DIP Episode 67 - Psych Pharmacology (Part 1 of 2)

Okay, welcome. My name is Divine. I am a T.Y. resident that's going into radiology. This is episode 67 of the Divine Intervention Podcasts. And today I'm going to be talking about psych pharmacology. This will be likely in two parts because one full lecture will just be too long and it will be too important. So I'll just do this probably in two lectures. So the first part today. Mainly I'll talk about all the depression drugs, all the anxiety meds and all the sleep meds. Okay, and again, I want to congratulate the listeners of this podcast. You've just made it to the end of the year. Right now it's about 8.54 pm at night. I hope you've had a wonderful year. And next year is another year. It's a new year. It's a new beginning. And if you didn't like the way 2018 went, change things around. Put your trusting God, do God's will, do your best. And you know, things can work out for the best in 2019. So let's jump right into it. So psych pharmacology right, obviously we're going to start with the antidepressants. And the thing is, if you're thinking about depression, there's this monomym theory of depression you've probably heard. Basically, the basic gist of the monomym theory is that if you have low levels of serotonin, low levels of neuropinephrin or low levels of dopamine, that can cause depression. Now, the thing with these antidepressants is that they are working some way shape of form to boost the levels of these neurotransmitters.

And the thing is pretty much every antidepressant has about the same side effects. But usually test one side effect in the giving context for a specific drug. So you see that for specific drugs, I'll see certain side effects. That is almost certainly what you need to know for your exam. So don't worry about like over this try to memorize every single thing. Like really, again, you can't say anything guaranteed. But I can almost promise you that if you know exactly what I talk about in this podcast, you probably know everything you need to know about psych pharmacology for all your USMLE exams. So just pay attention to this and you should be well on your way to cross in psych pharmacology. So the first drugs we'll talk about are the tricyclic and tidy presence. The way you think about the tricyclic and tidy presence is think of them as SNR Is. So they're almost like serotonin or epinephrine reoptic inhibitors. So they work at the sympathetic synapse, they inhibit the reoptic of serotonin and neuropinephrin. And the thing is they also have anti-ham side effects. What do I mean by anti-ham? It means they have the ability to block histamine H1, alpha 1 and moscarinic receptors. And it's actually kind of high to remember that these anti-ham side effects are also side effects that are observed with the low potency, fess generation anti-psychotics. So those are just one of those rare things you want to keep at the back of your mind. Tidy those two concepts together in your mind.

Now these tricyclic and tidy presence, the names all end in Pramine or Trip Telin. Although there's a weird one like doxapine, it doesn't really fit the mood. But it may Pramine, Chlomepramine, North Trip Telin, Amy Trip Telin, doxapine, those are all TCA's. Now the big side effects you want to know if you understand those anti-ham things I just mentioned, you already know the side effects. So these drugs are sedating because they block histamine H1 receptors. If you block the alpha 1 receptors, you cause visodilision, so these drugs can cause orthostatic hypotension. And then think about it, your parasympathetic system slows down conduction through your EV node. If you blocked most grainy receptors, you'll speed up conduction through your EV node. So tacky cardia, dangerous syrhythmias, and things you can observe with TCA's. And then again, remember, rest and digest parasympathetic system, your pin-pooping just fine. If you blocked most grainy receptors, you'll have your inner retention, you'll have a dry mouth. Again, that's why these drugs, because of the anti-colonelgic side effects, you'll try to not give TCA's to the elderly. And because they can cause confusion, they can cause the lyrium. And actually it's very high to notice your TCA's actually have sodium channel blocking activities. So if you're thinking about the myocardial electron potential, they block phase zero. Because they block phase zero, they can actually have some per-rhythmic effects.

And classically on exams, you'll see a wide-curious complexes. You have the wide-curious complexes, and then the person can die. Again, it's super, super high-yield to know that TCA overdose is associated with wide-curious complexes on EKG. This is phenomenally high-yield. Now, these drugs, because they block sodium channels, if you take five days worth, the person is pretty much dead. Five days worth of TCA's is lethal, at least if you look at a lot of the literature out there. Now, again, to remember the key toxicities of tricyclics, so remember tricycis, TCA's. You've probably heard this numonic somewhere, right? So like the cost cardiac issues, talked about those already, they can cause comas, and they can cause convulsions, right? They can cause seizures. And again, it's the blocking of sodium channels and the anti-moschronic effects that on the lining of the cardiac issues, people get with TCA's, right? And the way you treat TCA overdose is with sodium bicarb, because think about it, if you're blocking sodium channels, which is what TCA's do, right? If you give a ton of sodium bicarb, that sodium bicarb that's building up in the extracellular environment can overcome the block, right? It's like, oh, if you increase the concentration of sodium on the outside high enough, you can prevent that fast sodium channel block by the tricyclics. Okay, so again, very high you to know that.

Now, in me, per me, right, again, I told you many of these drugs, they can use it for many things, but it's usually like one high you thing you want to know for exams, for me, per me, in another TCA. The big thing you want to know is that it's used for nocturnal and ureases, right? So that's basically bed wetting. Now, on your USML, you need to be careful. Bed wetting does not happen until you hit the age of five. If you're four, and you're bed wetting, you're not bed wetting. It's normal behavior, okay? Per the USML. Once you hit the age of five, you start bed wetting, okay? And in general, the best intervention for nocturnal and ureases is to try like an ureases alarm, okay? I believe I read some studies, at least some literature that shows that it's actually more effective than pharmacological therapy and better tolerated. And you're basically treating, because nocturnal and ureases are very appealing on the bed, right? Basically, if you're essentially using the anti-muskronic effects of the TCA is to counter those effects, because by blocking most chronic receptors, you have a ureneurotension. So use the ureneurotentive side effects to fix those problems. Although I will tell you this, the first line treatment for nocturnal and ureases is desmopressin, right? Desmopressin is an ADH analog, right? So if you're giving a person ADH, right, they already absorb more water at the principal cell of the collecting duct, right? And that will prevent them from peeing, okay?

So desmopressin is first line, although desmopressin could technically cause like hypo-nextremic seizures, but is generally well tolerated by kids. Now, the other TCA I want to talk about is chlomypramine. Chlomypramine, it is like floridly high yield to know that this is used for OCD, okay? Obsessive, compulsive disorder. Chlomypramine can be used for many other things, but you don't care about those other things on your exams. All you care about is chlomypramine is used for OCD. In fact, the term OCD tells you the drugs that are used for the treatment of OCD. Start from the last letter and walk your way backwards, from first line to like third line if you make. So the D antidepressants, okay? Antidepressants, like SSR Is, a first line for OCD. And then the C is chlomypramine and then the O is ulanzapine. Ulanzapine is an atypical anti-psychotic, it can actually be used for the treatment of OC Ds. And then doxapine, this is kind of low yield, but I'll just mention it just in case you see on an exam. Again, it's basically an SNRI, like every other TCA, right? So that's how you get the antidepressant effects. But the thing is, it's also blocks dopamine receptors, right? It actually blocks dopamine receptors. So because it has dopamine receptor blocking activity, assuming you get like this weird case of a person having like psychosis and they have depression, you can maybe give them doxapine. But again, I've never seen this tested.

It's just one of those weird things you may see on an exam. And don't forget that TCA is actually used to treat neuropathic pain. And I mean since we're sort of talking about the adrenergic synapse, I'll just throw in the sidebar. I believe I've thrown it in at the previous podcast, but I'll just mention it here again. But don't forget clonidine. Okay, clonidine is an alpha-2 receptor. If I want to contrast clonidine with metasapine, metasapine is another antidepressant. Clonidine is an alpha-2 agonist. Okay, alpha-2 agonist. Remember alpha-2 receptors, if you go back to the ANS from ecology lectures, those are GI-copal. They are GI-copal. So because they are GI-copal, they are inhibitory. So if you activate them, you decrease the release of neuropinephyram from the pre-synaptic neuron. Now, clonidine is actually used to treat opioid withdrawal. I mean if you're in a hospital and you hear about the opioid withdrawal plan, the opioid withdrawal plan for all intents and purposes involves clonidine. Why is that? The thing is opioids. By working the bind-to-mear receptors, when the bind-to-mear receptors they decrease the release of cadecolomins like neuropinephyram at the adrenergic synapse. So if you give clonidine, you're giving an alpha-2 agonist. You're effectively decreasing the release of neuropinephyram at the adrenergic synapse. So it's like clonidine by acts in a different receptor is replicating an opioid mechanism of action.

So that's why clonidine is used to make opioid withdrawal feel better. And that clonidine is a street drug in certain localities because of this. Now, contrast clonidine with merthazapine. Merthazapine is an alpha-2 antagonist. Remember, I just said that if you activated alpha-2 receptors, you would decrease the release of neuropinephyram at the adrenergic synapse. If you block those alpha-2 receptors, you're inhibiting and inhibiting. So you'll actually increase the release of neuropinephyram at the adrenergic synapse. This is how merthazapine works as an anti-depressant. But the thing is merthazapine also has some sedidine activity because it blocks system in H1 receptors. So it can cause sedation and it can actually cause weight gain as well. Now, let's jump to the monoamin oxidase inhibitors. The key drug names you want to know here, just remember three. You can use an amonic pet, PIT to remember them, the piece for phenolzin, the ice for isocarboxazet, and the teas for trinosepromy. Now, monoamin oxidase inhibitors, that tells you that the inhibit monoamin oxidase, not a hidden fact here. Let's talk about the two monoamin oxidase enzymes. There's MEOA and MEOB. The thing is MEOA breaks down neuropinephyram and serotonin to basically enacting metabolites like HVA, VMA, whatever.

Now, the thing is you actually HVM here clinically relevant because you can measure those, the levels of those caracoloming breakdown products in the urine, to screen a patient or to make the initial diagnosis of a fiochromocyte tumor. That's in like an adult, right? Alternatively, you can actually measure the levels of those things to make the diagnosis of neuroblastoma in a kid. Remember, neuroblastoma have heart on this and multiple podcasts is one of those neuro tumors, right? So you would not see it in the anterior medias tighten them. You'll see it in the posterior medias tighten them very high to another for tests. And then also on pediatric shelf exams, they always describe it as a calcified mass that crosses the midline, very high odd. It's a calcified mass that crosses the midline. Contrast that with a Wilms tumor that is not calcified and it does not cross the midline on imaging. Okay? Remember, just like I said, neuroblastoma post-termidia stinam because it's a neurobiased tumor, your T's, your thymomas, your tereotomas, your lymphomas, those are all in the anterior medias stinam. And then MAB, right? Only breaks down dopamine. That's all it does. At least, that's what I want you to know for the USMLD. It only breaks down dopamine to an active metabolite. So, if for example you inhibited MAB with drugs like cellulogen or acetylene, you can boost a person's levels of dopamine. That's why cellulogen or acetylene are used in the treatment of Parkinson's.

I talked about those drugs in the neurophomacology podcast. And again, because these monamine oxidase, monamine oxidase enzymes, break down serotonin or epinephrine dopamine. If you inhibited them, you boost the levels of those things and you fix depression, basically. Okay? So, your MABO Is, your MABO inhibitors, right? So, they are non-selective inhibitors of both MABOA and MAB. So, you need to know that these drugs because they prevent the breakdown of serotonin, for example. They can actually cause serotonin syndrome. In fact, you don't want to give these drugs concurrently with an SSRI or an SNRI. In fact, you need to wait for about two weeks after stopping an SSRI SNRI before you start an MAB. Okay? It is extremely rare to ever say an MABOI ever prescribed. If an hotel has a physician, you probably should try to refrain from prescribing MABO Is and TCA's to patients with depression, right? Because again, these drugs have nasty, nasty, nasty side effects. Although, they are certain atypical types of depression, like depression that's associated with like lead-in paralysis, for example, that respond really well to drugs like MABO Is. But again, highly encourage you again. These podcasts are known for clinical decision-making, they're meant primarily for test-ticking, but I encourage you as a future physician, try not to use MABO Is on your patients. Now, one high-yield thing to know about inhibition of monamine oxidizes the drug-linisolid, right? So, linisolid, right?

It's a 50s inhibitor, it inhibits initiation, right? And it's used to treat like vancomycin resistant interococcus, right? And it's also used to treat MRSA, linisolid. That's the drug that's known as XI Vox in the hospital. The thing is, linisolid is also a monamine oxidize inhibitor. So, guess what? linisolid can cause serotonin syndrome. You don't want to take an SSRI and linisolid. It's a very small risk, but those risks are magnified on USMLE exams. So, so don't keep that at the back of your mind. Also, don't forget that St. John's worked, okay? If you take your SSRI again, it could also potentially trigger serotonin syndrome. And the thing is, if a patient is taking an MAOI, right, you don't want to give them a food that's rich in tyramine, like H.E.S., Me, Tswine, whatever. Again, this is another reason why you probably should not prescribe MAO Is for your patients. The thing is, tyramine is a sympatomymatic, right? And the thing is, you actually find, and it's actually broken down by monamine oxidize. Well, it so happens that monamine oxidize is also in the GI tract. So, the thing is, if you consume a tyramine rich food, the reason you don't get hypertension is that the monamine oxidize in the GI tract breaks it down for you. So, you're good to go. However, if you take an MAOI, right, that will inhibit the monamine oxidize in the GI tract. You're not break down the tyramine, it gets reabsorbed, and you get a tyramine crisis.

The way you treat the tyramine hypertensive crisis is to give phantolamine. Phantolamine is a reversible alpha blocker, right? Please don't confuse phantolamine with phenoxybenzamine. Phantoxybenzamine is a non-reversible alpha one blocker. Remember, you use these drugs to also treat, like, to pre-treat a patient for, like, before they go for phyocromocytoma surgery. You block the alpha receptors first with any of these drugs, and then you block the beta receptors. Now, let's jump to the SSR, right? So, SSR is the selective serotonin reoptic inhibitors, right? So, the big drugs you want to know here are drugs like citraline, fluoxatine, fluvoxamine, paroxatine, citaluperam, e-citaluperam, whatever, right? These drugs are pretty easy to recognize your names, right? But the thing is basically these drugs stop the reoptic of serotonin, so you increase the serotonin at their genetics and abs, and you relieve the symptoms of depression. Now, very classic exam question. You've given this patient an SSR, right? For two weeks, they haven't gotten anything, right? And they will try to give you an answer choice that says, oh, what's the next step in money man? They will try to get you to choose, like, oh, change the drug or do whatever, no. These drugs take four to six weeks to go into effect, right? So, you need to wait for at least four weeks before you start either increasing the dose or changing the medication or anything like that, okay?

These drugs are no magic pills, takes a while for them to work, but they do work, and I have certainly heard of stories of people, people whose lives have been changed by taking SSR rights. Now, again, because these SSR rights drugs are a pro-serotonergic agents, they can, again, cause serotonin syndrome, right? Serotonin syndrome, classic way, presents with, like, diarrhea and stomach upset, right? And, again, you know, like, definitely not remember the symptoms or attorney syndrome. How do I remember the diarrhea? Well, think about it. Carsinoid syndrome, right? Carsinoid syndrome, you have a tumor, usually in the appendix, making a ton of serotonin causing diarrhea, right? Remember, Carsinoid syndrome has BFDR symptoms, right? So, like, bronchospasm, right? Floshing, right? Diaria, that's the D, and then the R is for, like, right-sided heart lesions, right? So, the thing is that diarrhea, right? You see it as a component of a tumor producing, like, a serotonin-producing syndrome, right? So, it should make sense that in serotonin syndrome, you should probably have diarrhea as well. Now, so, in serotonin syndrome, you can get diarrhea, you can just look upset, you have, like, a fever, but it's usually not as pronounced as a malignant hypothermia, okay? And myoclonus is a telltale sign, very high yield. Myoclonus is a telltale sign of serotonin syndrome on exams, okay? And the way it's serotonin syndrome, usually you can give, like, a benzo or whatever, right?

But one drug you want to watch out for on your USML is this super-hyptodine. Super-hyptodine is an anti-hystem, but it also has serotonin receptor blocking activity, so it can be used to treat serotonin syndrome, okay? And remember that, again, carcinolid syndrome causes right-sided heart lesions, right? Because remember, the lungs have the ability to break down serotonin, right? So, it's only the right side of the heart that will fill the effects of carcinolid syndrome. And remember, carcinol usually arises in the appendix. That's the most common location where it arises in the GI tract. But the thing is, carcinolid has to metastasize to the liver for it to cause symptoms, because the thing is, the liver has the ability to break down serotonin, okay? So, all the carcinolid that's released in the appendix and travels through the portal system to the liver is broken down. But if you have liver ametes, then it's no longer broken down, you can get right-sided heart lesions. You don't get left-sided heart lesions because the lungs have the ability to break down serotonin. Remember, the lungs have a lot of metabolic activity, right? Like, the lungs have angiotensin, converting enzyme, right? That helps you convert angiotensin 1 to 100 tensin 2, the endothelial cells in the lung capillaries. So, SSR Is, right? So, what are the big side effects that can cause we gain? They can cause sexual dysfunction. We actually use this sexual dysfunction to benefit, right?

So, if a patient has, like, premature ejaculation, you basically use the sexual dysfunction side effect for SSR Is to, you know what I mean? If you have premature ejaculation, it means you get too excited too early, right? So, if you sort of call back that excite meter metal by giving an SSRI, you can actually use it to treat premature ejaculation. These drugs is actually high to know that they inhibited the cyrogram B450 system. This is one of those annoying details you probably need to commit to memory. Now, what do we use SSR Is for? In fact, I'll tell you this. If I take an acycic exam and you're blank out on, oh, like, what do I use to treat this disease? Just pick an SSRI. If a patient is here in Voices, pick an anti-psychotic, but pretty much every other disease, again, this is not perfectly true. But most other side diseases, pick an SSRI, you'll be right more than half the time. So, SSR Is actually first line for depression, right? They have first line for generalizing anxiety disorder, right? They have first line for OCD. Remember the other drugs for OCD, right? Clomypramine and ulanzapine. The first line for PTSD, right? Remember PTSD, flashbacks, hyperarousal, one month after, like a big stressor, like an accident, or coming back from deployment or something. If it's less than a month, that's acute stress disorder, right? And you can also use, but this is more for an OB-GYN-A, a shelf exam.

You can actually also use SSR Is for something called pre-menstrual dysphoria disorder. Basically, it's just like a patient that has a lot of psychiatric symptoms, like depression, weight, gain, blood, blood, blood, blood, blood, around the period of the amensis. Now, the next drugs I'll talk about are the SNR Is, the serotonin or epinephrine reoptic inhibitors. The big drugs you want to know here, you want to know vanilla vaccine, desvene-la-faxine, doloxetine, melnacepram, blood, blood, blood, blood. I'll just see some key things about these drugs. Again, these drugs, they have many of the same side effects as SSR Is, but again, one or two high-yield side effects they test for them. So I'll spill the bins right now. The thing is, doloxetine is used for fibromyalgia. That's the drug I believe that's known as sembaltah. Doloxetine, extrinsic neuropathic pain, diabetic neuropathy, extrinsic fibromyalgia. Because think about it, these drugs, if they increase your levels of serotonin and neuroepinephrine, neuroepinephrine causes a hyperadrenergic state. And the way I think about it, this is probably like a teleologic explanation. So by the word teleologic, I mean, it's probably no physiologic basis for this, but it kind of makes sense. So the thing is, think about it. Let's assume you have a big wound on your leg, right? And it's hurting so bad. It hurts you so bad. You're like, no, I can't move. This thing hurts so much, right? But you see a lion and a tiger running towards you.

I can almost assure you you will forget the pain in your leg and take off instantly. That hyperadrenergic state, that fight of flight state you get from seeing those, the lion and the tiger, makes you forget all your pain and your trouble and you run away. That's the exact same thing that I'm thinking about when I think of SNR Is. So you should potentially make sense that SNR Is, like Doloxetine, I used to treat fibromyalgia and neuropathic pain. And I mean, nasiopranols, which is fibromyalgia, that's super low yield. But side effects of SNR Is, the big one you want to know is that these drugs can cause hypertension. They can increase blood pressure. And the big one you want to know for these is vanilla faxin. Vanilla faxin raises blood pressure. It is mega mega floridly high yield to know this, for example. And again, don't forget, sexual dysfunction, stomach upset, serotonin syndrome, mentioned those already. I've talked about metasapine. Metasapine, I'll just say one more thing about it, right? So again, I told you that it's a good sleep aid because you can block histamine, H1 receptors, can cause weight gain. So the patient is anorexic and they have depression. Probably not a bad idea to give them metasapine. Metasapine increases appetite. Now, one weird thing I'll say here, it's not a psych med, but it's one of those weird things shows up on exams. Don't forget majestral acetate. It's a progesterone analog that can actually be used to increase appetite.

Whenever people have wasting syndrome like HIV or N-stage cancer or whatever, you want to spurs up the appetite, you can give them the progesterone analog majestral acetate. And then, don't forget your serotonin receptor modulators. These drugs, no one really knows how they work. Some people say they block serotonin receptors. Some say they increase the release of serotonin. Some say they prevent the reoptic of serotonin. It doesn't really matter. There are some big things you want to know about these drugs. The first you want to know their names. So drugs like trasodone, nephazodone, villazodone, whatever. They all end in zoodone. The thing is, it's super high you to know. Especially trasodone. Trasodone is the post-orchild drug here. Trasodone has alpha-1 receptor blocking activity. So think about it. If you block alpha-1 receptors, you get vasodilation. Well, if you're vasodiliv, if you're diliv, the vessels that feed your penis, you can get a very strong, smooth erection. So these drugs have prior pizm as a side effect. And if you know that the prior pizm side effect arises from alpha-1 medicated vasodilition, it should make sense that if you give an alpha-1 agonist like phenyl effring, you can actually treat the prior pizm side effect with alpha-trasodone. Because it doesn't matter if you have an erection for long. It doesn't cause any problems. That's the basis of blood in the penis. It can cause the Crocis. That's obviously not a good outcome. Don't forget bupropion.

Bupropion is probably the last anti-depersonal talk about. It's an NDRI. It's an orapinephrine, dopamine reoptic inhibitor. The big thing you want to know about bupropion is also known as well butrin. It doesn't have any sexual side effects. It doesn't cause weakening. It actually has a little weak loss. It can actually help with smoking cessation. But this drug lowers the seizure threshold. And again, the super-sweigh-youtu knows for example. If a patient has a disorder that increases the risk of electrolyte and normalis like bulimia or anorexia, you do not want to give them well butrin. You don't want to give them bupropion because again, because he lowers the seizure threshold. If you have any electrolyte disorder that can make you have seizures, don't give this drug. Again, it lowers the seizure threshold. Now, the anxiety treatment. I said that SSRI is a first line for the treatment of anxiety and please don't forget. You need six months. Again, very high yield. You need six months to be able to make the diagnosis of GAD. Many of the drugs that I used to treat anxiety are also used to treat insomnia. Because insomnia is kind of like a hyperaroused state, same thing with anxiety. Again, SSRI is a first line for anxiety. You can also treat anxiety temporarily, not permanently, temporary with a benzodiazepine. Remember, there is this pneumonia, you probably heard as you're studying for step one, that Ben likes to have it more frequently and Barb likes it to last longer.

So benzodiazepines Ben more frequently, increase the frequency of opening of the GABA E receptor. That's how your benzodiazepines work. If you're overdosing a benzodiazepine, well, you're not necessarily going to die. You can reverse those things with a flumazenial. Flumazenial is the antidote to benzodiazepine toxicity. Remember, your benzodiazepines are all end and palm and lamb. I believe I've talked about these drugs in a previous podcast. One rare thing you may see in many resources is that the benzodiazepines are luraza palm, oxazapem and temazapem, and not metabolizing the liver. That's not true. The thing is, if you have liver dysfunction, you can still take those drugs because even if your liver is on its last legs, you can still metabolize them. But believe it or not, those drugs are metabolized in the liver. Very high yield to know that for tests. Now, barbiterate. Barb likes it to last longer. These drugs increase the duration of opening of the GABA E receptor. Because again, remember, if you're potentiating the effects of GABA, that comes you down. You'll fix the anxiety that way. Barbiterate. The increased duration of opening of the GABA E receptor. But it's very high yield to know that barbiterate overdose is not reversible. Barbiterate overdose usually calls your friendly anesthesiologist. They can help you tube the patient. Those patients need to make sure they protect their airways. Barbiterate overdose.

You can not reverse flumazenial, unlike the benzodiazepines. Let's just say that I'm talking about anxiety meds and sleep meds right now. Let's talk about the sleep meds. They are the Z drugs. There's like Zopidem, there is Zaloplone, there is Zopiclon. These drugs are GABA E receptor agonists. Again, remember, GABA is an inhibitory neurotransmitter in the CNS. Real quick, what's the inhibitory neurotransmitter of the spinal cord? I hope you're seeing glycine. GABA, inhibitory neurotransmitter in the CNS. You give GABA agonist. You can stop neurons from firing and you sort of calm down and fall asleep. The thing is, remember earlier I said that benzoes, right? Barbiterate, they have a very high addictive potential. These drugs also have high addictive potential because guess what? They work just like benzoes. They are GABA E receptor agonists. They actually have an increased risk of addiction. In general, you don't give these drugs for more than 35 days. I think one of these Z drugs is Zopiclon, but I'm not 100%. In general, you don't want to use these drugs for more than a month. Because these drugs work like benzoes, well, if you overdose on these drugs, flomazineol can fix the problem. Very high you to know this. Flomazineol can reverse benzo overdose. Flomazineol can also reverse Z drug overdose. Then for sleep, other drugs you want to know, like your classic melatonin or melatonin. I mean, it can help with sleep.

Remember melatonin comes from the supra chiasmatic nucleus. It's one of those bizarre things. I'm using an exam. If you want to promote sleep, you can, because melatonin controls your sleep week cycles, you can give straight-up melatonin. Or you can actually give her a melatonin. A melatonin receptor agonist can be used to treat insomnia. These drugs, they don't have dependency issues, so you can use them for a prolonged period of time. One anxiety drug I guess I fail to mention is a bospyron. In the hospital, I believe there's no Biospar. It's a partial agonist that serotonin receptor is like a 5-HT1 A agonist. Again, it basically potentiates the effects of serotonin. It can be used to treat anxiety. It's used only to treat anxiety. You want to know about Biospar. I've seen Biospar. Many times on exams, they love to test it because they know SSR Is, everyone knows it. Biospar. Remember it for the treatment of anxiety. Now, flipping back to the sleep disorders. They fall asleep very easily. When they go to sleep or they get up from sleep, they have these weird, vivid dreams. These weird hallucinations. In fact, on exams, you want to recognize that there are two kinds of hallucinations they can have. They can have hypnagogic hallucinations or hypnapompic hallucinations. The hypnagogic hallucinations are the hallucinations they get before they go to sleep. Here is an easy way to remember which is we just remember one. Remember hypnagogic. Gorge is like gouging.

Let's assume you gouged on a very high carb meal. You feel sleepy. So, hypnagogic hallucinations are the right ones before you go to sleep. Contrast out the hypnapompic hallucinations. You're being pumped when you wake up because you've got any refreshing sleep. They get these hallucinations before they rise from bed. They can also have this phenomenon known as cataplexi. They can just like loose muscle tone. They can just fall all of a sudden. They can just drop and go right into sleep. These people have a decreased sleep latency. It's actually very high to know for exams that you diagnose, narcolepsy, and pretty much many other sleep disorders by doing a polysominal graph. Doing a sleep study. Now, that's not all you need to know. However, about the symptoms, narcolepsy is associated with low levels of something known as orexin. If you check the CSF of people that have narcolepsy, they have low levels of orexin, another term emission, an example, is hypochritin. They have low levels of these things in the CSF. So, think about it. If a person has a sleepy disorder like narcolepsy, you can see that they have low levels of orexin. If a person has a sleepy disorder like narcolepsy, you know that it's associated with low levels of orexin. If a patient has insomnia, it's almost like the reverse of narcolepsy. It's like a wake for the disorder. You want to try to induce a low orexin state. So, you can make those insomnia acts sleep better.

It so happens that there is a drug known as uvorexant. It's an orexane receptor antagonist that is actually used for the treatment of insomnia. Although, I mean, it's a new drug. It's probably not first line because it's probably super expensive. But it's one of those bizarre things you want to keep in mind for exams. And before I jump ship from narcolepsy, I mean, you can treat narcolepsy like stimulants like modaphineal. You can give them sodium oxybate. That's actually a higher thing to know for exams. Sodium oxybate actually is very helpful for the treatment of a cataplexi. And I mean, for refractory depression, let's assume a patient has depression and they're not eating and they're losing weight, they're having an electrolyte and normal ease. A person is depressed and pregnant and thinking of like, in fantaside or something like that. A person has like, a catatonia, right? And benzo is not cutting it. You can jump to ect. In fact, ect works really well for depression. I mean, the response rate is super, super high. And it's a very short procedure. Again, it's very safe, very effective. It's even safe in pregnancy. So I'm going to stop here. I'll pick up from here next time. And I will pretty much finish up the remaining psych meds. I'll start with the anticycotics next time. The thing is the anticycotics have to talk about all this like weird dopamine physiology, which I've again already talked about in previous podcasts, like the Neuro once. But it's fine.

I'll talk about it again. Repetition always helps. Okay, so I wish you the best. I wish you a very happy new year. And I will try to make as many podcasts as possible in the month of January. And again, just to throw this out there, I offer one-on-one tutoring for the USMLS Step 1, two-and-three exams. I offer tutoring for organic chemistry, alpha tutoring for biochemistry, and I offer tutoring for the Step 2 CS exam, and medicine in training exam. And maybe at some point in the future, maybe for the medicine board exams. And then, I also help with application prep, right? So either the Amcass application or the EERS application, I do offer prep for those like personal statements, and all that stuff. I take care of all those. I've done those with many people. And I have a ton of experience with the admissions process, but for residency and for med school. If you send me a message, I can go into more detail on the exact experience I have, especially for med school. It's actually very, very high-yield experience with med school admissions. So, I wish you all the very best. Have a happy new year. Again, remember, the new year is a first start. Do your best. Trust God. Do God's will, and everything will work out for the best. So I will see you in the next podcast. Have a wonderful evening, and God bless. Thank you.

They are SNR Is; they inhibit the reuptake of serotonin and norepinephrine at the sympathetic synapse.

Wide-complex arrhythmias due to sodium channel blockade (blocking Phase 0).

Benzodiazepines and Z-drugs (though they are metabolized by the liver, their toxicity/management is key). Correction based on transcript: The drugs themselves are metabolized in the liver, but the general principle of monitoring hepatic function remains critical for psych meds.

Sexual dysfunction (e.g., using an SSRI to treat premature ejaculation).

It is an alpha-2 agonist, and by decreasing norepinephrine release at the adrenergic synapse, it mimics the mechanism of action of opioids.

Myoclonus (muscle twitching) and diarrhea/GI upset.

Sodium bicarbonate, which overcomes the sodium channel blockade by increasing extracellular sodium concentration.

Clomipramine.

It acts as an alpha-2 agonist, decreasing norepinephrine release at the adrenergic synapse.

Megestrol acetate.

Orexin (or hypocretin).

Z-drugs (Zopiclone, Zolpidem); Antidote is Flumazenil.

Bupropion (Wellbutrin).

Sodium bicarbonate, which overcomes the sodium channel blockade by increasing extracellular sodium concentration.

Clomipramine.

It acts as an alpha-2 agonist, decreasing norepinephrine release at the adrenergic synapse.

Megestrol acetate.

Orexin (or hypocretin).

Z-drugs (Zopiclone, Zolpidem); Antidote is Flumazenil.

Bupropion (Wellbutrin).