens has been recording his thoughts and watching him around the clock. He says he has ideas to save humanity from them, but always forgets them quickly. After what type of thought disorders exhibited here. Mhm you. Most people have selected the right answer, which is Option A, which is delusional perception. So I'll go through each of the answers. So delusional perception is when a patient attributes a false meaning to a true perception perception. So, for example, they see a water bottle. But they say is a gun something like that and then thought broadcasting is when people, when patient thinks other people can hear their thoughts, thought insertion is, um, they think someone's putting ideas in the head and thought blocking. Um is when patient may speak. May stop speaking all of a sudden and this can last for a few minutes, and then the patient start speaking again. But when they start speaking again, they'll be talking about a completely different topic. And the key point for diagnosis is a change of conversation. Topic thought withdrawal is when patient believes, Um, in this example, um, patient believes aliens are accessing his thoughts. Um, but this can be tricky to distinguish on thought broadcasting. Um, but the key thing is to, um, differentiate. The key thing to differentiate is when they have thought withdrawal. They experienced disruption in the change of the thought and forgets their own ideas. And this is not the case here. Um, so schizophrenia defined by, uh, my CD 10 is two or more of the core symptoms for a significant portion of time, which is usually a one month period. I'm sorry for a significant portion of the time within one month. And at least one of these symptoms has to be the core core symptoms, which, which are thought disorders, delusions and hallucinations. Hallucinations can be visual. Um uh, What's the word for hearing? So they can hear, hear things, and more rarely is tactile hallucination, which is really where and when the percent is usually really severe. The condition is usually really severe, and secondary symptoms is, um anhedonia, which is inability to feel happy. Like we said earlier, a lodger is poverty of speech. Abolition is inability to motivate or be interested, And then flat affect is when they have an appropriate respond response to, um, emotional changes. So, for example, you tell someone, uh, the parents or the spouses have passed and they just go, okay? And yeah, and they don't seem to change, have a appropriate change in their mood. And then there's catatonic behavior is when patient's they don't move and they sleep all day speech blunting is again, less words, or they can't come up with appropriate words when talking. Now we're done with L4 now L5. This is quite short topic. Um, and I've allocated most of the SBA still last hellos because those are more important. Uh, we'll start with the first one. Which of the following feature is most associated with an increased risk of developing schizophrenia? Amazing. Everyone got the question right not one wrong answer, but that's okay. So the correct answer is, um, see where the patient, both both of the, uh, parents of the patient's are affected. Um, it gives them a 50% risk of developing schizophrenia, and just to go through the other, um, histories, All of these, um, increased increases the risk of you developing schizophrenia, for example, um, smoking marijuana, chronically. So you smoke marijuana a lot every day. That can increase the risk of developing schizophrenia, but just using it once is unlikely to increase your risk significantly. History of depression, Yes, but less so than the family history. Maternal grandfather With schizophrenia? Yes. And I'll explain the next slide. Um, that it's less risk, cause you can tell the the the genes are further away as a generation between them and then emigrating to more developed countries. That's, um, that's a risk factor for developing depression and schizophrenia Risk factors. Big thing is genetics. Family history attributes a lot. When you have a first cousin, that's 2% risk. When you have a grandparent, it's 5% risk. Parent, a single parents for a single sibling is 10% risk. Uh, both parents in identical twin Uh, well, you can figure out why, as both parents or identical twins, because they have, they will have all the same genetic material as you is 50% inheritance risk. And one thing I put in here is protective characteristics, uh, for schizophrenia, high IQ levels. Um, if the schizophrenia started suddenly, um, that's patients are more likely to recover from schizophrenia. And if they have an obvious precipitating factor, uh, I'm guessing that's protective, because that helps the clinicians to treat them and also, when they have supportive network a very strong, supportive network. And that's true across most mental illnesses and positive symptoms predominant, So positive symptoms are the core symptoms when they have hallucinations, delusions or thought disorders. Those are the positive symptoms and negative symptoms are Uh huh uh, the sides are quite far before, but negative symptoms are things like anhedonia elegy and abolition. Um, if you remember that if you remember that table and when they have more negative symptoms is less likely, they recover quickly. Okay, Next question. Patient is brought into the E. D. After Emerging department after walking on the edge of the roof. She firmly believes that she can fly and continues to think so. She has a history of depressive episodes to she has history of depressive episodes to not a sorry about my grandma. Her mother also has a history of similar, uh, of a similar mental illness. What is the likely etiology of her illness? Okay, so okay. And the pool here and most people has voted for either psychosis or Veronica's encephalopathy, which, unfortunately both incorrect and, uh, correct answers bipolar, effective disorder. And so, if you remember the criteria for bipolar risk taking behaviors walking on the roof, um, delusional, delusional beliefs and like, um, uh, grandiose ideas so such as she can fly and depressive episodes. So that's, um, qualifies for bipolar type one. So, um, history episodes of manic episodes, um, and depressive episodes, two of them separate. And also, um, bipolar. Bipolar effective disorder is also highly inheritable, like, um, schizophrenia. And the risk profile is here. Important thing to know is that it's equal risk for men, women or racist ethnic groups and social classes. But it's different presents differently in women, usually more rapid cycles and more severe depressive states. Uh, that's just something to bear in mind. It's unlikely you get a question on this, but it's an L0. So we'll cover it and anything I want to mention because this is the last slide. No, that's it. If you have any questions, please leave it in the chat, and we'll, uh, we'll start answering, Uh, and that's it for my presentations. Brilliant. All right. Thank you. Um, go in for that. So Okay, I will be taking open up. And are we talking about, uh, share my screen that we got perfect? So it's just basically stuff on appetite and sleep regulation, risk factors of mental illnesses and brain, um, maturing so adolescents to adulthood. A lot of it will be covering stuff from PCs, so it'll seem like revision for a lot of you. So first Low is going to be describing the mechanisms of appetite and sleep regulation. So first question, um, well, I'll give you 15 seconds to answer these questions just for the interest of time. Okay. I'm gonna start the poll now. Um, So which of the following is most likely to increase the sensation of hunger? Nice. I'm getting answers in. Okay, Few more seconds. Buying perfect right. So the answer is indeed be so, As we know, ghrelin is going to be known as the hunger hormone. Um, and can anyone drop in the chat? What other hormone is known as the hunger hormone? Um, And while you're here, I'll explain the other options. So cart is a neurotransmitter, which is inhibitory. Um, so that will decrease your appetite. Um, excess insulin also decreases appetite. Um, leptin is the big one is known as the the one that isn't the hunger woman. So it's anti hunger. Basically, um, that results in the loss of hunger alongside peptide YY. So P y y, which is which are Both of them are released in the gut. So they increased, uh, satiety. I think that's the word for it. Um, so no one's dropping anything in the chart, but I'll just say it anyway, So it directs in the the other woman involved. Okay. Nope. Okay. Right. Just painted it then. Um, so let me move the pole out of the way, because I can't see the Yes, it it's annoying. Right? Next question. Which of the following systems is involved in the regulation of the sleep wake cycle? um, for those who didn't see the spoiler just now. Okay, give you 10 more seconds. Okay? Perfect. Right. So it's going to be Hold on. I'm not so messed up. So last is gonna be be so a is, actually, um, not a system, um, is made up, Um, and see is, uh, forms part of the immune system that comprises of figure sites in systemically fixed tissues. That's going to be part of Case one, so I won't explain it now, Um, the place of role in blood pressure regulation that uses the RAAs system, and they'll be part of case 12. So I won't really go through that either. Um, is the respiratory system we know that's involved in breathing? So not really involved in this as such. Okay, next question. Which part of the brain is involved in the regulation of satiety? Okay, let's get a few more answers in. Nice. Perfect. Okay, so a lot of you have gone for C share the results, and the answer is indeed. See, So the hypothalamus does contain the Center for Appetite regulation. Um, and this is where the neurons would release the neurotransmitters involved in this process. um So the brain stem is is involved in a lot of unconscious activities. For example, breathing, heart rate, BP. So that's probably not the single best answer. Um, b is going to be involved in your voluntary movement, personality and planning. Um, and as I said, C is involved in satiety. Um, so D is actually involved in interpreting the amount of light received by the eyes. So that's more, um, to do with the ophthalmic system. And he is going to incorporate, uh, sensory information, learning and memory so less involved in some activity. Next question. Um, yeah. So a man is diagnosed with a deficiency of a hormone that affects appetite. His symptoms are hyperphagia to excessive eating and obesity. Which of the hormones is he most likely to be deficient in? So if you were focusing on SBA to there was a slight teaser into that. Okay, we got one person answering anymore. Yep. Got three answers. Let's get one more in. Nice. Perfect. Okay, so a lot of you have gone for D, and that is correct. Indeed. So, as I said, leptin is the hormone primarily involved in the sensation of satiety. When you lose this hormone, Obviously there'll be excessive eating. Um, and so obviously the side effect would be evident in a weight gain and obesity. Um, So, as I said, ghrelin is going to be involved in increasing hunger. Be is, uh, so that will be neuropeptide y or neuropeptide y, which we'll get into later. That increases hunger as well. Um, see, um increases hunger. So a g r p, um, and E is actually involved in the sleep cycle, but we'll get onto that in the next learning objective. So I think this might be the last one. Um, so the sleep cycle is primarily regulated by one hormone. Um, And where is that hormone released? Just a bit of your anatomy in this case. Okay. Very nice. Okay, we'll end it there. So a lot of you have gone for E. Um, I think, as I said in the previous answer is more involved in the opthalmic system. Um, the actual answer is See, So this is gonna be the release of melatonin. So that's the whole meaning question. Um, and the pioneer gland primary primarily releases, um, melatonin in this. Okay, Right. Let's talk a bit about appetite, then. So this will take us back to PCs. Um, I won't be talking through cephalic phase gastric phase intestinal. That's not relevant to this case. But be in case. Six. If you want to join us, then however, let's talk about the neural and hormonal control, Um, in appetite. So there's going to be the appetite control center in your arcuate nucleus, and that is in the hypothalamus. Um, you're gonna have excitatory versus the inhibitory, um, neurons in this case. So neuropeptide Y is going to a beauty related peptide to a G R p um, those are going to be excited, Torrey, whereas POMC and CART are going to be inhibitory in this case. So the hormonal controls has two main origins. So your gastrointestinal tract and the rest of the body, um, the GI tract will release the ghrelin, which acts on your excited neurons. Um, that increases your hunger whilst peptide yy leptin, an insulin. So all three of them will act on inhibitory neurons, which will increase your sorry will decrease your appetite. Um, erection is going to be released in the hypothalamus alongside, and that will stimulate the sensation of hunger okay. And this is just the table to sum up all of that. You can read this in your own time and screenshot it, putting any notes wherever that's there for you, for me to run. And this is just a brief pathway about what happens when you ingest food and how there is a negative feedback system. Um, there's gonna be long term control, short term control. Um, fat storage increases your leptin, whereas when you're digesting a meal, you're going to have more peptide y y and incident involvement. But that's just a some version of it. So if we talk about sleep, sleep is defined as sort of an altered state of consciousness. Um, and this is sort of a multi step process. Um, so the sleep wake cycle is called the circadian rhythm, and this is just a cyclical pattern of being awake and then going back to sleep. Um, this all just basic represents that throughout the day, that's what it is. Yeah, Throughout the day, you become more more sleepy, and it's gonna know it's a cycle that happens. So sleep has to neural mechanisms of control and one endocrine, uh, control mechanism. So we talked a bit about the reticular activating system. Um, so this is involved in weightfulness consciousness and arousal. Um, so this center is located in the anterior brain stem. Uh, there's a bit more information on the slides, but these are the sort of the main points. Really? Um, the hypothalamus governs the circadian rhythm, and this is sort of responsive to light. Uh, more specifically, the super cosmic nucleus controls this circadian rhythm. Um, erection is going to be involved in weightfulness as well, and that is secreted in the lateral hypothalamus. Um, so erection sort plays two roles in this case, um, one of which is appetite, regulation and weightfulness. Um, just actually an extra added note. Narcolepsy type one is caused by the lack of this erection, and that sort of explains narcolepsy type one. And the ventral lateral preoptic nucleus will inhibit this or a system to promote sleep. Um, so the key points here, really is that the rashes involved in arousal whilst the hypothalamus is involved in regulating this sleep. Essentially. So if you talk about the endocrine regulation of sleep, melatonin is going to be your main hormone in this, um, and As I said, the pioneer gland will secrete this, um, and the higher the level of melatonin, the sleepy of the individual. Um so blue lights will inhibit melatonin. Then it's another thing. Another chemical to be wary of is adenosine. So this will come up more and more during pts. Um and I might It might come up in s too as well. Um, but this is released in the basal forebrain. Um, but that's less relevant. But what you need to know is that is that it binds to adenosine receptors in the neural membrane. Um, so this a dentist in will accumulate throughout the day. And that explains why you become more and more tired throughout the day. Um, and one clinical application is that caffeine will block these identity receptors. So that blocks the cycle momentarily, and that's all stops the action of adenosine for a period of time. Next. So, yeah, this is just all of it in a nutshell. So just generally summarize it. Hypothalamus makes you sleepy. Melatonin makes you sleepy. But the last week's you up, and that's a very stripped down version of it. Okay. Next. Hello. Right. Fly through this basically. Okay, So which of the following is not an adverse childhood experience watching the polls know they. So being adopted, being hit, being made to feel like a burden, having depression and having a parent with depression. Okay, any takes on this? Okay, we got one. Okay, You got three. Nice. Okay, perfect. So a lot of you have gone for a Sorry. So a lot of you have gone for a, which is indeed correct. So, uh, a is, um, not in a known adverse childhood reaction. Um, be encompasses physical abuse. Uh, C will encompass emotional abuse. D encompasses a mental illness, and, um, e will encompass a family history of mental illness. Is there is a nice table at the end to summarize all of it, but we'll get there when we get there. Cool. So next question. So which of the following is a known protective factor against mental illness? Development? Um, so healthy diet, Regular contact with health professionals, supporter friendships, married parents or guardians or a well paying job. And give you 20 seconds. Stop to this. So we've got one answer on that. Two answers. Three answers. Four. We'll wait for one more and then we will. Okay, Never mind. Okay, so the answer is seen, Um, so a good support network is a known protective factor, and the others are not really well researched factors. Because if you think about it and there are other things that will come into play that might, um, completely get rid of it, for example, regular contact with health professionals. You know, it depends on the quality of that Married parents and guardians is not necessarily, um it depends on the marriage as well. And a well paying job, not neces, is not necessarily key to being protective against mental illnesses. It might in fact, be the opposite, depending on the job. So next question a 25 year old female presents, although mood loss of interest and poor sleep over the past three weeks. A month ago, she moved houses, lost her job and took up reading as a hobby. What is the strongest risk factor for depression in her history? And i'll give you 20 seconds to answer this question. Okay. We'll wait for about three more answers. Um, so currently at two. Nice. All right, cool. We'll end it there. Fine. So a lot of you are going to be, and that is correct. So unemployment is a known risk factor for mental illness. Um, and the others are not, uh, exactly, Well, research factors. Um, so, for example, female sex There might be a link, but it's once again, not a very well researched factor. Um, cool. So this one, I'm going to give you a bit more time to unpick because there is, um there is more reading in between the lines as such. So, uh, Mr Jones is a 35 year old person who is being assessed for adverse childhood experiences. So in their childhood, they were often left alone and made to feel like a burden. Um, Mr Jones was not a victim of domestic violence, but their mother was their parents was imprisoned, uh, pausing away. So they're parent. Their father was imprisoned when they were 11 when they were 20. For they became addicted to opiates. How many? How many aces does Mr Jones have? And I'll give you about 40 seconds. Answer this one because there's a bit more thinking to do. Okay, I've got two answers in, okay. We'll wait for one more answer, and then we'll record it there. Okay? Right. We'll just call it then. Okay. Perfect. So, uh, the majority of of you have gone for three, so option deed, and that is correct. So I've highlighted what I think might be the, you know, the many aces involved. So that will consist of the emotional abuse. So feeling like a burden, the witness of the domestic violence. So the mother and the familial imprisonment, The father. Um, So the only thing is, um, I know someone's gone for e, um, and that that might have been down to becoming addicted to opiates. Now, with that, obviously, aces are adverse childhood experiences. And I think when it says when they were 24 so that already goes beyond the age. So, um yeah, that's that. But I think, you know, mistake making is less than learning, so it's better to make that now than to make it in s to where it does matter. So the final SBA of this L0 um, is going to be this one. So interpersonal therapy is a management of option is a management option in depression. It involves identifying and fixing problems in close relationships. What aspect of depression risk does this address? So does it, uh, deposing away again? Does it improve the strength of support networks, improve problem solving skills, allow the person to assign extra personal blame, reducing self hatred? Um, allow development of a strong cultural identity, Or it does it improve self esteem? And I'll give you guys 15 seconds to answer it. All right. Perfect. So I think there's only four people that engaging. Oh, there's five. Nice. Okay, so there's five engaging, which is perfect. So, um, the answer is actually a, um this is this is basically the primary aim of interpersonal therapy. Um, and we'll explain that more later on. Um, but the other ones, uh, are not so addressed. Too close, close relationship nations. Cool. Um, so just to talk a bit about risk factors of, uh, mental illnesses, this is sort of a summary of the risk factors involved. This list is obviously not exhaustive, but there are some common risk factors to read in your own time. So these ones as such and there are also protective factors of mental health illnesses, which makes a person less likely to develop a mental health illness. It's not saying they won't, but it makes them less likely to develop one going forward. And I'll let you read this in your own time when you receive the slides. Cool. Um, and this is talking a bit about aces now, so these are experiences that a child might undergo. Um, and this will have a long lasting biological, social and psychological impact. Um, and as we know, this is the definition of health. But there is a theory that, uh, four or more of these aces will predispose the individual to lots of adverse life consequences. So that will include, uh, 14 times more likely to attempt suicide 11 times more likely to use IV drugs 4.5 times more likely to develop depression four times more likely to have had sex by age 15, 3 times more likely to have lung cancer and two times more likely to have liver disease. Um, so in a nutshell, four or more, you have more consequences as such, um, and people with six or more aces will have a life expectancy of 20 years younger than those with none. So that just goes to show the more cases you have the longer lasting this impact and finally from me. We're going to talk about the brain changes during development and maturation. Maturation. Um, so what is the paradox of adolescence? So we don't report. And just to, um just to clarify this session is sort of a will act as a consolidation section session. So if there are any things I've skipped over, do drop me a message or drop me an email, um, you'll find me somewhere and, um, I think I'll be more than happy to answer the questions, but, uh, this would just be a sort of a quick overview as such. Okay, so you got one answer. Two ounces Nice. I'll wait for five because I know there's about five of you engaging there and we'll wait for one more. There's a tire currently between B and C. Wait for five more seconds. Okay, Perfect. So we have gone for B. However, the answer is be nice. OK, so in adolescents, the people are at their maximum health and cognitive performance is, but there is a higher rate of mortality than in others. Um, the others are going to be incorrect as such cool. Next question. Which neuro phenomenon contributes to the increased risk taking observed in adolescents. And if you don't get it now, there is quite a It's quite clear explanation later on that. So I'll go through. Um, OK, got one answer in. Nice. Good. As a tie. There's a tie now, see? Okay. Interesting. Wait for one more. See if you can push it over the edge. All right. Never mind. So if you've got a tie between, uh, right, we've got majority going to see Perfect. Right. Um, so the risk taking in other lessons is attributed to the early development of this limbic system, which is going to be more emotional, um, and the underdevelopment of your prefrontal cortex. That doesn't really develop till the age of 18 to 25. And when I talk about development, it's more like myelin nation. Um, so you've got the ratio between, um emotional thinking versus rational thinking because that ratio is a bit offset. You're going to have more risk taking, um, risk taking emotionally driven behaviors. Basically, um, the next one is which behavioral phenomenon contributes to the increased risk taking in adolescents. Right. Ok, Got two answers in. Mm. We've got five people engaging. I wonder where the rest of us are. Uh, no, it's a pretty cool. So, um, the answer is B. And that's the majority vote. Very nice. So, um, it's been well researched that adolescents are going to be more susceptible to social pressure. Um, and not increased aggression at this point. Um, cool. This will be further explained in a in the slides later on. Okay. Last question of my, um, presentation with the so a 17 year old presents to a any with a posterior hip dislocation following a high speed track road traffic collision. Um, with their friends who egged them on which of the following is most likely. It's almost like risk factor for their presentation. Um, loss of control due to seizures. Increased risk taking due to adolescents. Poor judgment used to, uh, substance misuse. Um, increased risk of pathological fractures Do too early onset osteoporosis or attempted suicide. Okay, wait. We'll wait for about one or two more answers. Nice. OK, perfect. Majority have gone for. Be perfect then. Um, so as you can tell, in this current history, there is not any re disposing factors to any seizures? Um, substance abuse or any pathological fractures? Um uh, or any attempted suicide of such, um, and the history source says that they egged them on, so that sort of gives it away. Really? Right, So this is the final slide from me, But let's talk through it, because I think this might be quite helpful. So this is a summary of the development in the brain, from a child to an adult. Um, and the trend is that at the start of life, we are sort of getting to grasp his life. So that involves the coordination and your cooperation. Um, corporation being teamwork and talking like, um, cooperative play as such. Um, And as we age, we become more emotional and aware of those around us including, um, friends, which then introduces your aspect of peer pressure. Um, and as we move into adolescence, um, this is where the risk and behavior and aggression comes into play. Um, but at the end of this, um, we begin to calm down, and therefore we have a more rational approach to life. But that is just a very quick summary. Um, if you want to talk about the active brain changes. So from infancy to seven, the brain will increase in size and the cranial nerves that come to mind innate. From 11 to 14, you have this thing called. You have this phenomenon called synaptic pruning. Um, and this is essentially a phenomenon where useless information is pruned. So as a child learns and grows up, their brain is all like a sponge. Um, but as we age, we need to hone down on this information and cut out whatever is unnecessary. Um, so that will basically allows the whole now information and retain What's important? Um, and the limbic system begins to develop faster than the prefrontal cortex, and that will shift your balance of emotion over logic. So that introduces as to the age range of 15 to 17. So brain myelination is complete, um, apart from the prefrontal cortex and this center is involved in inhibition, which does explain why adolescents are more at risk of risky behaviors and aggression. And this possibly introduces an identity crisis. Um, and from 18 to 25. So the final stretch, Um, and this is where the prefrontal cortex is actually completely myelinating. Now, um, the individual would engage in more rational thinking over emotional thinking. Um, and this will increase that identity or self confidence. Um, and this is a lot of the time This is where the parent and child conflict will resolve. Um, so, yeah, because of, you know, the whole rational thinking idea. But that is a very quick rundown of that. So if there's any questions, I'll be happy to answer in the chat. Um, feel free to drop it. Anything. However, I'm going to hand over to John now, we will talk about his slides. Cool. Don't either. Yeah. Do you hear me? Nice. Yeah. Uh, yeah. Uh, show us green. Are you gonna stop sharing for me to, uh you see that? Yes. So yeah. So I'm John. Hello. I've got you for the next bit and the last bit. I'll try to make it quick punches of the time that we are running over. Um, the SBA is actually after the explanations, Um, for for my slides. So I'm just gonna ignore the S p A for a second. Uh, but the first L0. Uh, I've got is just to describe physiological mechanisms like stress and disease. including neural endocrine factors, and it's a lot simpler than it sounds. What? What? Okay, so we got to talk about the HBA axis. Uh, so we're looking at the hypothalamus, uh, the anterior pituitary gland and the adrenal cortex. Essentially, all that happens physiologically speaking is the hypothalamus is going to secrete, uh, CRH that actually anterior pituitary, which is gonna secrete ACTH that's gonna act on the adrenal cortex, which is gonna release cortisol, which is effectively your stress hormone. Um, and the key part is that protocols got negative feedback mechanisms, and it negatively feeds back on the hypothalamus. Um, and the anterior pituitary. Okay, so it's kind of like self regulating almost is that this can go wrong. Uh, like many things, um, so adverse childhood experiences, which we spoke about earlier, Um, early life stress and traumatic stress. They can all lead to kind of disregulation and subsequent dysfunction of the H p access. Um, and that essentially results in a prolonged stress response. What ends up happening is is that core source ability to negatively feedback on the anterior pituitary and the hypothalamus becomes impaired. Um, because of that, you end up with like, exceedingly high CRH levels and exceedingly high ACTH levels, which puts the whole system in a vicious circle and you end up producing excessive cortisol. Um and so you end up with excessive Circulatory Chorzow, and that causes a lot of problems. Essentially, in a nutshell, you end up with a prolonged, uh, stress response because of the high Secretary forces, all implication of this is quite serious. Uh, so you end up with, uh, suppressed immune response. Um, and actually, uh, the effects of chronic trust can last beyond childhood, even if you have, uh, cases and they can manifest in adulthood. Um, uh, cabbage is is that those adults end up with high inflammatory markers and then with increased risk of metabolic syndrome and can end up with diabetes, hypertension and obesity. So it's a risk factor for that, Um, something quite interesting as well Is that prolonged HP? A access activation that we can see here actually suppresses the secretion of growth hormone. Um, in Children, uh, and so you end up with all these Children with very short statues and can also predispose them to mental health risks. Um, in the adult hood. Um and it also impairs brain development. So look at your neurogenesis, your neuroplasticity metastatic control, coordination of stress response. It all becomes affected all when this HPV access becomes, uh, dysregulated. So we're looking at to relevant conditions here. Um, you've got fishing syndrome and Addison's disease. Um, so I've put in brackets just in a nutshell. What they are with fishing syndrome, you're looking at I cortisol and Addison's disease is looking at the know cortisol. There's a bit more to the story than that. It's like a Cushing's syndrome first. So half of pathogenesis for Cushing's syndrome is you might have a pituitary adenoma. It's benign. Uh, that's gonna allow the opportunity to secrete excessive amounts of ACTH. So if you remember ACTH from over here, and that's gonna need to excessive circulatory force, So So it's going to keep on going on the atrial cortex and you have way too much cold still okay, The access, of course. So is what's gonna lead to the symptoms experiencing cushion syndrome. And you've got Hallmark, uh, symptoms that you should remember. Main ones are moon face weight gain, which is predominantly around like like centrally and, uh, look at the net get it with glucose intolerance, hypertension, uh, purpose. Try, uh, depression, anxiety and as a whole slew of other symptoms as well. But I think these are the main ones, and they're just a small note is that although cortisol is a glucocorticoid and it binds to, uh, glucocorticoid receptors, uh, in super high abundance ease such as cash, um, syndrome, uh, it can actually binds to mineralocorticoid receptors like that except their effects. So that's where the hypertension and the HYPOKALEMIA comes from. Okay, so now we're looking at Addison's disease. So remember, we said, this is effectively low cortisol. So in many ways, it's kind of the opposite to Cushing syndrome. Uh, but this is autoimmune destruction of the adrenal cortex. So because the adrenal cortex has become destroyed, you get drastically low cortisol automatically low cortisol or just complete lack. Of course. Seoul. Okay, So, in contrast to Cushion Patient's who who experience hypertension and central obesity, uh, these patient's experience anorexia and hypertension, so it's very different. The Hallmark symptom, though, of Addison's disease, is, um, this thing called bronzing or hyperpigmentation of the Palmer creases in the mouth. Uh, reason why that happens is because when there's really little cortisol, the levels of ACTH is gonna rise. And that's because of the negative feedback mechanism. Um, from over here. So if cortisol is really low, ACTH is going to go up because that negative feedback almost isn't acting. So it cuts both ways. Okay, Um so local does also end up with high ACTH, precursor of ACTH, which we spoke about earlier called propio Melanie Corton or punk. So I'm going to call it from now on. Uh, it's also a precursor of something called melanocyte stimulating hormone, or MSA, and that causes darkening of the skin. So an increase in ACTH is gonna result an increase in punk. This is the precursor for ACTH. So we need the precursor for ACTH, which is what we're producing lot of. Because of that, we're gonna have a byproduct of increased MSH, and that's gonna that's what's going to lead to the darkening of the skin. Okay, it's a small note for these. Addison's patient's is they can experience a serious complication called Addisonian crisis. Okay, so if we're talking about someone who doesn't have Addison's, typically they're able to mount a stress response, uh, to a stimulus via the HP access. Um, and call dissolve. That's your fight or flight response. Um, Addison's patient's can't do that. They can't mount. An adequate response to stress is, um, and they end up experiencing electrolyte dysfunction and severe hypertension instead. Um, and that's a medical emergency. And what these patients need is urgent. Hydrocortisone or could be fatal. Okay, so it's very serious. Okay, so now we're onto the SBS. Um, just try your best. Uh, we're looking at the first SBA soap. CRH is a hormone with the pulse covering question. CRH is a hormone that acts on which structure to stimulate secretions of a CT. Hate. Just try your best or just pick any answer. Cool. Uh, we'll end it there. So most people have, uh, right. So it's the end. So most people picked the anterior pituitary. It's correct. So if we shift all the way back, you see the CRH. It's secreted by the hypothalamus, but it acts on the anterior pituitary. Okay. The anterior fertility, those What? Uh, what stimulus description of ACTH. Good. Okay, it's be a two. So me starting year seven of high school him. He's got many known cases he's super stressed, and he's anxious about being bullied in secondary school. So using your knowledge of the H P axis, which of the following is more likely to be suppressed? Remember, Timmy is quite young. Try your best. Just pick anything. Great. Well, under that thing off or your kid or the engagement we're gonna get. Um, so most people have gone for B. It's the correct answer. Yep. So, uh, belonged activation of the H P axis leads to growth hormone secretion suppression. Um, and Timmy, who's got many known aces and a super stressed There's a good chance his h payer accesses gonna be dysregulated. Um, so it's a good chance he's also going to have growth hormone suppression, too. Okay, looking at the third one. So Joe is a 58 year old male, okay? He presents to his G p with purple stray on his abdomen, moon face and hypertension. Joe also explains how he's been feeling very depressed from his uncontrollable weight gain recently. And you notice that most of his weight is central has a past medical history of pituitary adenoma. So what's the most likely diagnosis for Joe? Just pick one Brilliant So everyone has, um, everyone has voted has gone for, uh, a which is the correct answer. So yeah. So purple stripe, uh, moon face, uh, hypertension. It will like screaming Cushing's and then the pituitary adenoma past medical history is just, you know, the the cherry on top to give you the answer, so well done. OK, SBA four. So J presents to her GP with bronzing of decreases in her hand. She also reports not eating as much as she used to and now only eats one banana a day. Okay, He's hypertensive, and she's got a past medical history of autoimmune disorders. So based on these facts alone, what is the most likely diagnosis for Jane? Anything? Uh huh. Well, so most people have picked, uh, Addison's disease. Uh, that's correct. Uh, so someone pick no significant diagnosis. Uh, someone who's hypertensive and is only eating a banana a day and got bronze increases in that hand is, um definitely something significant. It definitely is. Added disease. The bouncing of the Christmas in the hand is what gives it away. Uh, passed by the country of autoimmune disorders, uh, predisposes this patient to other autoimmune disorders and we know that in Addison's, the other physiology is autoimmune destruction of the adrenal cortex. Uh, so, yeah, good stuff. Got a bonus question, But based on the engagement, I'm going to give you the answer. But if Jane suffers from Addisonian crisis, what is the urgent treatment required for Jane in this medical emergency? I'm just gonna give you the answer. It's hydrocortisone. Okay, so Addisonian crisis you give hydrocortisone, um, as an urgent remedy, who So we're gonna look at personality, and we're going to outline how personality can image what's the course of disease and its treatment and also an official L0 whoops. So, firstly, what is a personality? Uh, so there's many different definitions of personality, honestly, and the main, uh, the main thing to understand is just the grass. The general idea of what is, um, and all the different personality definition is just referred to individuals, general characteristics and how those characteristics just influence and behavior. Um, so you don't need to go learning all the different definitions. Just get a general idea of what it is they're talking about. Okay? So why is personality important? Why bother? Okay, uh, and the reason is is because personality traits are breeding. As for predicting life outcomes and actually just as important as other factors like socioeconomic status and cognitive ability, that's been proven. That's why we study it. That's why we give attention to it. Okay, so series of personality. So there are six. Okay, you've got biological trade theory, psychodynamic theory, behavioral theory, humanistic theory, social learning theory and type theory. Uh, and I know what you're thinking is that's a lot OK? And honestly, don't be intimidated. It's a lot simpler than you think. OK, and we'll go through them one by one. Okay, so let's start with biological trade theory. So in biological trade theory, personality is made up of a number of grades that are distinct, inheritable and stable across time and context. Okay. And these trades can be used to pick behaviors. Okay, that's what biological trade theory says behavioral theory. So an individual's personality is formed based on the interactions between the individual and their environment. So the individual is gonna respond to an external stimulus, and the consequence of that response is what determines individual's behavior. Social lighting theory. So it's when personality shaped by the interactions between the individuals, coalition and their environment through the process of modeling. So our individual interact with their environment, so the dynamic theory. So this is where personality develop from numerous attempts to resolve conflicts between unconscious and societal demands. Okay, so the main emphasis is on the unconscious mind, the unconscious motivation. So this is more of a personality becoming developed just from somebody's unconscious mind. So not something that's within their control. Humanistic theory. So this is where individuals have the freedom and we'll to change their behaviors and their attitudes, and they're responsible for their own lives and actions. So, almost in contrast to psychodynamic theory, humanistic theory is individuals have the freedom and the control over their own personality development. And then you have type theory, which is probably one that you're more exposed to than the others. But in type theory, instead of traits being designed to an individual, the individual's place under a category or a type, and that comes in a pre established static set of attributes that determined personality. So you've often heard, uh, this person is the type of person to do X, y or Z. That's effectively type theory, so When we talk about personality, we need to talk about personality traits, right? That's gonna send a lot of biological trade theory. It's because the most commonly accepted model is called Big Five, and that comes under the biological trait theory. Okay, Uh, what the Big five are there five, uh, rates that underline, uh, personality. Uh, and what we've got is openness. And it's openness to experience and experience things. Uh, conscientiousness, which is just like being organized Extra version gratefulness and neuroticism. Okay, really easy way to remember this ocean. Okay, openness, conscientiousness, extra version agreeableness, and you're citizen ocean. Okay, so it's a little bit deeper as to what they are so open is to experience. So you'll be able to identify if someone's got a high, uh, score and openness. Uh, they've got wide ranging interests. If they're intellectually curious. If they're imaginative, creative people conscientiousness. As I said, it's just being organized, thoughtful, self disciplined and a dependable person. Extra version. So, uh, attributes associated with ice assertiveness. Someone who's sociable, emotionally expressive, enthusiastic agreeableness is different to openness. It's someone who's trusting empathic, synthetic, friendly cooperative. Also, talk about agreeableness is different to conscientiousness. as well a little bit of overlap that, uh, there's not. And then neuroticism is anxiety, emotional instability, tension, moodiness and easily upset. So we're talking about, uh, that spectrum of attributes. So, as I said, all individuals are given a score based on each section, Um, and depending on how well their attributes compared to the traits above right. So if someone's got a higher score and openness, that means they're more open. If someone's got a high score in neuroticism, that means they are more aligning with someone who's anxious and emotionally, uh, stable. Okay, so how is health link to personality that? Okay, so there's four possible parkways, and it sounds a lot more complex than it is, but it's common sense, okay, so either you have a direct personality to illness link. So an individual's trades represent biological differences that cause different outcomes. So someone's personality, uh, personality traits is what's gonna lead them down to different biological differences, and that's going to result in different outcomes. Um, or you might have a causal chain linking personality traits, health behaviors and outcomes. So health, uh, health attribute of some of someone is gonna directly linked to a change in their personality and subsequent health outcome. You might have a correlation of link rather than a causal link. So two things that don't cause each other, but they just correlate, um, in data and you might have an illness that leads to a personality change. So if somebody gets diagnosed with, uh, serious illness and then it with the depressive change in their personality afterwards as a result of that a bit deeper. And I think this is where you'll find things more relevant for your exams, um is individuals with high conscientiousness, which is what we spoke about as part of the Big Five earlier? Uh, these people are more likely to commit to health promoting behaviors. Um, and this includes stuff like regular exercise diet, and they're also less likely to commit to health harming behaviors like alcohol abuse and other substance abuses. Okay, So high conscious, Interesting. Uh um, high conscientiousness is also associated with good adherence to treatment as well, because they were organized high levels of neuroticism. So that's been associated with this regulation of the H P axis, which we spoke about earlier. Um, and we know that chronic activation of the H P axis contributes to hi Alice static load, which is likely just excessive stress. Okay, so high as static load just means stress load. It's just that the h p access of individuals high rates of neuroticism, they're more vulnerable to stresses or the experience more stresses or have higher levels of HP access activation generally throughout the day. So basically what this is trying to say is that people who've got high levels of neuroticism are more likely to have chronically activated HP access or HP access disregulation, um, and subsequent dysfunction and that prolonged stress response. And you can see that it makes sense when we look at the attributes of someone who's typically anxious, emotionally unstable or Ted someone who's moody, someone's easily upset. You can understand why they're, uh, treated and linked. So how do we treat it? So we've got CBT and CBT is good. There's a very problem with CBT. Hard to access, Um, and that's just because of the state of the NHS right now. But it's an unfortunate proof. Um, another aspect of why sometimes it doesn't work is that if an individual's got poor agreeableness and poor openness to experience new things. Uh, it's far less likely to actually work. Uh, if the patient isn't cooperative, that's part of the agreeableness. And if the patient isn't, uh isn't open to something new and reasoning that word if the patient isn't willing to try something that's part of openness. Okay, so it's less likely to work. Okay, let's go into SBS all your best. So which dairy of personality describes how personality is comprised of distinct, stable and inheritable greats? Try your best and just pick one. There's a big clue in the question. So in the interest of time, I'll end it there. So the answer is biological trait theory. Uh, so remember Barnicle. Trick theory says that an individual personalities are made up of attributes. Rates? Um, um that are, um, the artist ST stable across time and context. Also inheritable. Okay, next one. What are the big five? Try to remember the, um I don't know what the thing's called. What? You remember, ocean. Here we go. Just tell it to let's remember ocean or the Big Five. We have the polar. Yeah. Brilliant. You guys have got it. So yes, be so it can't be a because Peacefulness and carelessness are not part of the Big Five. Not see, because controllable, empathic, outgoing and nose er are the big five. The only has four attributes, and he's not true because he's correct. Cool. Let's be a three. So this regulation and dysfunction of the H P access resulting in prolonged activation is associated with high schools of which of the Big Five. Oh, cool. So, yeah, you guys gotta rights neuroticism. I don't think anybody got this question wrong. Okay, Number four. So 65 year old man he's brought to the g p by his daughter. His daughter explains that after he was diagnosed with prostate cancer, he's been far less assertive and unsociable. Which of the following personality changes is he experiencing? So he's got diagnosed with a serious illness. I know he's had a personality. Change is less assertive, and he's more unsociable. What personality change. I agree. Good. So yeah, so it is lowered extra version, so we'll put load openness, and I can understand why you would put that because it almost, uh, like, if we're speaking kind of, uh, locally. If there's someone is not that open, it's almost like they're not opening up. And we see that as we conflated someone being quite sociable. Uh, remember, when we say openness and we talk about the big five, it's openness to experience. Um, so it wouldn't be openness. In this sense, it would be extra version. So this, uh, this particular person is experiencing load, extra version. Um, so just just watch out for that. It's something that you can easily get stepped up on. Okay, uh, and then we've got 50 s p A. Uh So which of the following traits associated with poor adherence to treatment Really interesting array of results. So we got a split basically across everything. Uh, but the correct answer is lowered conscientiousness. Uh, so I'll go through this one. Uh, the reason is is because someone who's quite conscientious is quite organized and quite disciplined. So if someone's got load conscientiousness, um, there are a lot less likely to adhere to the treatment that they have at home to their big tablets. Or uh, that's a different time of the day or whatever the treatment might be. Uh, they're a lot less likely to stick to it, either by choice or just by unfortunate outcome. Uh, openness wouldn't be, um, a terrorist. The treatment, I think that would be more kind of in accordance with with with the doctor and not starting the treatment in the first place. Uh, but I can understand why you would put that That wouldn't be the best answer in the situation. Uh, it wouldn't be extra version, because, uh, this is just pour it into treatment. And it's less about, um, an individual's, uh, interaction with relationships and, uh, surrounding in, um, environment. Not gonna start. Why be agreeableness? That is more cooperation. Um, whereas this is just a treatment, there is no other person to cooperate or be empathetic or sympathetic with, so it wouldn't be agreeableness. It would be depending on how disciplined the individual is. Um um and how organized the individual is so it would come under lower conscientiousness. Okay, we got the last ever, though, we'll try blitzing through this. Um, so this is about stigmatization of mental health and how that can affect patient's opportunities. Uh, it's a stigmatization. Uh, discrimination is also included. So start off which need to just say something obvious about stigma. And that's before you even become unwell before you become diagnosed with anything, you already become exposed to different stigmas in society. Okay? And you learn what those negative attitudes towards, um, those different conditions, maybe so towards, like, mental health disorders. And when you do become diagnosed, if you do become diagnosed with those, um, disabilities or mental health disorders, you are very well aware of the, uh, negative attitudes and the stigmas within society. And you almost expect them, uh, to be, uh, did upon you and that expectation that red is what fuels, um, type of stigma called self stigma. Okay, so I pray fell on slide. Um, but don't let it scare you, OK? We just call the different types of Stigma, and we're gonna talk about them a little bit. Okay, so we've got three types of stigma that we're going to be talking about, uh, self stigma, which can also be called felt stigma. They're the same thing enacted stigma and cultural stereotyping, which is a form of stigma. Okay, so let's talk about self stigma First. We mentioned it seconds ago. Uh, so this describes the fear or shame. An individual has that their condition or personal circumstances being negatively viewed by society. Um so that is a very individual sort of inside that person's sense, um, and less of an interaction between an individual and their environment. Uh, it's a fact is, is that in my result in people avoiding healthcare and not seeking help when they actually need to and not following through with better constructions because they believe they're not deserving of help because they can be affected by their own stigma and talk about self stigma? And you can also look at it as if they are feeling the stigma, which is why we call it felt stigma. Um, and I feel like that just makes it really easy to remember. So then we have an active stigma. This is firsthand stigma. Okay, so this is what happens when the individual is shunt, denied protection under the law or the humanize. Uh so, for example, individuals with particular health condition being treated differently by society. But other individuals you probably heard of how individuals living with HIV or AIDS are done by society and pretty differently by society, are distant by other people in society. Um, that's a form of an active stigma. It's the first hand experience of stigma between an individual and somebody in their immediate environment. Then we've got cultural stereotyping. So this is when you've got groups or categories of patient's, uh, within the healthcare system. So they might be sick, critized according to the agenda of race, age, socioeconomic status or just any other, uh, protective factor. Um, and because of that prejudice, um, they have lower health outcomes. So there's people know stigmatized groups. Okay, let's come back on. Uh, information for you to read in your own time when you get these slides that if you're interested, okay, then we're going to talk about discrimination. Uh, so you've got two main categories of discrimination. You've got direct discrimination, and you have indirect discrimination. But we can split up direct discrimination into, uh, two different forms of discrimination, uh, discrimination by perception and discrimination by association. They're both forms of direct discrimination, uh, an indirect discrimination. It's just its own category. So let's talk about them. So discrimination by perception. So this is when a person may be discriminated against because there is a perception or belief that they are disabled and that can be true or false. Okay, So, uh, they might be discriminated against because they may be perceived as having, um, muscular dystrophy. Uh, but they may have muscular dystrophy, or they may not. Either way, the fact that the person the perpetrator who is doing the discriminating is perceiving that they are disabled. Um, and that's what scribing the discrimination. That's what makes it discrimination by perception. Whether or not that interpretation is true or that perception is true, it doesn't make a difference if it's a discrimination by perception. Okay, um, I don't need to read out the examples with time on time. They've got discrimination by association, so a person may be discriminate against because of their connection or association with a disabled person. So, for example, if a coffee shop refuses to serve someone because they were accompanied by their friend who's got a visible disability, so personal question doesn't have, uh, predicted factor or the disability. Uh, they're associated with someone who does, and they discriminate against. Because of that fact, we've got interact discrimination. So this is one of just all system occurs to be neutral and non discriminatory, But it does, uh, disabled individuals particularly disadvantage to people who are not disabled, who have a protective fact that people who don't So this is a much more of a systemic effect compared to a direct discrimination by a person. Um, this is more of like a design flaw is the way I like to think of it. The example I've given I I quite like this example. So, um, and if I center that only agrees to see individuals face to face, that's just their policy and not over the phone or email. That's gonna put people with agoraphobia a major disadvantage because they'll find it difficult to leave their homes so they won't be able to get advice. And that's not because of an individual's decision. Uh, but that's just because of a systemic, um, systemic flaw puts these people at a disadvantage. And, as I said, it can doesn't have to be a disability. It can be any protected characteristic. Um, and we've got some examples there, but I'm sure you know particular characteristics are all right. Final stretch is the last SBS. So, uh, Ronald is living with HIV. Last week, he wanted to meet with one of his old friends from secondary school. However, When his friend learned that Ronald has HIV, they became very cautious and they kept their distance from Ronald. So which type of stigma best represents this Both. I'm not sure where the poll is. We'll just go through it. Um oh, that's the goal. Okay. Yep. So most people have gone for, uh, enacted. Stigma is true. So remember we said enacted stigma was firsthand experience of stigma. So Ronald has experienced the first hand experience of stigma from his friend. He's looking very cautious and kept their distance from him. It's a piece, uh, condition. Okay, so now we're gonna move on to Brian. So, Brian, he's 20 years old. He's a male. He's recently diagnosed with depression by his G. P. He's worried that he's going to be judged by his friends, and he feels ashamed. He's worried that his friends will make fun of him, and this has been bothering him a lot. So what type of stigma is Brian most likely experiencing? Cool. So, yeah, everyone got it right. It's self stigma or felt. Stick with that. The same thing. Okay, very good. Okay, let's move on to Shane. So Shane is an individual living with agoraphobia. Okay. He calls the G P reception to see if he can get a telephone consultation with this G. P. However, the receptionist tells Shane that they're only offering face to face appointments at this time. So what type of discrimination is Shane facing, If any you can get one more. Answer it. Brilliant. So you're overwhelming. Majority went for indirect discrimination, which is the correct answer. Uh, you had someone go for E? Uh, I mean, I can see why you would go for e. Uh, but within this context, uh, the question is leaning towards discrimination. Uh, just because this is, uh, really a design flaw where this is a patient who is seeking advice. You can't get advice just because of the way the system is designed. So although it is a form of discrimination, um, it can be different to other forms of discrimination that you might be exposed to. Okay, Number four. So we've got Bobby. So Bobby comes into the pharmacy with his son Robbie, who's living with cerebral palsy. So Bobby is here to collect a prescription for his son Robbie. The dispenser refuses to give Bobby the medication for his son because they don't like Children receivable policy. So which specific type of discrimination best describes this inappropriate behavior? Don't will end up there. So most people have gone for a Everyone else went for B. Um, although although B is a form of direct discrimination, the question did say which specific type of discrimination. And if you're going more specifically, this is a discrimination by association. Um, so that would be the single best answer. The direct discrimination is correct. The single best answer is discrimination by association. So just make sure you read the final line of the questions a bit a bit more careful when you get to exams, because they do. They do like to do that on purpose. All right, this is the last question. Okay, So Peter is a Middle Eastern Christian living in the UK because of C S d. G p. For the first time due to a new pain he's been experiencing in his head on arrival. The GP refuses to see Peter because he doesn't like Muslims. So which specific type of discrimination is Peter facing? Wait for one more. Okay, So correct answer. Here is discrimination by perception. Uh, again, Although direct. Although discrimination by perception is a form of direct discrimination, the question did say, which specific type of discrimination is Peter facing? So although direct discrimination is direct answer, it's not the single best answer. Uh, it is discrimination by perception. So even though Peter isn't a Muslim, he's perceived to be one. And that's why he's become discriminate against. So it's a discrimination by perception. So I've always wanted to say this, but that was just a whistle stop tour. I'm just for listening. I'm sorry we went over, like heavily. Uh, really do Thank you for, uh, spending your time here. Appreciate it a lot. So thank you. I hope this helped. If you've got any questions, put them in the chat, or you can just stick around. And I'm happy to happy to answer them. Um and yeah, I appreciate it. All right. Perfect. Thank you so much. The feedback form is actually a bit messed up. Give me a second. Um, I will need to. So if you guys can bear with me just for a few minutes, um, I'll post a new link out. Um, apparently, but no. Uh, yeah. If there's any questions? Do you let us know? Um, that's 19 a second. Wait, Um, John, you know, and so I think you're currently in here too, right? Uh, yeah. Yeah. Uh, for this second part, I don't remember having it in our in. Our thing is, it is a new thing that they've added. Uh, what do you mean? Um, the personality stuff? Because I think I don't think we got it in hours. It was It's in a It was an e learning module. Oh, Okay. Thank you for that. Um, definitely learned a lot from that. Everybody ignores. Nice. Thank you. I'm sorry, guys. Just almost there with the feedback forms. Just give me a sec. It's, uh I put the wrong name in, so it's a bit orcs, but, um okay, Perfect. I think that's done. Okay. Perfect. Um, so this is the new link. Sorry, guys. I hope everyone still around. Okay. Yeah, everyone is still around. Perfect. Yeah. Sorry for the wait. That you are. That's a new link. Hopefully, everything should be set, you know? Just double check it. Yeah. Perfect. Yeah. So that's a new link. Um, if you feel that said, we'll send all the other stuff as well. The the slides and resources, but so, yeah, thank you all for attending. Um, yeah. Please do. Fill fill out the feedback form. It will be of great talk to us. So I'll just stay on here for a bit longer just for you guys to fill out the feedback from's. And, um, if you have any questions, do you drop it in the chats as well? All right. I'll close the chart in about I mean, I'll close a call in about a minute or two. So, um, if anyone hasn't filled it in yet, please do fit it in, but yeah. All right. Perfect. Thank you. Everyone for attending. I'm going to close the chats now, so we'll see you in the next. Um, yeah. We'll see you in case 11. If you would like to join us, then. So yeah. Thank you, guys.