DIP Episode 349 - The Clutch Psych Pharm Review (for the psych shelf, Step 2CK, and Step 3)

Okay, welcome everyone. My name is divine. This is episode 349 of the Divine Intervention Podcast. This podcast is going to be a psych from a college review. In fact, I'm going to call this the clutch psych from a college review. So let me tell you who this is targeted towards. This is for people taking step two, CK, step three of the psych shelf. That's it. If you're studying for step one, you shouldn't be listening to this. Go to the specific psych from a college podcast. I've made a dedicated for step one. Okay, this is supposed to be a very high level clinical review that is more tuned to again the psych shelf, step two, CK or step three. If you know what I discussed in this podcast, or I guess I just are calling them podcasts since I'm going to be posting video versions and audio versions of these podcasts, I will be really surprised if you somehow happen to get a psych from a college question wrong on your shelf and believe it or not, from a college is going to be a big chunk of your psych shelf. If you're taking the psych shelf exam, probably about 30% of your questions are going to be from our college questions. Easy. And then for those of you that are studying for the USMLA exams, so I have two sets of review courses. I have a set for step two, CK step three. If you're interested in that, he starts as an MBME Testicking Strategy course. That's going to be taking place on the sixth of December from 2 to 4 30 p.m. Mountain Time.

Again, I've had tons of people take these courses. And again, we focus on test taking process just being good at taking tests and test taking strategies, especially pertinent to step two, CK step three. And I've also had some people just taking their shelf exams, take this test taking course. And they found you to be extremely helpful. The second course I offer for step two, CK step three is the review course, the 24 review course. That will be taking place from the seventh to the 10th of December. Right? So basically next month, if you're interested, just shoot me an email through the website. Or you can send me an email at Divine Intervention podcasts. So podcast with an S at the end at gmail.com and I'll give you some more information. And then I have an 81 hour step one course. Again, that will be taking place from the 27th to the 30th of December and from the 3rd to the 6th of January. If you're interested, again, it's going to be a case-based review. That's the thing that makes it very different from pretty much every other step one review course you'd see out there. It's going to be a case-based review. There's not going to be any stop lectures. And the goal is to just use cases and examples and context and integrations to expose you to the vast majority of the high-year things that are tested on step one. If you've listened to any of my podcasts, you know how I love to teach. You know how I love to use examples. You know how I love to use scenarios.

You know how I love to use integrations to drive my points home. That's basically what you're going to be getting for about 81 hours. Although we're also going to be spending a lot of time answering people's questions for the step one course itself. There's going to be a limited number of spots because I want to be able to heavily invest in every single person that attends. So again, if you're interested in any of these courses, go ahead and shoot me an email through the website and I'll be happy to give you some more information. So this review, let's just jump right into it. So what are the first few drugs I'm going to be talking about? Well, the first ones I want to talk about, right? I want to talk about the atypical anti-depressant. Right? So the first drug I'll talk about is bupropium. Right? We only bupropium. Bupropium is an NDRI. Right? It's a neuropinephrine dopamine reoptic inhibitor. This is the kind of thing that will give to a person that has depression and the person potentially smokes, right? Because it helps with smoking cessation. And also bupropium is pretty amazing because it does not cause weight gain. If anything actually causes weight loss, right? So if you have a person that has depression and they have like really huge weights, then bupropium is amazing for those people. Right? So bupropium, it helps with weight. It helps you lose weight. It helps with smoking cessation.

And another good thing with bupropium is it doesn't have those sexual side effects that we fight with the other anti-depressants. So if you see a person that is beginning to have like low libido or they're beginning to have like sexual dysfunction because they are being treated for depression. A very good drug to start those people on or to even add on to their SSRI therapy is bupropium. Again, bupropium is an NDRI. It's a neuropinephrine dopamine reoptic inhibitor. And then it's very high yield to remember that if a person has like an eating disorder, right? So let's say for example they have something like anorexia nervosa or bulimia nervosa. People with these eating disorders, they especially prone to developing electrolyte abnormalities, but then cause them to have seizures. These people should not be touching bupropium at all. If they touch bupropium, then unfortunately you're gonna be setting up those people for seizures. Remember bupropium can lower person seizure threshold. So that is something you absolutely try to avoid in a person that has again something that will just say them up for seizures. Either they have like an eating disorder that can cause them to have electrolyte abnormalities that can cause seizures or you just have seizure disorders for whatever reason. In those people, you want to make sure you go ahead and avoid bupropium.

Now what if they give you a question about a patient and they tell you that this patient is fed up with their SSRI because it's been causing a lot of sexual dysfunction and you're trying to find a new drug for them. That doesn't cause that sexual dysfunction. And then you look at all the answer choices on the exam. You don't superpropium as an answer. What do you want to go with? I hope you're saying oh divine, I'm gonna go with meritazapine. Meritazapine is a very powerful anti-depressant. Right? Meritazapine is an alpha-2 blocker. Remember the alpha-2 receptor is an adrenergic receptor that when you stimulate it, that decreases neurobeneferin release. So if you block it, that's actually gonna increase neurobeneferin release. That's how it helps us an anti-depressant. So the thing is meritazapine. This is one of those little non factoids that is very important to know for your shelf and step 2, see key step 3. Meritazapine actually does not have sexual side effects. So you can make those seem sort of similar no-sexual side effect claims that you make with bupropium for meritazapine. Meritazapine does not have sexual side effects. Now one thing when meritazapine though is that it causes people to sleep. Meritazapine is essentially an anti-histamine because believe it or not, it has the ability to block the histamine-H1 receptor. Remember if you take an anti-histamine, you're gonna feel sleepy. So it blocks the histamine-H1 receptor so it can cause sedation.

But meritazapine also causes you to gain weight. So again, if a person has depression and they're like anorexics or they have depression and they don't eat very much, meritazapine is a very good choice in those people on MBME exam. So this is a big thing to do about meritazapine for your test. Now what if they give you a question about a patient and they tell you that the patient will start on a side drug. And they tell you that this person has noticed like a blue-black discoloration of his penis over the last few hours, right? If you see something like that, what are you thinking about? But I would really hope you're saying, oh, divide. Oh, this is probably gonna be trasodone, right? Remember trasodone is a drug that has many different mechanisms of action. The big thing I want you to remember for your exams is that it modulates serotonin receptors. So because it has the ability to modulate serotonin receptors, it has so many different kinds of effects. The big thing to know about it is it's very sedating, but in addition to that, it can cause pre-epic. Remember, if you have an erection, that thing is supposed to cool down after a few hours. If it doesn't cool down, that's a big problem, right? Because if the penis is so engorcery blood, over time, that penis can undergo necrosis. And that's obviously not a good thing, right? So actually, how do we treat the prior pizm? That's a seducido trasodone.

The thing you want to pick on an embankment exam is I want to inject an alpha-1 agonist into the penis, right? So you can inject, like an intra-carver nozzle injection of something like phenol effort. Phenol effort is an alpha-1 agonist, right? Again, by doing that, you're going to be decreasing blood flow to the penis, right? So that will prevent it from, you know, essentially getting bigger, right? With all that blood that is engorging it, essentially. Right? And remember, prior pizm, is there some genetic condition that's associated with the prior pizm? On an embankment exam? Well, I really hope you're saying, oh, divine. For person who has sickle cell disease, those people can get prior pizm. That's something that's very high yield to know for purposes of your test. Now, what if they give you a question about a patient and they tell you that this patient has been, you know, for the last, you know, for the last two, three weeks, they've been having like various severe headaches. They've been having a lot of insomnia, right? That, you know, they've been trying to quit smoking and this quit, like, cold turkey, like two, three weeks ago, right? And then they say, oh, what's your next best step in management for this person? Well, this person obviously is withdrawing from, you know, this stopped smoking, right? So they're having some kind, they're having all these urges and things like that. Again, many times, right?

The thing that is very addictive in cigarettes is the nicotine, right? So many times you can do some kind of nicotine replacement therapy in these people. You can use like a patch, you can use like nicotine and osangies, things like that. But other things you can also consider using, you can use again, a drug like bupropion, remember bupropion is very good for helping with smoking cessation. And the thing that can help is the drug called varanic clean. Varanic clean works like nicotine. It's a partial agonist at nicotine receptors. It's very amazing for the treatment of smoking cessation, right? So that's something you can consider using on an NBM example for smoking cessation. And then two drugs that are kind of anti-depressants that I think I should talk about are these drugs of villazodone? They are both, they start both started with V's, right? So there's villazodone and then there's vodoxetine, right? Vellazodone is V-I-L-A-Z-O-D-O-N-E. And then vodoxetine is V-O-R-T-I-O-X-E-T-I-N-E, vodoxetine. Again, the key thing to know about these drugs is that they can inhibit serotonin reupti-crit, so you can potentially use these drugs for the management of measured depressive disorder. They are one of these newer sets of drugs that are starting popping up on the NBM exams in recent times. And then don't forget, if they give you a question about a patient, they tell you that, oh, this patient has been found was found down at a party, right?

And you know, they tell you that this person is very arahensible. I noticed that they have like bilateral popular meiosis. I you notice that their respiratory rate is like four. If you see stuff like that, I really hope you're saying, oh, divine. This person potentially has opioid intoxication, right? Opioid intoxication. What are you going to do in those circumstances? Well, you're going to give the person maloxone. Remember, maloxone is a new opioid receptor antagonist that can be used for the man that can use to, you can use it to essentially rescue that person very rapidly from that opioid intoxication. So I know some of you may be like, ah, divine. How do we differentiate opioid intoxication from benzoyntoxication? Remember, benzoyls will cause a respiratory depression, but you will not get any popular findings, right? That's how you differentiate those two things on exams. And remember, for presently intoxicated with benzoyls, you're going to be giving those people flomazineal, right? Remember flomazineal is a gabber receptor antagonist that can be used to rescue people from benzoy overdose, right? And remember flomazineal, you don't only use that to reverse benzoydaisy pins. You can also use flomazineal to reverse toxicity of the z-drops. These are drops for insomnia. The essentially work as gabber receptor agonists, but those things can also cause a profound respiratory depression. So these are going to be drugs like zopidem, zaleplon, and is zopiclone, right?

Zopidem, zaleplon, is zopiclone, right? So again, you can rescue people from those drugs with flomazineal, okay? But again, remember, an aloxone is how you rescue people from opioids, right? And let me just maybe throw in one bonus question for you here, right? So what if you tell you that, you know, this person, you give the person that aloxone, they came right back, but then this person is completely echinetic. They are not able to move. And what do you want to think about on your exam? I'll really hope you're saying, oh, huh, divine. Maybe this person doesn't have the gifting of water white from breaking bad in cooking those opioids. This person has MPTP toxicity, right? That MPTP has damaged the substantione migra, right? And because it's damaged the substantione migra, the person is having signs and symptoms of Parkinsonism. Now, don't forget the close causing of an aloxone is now trexone. But now trexone, even if it works like an aloxone, you know, it's an opioid receptor antagonist, we cannot use now trexone to treat opioid intoxication. If you try to give now trexone, your patient will be long dead before he kicks in. Remember, we use now trexone on MBME exams for treating alcohol use disorder, right? So when a person is like saying, you know what, I used to watch alcohol. I really, really want to stop, right? One thing you can do for them is you can put them in alcoholics and non-immers, but you can place them on one of two drugs.

One of those drugs is now trexone, right? Now trexone helps with a person trying to stop drinking. Another drug you can also use is e-compress it. E-compress it. To be honest with you, the drug that I saw from is something that I'll encourage you to think a few times above before you consider using on your exam, right? Because dysopharyn, you know, in some circles, people think that the use of dysopharyn is on ethical, right? So that's something you kind of want to keep in mind, for exams. Remember, dysopharyn, the way it works is that it inhibits acetaldehyde dehydrogenase. I'm just saying this for completeness sake. And inhibits acetaldehyde dehydrogenase, but inhibiting that enzyme, right? Acetaldehyde is going to build up. So if you drink, you're going to feel terrible, terrible, terrible, terrible, right? And remember, it's not only dysopharyn that can do that. There are many drugs that can do that, especially in metronidousine, right? So they can give you a question about a person that is being treated for either like giadial infection or whatever. And then the person is coming in with like vomiting, abdominal pain, altered mental status, stuff like that. That's a dysopharyn side effect, right? Remember, when you're taking a drug like metronidousine, the incoherty not to take alcohol, if not, you're going to get that dysopharyn side effect again from where? From the inhibition of acetaldehyde dehydrogenase, which can cause the person to have a build up of acetaldehyde.

And then you'll have those nasty, marly symptoms, right? Now, what if they give you a question about a patient that has used opiars for a long time? And they're like, you know what? I'm trying to quit. I'm trying to quit. What can you do for me? Well, one thing you can do for those people is you can put them on methodone, right? Methhodone is a long-actin opioid receptor agonist, right? It's a long-actin opioid receptor agonist is very good, but one thing you want to keep in mind with methodone is that it has the ability to prolong the cutine interval. So many times on these exams, they will say, oh, in prior to studying methodone therapy or prior to studying like long-term therapy, what is the next best step in management? And the right answer may be to get an EKG to check the cutine interval. If the cutine interval is more than 440 milliseconds, you want to think twice before you put those people on methodone. You may want to consider another drop like buprenorphine, for example, right? You want to consider another drop like buprenorphine, things like that, right? Now, what are the first line medications for treating depression? Notice I'm just going almost like freestyling this, right? So what are the first line medications for treating depression? Well, I hope you're saying, oh, divine, SSR Is, right? So again, SSR Is, they are very high-value drops.

In fact, if you take your side shelf and you don't pick an SSRI as an answer, by the time you're done with the exam, something that's probably going horribly wrong with the test that you just took, right? So remember SSR Is, there's many, many times, there's like Citarlopram, E-Citarlopram, Fluoxetine, Paroxetine, Fluvoxamine, right? Setyrlin, there's many, many SSR Is, right? And again, the inhibits the reoptic of serotonin. Now, what are some key high-value things to love about SSR Is? Well, remember SSR Is as a class can cause sexual side effects. That's very high you to know. SSR Is as a class, right? They can occasionally also cause SID, right? That can potentially cause hyponitrimia and seizures, right? Because you're sucking up a lot of water from your urine, right? And then don't forget that SSR Is, they also have this discontinuation syndrome associated with them. If you take an SSRI, right? And you stop it abruptly, that can cause you to have this discontinuation syndrome. Although, that's not something we worry about with Fluoxetine. The thing is Fluoxetine has metabolic, they have a very long half-life, right? So you can stop Fluoxetine abruptly. You're not going to get, you're not going to get one of my thinking about here. Discontinuation syndrome from Fluoxetine, right? Well, don't forget your other SSR Is. Or remember, you have things like Setyrlin, Setyrlin is a great SSRI in pregnancy, right?

If you look at a drug like Citaloprom, is the SSRI that has the fewest, like, the best side effect profile, right? If you look at peroxetine, you certainly don't want to give peroxetine to a pregnant woman, right? I believe it's like pregnancy category D from Lomins Stake It, right? You can postpone her hypertension in the fetus, right? So those are all things you want to keep in mind with SSR Is. I mean, what do we use these things for? They're first line for, like, measure the perceived disorder. First line for generalizing anxiety disorder. First line for pre-manstrual syndrome, right? They're the first line for OCD. They're first line for PTSD. They're first line for panic disorder. They're first line for, if a person has like premature ejaculation, right? Because again, they're essentially using the sexual dysfunction to your benefit. If a person's sexual function is too great, they can kind of slow them down a little bit by giving them an SSRI, right? So SSR Is are very good for many of those circumstances. Now, the close cousin of SSR Is, at the SNR Is, right? So if they give you a question about a patient and they tell you that this patient was recently studied on some kind of anti-depressant, and this person is having a lot of trouble, like, sleeping, for example, right?

Having a lot of trouble, sleeping, and they tell you that this patient's blood pressure has been going up over and over, like, over time, if you see that you want to think about an SNRI, your SNR Is at the serotonin, neuropinephrine, reoptic inhibitors, right? SNR Is, serotonin, neuropinephrine, reoptic inhibitors. So how do these drugs work? They prevent the reoptic of serotonin and neuropinephrine, right? Now, it's actually very high you to know for purposes of the USML exams, right? That these drugs can raise blood pressure, right? These are going to be drugs like vanilla vaccine, desven la vaccine, melmassi-pran, duloxetine, right? Those are all drugs that fall into that category, right? Now, the big thing with these things again, the raised blood pressure, and they also have sexual side effects, right? The cross-sexual dysfunction. That's something to keep in mind. But one other thing I will say about these drugs is it's actually kind of high you to know that you can use them for, like, diabetic neuropathy, especially like painful diabetic neuropathy. Duloxetine is a great drug for that purpose. But then the other drug melmassi-pran in addition to duloxetine again via SNR Is, you can actually use these drugs to treat fibromyalgia, right? So that's going to be a lady, right? Again, can men get fibromyalgia? Yes. But on MBM exams, no, right? So if you see a woman and she has tenderness like everywhere in a body, they'll say like multiple points of tenderness.

That's fibromyalgia. You want to go ahead and use duloxetine or melmassi-pran in those people. Although you can also consider using a drug like pregabaline or gabapente, right? And then what if they give you a question about a patient? The teller that this patient was recently started on an antidepressant and then they find a suicide note by the patient's side. And the patient is altered. The person says that, oh, he has had a few generalize the tonic lonic seizures. And then we show you an EKG. You notice that the QRS complex is wide. If you see that, what are you thinking about? I'll really hope you're saying, hmm, divine. This looks like TCE toxicity, right? Remember, you're tricyclic antidepressants. I'm going to be drugs like not triptiline, amitriptiline, clumipramine, right? They either end in triptiline or premin. Now, these drugs tricyclic antidepressants, they do a lot of stuff, right? But primarily, they use the treatment of major depressive disorder, right? But in addition to being used for major depressive disorder, you can use them for nocturnal and eurysis, right? Nocturnal and eurysis, they're like a second third line agent for the management of nocturnal and eurysis, right? Now, what are the big toxicities with these drugs? Remember, these drugs are cardiotoxic, because essentially, they are sodium channel blockers. Think about it. When you take a TCA, it's almost like you're taking a class one anti-rhythmic, right? Those things are pro-irhythmic.

They can cause people to have arrhythmias, right? They can also widen the QRS complex, right? They can widen the QRS complex. That's like the big, big, big thing. And whenever you see that white QRS, the first thing you want to give those people is sodium bicarbonate. Sodium bicarbonate is the drug of choice for treating the cardiotoxicity, right? The widening of the QRS, the prolongation of the acute interval. That's a associated with taking a tricyclic antidepressant. That's very high yield to know for the purposes of your exam. Now, it's very high yield to know as well. If you tell you that, oh, people were studied on these drugs. And then whenever they rise out of bed, they feel very busy. If you see that, think of orthostatic hypotension, right? Orthostatic hypotension arises because tricyclic antidepressants have the ability to block alpha-1 receptors. So they block alpha-1 receptors. So they can certainly cause those problems, right? And again, these drugs can trigger the lyrium, right? Because they have anti-cool energy activity. Remember, anti-cool energy are big drugs that can trigger the lyrium, right? So like, diphenhydramine, for example, is an antistamine, but it has very powerful anti-monstrino activity, right? So you can also trigger acute lyrium, right? So those are all high yield things you want to keep at the back of your mind with TCA's. And one thing I want to say about TCA's is that there's a special TCA that we use for the management of OCD.

In fact, it's a second-line agent for the management of obsessive-compulsive disorder. This TCA happens to be clomypramine, right? Clomypramine is a second-line agent. Remember, I said first-line for the management of OCD is an SSRI. What second-line is going to be clomypramine, right? Clomypramine, clomypramine. Although, remember, the president has OCD. In addition to drugs, you should also consider like CBT, the CBT for OCD, right? What do you think it is? Well, I would hope you're saying O-Divine. This is something we call exposure and response prevention, right? Exposure and response prevention, you expose them to the thing that kind of gets them going. And then you try to get them to make better choices in those circumstances, right? Exposure and response prevention. Now, one high yield thing, other high yield thing to know about TCA's is if you're stopping an SSRI and you're studying at TCA, you need to wait for at least two weeks. You need to give like a two week washout period. If not, you have a very high risk of triggering serotonin syndrome, right? Now, what are the close causes of TCA's? Well, think about the MOI's, right? So this is going to be a person, this is going to be like a hypertensive urgency or emergency question in the setting of a person that you know is eating at some restaurant and we recently started on an anti-depressant, right?

Remember your MOI's are going to be drugs like trinocipromine, isocarboxazide and phenols, and I'll say that again, right? Isocarboxazide, that's ISO-C-A-R-B-O-X-A-Z-I-D, right? Isocarboxazide phenols, right? PHE-N-E-L-Z-I-N-E, right? And also trinocipromine, right? So T-R-A-N-Y-L-C-Y-P-R-O-M-I-N-E, trinocipromine, right? So this is your MOI's, right? So these drugs, right? They essentially prevent the breakdown of your, of your, you know, your serotonin, your neuropinephrine, your dopamine, right? So that's why they're great as anti-depressants, but remember these drugs, they can cause hypertensive problems, right? Because again, M-E-M-M-M-O-M-I-N-O-X-D, right? It's an enzyme that also breaks down thyroid. Tyramin is a, is a, is a substance that we can find in certain foods that says the empathomimetic, right? So it can cause powerful, powerful, powerful hypertension. So when you eat, it is normally broken down by M-M-O-M-I-N-O-X-D, right? But if you dig in the M-M-O-M-I-N-O-X-D, inhibitor, then all these tyronin rich foods can cause problems, right? So like cheese, wines, smoked foods, things of that nature, right? So that's something you certainly want to keep at the back of your mind for purposes of the USMLE exams, right? And then again, I said that we can use SSRI, SSRI, SNR Is for the management of generalizing anxiety disorder. Well, what else can we use for GAD? Actually, the second line agent for GAD is BUSPIR, right?

Many people call this BUSPIR in the hospital, right? BUSPIR. Remember, BUSPIR works as a partial agonist at serotonin, 5-HT-1-E receptors. So it's very good from that perspective. And then what if they give you a question about a patient, they tell you that the person comes in, is brought in by their spouse because they've been only sleeping for like two hours a night, they have like, you know, very rapid speech, they have just been very go-directed and activity-directed. If you see those people, right? This person clearly has bipolar disorder. Well, we know that if a person has bipolar disorder, you should probably put them on some kind of mood stabilizer, right? But let me tell you this, this is something that's very high you to know for exams. That many people mess up on tests. Let me tell you this, when a person comes in and they are cutely manic, what is the first drug you're supposed to put them on? You're supposed to put them on an anti-psychotic, anti-psychotics at the drugs of choice for acute menia. Because the thing is the mood stabilizers before they will kick in, it's going to take a long time, right? So you put the person on an anti-psychotic first to calm them down and then you add on some kind of mood stabilizer, right? You can add something like lithium, lithium is like the poster child, most stabilizer, right? So what's the big thing with lithium?

Well, the thing is, good thing is, we don't know how lithium works, you know, it does some stuff with in acetotryphalcy, but that's beyond the scope of our discussion. But lithium, you kind of need to know the side effects, remember, lithium, the big side effects with it and the tremors, right? Lithium causes tremors, those tremors actually respond very beautifully to what? A beta blocker, like perpranolop, for example, right? So lithium causes tremors, lithium can cause renal dysfunction, right? So if your kidneys don't work well, want to think twice before giving a person lithium, because if you're a pyrrepolytic index of lithium, it's very narrow, right? It's very narrow. And don't forget, lithium can also cause hypophyroidism, right? And again, remember, if one is pregnant, you want to think twice before giving her lithium, because it can cause Epstein's anomaly, right? So it's going to basically mess up the right side of the person's of the fetus is heart, right? Now, actually, one weird factoid about lithium, that is very high yield to know, is that lithium actually has the ability to, it actually reduces the risk of suicide, right? So it has like a survival benefit, right? Lithium does in fact have a survival benefit, right? It's one of two drugs in all of psychiatry that you need to know for your exams that has a survival benefit. Lithium is one of them. The second one is going to be command of, I think, clasping, right? Closipping.

Closipping also reduces the risk of death. And problem is, clasping also kind of causes other problems that I'll probably talk about shortly here. So it's very high yield to know those things about lithium, right? All these things have said, lithium very high yield to know. Remember lithium, again, one big side effect, obviously, right, is the nephrogenic diabetes and sypidus, right? So if we go back to our renal from ecology, we know that in the distal part of the nephron, we have the principal cell that of the collecting duct, right? That principal cell has an inek channel, right? ENAC channel. Lithium goes in through that channel and messes of the signaling cascade of the of a ADHD, right? You know, those visual present V2 receptors of ADHD, right? So if you want to prevent that from happening, well, the thing you can do is you can block those inek channels, right? You can use drugs like a milleride or triamterine to block those inek channels. Lithium won't come in and cause cause havoc, okay? And one thing I guess I would say is if a person is having really bad lithium toxicity, one thing you can do to really bring to bring down the lithium levels very quickly, is actually hemodialysis. Dialysis is amazing, amazing, amazing, amazing, for bringing a person's lithium levels down quick, right? Bringing a person's lithium levels down quick. Now let's be going to antipsychotic country, right? So we know that we use antipsychotics for many things, right?

We use them for treating the lyrium, we use them for treating schizophrenia. Remember, that's where you have, you know, your hearing voices for more than six months. We also use antipsychotics for again acute menia, right? If a person has like PCP intoxication, again, antipsychotics are great for those people. So remember the antipsychotics they call them many different flavors, right? So there's the first generation and in the first generation there's two main categories, right? The first category are the hypotency ones, right? So this is going to be drugs like jaloparidol, flufenazine, right? Trifluoparazine, right? Those are the first generation, you know, they're very powerful, right? jaloparidol is actually the most powerful of all of them, right? They're very powerful antipsychotics, but we have the, and those ones, they just, they blocked dopamine receptors, they're very good at it, very amazing at it. The only problem is they have a very high risk of extraperamidol side effects, right? We'll talk about those extra pyramidal side effects in a bit. But under that first generation, we also have the low-potency ones, right? So the low-potency ones, they are going to be drugs like clopromazine, right? CHLOR, PRO, N-A-Z-I-N-E, clopromazine. And then another one is fireridazine. It's a low-potency, first generation antipsychotic. Fireridazine is spelled as, I believe, THIO, fire-RI-D-A-Z-I-N-E, fireridazine, right? Fireridazine, right?

So the thing is, what are these drugs called low-potency? The thing is, they are low-potency because they don't only block dopamine receptors, they block other things, right? In fact, remember when I talked about tricyclic antidepressants, I said, we have anti-harm side effects. Well, what in the world are we mean by anti-harm? Well, the H means anti-H1 sedation, anti-alpho-one, right? Orthostatic hypotension, anti-M, right? The M is musketic. Well, the thing is, those anti-harm side effects, you also find them in the first generation, low-potency antipsychotic, again, drugs like clopromazine and fireridazine, right? So these drugs can cause all those things like sedation, orthostatic hypotension, they can trigger delirium, right? So giving a drug like clopromazine or fireridazine, for a person that has acute delirium, it's not a smart idea. You want to go more with a hypotency, first-generation agents in those circumstances, although you can also use the second-generation agents for those circumstances. Now, one weird, bizarre thing that's high you to know about the first-generation low-potency antipsychotics is for whatever bizarre reason these things love to mess up a person's eye, right? So what are the big things to remember? Clopromazine remembers C in clopromazine for the C in your cornea, right? Clopromazine can cause problems in the cornea, it can cause deposits in the cornea. Remember, amyldoron is also a mice fancy drug that can cause a corneal deposits.

And then don't forget fireridazine, remember the teeth fireridazine for the teeth right now, right? It can also cause something that looks almost like a red mitis pigmentosa. As you will see when we get to the atypical antipsychotics, quityapine can also cause eye problems, it can cause cataracts, right? It can cause cataracts. Again, that's very high you to keep in mind for your exams. Now, let's talk about the first-generation of the antipsychotics. Now, let's hop over to the second-generation of antipsychotics, right? So the thing is, again, these drugs, they're good for positive symptoms because, you know, they block dopamine receptors, but they also good for negative symptoms because they block serotonin receptors, right? So is that serotonin receptor blockade that makes them very good at dealing with negative symptoms? Because the first-generation antipsychotics, they are amazing for treating positive symptoms. In fact, they work better than the second-generation for treating positive symptoms. But these drugs, they're not very good for negative symptoms, right? In fact, they were saying the first-generation agents, they were saying negative symptoms. The second-generation agents are way better than the first-generation agents at treating negative symptoms, right? Because think about it, you may see, I'm not divine. But, you know, first-generation antipsychotics, what do you mean by negative symptoms? Well, think about it.

If you notice a person that has been placed on, like, Hallopere dole, how do you think those people are at the end? You see, they are very mute, they're very calm, they're very docile. That thing you're seeing is actually a worsening of their negative symptoms, playing out right before your eyes, right? Literally playing out right before your eyes, right? So, again, the first-generation agents, they are amazing for positive symptoms, they are better than the second-generation agents, but they are awful for negative symptoms, right? So, they are good for positive symptoms, awful for negative symptoms. But the second-generation, they are good for positive symptoms, not as good as the first-generation, but they are amazing for the negative symptoms. That's why many times when people have schizophrenia, and they are being started on an antipsychotic, most times you go with a second-generation agent first, right? Now, the second-generation agents, they have some unique things about them that I think we should discuss, right? So, like, the first one I think I should discuss is going to be a drug like RIP, right? RIP, RIP, RIP, RIP, RIP, RIP, RIP, is all, again, is an atypical antipsychotic, but one thing that's very high-youtes on about it is that it's not a classic dopamine receptor antagonist. What it does is, it's actually like a partial agonist at dopamine receptors. Next one I'm going to talk about is going to be respiratory doom, right?

Remember, again, respiratory doom, the big thing you want to know for purposes of MDME examines of all the second-generation antipsychotics is the one that has the strongest association with extra pyramidocyte effects, but it can also cause you to have Ghanaic homostia and Galactorea, okay? Is the one that has the strongest association of all the antipsychotics? First-generation second-generation doesn't matter, right? With hyper-prolectinemia, right? With hyper-prolectinemia, remember, that is something that arises from the tuberoo-informedibular pathway, right? And then don't forget clasopin, right? Closopin, again, is one of those drugs I said reduces the risk of suicide in psychiatry, right? Kind of like lithium, right? Now remember, clasopin, actually, of all the antipsychotics, it is the most effective. It's even better than halopyridone, but clasopin is like a third-line agent, why? Because it causes a lot of problems, right? It can cause like a metropinic fever, right? Because it can cause the endocrinolocyteosis. So if you see a person having a fever, after they were studied on any psych med, it's clasoping their asking you about on your exam, right? And then remember, it can also cause myocarditis, it can cause inflammation of the heart, and that can lead to heart failure, right? And remember, clasoping can also cause a person to have hyper salivation, right? So again, those are all the high-yield things to keep in mind with clasoping, right?

Again, you need to monitor a person's blood levels, like the white blood cell counts, if you're on clasoping, right? If you're on clasoping. Now, don't forget Ziprasidone, right? If you look at all the etymiculanticycotics, all the anticycotics can prolong your cutie interval, but Ziprasidone, I think this is the drug that's called geodone in the hospital, right? It's pretty amazing. Like, if your cutie interval is prolonged, if it's more than 440, you should not be on Ziprasidone, right? Because if you put a person on Ziprasidone, they could potentially get a prolongation of the cutie interval, the whole way to truss out the plant, and then they will die, right? And obviously, that's not an ideal situation. And then, if they give you a question about a patient, and they tell you that this patient has like diabetes or the metabolic syndrome, or, you know, they fall a lot, right? Like an elderly person, and they say, oh, what anticycotic is contraindicated in this person? I really hope you're saying, oh, divine, let's not put this person on ulansapine. Remember, ulansapine can cause very big time with gain, right? It can cause with gain, it can cause the metabolic syndrome, right? So that's something you want to keep at the back of your mind, for example. And then, I think another one I should talk about is quethyapine, right? So, quethyapine, quethyapine, quethyapine, it's a high-yout ATP-guelanteicycotic to know, because we use it for a few things, right?

Obviously, we use it for schizophrenia, right? But another thing with quethyapines, if a person is on Khabidopa, Livo Dopa, for Parkinson's, and they start having like hallucinations, I mean, obviously, the first thing you're going to try is you're going to try to lower the dose of Khabidopa, Livo Dopa. Many times, they can tolerate that, right? So, your next step is to give them quethyapine. You cannot give them any other kind of anticycotic, because all the anticycotics are just too powerful, right? They're too powerful, right? So, quethyapine, you know, it's like kind of like a mild mellow anticycotic that you can use in those people, but again, don't forget, with thyapine also has the ability to cause cataracts, okay? Has the ability to cause cataracts, right? So, let's talk about these extra pyramidal side effects, well, how do these things work? Essentially, with the extra pyramidal side effects, right? They can give you a question about a person starting on an anticycotic, and then you notice the person, right? He's having like this very, you know, like stereotypical, like neck movement or whatever, right? Like a day or two or a few hours after standing on an anticycotic, think about Cudestonia. How do you, how do you should a Cudestonia? Well, you can use biphenhydramine, again, remember, it's a powerful antihistamine, but it's also a very powerful, most greenery receptor blocker. Another drug you can use for these purposes is Benstruoping.

Benstruoping can also be used for acute dystonia. And then remember, if they give you a question about a person, they can't seem to, they feel like their body is jumping everywhere, right? They can't seem to stay in like one particular place. That's gonna be a caticia, right? A caticia is treated with beta blockers, right? Beta blockers are the first line agents for the management of a caticia, but if whatever reason, the person has the contraindications of beta blockers, maybe they have like bad asthma, right? Where if you give them a beta blocker, their earwaves will close, then given a benzodiazepine in those circumstances will be smart. Now, let me tell you something. There are three high-yield things you want to keep at the back of your mind for MDM exams with beta blockers, psychic exams with beta blockers. Beta blockers are good for tremors. Including the tremors you get from taking a lithium. Beta blockers also good for stage fright, and then beta blockers, they are also an amazing, amazing, amazing, for the management of, of, so I've said tremors, stage fright, and then acathesia, right? They're good for acathesia, but again, remember, the second line agent for acathesia is gonna be a benzodiazepine. Stage fright, actually, the second line agent also happens to be a benzodiazepine. So, again, if you cannot take a beta blocker for whatever reason, you can go ahead and put that person on a, on a benzodiazepine, okay? Put them on a benzodiazepine.

And then remember, Parkinsonism is also an extraperimidocyte effect, right? So, that Parkinsonism, what can we treat it with? Again, remember that Parkinsonism arises from the migros trytopathway, right? I guess maybe I should mention the pathways because I've gotta talk about them, right? So, remember the, hyper-productimemia pathway is the tuberoid formibular pathway, right? The positive symptoms of schizophrenia, gonna be controlled by your mesolimbic pathway. The negative symptoms are gonna be controlled by your mesocortico pathway, right? And then the movement symptoms, extraperimidocyte effects, try to discontentia, that's gonna be more in migros trytopathway, right? So, Parkinsonism, right? With anti-psychotic, right? You want to think about that with a drug line. You want to consider treating that. First line with a benzodiazepine. The first line agent, you can use benzodiazepine or you can use a drug called trihexifenidial. Trihexifenidial is spelled as TRIHEXYPHNIDIL, trihexifenidial. Those are both muscronic receptor antagonists. But if you don't see that as an answer, you can consider using a dopamine agonist, a drug like bromo-cryptine or carburegoli, right? And then don't forget, right? If you notice like months, years after a person was started on an anti-psychotic, they, you know, they have like these movements that, oh, if they are aware of it, they can control it.

But when they are not aware, they do these things like, let's say they keep moving their tongues or whatever. If you see that, that's tardive dyskinesia, right? Tardive tardy comes late, tardive dyskinesia, right? You can treat that with a drug called valbenazine. You can either use valbenazine or you can use the drug called tetrabenazine, right? So valbenazine or tetrabenazine. Although many times, if you don't see that as an answer on exams, one thing you can do is, if a person has tardive dyskinesia and they are on a typical anti-psychotic, you can go ahead and stop that typical anti-psychotic and then switch them to an etypical anti-psychotic, okay? And then don't forget that you can also get these etroperamidol symptoms from taking the drug-medal clopromide. So they can give you a psych question about a person that's like a, like a diabetic, right? And they have like gastroparesis and they took a drug and they have any of these etroperamidol side effects. If you see something like this, think about middle clopromide. It's a dopamine receptor antagonist that can certainly cause these kinds of problems. And then it's also very high yield to know that these anti-psychotics, right? If they tell you that, oh, a person, you know, was studied on an anti-psychotic and then you notice that they have like muscle rigidity, lupus, cytosis, you know, like a high-wide blood cell count, high-fifers.

If you see that, you want to be thinking about your elliptic malignant syndrome, right? Remember, your elliptic malignant syndrome, the first line drug for treating that is dantrullin, right? Dantrullin. Dantrullin is a calcium channel blocker. It's a ryanodine receptor antagonist. It prevents you from releasing calcium from the sacroplastmic reticulum. It's very helpful, helpful in those circumstances. And then serotonin syndrome is a close causing, right? Of, I guess dantrullin is not just for NMS. You can also use it for malignant hyperthermia, right? Remember, serotonin syndrome, right? We can treat it usually with benzodiazepines. Benzos are the first line agents for treating serotonin syndrome. If you don't see that as an answer or if that doesn't work, you can then consider superheptidine. CY-P-R-O-H-E-P-T-A-D-I-N-E, right? So superheptidine, right? It's an anti-histamine that has the ability to block serotonin receptors, right? So you can use superheptidine on the dose of circumstances. And then since we're talking about benzos, right? Let's go into benzos, right? Malas will do that, right? So remember your benzos, right? In fact, maybe I should talk about these three as at once, right? So let's talk about the benzodiazepines, the barbitrate, and the z-drugs, right? The z-drugs, right? So remember your benzos, right? Your endympamolab, right? Although there's one weird one called chlorides epoxide. It's a long acting benzodiazepine.

And your barbitrate, your endymbabinol, or pentol, or thaw, right? And then we have the z-drugs, right? These are drugs for insomnia, right? These are going to be drugs like zopidem, zalaplon, and zopiclone, right? So zopidemzalaplon is zopiclone, right? So remember, your benzos, the increase the frequency of opening of GABA receptors. Remember, those GABA receptors are chloride channels, right? Now your barbitrate, the increase the duration of opening of those GABA receptors, right? Again, those GABA receptors are chloride channels. Your z-drugs like zopidem, zalaplon, and it's zopiclone. These are drugs that are GABA-A receptor agonist, right? GABA-A receptor agonist, right? GABA-A receptor agonist. Now, remember, we've talked about how you use flomazinol to rescue these people, right? But again, remember, you can use benzos for quite a number of things. You can use it for alcohol withdrawal. You can actually use like a light benzoyl like a clonazapam to help people that have like sleep problems with adjustment disorder, right? You just give them like a very small dose for a very sharp period of time, right? And that can help those people. And then remember, benzos are the drugs of choice for, for patients like cocaine and toxication, right? You actually give them benzos first. Benzos are going to calm them down, right? And actually, benzos will lower those people's blood pressure, right?

And they remember, we said benzos are second-line for acothhesia, they are second-line for stage fright, right? Remember, benzos can cause a profound respiratory depression. And you can rescue those people with flomazinol, right? With flomazinol. With flomazinol. Now, what if they give you a question about a person that has this irresistible urge to sleep? That's an aqualepsy, right? Remember, it's a sleep disorder. So we're going to do polysomography to make the diagnosis. Well, how do we treat narcolepsy? We can treat narcolepsy by giving us stimulant, right? So we can give like dextramphetamine, right? Or we can give a drug called modaphineal, right? Modaphineal. Now, one of the drugs you can use in narcolepsy is there's this thing that happens in narcolepsy called, what is it called? Caterplexy, right? We call it caterplexy. Caterplexy is where like if you see like blood or you express emotion, you go straight into REM sleep. So you're like, let's say I'm laughing. And then I go straight into REM sleep, right? That's caterplexy. The drug you used to treat caterplexy on MBME exams is a drug called sodium oxybit, right? You can use sodium oxybit for those purposes on MBME exams, right? So those are the things you use for narcolepsy. Now, what if they give you a question about a person that is having sleep problems and they tell you that, oh, they feel like something is moving on their legs at night?

If you see something like that, one thing I really, really want you to think about on your exam is restless legs syndrome. Remember, restless legs syndrome has a strong association, right? With, um, come on divine thing, has a strong association on iron deficiency anemia, right? But how do we treat restless legs syndrome? Remember, one set of drugs you can use, you can use a dopamine agonist. So I know some of you may be like, huh? Bremocryptine carbonyl, well, the answer to that is no, you cannot use Bremocryptine carbonyl. The drugs you're going to use for restless legs syndrome are going to be drugs like, um, primary pexol and rupeinero, right? Primary pexol and rupeinero. Those are dopamine agonists that are indicated for treatment of restless legs syndrome. Another set of drugs you can use to treat restless legs syndrome is a babiterate. It's actually known as premedone. P-R-I-M-I-D-O-N-E. Premedone is a babiterate that can be used to treat restless legs syndrome, right? Most people that have restless legs syndrome, you're going to work them up for iron deficiency anemia. Again, that's kind of high yield to know for exams, right? And again, remember for pressing house Alzheimer's, what part of their brain is messed up? Well, don't forget is the basal nucleus of maynard, right? That's the part of the brain that makes acetylcholine, right? So how can we treat that? Where we can treat that, by giving an acetylcholine esterase inhibitor, right?

Because that will boost up your levels of acetylcholine. Again, it's not just any acetylcholine esterase inhibitor. There's only three, you should pick on your exams, right? So what are those drugs? Well, these are going to be drugs like dunepezero, right? It's going to be drugs like galantamine, going to be drugs like reverse teemine, right? And then what if they give you a question at this point, I'm just kind of freestyling to kind of wrap up this video, I've definitely gone on for a long, but again, unfortunately, there's a lot of drugs in psychiatry, right? So let's see, if they give you a question about some child, right? And this child, you know, always talks out of his turn, cannot stay put, you know, having educational problems. But if you see that, that's ADHD. Well, how do you treat ADHD? Remember, the first line treatment for ADHD is going to be a stimulant, right? So something like, again, like methylphenidate or dextramphetamine. Second line, I'm going to be your non-stimulants like atomoxetine. Atomoxetine is essentially an SNRI, believe it or not. And then the third line agents are going to be your alpha two against, right? So these are going to be drugs like clonidine or guanfacin, right? So clonidine or guanfacin. Now remember, clonidine is also used for something else on exams. We can use clonidine, right? To treat opioid withdrawal. Remember, opioid withdrawal is not fatal. If you want to make those people feel great, you can put them on clonidine, right?

Because again, many of those opioid withdrawal symptoms are hyperadenergic symptoms. Clonidine being an alpha two agonist can really calm those people down, right? Can really calm those people down. And then don't forget, if a prescience PTSD, remember, we said first line is going to be an SSR, right? But if you're having nightmares, remember nightmares or curtailing REM sleep, if you're having nightmares, the drug you can use for those people is going to be a drug like prousocin. Remember, prousocin is an alpha one blocker, right? But again, because it's an alpha one blocker, it can potentially cause autostatic hypertension, especially with your first dose, right? It can potentially, on MD exams, cause some kind of autostatic hypertension, right? And then again, your mood stabilizers, every now and then, they like to throw in a question or two on these things. Again, I will go memorizing tons and tons of stuff, but don't forget things like our pre-carset, right? If our pre-carset, you shouldn't give it to a pregnant woman ever, right? And remember, for our pre-carset, there's hepato toxic, right? It can cause a lot of liver toxicity. Carameezapine is another most stabilizer, right? Remember, it can cause SIDE, so it can cause hyponitrine, and you don't forget carameezapine can also cause agronolusitis, right? It's very high, you know, the carameezapine can cause agronolusitis. So don't forget your two drugs, like, they're your side shelf, but then cause agronolusitis.

This is going to be drugs like carameezapine, and you don't forget your second generation anti-psychotic, like closapine, right? Like closapine. And then, remember, if a person has really bad hypertension with cocaine intoxication, again, I said, Benzos at first line, but if you don't see a Benzos and answer, you can actually consider giving an alpha-1 blocker, like Fentula-mean, right? Fentula-mean is a reversible alpha-1 blocker that can really help with really bringing down a person's blood pressures, right? When they have cocaine intoxication. So, I think I'm going to go ahead and stop here. Well, thank you for listening to me. I think I've blabbered a lot. I mean, this is almost like, this is just over 47 minutes. At this point. But again, I'm telling you, this podcast is very, very high yield. If you know the stuff here, you're going to do really well on the pharmacology portion of your side shelf. I feel like I even talked about a bunch of weird pathologies along the side. Again, as I do, at the end of every podcast or video, I do offer one or one tutoring for many exams, step one, step 2ck, step three, pre-clinical med school exams, 30-ish-off exams, offer review courses for step one. Remember that one is coming at the end of December. That's at the end of next month. Then I also offer like a step 2ck step 3 review course, right? It's 24 hours long. The step one course is an 81 hour course. And also for step 2ck step 3, I offer a test-taking strategies course.

And again, please hit the subscribe button, right? This You Tube channel, Divine Intervention, the USMD podcast and videos. Again, any little bit of support certainly helps. And then also, I have all my podcasts on the website, Divine Intervention Podcasts.com. In fact, if you subscribe to my podcast website, whenever I make a new podcast, you're actually going to go ahead and get an email notification. And then I have these podcasts, at least the most recent 150 on Apple podcasts, on Google podcasts and on Spotify, right? So I have it on those three podcast platforms. So again, if you want to listen to the most recent 150, that's a good place to go. But if you want to see everything from episode one, then you want to go all the way to my website again, Divine Intervention Podcasts.com. And then, I know I, you know, this was probably something that started last year. So I get in tons of emails from people saying, Oh, Divine, I really love the life lessons that you give at the end of your podcast, right? So I decided to start another website completely, right? It's called Divine Intervention Life Lessence.com. If you go on that website, you're actually going to see life lessons podcast, right? So many of you know I'm a Christian, right? So just a lot of bible basteach in some of it is like 10 minutes, 20, so much 20 minutes. I actually made one on marriage, relatively recently, believe it or not, like, you know, how to find a person to marry, basically.

I guess it's made in my matchmaking podcast. But essentially, I have about 36 episodes, I think now, right? And actually, it's also an Apple podcast. If you look for Divine Intervention Life Lessence on Apple podcasts, again, just bible basteaching that is targeted towards like some common problem that humanity faces like I've had podcasts on how to keep the money that you make, right? Podcasts on being diligent, podcast on being patient, stuff like that, right? Just common things that people kind of foreshort with, including myself, right? I'm still working on those things as well, right? But again, I feel like many people that I've listened to, those have found them to be really, really helpful. So I wish you all the best for those taking your your psych shelf or if you're, or if you're studying for Step 2, Step 3, I really hope you find this podcast to be helpful. So thank you for listening. Have a wonderful evening. God bless you. Thank you and goodlakers.

Bupropion. It helps with smoking cessation and does not cause weight gain; in fact, it can promote weight loss.

Mirtazapine. Its $\alpha_2$ blockade increases norepinephrine release, and its H1 receptor antagonism causes sedation/weight gain.

Naloxone. It is a pure opioid receptor antagonist.

Tricyclic Antidepressants (TC As). The primary antidote for TCA-induced widening of the QRS complex is Sodium Bicarbonate.

Agranulocytosis (low white blood cell count). This requires mandatory monitoring of WBC counts.

SSR Is/SNR Is are first line. Buspirone (Buspar) is a common second-line agent.

Benzodiazepines increase the frequency of opening; Barbiturates increase the duration of opening; Z-drugs are $\text{GABA}_A$ receptor agonists.

Benztropine (or other anticholinergics). They are muscarinic receptor antagonists.

The mesolimbic pathway. First-generation antipsychotics primarily block dopamine receptors in this area.

Opioid intoxication causes miosis (pinpoint pupils) and respiratory depression; Benzodiazepine intoxication causes respiratory depression but not pinpoint pupils.

Clozapine. It is critical to monitor WBC counts due to the risk of agranulocytosis.

Donepezil, Galantamine, Rivastigmine. They boost Acetylcholine levels.

Benzodiazepines increase the frequency of opening; Barbiturates increase the duration of opening; Z-drugs are $\text{GABA}_A$ receptor agonists.

Benztropine (or other anticholinergics). They are muscarinic receptor antagonists.

The mesolimbic pathway. First-generation antipsychotics primarily block dopamine receptors in this area.

Opioid intoxication causes miosis (pinpoint pupils) and respiratory depression; Benzodiazepine intoxication causes respiratory depression but not pinpoint pupils.

Clozapine. It is critical to monitor WBC counts due to the risk of agranulocytosis.

Donepezil, Galantamine, Rivastigmine. They boost Acetylcholine levels.