DIP Episode 68 - Psych Pharm Part 2 (Final Part)

Okay, welcome to the 60th episode of the Divine Intervention Podcasts. This is the 7th of January. I'm going to be continuing our review of Psycho Pharmacology and I will just get going right away. So I said we'll basically talk about the anti-psychotics and some other stuff like the drugs of abuse in this episode. So we're going to do that. So basically I'm going to round up psych farm right here right now. So let's begin. So anti-psychotics, right? Obviously we know they are used to fritzkits of frenia, right? The thing is you can also use them to frid bipolar disorder. You can use them to frid like Tourette syndrome. You can use them to frid like a delirium in the elderly. Remember you want to avoid benzos because of the problems they cause. And one thing I'll just say is if you want to treat bipolar disorder in pregnancy, I will encourage you to go with Hallopereidol as a first-line agent over lithium. Now, so schizophrenia, right? Let's, I mean because the thing is I'm not going to jump straight into the pharmacology of schizophrenia. I'm going to talk about some pathophys because it will make the pharmacology super easy to remember. So the thing is schizophrenia is a disease that's characterized by positive and negative symptoms, right? And the positive symptoms are like auditory hallucinations. So basically here in voices, please contrast this with the visual hallucinations, like seen things that are not there in the setting of a Louis body dimension, right?

This organise thinking, right? This organise thought speech, those are all positive symptoms of schizophrenia. But if you jump into the negative symptoms, we have things more along the lines of like you know like social withdrawal, flat effect, stuff like that. And the thing is if you have these symptoms for more than a month, I mean for more than six months, that's schizophrenia. If you have them for between one to six months, that's schizophrenia form disorder. And then if you have them for less than a month, that's brief psychotic disorder. And to understand schizophrenia from a pharmacology, you need to understand some dopamine-nergic pathways. The thing is the positive symptoms of schizophrenia that I just talked about, they are controlled by the misolimbic pathway. Okay? They're controlled by the misolimbic pathway. And the thing is if you increase dopamine in the misolimbic pathway, you have more positive symptoms, right? So, anti-psychotics, they block dopamine receptors. So they should have the ability theoretically to decrease dopamine activity in this pathway, right? So again, to summarize, if you have two more dopamine in the misolimbic pathway, you have more positive symptoms of schizophrenia. Now, if we're talking about the negative symptoms, right? So the negative symptoms, they are controlled by the misocortico pathway. Okay? They are controlled by the misocortico pathway.

If you have high levels of dopamine in the misocortico pathway, you actually make the negative symptoms better. Okay? So low levels of dopamine in the misocortico pathway is what causes negative symptoms, right? So obviously, you want to increase the amount of dopamine in the misocortico pathway to treat the negative symptoms of schizophrenia. So to summarize, if you have two little dopamine in the misocortico pathway, you have more schizophrenia. So again, let's just summarize this again, because it's very important. More dopamine in the misolimbic pathway is responsible for positive symptoms. Less dopamine in the misocortico pathway is responsible for negative symptoms. Okay. Now, some other high level dopamine pathways, right? So there's a migratory pathway. This is basically the pathway that is responsible for all those extra pyramidal symptoms with schizophrenia, right? So things like acute dystonia, that's usually the one that occurs first, and then acathesia, that's the one that usually comes second, and then packing senesem is another one, and then tardive dyskinesia, right? So tardive like tardy sort of coming lead, although tardive dyskinesia could potentially technically show up at any time in the course of schizophrenia treatment. Okay? And again, these extra pyramidal symptoms, migratory pathway, they arise from low levels of dopamine. Okay? In that pathway. Now, the other dopamine pathway I'll talk about is the tubero-informed developed pathway, right?

So this is the pathway that when you block it, you get hyper-prolactinemia, right? Because remember, there's another name for dopamine. Dopamine is also known as prolactin inhibiting factor, okay? So if you block dopamine's activity, then you will no longer have the ability to inhibit the activities of prolactin, right? So you'll then have hyper-prolactin emia. That's classically as with a respiratory donor, you see when we get to that. So the thing is, if you want to understand schizophrenia drugs, I think there are a few principles I should probably try to establish. So some of these things are teleologic, but I'll say the great majority of them are actually rooted in truth, from just mirroring the literature and reading a lot of pharmacology works basically. So some of this is teleologic to help with understanding and for tests. Again, that's why I said these podcasts are for a test-taking purposes. But I will say that if you really understand what I'm saying here, you should be able to tackle essentially an it's schizophrenia drug question you encounter. So let's establish a few key principles. First principle is that there is a chemical equation if you may that relates dopamine to acetylcholine. It's an inverse relationship. Whenever you have low dopamine, you have high acetylcholine and vice versa, okay? Now the next principle you also want to establish in your mind is this principle regarding this receptor. It's the serotonin 5-HT2-A receptor, okay?

Serotonin 5-HT2-A receptor, okay? The thing is, this is a receptor that actually regulates the release of dopamine. If you activate this receptor, if you activate the 5-HT2-A receptor, you actually decrease the release of dopamine. But if you block this receptor, you actually increase the release of dopamine, okay? So antagonism of the serotonin 5-HT2-A receptor actually causes an increase in the release of dopamine. Now, the thing is most treatments for schizophrenia, right? Work by blocking dopamine receptors, not a huge deal, right? So you block these dopamine receptors. And when you block those receptors, you relieve many of these positive symptoms that you see with schizophrenia. But the thing is, for these different pathways, at least the four different pathways I talked about, right? So like misolabic, misocortical, tuberculosis, and migrostriol, I want you to think of ratios of two types of receptors, okay? Ratials of two types of receptors, right? So basically the two types of receptors are the ones I just introduced. The serotonin 5-HT2-A receptors and the dopamine D2 receptors, okay? Now, the thing is, and let's put the dopamine receptors on top of the, because we're talking about a ratio, right? It's a fraction. So in the numerator, we have the dopamine receptors. In the denominator, we have the serotonin 5-HT2-A receptors, okay?

The thing is, this ratio of D2 to 5-HT2-A receptors is low in the migrostradal pathway, the tuberculosis of the dipolar pathway and the misocortical pathway. Again, very high you to know this. The D2 to 5-HT2-A ratio is low, okay? In the migrostradal pathway, the tuberculosis of the dipolar pathway and the misocortical pathway. So by me saying the ratio is low, it means that there are more 5-HT2 -A receptors in those pathways in comparison with dopamine. It may not necessarily be number, it may more be a function of just a concentration kind of effect, but to make it simple, and because again at the end of the day, you want to have the understanding for your exams. To make it simple and easy to understand, just take it that there are more 5-HT2-A receptors in those three pathways in comparison to dopamine-D2 receptors. So that D2 to 5-HT2-A receptor ratio is low in those three pathways. Now, in the misolimbic pathway, right? The misolimbic pathway that controls the positive symptoms of schizophrenia, the D2 to 5-HT2-A ratio is high. The D2 to 5-HT2-A ratio is high. So you want to take this away from me that, oh, there are more dopamine-D2 receptors in that pathway in comparison with the serotonin receptors that you find in that pathway. Very, very, very high yield to know that. Now, we've established those facts. So now, let's talk about the two categories of antipsychotics. Right? So the thing is, we have the typical antipsychotics, and we have the atypical antipsychotics.

So there's the two big categorizations. But the thing is, under the typical antipsychotics, we have those that are hypotency, and we have those that are low potency. Okay? So let's talk about the typical antipsychotics, and the two subcategories, like the hypotency, low potency. The thing is, the typical antipsychotics, the hypotency ones are those that are very strong. Okay? At blocking dopamine-D2 receptors. Okay? They are super specific. They block their receptor like super well. And because they block their receptors super well, they are awesome for treating the positive symptoms of schizophrenia. But they are not awesome for treating the negative symptoms. If you understand what I've talked about earlier in this podcast. And the drug names you want to remember here is like Halopere doll. Okay? Halopere doll is like a phenothlyzing. That's like the chemical drug class. There's Halopere doll. And remember, it has a soft allergy with it. There's flufennazine. There's a trifluopereazine. And then there's another drug known as a PMOSI. PMOSI is a hypotency, typical antipsychotic, but it's used mostly for turret syndrome. That's how you see tested on exams. And then the low-potency, typical antipsychotics. So again, these antipsychotics that they block dopamine receptors, the D2 receptors primarily, but they are not as good at blocking those, they're not as good as blocking those receptors as the typical, like the Halopere doll, for example. Okay?

Because the thing is, I sort of think of it this way. Right? If for example, you're good at one thin, that's all you focus on. Then you will be amazing at that thin. But if you're spreading yourself too thin, that's when you begin to get into trouble. It's like your jack-of-all traits, what your master of none. So same thing happens with these drugs. So the thing is, yeah, they block dopamine-deter receptors, but they also dip their feet in other waters. Like they block histamine-hitch one receptors, so they can actually cause a sedation. They block alpha-one receptors. So they can cause orthostatic hypotension, because that's causing visual dilution and decreasing systemic vascular resistance. They also actually block most scurineic receptors. So they have anti-cholenergic effects in essence, where they can increase the speed of conduction down the AV node. They can cause arrhythmias and all that stuff. So there's just one of those bizarre things you kind of want to keep at the back of your mind. Because they block so many other kinds of receptors, they lose specificity. So they are not as good at blocking de-turiseptors as the typical anti-psychotics. Super, super, super high you to know that. And the drugs you want to remember here, and I guess, I'm just sort of tied this into something I've talked about before. These anti-hamside effects, you also find them with the tri-cyclic antidepressants. So just link those two drug classes in your mind.

The low-potency typical anti-psychotics and the tri-cyclic antidepressants. And the drugs you want to remember under this purview with the low-potency typical anti-psychotics. Drugs like clopromazine, just go ahead and see this here to save time. Clopromazine actually causes a blue-green, I mean blue-grade discoloration of the skin. And then also thyroidazine. Thyroidazine, it can also cause a software allergy. I mean, it has thio in the name. And if you were, if you remember, a reanic chemistry from college, thios, right? Things that it's a functional group. If you remember your functional groups from OEM, it's a functional group that contains a software. So you make sense that you get a software allergy with that. The thing you want to remember about a thyroidazine is that it can cause a retinitis pigmentosa, right? It can actually cause a retinopathy because it can deposit in the retina. Okay? So again, these drugs, they're good for treating positive symptoms, but they're not as good as the typical high potency, the your how-doll and stuff. They're not as good as those at treating those positive symptoms. And because they don't block dopamine receptors super strongly, they don't worsen your negative symptoms as much. They still make your negative symptoms worse, but you don't worsen them as much. Okay? Now, the second big group of anti-psychotics at the atypical anti-psychotics, okay?

These atypical anti-psychotics, they actually are very good at treating both positive and negative symptoms. So again, I said that typical anti-psychotics, they are awesome for treating positive symptoms. They are not awesome for treating negative symptoms, but the atypicals, they are great, not as amazing the word, awesome. They are great for treating the positive symptoms, and they also great for treating the negative symptoms. So why is that? The reason behind that is that these drugs have two mechanisms of action. The thing is, they are very good at blocking those fancy schmancy serotonin 5-HT2 A receptors. I talked about earlier. So because they are very good at blocking those receptors, they increase the release of dopamine. Now, these drugs also have the ability to block dopamine D2 receptors. They are not as potent as the high levels of this world, but they are very good at blocking dopamine D2 receptors. Okay? So let's analyze the effects of these drugs on the four dopamine energy pathways. So the thing is, because they block 5-HT2 A receptors, they will cause the release of dopamine in the two-barre-informed developed pathway and decrease hyperprolectinemia. Because again, remember, they are more 5-HT2 A receptors in that pathway compared with dopamine D2 receptors. They will also increase the release of dopamine in the mesocharical pathway, because again, there are more 5-HT2 A receptors there than D2 receptors. So they treat the negative symptoms pretty well.

They also somewhat decrease the activity of dopamine in the mesolimbic pathway. Because I said, they are more D2 receptors, they are than 5-HT2 A receptors. So because they have the ability to block those D2 receptors, you can see that they potentially help with treating positive symptoms. Now, again, they are not as good as the typical, you may see divine, come on, you say this like 10 times. I'm repeating this over and over again, because these anti-psychotic pharmacology is just one of these things that will progressively hunt you if you just never get it down. You'll get hunted on step one, on step two, on step three, and on shelf exams, if you don't understand this. And this is not just a side shelf, like a medicine shelf and OB gang shelf, they test many of these things in many different contexts. So just sort of go ahead and just know it right now. So these drugs, they are essentially giving you the best of both worlds, right? You don't get watching the world of extra pyramidal side effects, okay? And you also treat your positive symptoms, right? So it's like the best of both worlds. Although they are not the best, again, at treating positive symptoms. So what are the drugs you want to know here? The thing is, many of these drugs in this class, they have multiple, like many of them have very similar side effects, but I will encourage you to keep this at the back of your mind.

For each drug, the side effects I mentioned here are essentially the only ones they ever test, because it's like every drug in the typical class, they all have the same side effects blah, blah, blah. But I'm telling you, the side effects I mentioned are the ones you want to know, right? You may have memorized the long list of blah, blah, blah. No, it doesn't matter. Just know what I'm talking about here. First one is clasping, okay? Closepin shares a similar side effect profile with PTU and methamazole. Those are your anti-thyroid medications, right? The side effects of agronoloseitosis, right? So if a patient is put on clasping, you want to check the white count pretty much every week, okay? Because agronoloseitosis can show up in about 2% of patients that are taking clasping. Now, all the higher things you want to know about clasping is clasping actually decreases the risk of suicide. It's one of two drugs inside that has that benefit. The other drug that has that benefit is lithium, okay? Remember, lithium is for bipolar disorder. And again, the thing with clasping is actually it has zero risk. I mean, we will not say zero, but almost a non-existent risk of extra pyramidal side effects. Closepin is an amazing drug. It's just these side effects that just make people not use them with comfort, okay? But there's essentially no risk of EPS effects with clasping.

In fact, I'm telling you this, there have been many, at least if you read the literature, there are many pharmacology texts to see that the best unsized psychotics is clasping. Like if you're like saying, oh, clasping versus how dull versus whatever, clasping is essentially the best. Like if you look at the data for clasping, it's really the best anti-psychotic, but the side effect profile just makes it really hard to prescribe. Other things you want to know about clasping, it can cause hyper salivation, okay? So they call it like the wet pillow syndrome, and it can also cause amaryacriditis. Respiriedone is the next one. The only thing you want to know about is the most associated with prolonging the QT interval. It prolongs the QT interval, so obviously it can cause a torsad point, which is not an ideal outcome. And then, o'lanzepin, the big thing is that the big thing you want to know about o'lanzepin is that it can cause the metabolic syndrome, okay? In general, before you prescribe o'lanzepin, you want to go ahead and check up the patient's hemoglobin A1c. But another high-yield thing you want to know about o'lanzepin is that it can actually be used for the treatment of Oc, and it can cause the metabolic syndrome, okay? In general, before you prescribe o'lanzepin, you want to go ahead and check up the patient's hemoglobin A1c. But another is that it can actually be used for the treatment of OCD. Remember, I talked about that in the previous podcast.

I said first-line OCD is an anti-depressant like an SSRI. You can also use clomi premin. It's a TCA that can be used to treat OCD. But like third-line-ish is o'lanzepin, okay? The next drug is a repy-prosol. The big thing you want to know about a repy-prosol is it's a partial dopamine, a de-tur receptor agonist, okay? So in the presence of like full dopamine, it acts as an antagonist because it's a partial agonist. And then quethyapin is the next one you want to know. There are two high-eal things you want to know about quethyapin. One is quethyapin causes cataracts. I mean, there's this one you've probably seen in many texts quethyapin causing quadaracts, right? So it can cause cataracts. And the thing is, in general, before you start a patient on quethyapin, usually on exams, you want to go ahead and do like a slit lump exam or something of that sort, okay? Now the next thing I want to say about quethyapin is if a patient has a history of Parkinson's disease, right? I mean, obviously, if a patient has Parkinson's, the way you treat those Parkinson's is by essentially giving them pro-dopamine-nergic drugs, right? So drugs that boost dopamine activity. But we just said that if you have a ton of dopamine on board, that's what causes the symptoms of schizophrenia, at least the positive symptoms, like the like the auditory hallucinations, right? Like hearing voices and whatnot.

So the thing I want to say to that is if a patient has Parkinson's, they're being treated for Parkinson's and they have psychosis as a result of that, go ahead and give them quethyapin, okay? Quethyapin, you know, you may be like, that's a super-spiritual scenario. I know I am going over this concept. It's something you definitely want to know for tests, okay? Quethyapin. So let's then talk about the extra-parameterocyte effects of the anti-psychotics. If you've made it through this part, at least this anti-psychotic part, you're over the more difficult part of this podcast. So the extra-parameterocyte effects, again, they all arise from the nigrosyroidopath way. The first one I guess I'll talk about is acute dystonia, right? Shows up like hours to days after studying these drugs, okay? And basically the way you can shop is like a stiff extremity or like weird-core reform movements of the extremities or like severe contractors. Basically, you treat it with a drug that has acetylcholine receptor blocking activity, okay? Because the thing is, if you think about it, I told you that, you know what, I'll probably confuse you more. So let me just let it go. But actually, I've talked about this point in my neuro podcasts, at least my neuro-phomacology podcasts. So I would let it go for an eye.

If you really want to understand it, go and listen to my neuro-phomacology podcasts where I talk about like how that dopamine acetylcholine ratio affects extreparameteros symptoms and all that stuff. That's like 10 minutes of stuff I don't want to deal with right now. So acute dystonia, if you're doing a acetylcholine antagonist, drugs like benz-tropin, okay? Remember, benz-tropin is also for Parkinson's, right? Like the tremors in Parkinson's. And then diphenhydramine, diphenhydramine is an anti-estamine that has powerful anti-choline energy activity. So you can also use it for that purpose. Now, acetygia. Acetygia is the next one. Acetygia, Parkinsonism, I'll just discuss both of them together. Acetygia is basically like this feeling like you cannot sit still, like you have to sort of, like move around all the time, like always pacing about. You treat acetygia with an adrenergic blocker, right? So like an unselected bit of blocker like proprenolol, okay? Remember, proprenolol is also used in thyroid store because it has the ability to inhibit that 5 prime diodeonis, right? That peripheral 5 prime diodeonis that converts a T4 to T4 to T3. And then don't forget that you can also use benstruoping for acetygia. And then you can also use benzoid diesapines as well, okay? But I'll say in general, acetygia on exams, the first line drug you want to go with is proprenolol. If that is not an option, if that's not an option, go with benzoid diesapine, okay?

Although I will say in general, so this is, I don't see them doing this to you on an exam, but you never know, you never know. The thing I will say is if, if, if, if I how do I put this? So I don't confuse you. I'll just put it this way. If you get an exam question about acetygia, and one option is proprenolol, I don't see them ever doing this. Well, let's assume they did this. I want you to be prepared. If they tell you that the persons, they give you the option to choose proprenolol, but also as an answer choice, you see decreasing the dose of the antipsychotic as an answer. Pick decreasing the dose of the antipsychotic and go with that over starting proprenolol. Although again, I don't ever see them putting that on an exam, okay? Now, for the Parkinsonism, like tremors and all that stuff, just go ahead and give a, give a benchroping. Remember, park my bench. That's the nice, no money for that. And then for tired of dyskinesia, usually shows up months after you study antipsychotic. For this, you always stop the antipsychotic, and your next step in management is always to switch to an e-tipico. Okay? Switch to an e-tipico. Now, let's jump to bipolar disorder. They shouldn't take too long. So bipolar disorder, you treat it with lithium. No one knows how lithium works, so that's easy enough. Lithium can, basically, the big things you want to know about lithium at a side effect, right? So lithium, it can cause hypothyroidism, right?

Lithium can, I mean, actually let's think about this for a second, right? So lithium is kind of like sodium, right? So if you remember back to Genkamp from college, lithium is a group one element just like sodium. It's just smaller, right? It's like element number three. The thing is lithium, because of similarities to sodium, it can actually cause neurons to depolarize. So this should help you remember that lithium could potentially cause tremors as a side effect. And in general, you'd want to avoid given lithium, although I mean, this is done all the time in the real world, but in general, I'll say for USMLE purposes, you want to try to avoid given lithium to a pregnant woman, because lithium, right, can cause, it's a teradogen, it can cause Epstein's anomaly. That's basically where you have like a downward displacement of the tricospit valve, like the boss phrase, it uses apical displacement of the tricospit valve. So in so doing, it causes like an underdevelopment of the right ventricle, so you have something that you call like etralization of the right ventricle, if you may. That's a classic side effect, like teradogenic side effect of lithium. And again, lithium, because it's clear through the kidneys, or patient-ass kidney disease, do not give them lithium. If they give you a question about a patient that's on lithium, and they have like hyper or smaller blood, so they have like hyper and extraneous, for example, what they are urine is very high, poor or smaller.

Think about it for genetic diabetes and sypidus, right? They have the high serimos molarity because they are losing a ton of water in your urine, right? The thing is, how do we treat this lithium in use nephrogenica, diabetes and sypidus? The thing is, you treat lithium in use nephrogenic diabetes and sypidus by giving drugs like amyloid or triameterine. Why is that? Right? So let's think about the pathophys. The thing is, we have the principle cells, right? They are part of the collecting duct. On the urine side, there is like this inect channel that brings in sodium, and that inect channel is actually activated by those two runes. And then as sodium comes in, you create a negative charge in the lumen of the, like the urine side of the principle cell, that negative charge draws out potassium, right? So you waste potassium in the urine that way. The thing is, because lithium has very similar chemical properties to sodium, it can actually pass through that inect channel, and basically scrub the signaling cascade of a visopressin of ADHD, right? That adds on visopressin vitro receptors at the principle cell. So because you have those problems, you scrub the signaling cascade of ADHD or so-called visopressin, you will not be able to insulate our pores on the urine side of the principle cell, and you begin to waste water in the urine, right? So that's why you treat this condition with amylluride or tramtering.

Amylluride and tramtering, they are both inect channel blockers, right? So they block that inect channel, and lithium will not be able to gain access into the, into the, into the principle cell. Sorry, I apologize for the omzanars, give many of these lectures from memory. Okay, so one thing you should try not to fall for an exam is this. So many times, right? If you see diabetes in sypitus, the first thing you think about is, oh, diabetes in sypitus, give thazide diuretics. That's how generally you treat diabetes in sypitus. Well, the thing is, diabetes in sypitus that arises from lithium toxicity, the last thing you want to do is to give a thazide diuretic. Why is this? Think of lithium, again, as a sodium analog, right? The thing is, whenever you lose sodium in the urine or whenever your volume down, your body will rev up the urine and your tensin outosterone system. And when your body revs up the urine and your tensin outosterone system, you will increase the activity of that inect channel that you find out the principle cell. If you increase the activity of that inect channel, that you find out the principle cell, right? Anything that goes through that inect channel will be brought in in greater quantity into the body. And that thing, I'll be writing with greater quantity of lithium, if you're on lithium, right? So you can see how that will potentially be a problem.

So the thing is, many people like have a lot of trouble, at least in my experience teaching a ton of people, many people have a lot of trouble sort of remembering what can cause lithium toxicity because there's like this long, laundry list of drugs that can do this. Let me make your life simple. Basically, remember this one fact, if you remember this one fact, this thing will click in your, or clicking your head. Anything that increases the activity of the renein and your tensin outosterone system makes you get more lithium toxicity. Just leave it at that. I mean, for example, if you take a thiazide, thiazides are diuretics, diuretics will make your volume down. If your volume down, guess what? You rev up, you'll hyper-perfuse your afternoon material, you will increase the activity of your renein and your tensin outosterone system. Endsets can also cause lithium toxicity. How's that? Well, endsets are coxane hybeners. If you need the activity of cycloxyginis, you don't make presteglandins. If you're making less in the way of presteglandins, you do not die leave the afrin materials. You constrict them. When you constrict the afrin materials, you will hyper-perfuse your GG cells. When your GG cells are hyper-perfused, guess what? They will start making more renein and now kick start the renein and your tensin outosterone system. You get into trouble with lithium toxicity. That's one of those weird, bizarre things you want to keep at the back of your mind.

That's probably the one principle you want to remember. Then you can boil down any exempts in your your get to that principle. If that exempts in your your get, revs of the activity of the renein and your tensin outosterone system. That's something that could potentially increase lithium toxicity. Now to round up this presentation, let's talk about the drugs of abuse. The big ones you want to know for exams, you want to know marijuana. The classic describe this as a patient that has like a person that has like red eyes and they're hungry. The thing is marijuana causes hunger because it actually antagonizes the activity of leptin at the hypothalamus. I remember leptin, I know I've probably never talked about this in a review before, but leptin, it actually inhibits the lateral nucleus, which is like a hunger center in the hypothalamus and it activates the medial nucleus, which is actually like a slightly center in the hypothalamus. The thing is marijuana, it acts on the cannabinoid like CB1 receptor. By doing that, it decreases the activity of leptin. By decreasing the activity of leptin, you have less inhibition of the lateral nucleus of the hypothalamus and more activation. So you have less inhibition of the lateral nucleus of the hypothalamus and you have less activation of the medial nucleus of the hypothalamus. So in effect, you promote hunger. That's the pathophysiology behind marijuana potentially causing a hunger. I may see divine.

I've never heard of these hypothalamus nuclei. The lateral nucleus, the medial nucleus, who cares about that? Let me tell you why you should care. If you're taking step one at any point in the future or in neurology shop, you should definitely care. I promise you these hypothalamus nuclei are like they're like slyridly high yield for the USMLS step one exam. Okay, now continue in our discussion. Dronebino is a one drug that's peripherally related to marijuana. You usually give it to cancer patients to increase appetite because again, it's a cannabinoid receptor agony. So basically it is like pharmacologic marijuana almost if you make. Okay, so it increases the lateral nucleus activity promotes hunger. Okay, you can also actually use dronebino for chemotherapy induced MSS because it so happens that whenever you have activation of the cannabinoid receptor, you actually decrease the activity of the chemoreceptor triggers that controls MSS in response to chemotherapeutic agents. And then the next drug of abuse is a PCP. Right, so PCP, they'll present this person that's like super angry, super psychotic, super violent, almost like Superman. They want to like jump off a building or something ridiculous. You know how these people are in the ED if you're an ED doc. But basically, and they will also have like mastagmas on physical exam. We can even have like hypothermia just from the increased activity of their muscles.

In general, you treat this with like haloparydol and usually like a benzodiazepine. Okay, so sort of calm those people down. LSD is another drug you want to associate this with hallucinations and flashbacks, okay, like intensified experiences if you may. Opioids, right, opioids have talked about this a bunch. They cause respiratory depression, they cause pinpoint opioids, right? Cocaine and Fedamines think about like tachycardia, think about my dryasis, right? So like, publicary dilation because remember, these drugs prevent the reoptic of neuropinephyen and the adrenergic synapse. And I guess to sort of like just review a lot of stuff real quick because I know psych farm is a bugger booth for many people. So let's just review like a lot of the high-yield information real quick in like two minutes. And remember that opioids are mu. So this is me. I'm going to start talking like like sports commentator. Remember, opioids are muoreceptor agonists, okay? Remember the other endogenous muoreactivators of muoreceptors in the body, things like betaendorphine, dinorphine, dinorphine goes after, betaendorphine goes after the muoreceptors, dinorphine goes after the copper receptors, and catholine goes after the delta receptors. Those are endogenous opioids. Those are frequently tested on the USML Es. And then don't forget your MEO Is, okay? You're nonselective monoaminoxidine inhibitors, drugs like phenylzene, traneusepromine, and isocaboxazine.

Don't forget your cellulinous Agilinous Agilin, they are MEOB inhibitors, they can technically trigger serotonin syndrome. Don't forget your tricyclicantide presence, they act like SNR Is, they act like selective, they act like serotonin or epinephrine reoptic inhibitors, okay? They also have those anti-hamside effects I talked about. And don't forget that they can cause comers, they can cause convulsions, they can cause seizures, they can cause QRS up widening on an EKG that is true with sodium bicarbonate. Remember that in mepromine is used to treat nocturnal any recess. Remember that doxapine is a drug that can be used for psychotic depression because it's broken down into two sub two. It has two breakdown products. One acts as a TCA and the other acts as a dopamine receptor antagonist. Don't forget chlomypromine that you can treat OCD, it's the C in OCD, and remember you can also use your tricyclic to treat an neuropathic pain. Also don't forget your SSRI, they can cause weight gain, they can cause sexual dysfunction, you can use that as a means of treating a premature ejaculation. They also cause insomnia, and they take four to six weeks to have an effect. Don't forget about the serotonin syndrome with those. Remember your SNR Is, especially when the vaccine can elevate blood pressure. Remember your serotonin receptor modulators like Nephazodone and Trasodone. These drugs have the ability to block the alpha one receptor, so they can cause pre-apisim as a side effect.

You can treat that with phenol effron. Mertazapine, remember that it's an alpha two antagonist, so by blocking alpha two receptors, it actually increases the release of neuropein effron. It's a powerful sedative, but it also causes weight gain. You can use it very nicely in an anorexic patient. Don't forget your bupropion. It's an NDR, it's an neuropein effron dopamine reoptic inhibitor. It has no sexual side effects, it causes weight loss, and it can actually be used for smoking cessation, but you want to avoid any patient that has any disorder, like an electrolyte imbalance, or like an anorexic patient, where they can have problems that increase the risk of seizures. You don't need to use bupropion in those patients. Then your typical anti-psychotics with low potency, remember they block like clopromosin and thyridazine, they block dopamine geturiceptors, but they also block have those anti-hamside effects that you get with the TCA. Then, typical anti-psychotics like haloparidol, fluffenosine, pimoside, and triphloparasine, those have very powerful activity against the dopamine geturiceptors. They are used for treating the positive symptoms of schizophrenia. Remember that pimoside can be used to treat syndrome. Don't forget clasoping, it's a needypical anti-psychotic, it's a powerful 5-HT2 A receptor blocker, it's good for negative symptoms, it's also a very strong dopamine geturiceptor blocker, so it's great for positive symptoms.

Don't forget that it can cause myocarditis, it can cause hypercellivation, it can cause agrenolocyteosis, and it actually is one of two drugs in psychiatry that decreases the risk of suicide, along with lythium. Don't forget that RIP-Persol is a partial agonist at dopamine receptors, but it actually acts as an antagonist in the presence of full dopamine. Remember that Rolanzapine can be used to treat OCD, and also it causes the metabolic syndrome. Lythium, remember, can cause the phrygienic diabetes in sypedas, you want to avoid the impregnancy if you can, because it can cause Epstein's anomaly, and treat lythium, induced in a phrygienic DI with a triamterin or amylo-right. Remember that lythium can also cause hypothyroidism. Don't forget your Z drugs, like Zopidem, Zaloplone, and Zopiclon, they have a risk of dependence like benzozambapitrorids, and you can reverse the effects with flumazanel. Don't forget Ramyotion. Ramyotion is a melatonin receptor agonist. It has no dependency, so you can actually use it long-term for the treatment of insomnia. Don't forget your vorexant. Your vorexant is used to treat insomnia because it's a blocker of Rxn receptors, because remember, having low levels of Rxn, also known as hypocretin, is as result of the sleepy disorder, basically in our colapsee. So if you block those receptors in a patient that's in some meach, you could potentially make them sleep better. Don't forget Bospiron.

Bospiron is a partial serotonin receptor agonist that's also used to treat generalize anxiety disorder. Don't forget cocaine and phedamine, they can cause my drases and tachycardia. Don't forget clonidin. Clonidin is an offer to receptor agonist. It causes a decreased release of neuropinephrine, and actually makes opioid withdrawal feel better. Don't forget PCP, PCP, super violent person with nice stagmus, that's how it presents. LSD, don't forget flashbacks and intensified experiences. Don't forget marijuana and cannabinoids like dronabino. They can cause red eyes, they can cause hunger. You can use them to treat chemotherapy and use MSS, okay? And you can use them to increase appetite in a patient that's caquectic. Remember, you can also use my gestural acid tit for that purpose. nicotin, right? Activates an nicotinic acetylcholine receptors. Remember that while we're on this topic, theophilin, right? Has an antagonist effects on adenosine receptors, okay? So if a patient has an SVT and they have a ton of caffeine, you don't want to give them adenosine for that SVT because they will not break the SVT because caffeine has like theophilin-like activity and theophilin, right? So they're methozank things, the antagonized effects of adenosine. Don't forget marijuana and clonidin. It's just for smoking cessation. It's a partial agonist at the nicotin receptor, so it's effectively an antagonist. And again, don't forget you have phedamine and methylphenidate based on 3 D-GHD.

Having those high levels of neuro-epinephrine can really help you focus, right? I mean, like if you're running from a lion, you better be focused. So that's probably an easy way to remember that. And then don't forget out amoxetine. At amoxetine actually inhibits the reoptic of neuro-epinephrine. Shockingly, it's used to treat ADHD. In fact, I'll say it's probably becoming more commonly used because it's not a stimulant, right? It's a non-stimulant that actually works pretty well for the treatment of ADHD. So all those insomnia side effects, you get what the ADHD drugs are like weight loss. You don't necessarily observe them without amoxetine. And then remember, alcohol, booze basically, can cause respiratory depression. If you combine it with a bensoribabiterate, remember if a patient is hypochloric from chronic alcohol abuse, give them in first before you give glucose so that you don't precipitate or wear any keys or curse or coughs. So I know this is probably like a new format, but if something I've done a lot in the past, I call them like flush reviews where just like in between two and five minutes, I review like a crop tone of information that just summarizes the salient points from what I've discussed earlier in my presentation. Maybe I'll try that in another podcast. Let me get some feedback on this. Let me see what you guys think and I'll go from there. And to round this out, I promise I'm pretty much done.

There's one of the thread out there that I offer to the ring for many exams. For the USML, step one, step two CK, step two CS, step three, medicine training exam, and in a few weeks to a month, the medicine board exams as you'll see. And I also do application prep for an application and interview prep for like Amcass applications to med school and ERAS applications to residency. That's something I've done with tons of people and I have like admissions committee experience. So I can definitely help with that purpose. So feel free to reach out at any time if you want any of those services. And if there any particular podcast you want me to make, just send me an email or something. I'd be happy to oblige if I have the time. Or if it's something I deem appropriate. So I wish all the best, have a wonderful rest of the day and I really hope the week lakers win their game tonight. And LeBron comes back. Okay, good night for now. God bless. Thank you.

Increased dopamine in the mesolimbic pathway.

The mesocortico pathway (low dopamine levels cause negative symptoms).

Clozapine and Lithium.

Blocking 5-HT2 A receptors (increasing DA release) while also blocking D2 receptors.

Tricyclic Antidepressants (TC As).

An acetylcholine antagonist (e.g., Benztropine or Diphenhydramine).

Thiazide diuretics are contraindicated; instead, use carbonic anhydrase inhibitors like Amyluride or Thiameterine.

Mesolimbic pathway has a high D2/5-HT2 A ratio; Mesocortico pathway has a low D2/5-HT2 A ratio.

Epstein's anomaly (downward displacement of the tricuspid valve).

Chlorpromazine (and Clozapine, though chlorpromazine was mentioned in relation to this side effect).

Quetiapine.

Risperidone (or Aripiprazole, though not mentioned, the principle applies).

Tricyclic Antidepressants (TC As) due to anti-histamine/anti-cholinergic blockade.

Amoxetine.

Mesolimbic pathway has a high D2/5-HT2 A ratio; Mesocortico pathway has a low D2/5-HT2 A ratio.

Epstein's anomaly (downward displacement of the tricuspid valve).

Chlorpromazine (and Clozapine, though chlorpromazine was mentioned in relation to this side effect).

Quetiapine.

Risperidone (or Aripiprazole, though not mentioned, the principle applies).

Tricyclic Antidepressants (TC As) due to anti-histamine/anti-cholinergic blockade.

Amoxetine.