DIP Episode 164 - The Clutch Toxicology Podcast (Drugs of abuse, overdose, withdrawal, toxidromes)

Okay, welcome. My name is Divine, I'm a resident. This is a piece of 164. I believe of the Divine Intervention Podcast. And in this podcast I'll be doing a series that I will call, I guess I'll go ahead and call it the Clutch Drugs of Abuse, Slash Toxie Drums Podcast. It's been a while since I've been here last, it's just been a very extremely busy, apparently my life. But I'm glad to be back and I think we can get really on some high-yield things that have been kind of stuck in at the back of my mind for the last couple of weeks. So let's go ahead and jump right into it. So what if you get a question about a patient, right? And this patient has a history of diabetes and then this patient is found, you know, all sprout out on the ground, has lost consciousness, not a responsive. What is your next best step in management? Well, that will be to go ahead and give the person glucose, right? That will be to go ahead and give the person glucose. Although remember, this person has like symptomatic hypoglycemia, right? Again, that's the classic way they'll put it, they'll be a diabetic, like a person with a history of diabetes, and then they're all like knocked out or whatever lost consciousness. And all that crap. So I'll let those circumstances your next step in management will be to go ahead and give those people glucose, right? So you give them the extra solution.

They will try to give, because the thing is your friends at the MBA and they love doing this thing where they write answers that are closely related but don't answer the question. They'll give it insulin as an answer choice. Don't pick insulin, right? Don't pick insulin. Because the thing is, I promise you if you're picking insulin, the patient is going to die, right? So you don't want to do that. That's not a great outcome, right? So actually, that's not an outcome you want. Let's put it that, not an outcome you want, right? I remember another alternative, right, for treating hypoglycemia. In fact, actually the quickest means of a reason a person's glucose is to give glucose. So that's one thing you want to keep on the back of your mind on tests, right? Then what do they give you a question about a patient? Let's see, this patient was found on the ground on responsive. And this person's respiratory is four, right? And this person has like bilateral popularly meiosis. And this person again is not responsive and they will give you like AB Gs. And maybe let's say like the oxygen tension is like 50. And let's say the PCO3 is like 70 or 80. So you know, pretty high, the person is pretty high-boxic. And let's say the person's pH, right, it's like 7.21. To tell you that they have like, you know, quite severe respiratory acidosis. And that is circumstances. What's your next step in management, right? So they will try to trick you.

They will give you an answer that says to be the patient. They will also give you an answer that involves giving a loxone, choose a loxone. Okay? This is one of those situations where a patient is profoundly hypoglycemia barely breathing. We want to try the loxone first before you jump to intuition because now loxone can probably rescue the patient a lot faster than intuition will. Obviously, I would hope you're thinking that this person has some kind of opioid overdose. Okay? So that's one of these high-yield things you want to keep at the back of your mind. Now loxone is the drug of choice for treating an opioid overdose. Again, try to make sure that you don't pick now trixone. Right? Now trixone is not the answer. You want to pick on your exam. And the final trixone keeps in the patient again will be long dead. So you don't want that. And then, what if they give you a question about a patient? You know, this patient has a history of multiple episodes of like acute pancreatitis. Or they can show you like this person's you know, imaging and you will see like a calcifications kind of lining the pancreas. Right? And then they tell you that this person comes into the ED and this person has like, I don't know, like a stagmus and this person has, you know, has like trouble like walking appropriately. And maybe it's like, seem weird things and all that crap. If you see that, what is your next step in management?

Well, I would really, really hope that you're thinking about when keys and cephalopathy. Right? Remember when keys has a triad, right? So confusion of thermoplysia and etaxia. And again, the input, the patient has a thermoplysia on your exam. Not right. No, no, no, no, same question. I don't do that. Right? So the authentic like a stagmus. So you can know that they're putting a stagmus. They'll put light. They'll just put basically once you see like I find in walking, finding sweetaxia and then confusion. They don't know those circumstances. Think about when keys and cephalopathy. And remember that when you add a confabulations so the patient is making stuff up an amnesia, right? Then that gets you into the world of a Corsa cough cycle. So you kind of want to know that for you exact. Right? So that's what important thing to know. Now the next important thing to remember is that remember the neuro and atomic wall association, right? They love to test the stuff all the time. You're neuro and atomic wall association. You want to remember that when you key cross the corsa coughs, right? So she they would like problems with mammillary bodies, right? With like problems with the mammillary bodies, like hemorrhagic infarctions of the mammillary bodies. And obviously the way you want to go ahead and treat this is you want to go ahead and give them a vitamin B one right fine. You want to give them a vitamin right?

So they would try to treat you by giving you like an answer that says oral thymine and then they would give another answer that says IV thymine. IV thymine, okay? It's the drug of choice for treating when you suspect or when you go ahead and give those people a IV thymine. Because remember if you go back to step one, people believe that dysfunction of a transkydolise gives rise to some of the troubles that you see in people that have a when you key cross the cough syndrome. Right? So transkydolise remembers the real meeting in some of the nonoxididies fees of the pentose possibly pathway. So again, when you key cross the cough syndrome, you can think about a person that is that has a deficiency of thymine. And again, many people just think that, oh, to find people that get when you key cross the cough, you know, that must be like just the alcoholics. Yes, it's the alcoholics a lot of the type on in the exams. We don't forget that people that have anorexia nervosa also classic patients to get when you cross the coughs from like B1 deficiency. And then also don't forget that people that have like chronic malnutrition, like people that have like osinimofissa, OB-Dyandasodar, where they puke a ton. Come on, divine think. Hyper-MS is gravity, right? Those people tend to get invited in B1 deficiency as well.

In fact, those people come into the ED and they are trying to get you to pick an answer that involves, you know, they're getting, trying to get your pick an answer that involves like supplementing a vitamin. You want to go ahead and supplement B1 in those patients. Just again, a high-ealth thing, you want to keep at the back of your mind on the exam. Okay, now, okay. So what if you get a question about a patient? And this patient has been on an hydro-perside infusion for a while. And then they tell you that this patient has, is developing like this, like they give you like, you know, like a peach of like 7.19 and a bicarb of 10, right? So like your profound metabolic acidosis and a person that has had a long time an hydro-perside infusion. If you see that, I want you to think about cyanide poison, right? You really, really want to think about cyanide poison. And remember that cyanide poison, right? There is a, that's like, again, one classically will present. They may have like, you know, like a lactic acidosis in the setting of like long-term, like not even long-term. You just be like, you know, just three days of, what is it called? Three days of, like nitro-perside infusion. And then they ask for your next best step in management. Your next step in management will be to go ahead and give those people a hydroxycobalamine, right? Or you can give a combination of emo nitrite and sodium thiosophage, right? Because remember, cyanide, right? It binds really well to ferric iron.

So iron in the FE3 plus 4. And if you want to go from FE2 plus to FE3 plus, right? You need a, you need a, it's an oxidation reaction. You essentially looking for that oxidation reaction, who happen on the, happen on the thiosophage of a good oxidizing agent like emo nitrate. So you convert ferrocyan to ferric iron. And then that FE3 plus, right? So you form like, that will bind up the, bind up the cyanide, right? And then you give thiosophage, that will convert it to thiosyanate. And then you can put it out or whatever, and you get it out of the body. But under the drug emission, the example treating toxicity of cyanide is hydroxycobalamine. So that's something when you keep at the back of your mind. And then what if they give you a question about a patient that consumes antifreeze, right? And this patient, you know, is now completely no flung, being ready to into the groin. I hope you're thinking about like oxalate nephrolithiasis, right? Remember, oxalylithylithiasis is common in people that are taking that drink antifreeze. But there's also people, common in people that have Crohn's disease, right? Because remember when you have Crohn's disease, you have increased reabsorption of oxalate because the terminal helium has been torched, right? So that can cause a high proxyloriya. But again, specifically for the case I described, person drinking antifreeze, remember antifreeze contains a thylin glycol. What do you, what your next step in management beyond the circumstances?

Well, I hope you're saying to give a form of epizome, right? Because remember, ethylene glycol and I guess to sort of like streamline things, ethanol poisoning and methanol poisoning, right? Those things all cost trouble because they are metabolized further by the enzyme alcohol dehydrogen. So if you wanted to prevent the sequelae, like this person that has like ethylene glycol poisoning, you would want to give an alcohol dehydrogenase inhibitor, like form epizome. Okay, give form epizome. It's a competitive inhibitor of alcohol dehydrogenase so that you don't make like the nasty stuff that causes many of the symptoms with three of these toxicities. Because remember, methanol classically will present on mbiming symptoms as a person that has a lactic acidosis and visual difficulty. You see, lactic acidosis, visual difficulty. I really want you to think about methanol toxicity. I mean, I think I remember back in the day in college, I think I read this book or whatever or this lecture I went to where they said that if a present takes like very small amount of methanol as little as I think like 15 cc's, either 15 or 100 cc's that can cause like permanent blindness. So you want to get on that, you know, go ahead and give the form epizol sooner or later. And then alcohol poisoning, right, it will just be a person that it almost looks like a benzodiazepine toxicity.

The person, you know, like they may have like sort of kind of like they're like sleepy or like poor your responsive, but they will not have any popular findings, right? That's what helps you differentiate that from from opioids, right? And I guess something I'll go ahead and mention. How do we treat benzodiazepine toxicity? Well, I would hope you're saying to give a flomazineal, right? Flomazineal. Again, remember benzotoxicity, profound respiratory depression in the absence of popular findings. And it will really be a person that has a history of like some psychiatric disorder. Whenever you see that under those circumstances, go ahead and give flomazineal. A flomazineal, right? Again, like I said, it's a it's a GABA receptor antagonist, right? So it can help under those circumstances. Another high you think you want to keep at the back of your mind is that flomazineal can also be used to reverse. Like the Z drugs, right? So like Zopidem, Zaloplone and Zopiclone. Remember those are GABA B receptor agonists? Those drugs are used to they're used to treating insomnia, but again, they have a abuse potential. So they are typically not prescribed for long periods of time. Unlike the melatonin receptor agonist from out here and stuff like that, they can be prescribed a long term. So that's just something high you would want to keep at the back of your mind. But yes, those Z drugs again, Zopidem, Zaloplone, Zopiclone. You can reverse their toxicity by giving flomazineal.

Although don't make that knowledge leave that, oh, you know what? Since Babiteri is also agonist, GABA receptors, that means they must be reversible flomazineal. No, that is not true. That's not a thing. So that's again, high you think you want to keep at the back of your mind. And then what if they give you a question about a patient? And this patient has a body temperature of like 103. And this patient has like super diluted poopy, skinny, super dry, red. This person has like super pubic fullness. That's like MgMe code word for urinary retention. And that those are circumstances. What are you thinking? What are you thinking about? What kind of toxic drum does this person have? Well, this person clearly has an anti-collinergic toxic drum, right? Remember like this hot as a hair, blind as a body, yada yada yada. You do personally, I've never seen the utility of that numonic. Because most of the findings make perfect sense if you just kind of think about them. It's like if you knock out your parasympathetic system, where your sympathetic will hold sway, right? So you have a pulmonary dilation. If you've blocked most carinic receptors, your sweat glands won't work. So you're going to have dry skin. You're not going to be sweating. Because you're not sweating. You're not distributing it very well. Right? So you'll be hyperthermic. You have redness of your skin. And again, if your parasympathetic system is knocked out, you're going to have urinary retention.

You're going to have constipation. Right? And these people tend to be tacky cardic as well, right? Because again, if the parasympathetic system has been knocked out, right, then your sympathetic will hold sway. So you have increased conduction down the EV node. Or here's the thing. There are many things that can cause this anti-parasympathetic, or you can see anti-collinergic toxic drum on NB Ns, right? Remember, the fact that you love to do this stuff with like some of the psych drugs. Remember, you'll try psychically, anti-depressants, right? Those have an association with anti-collinergic toxic drum. Because remember, they have anti-hamm side effects, right? Anti-hamm side effects. So those anti-hamm side effects are things like, like ham, right? Like the heach stands for heach one. The heach stands for alpha one. And then the instants for anti-moscarinic, right? So like anti-heach one. So the cause, so anti-heastamine, the energy, so the costed edition, anti-alpha one, because of orthostatic hypotension. And the anti-moscarinic, right? They have anti-collinergic effects essentially. Although remember, your tricyclics, when a person overdoing a tricyclic, like classical NB Ns, they may also give that a person has like a white QRS on ITG. And obviously, under those circumstances, right? You want to go ahead and give those people a sodium, sodium bicarbonate. Also, don't forget, right?

Like, again, anti-heastamine is that have powerful anti-collinergic activity, like diaphne hydramine. Those can cause an anti-collinergic toxidrom on NBN exams, right? And then if a person is exposed to like the Beladona plant, remember, the Beladona plant contains an atropine, right? So that can certainly cause a lot of problems with anti-collinergic toxidrom. So again, that is something very high you want to keep at the back of your mind on the exams. So if a person has like atropine overdose, right? So how do you fix that, right? Remember that you fix an atropine overdose with phyzo-steegmin, right? You fix an atropine overdose with phyzo-steegmin, right? So that's a high-yalthine one, remember? Because how those phyzo-steegmin work. Remember that phyzo-steegmin, it's an acetylcholinestery inhibitor, right? So because you have an acetylcholinestery inhibitor, that will bump up your levels of acetylcholine, and that will outcompete those atropine molecules that you find on the surfaces of all mascarinic receptors, right? So that will help you on those circumstances. Now, I just talked about the anti-collinergic toxidrom. The collinergic toxidrom is almost like a reverse case, right? So this person will be like bepine, a ton, they'll have pupillary maiosis, right? So again, remember, my dry ass is this plant, I call an anergic toxidrom. Myiosis is for collinergic toxidrom.

So they'll have like diarrhea, they'll be sweating, because again, they have sweat glands that are like an overdrive. They'll have, you know, they'll be making a lot of saliva, so they'll have like laparamation. They'll have, they can have bronchospasim, right? I mean, that's why we treat... As... I mean, yeah, that's why we treat like COPD or all these like reactive area diseases with mascarinic receptor antagonists, like Ipertropium or tyotropium, right? So whenever you see this collinergic toxidrom, right? The big causes you want to think of when you accept, right? You want to think about a person that is, let's say, they give you a question about a child, where maybe I don't know, like, mom has my astenia gravies or some weird crap, right? And then, because that child's mom has my astenia gravies, maybe the child, you know, mom left the child alone, and then the child took something from mom's pill bottle. Obviously, on the NBM, the contents of the... the names of the drugs are never known, right? But they will give you all these fancy flashy symptoms that you need to essentially figure out, right? So that's something you want to keep at the back of your mind. Remember that if they talk about like a terrorist attack with like nerve gas, nerve gas, right? Like siren, nerve gas, for example. That has, you know, powerful anti-colonestraiser activity, right? So organophosphates essentially, right?

Organophosphates, carbamates, those things, it'll cause a lot of trouble with colonelgic or toxic syndrome, because they only inhibit acetylcholonestorase, right? So, obviously, how usually under these circumstances? So we know that having high levels of acetylcholin is causing all the trouble. So one way you can try to, you know, fix that, is to give atropine, right? Because again, you have too much colonelgic activity, right? So that's causing a lot of trouble. So you give atropine, atropine will block the most creative receptors, right? And then you can also, especially if it's organophosphate poisoning, you give atropine first, they will try to trick you to give pre-dedoxine first. They will not give pre-dedoxine first. It is the initial atropine you give that will see these people's light first. So you give them atropine first. And then after that you give pre-dedoxine. That pre-dedoxine, right, will help you regenerate acetylcholinesterase. But that comes after you have given atropine. That is very, very high yield to keep at the back of your mind. Now, what if you get a question about a patient? And this patient has, this patient, you know, has a histone diabetes, and they have gastroperesis. And they tell you that this patient is having trouble. This patient is having trouble, has been having, you know, like, muscle rigidity. And this patient has been, they show you, like, a temperature of the person's temperature is like 105.

And this patient is not doing very well, and all that, yada, yada, yada. And they tell you that a new drug will start it recently. What's your diagnosis under those circumstances? I would hope you're thinking about your electric malignant syndrome, right? Again, that's why the USML is right. Just like, this is the, you know, people say it's a little hard. They're just unusual presentations of things, right? That people will mean not necessarily, like, people like know the concept, like, the things that are kind of obvious and mixed sense. But they may not necessarily have, you know, like, made that, like, mind connection, right? It's something, probably, remember, like, if you thought through a path of physiology, wise, you know, you feel comfortable with. But it's maybe not necessarily something someone has thought about. So that's, like, classic, classic, NMS, right? Remember, that very gastroperesist, you can treat it with metal clopper mind. Metal clopper mind, remember, it's literally, it's essentially an anti-psychotic, right? It's an anti-psychotic. So it can cause many of those, you know, very similar extra-peramidal symptoms, like the neuroleptic malignant syndrome, for example, right? Like NMS. And remember, right, the way you treat NMS, right? Obviously, it's to go ahead and give the person a... You can give a... you can give a benzodiazepine, right? That's all you can treat that. You can give a dopamine agonist, like carburetolino brumocretin, right?

Those are all means of treating a neuroleptic malignant syndrome, right? And again, remember, the presentation is eerily similar to serotonin syndrome, right? The exposure is different, right? The exposure is an agent that is serotonergic, right? Like a combination of, you know, one or two agents and a serotonergic... And what could those serotonergic agents be? Right? It could be something like... St. John's word, remember, St. John's word has serotonergic activity, right? Another thing that can cause serotonin syndrome, lignisolid. Right? Remember, lignisolid is used to treat MRSA. But in addition to being treatment for MRSA, lignisolid also has a... monoamino-CDC inhibitor, like, weak mui activity. So you can treat a serotonin syndrome. Another classic one is a person that has... Has migraines, right? And get taken so much triptans. Remember, those triptans are serotonin receptor agonists. We even, like, are got amine, right? So like, they're ergot... Ergot agents. Those things also have serotonergic activity, right? So again, all those things can all trigger serotonin syndrome. Or they may give you a question about a person that is actually, like, let's see... Maybe they were some kind of side-drog, like, you know, let's say they've been on an SSRI for like the longest time possible. And then they tell you that, oh, the... The stop that SSRI, and then, like, a few days later, they will start it on, like, an MUI or some other, like, a serotonergic agent.

That can also be a presentation of serotonin syndrome. That's kind of like a nice way for your friends at the NBME too. Give your serotonin syndrome a question in a patient that is not on two serotonergic agents at the same time. The thing is, if a person is on an SSRI, especially, like, fluoxetine, remember, fluoxetine of all the SSR Is, it has the longest half-life, right? So you typically have to wait at least two weeks before you start, like, a TCE or an MUI, right? You need to wait for all that stuff to wash out of the system if not guess what. You're gonna get your patient into a... You're gonna get your patient into serotonin syndrome. And again, remember, serotonin syndrome, classically, right? It will present with a person that has myoclonus. That's the classic thing. You'll see on exams. So you see myoclonus. You'll see hypothermia. And again, really, the way you treat serotonin syndrome, you can actually give a benzo. Right? Believe it or not. You can try supportive care that actually works pretty well, right? But on that thing, you may also see what serotonin syndrome is to give super-hyptidine. Membership-reheptidine is an anticholinergic... I mean, sorry. It's an antichristamine that has serotonin receptor blocking activity, right? So again, that's a high-yield thing you want to keep at the back of your mind on exams. No. So again, remember, serotonin syndrome, hypothermia, right? But the person may not necessarily have most originality. They may, though.

They may, though, in your exam. You just need to look at the context because it has many similarities to your electric malignant syndrome on exams. Right? So again, serotonin syndrome, hypothermia, you usually have diarrhea, right? I mean, think about it. If you're trying to make a parallel here, the person has carsmoid syndrome. Right? Carsmoid syndrome, right? Remember, there's this pneumonia BFDR for the findings in carsmoid syndrome. Right? So brunco-spasming is one. Flushing is the other. Diarrhea is a third. Right? And then, right-sided heart lesions. Right? So diarrhea. Okay, whenever you have over-secretion of serotonin, that tends to cause a GI issues, right? So that will cause diarrhea. So if the person has a serotonin syndrome, they can have diarrhea. They can have like the myoclonus. Again, those are big things you want to keep in mind. And again, don't forget your MEO Is, your TC Es, right? You can try to cycle your tiny presence, right? Because they have serotonergic properties, your SSR Is, right? Some of you are opiate, opiate analgesics, right? Like trasodone, for example, again, these cannot trigger serotonin syndrome. They can even give you a person that has a histone depression and is taking like cough medicine, right? Because again, remember, when you have these cough medications, they have like some slight serotonin agi- activities, right? And then some of these drugs that I used to like lose weight.

Believe it or not, they can also trigger serotonin syndrome. So again, let me see, divine, you're presenting all these unusual scenarios in this podcast. I'm just doing that to prepare you for the realities of the new state to seek exam that is oponus. So again, those are all high-yield things to keep at the back of your mind, right? And then, what if they give you a question about a patient, you know, that a patient that, you know, was studied on a side drug recently, and then it's in like, like some myths, like a waterfront restaurant or whatever. And in this patient's blockages, like 250 over 130, like some ridiculous number, right? I would hope one of those circumstances, you're thinking about like a tyramine crisis from having, you know, taking like a tyramine-rich food, I mean, the decision of like a M-O-I exposure, right? So you're taking an M-O-I, you're not supposed to eat tyramine-rich foods. So the person can have a hypertensive crisis. And then they ask, what is your next best-estepin management on exams? Your next best-estepin management will be to give like a phentulumine, right? And give an alpha one antagonist like phentulumine. And remember, it's a reversible alpha one inhibitor, right? So that can help with the block pressure. But let me just take a quick sidebar here. I guess it's kind of important. Like, how do we, in general, treat hypertensive crisis? Because I don't know for whatever, I don't know, it still baffles me to this day.

I don't know why people never talk about this stuff. Or like, you know, put it in one spot, right? But in general, if a person has hypertensive emergency on NV Me exams, there are very limited number of drugs you should give, right? You should give either my trope or side, that's one, or you can give my cardiopine, that's two, or you can give clevidipine, that's three, or you can give labidolone. Those are the four drugs you should use for hypertensive emergency or urgency on NV Me exams. They will try to trick you into giving my phydepine or whatever. Don't give my phydepine. I promise you that I'll end in disaster. At least you will essentially get the question wrong. So there are really only four drugs you should choose for hypertensive emergency, my cardiopine, clevidipine, labidolone, and sodium nitroforside, right? Again, don't pick my phydepine, don't pick hydrozene. They will give you, although, he has those drugs lower blood pressure, but they don't treat hypertensive emergency on NV Me exams. And again, I'm promising you I'm seeing this from years and years of experience taking NV Me exams. I don't think I have truly ever seen a hypertensive emergency situation where it was not one of these four drugs, that was the correct answer. So that's something you want to like just screw into the back of your mind. Again, there is an exception right with this like tyramine crisis with taking an NV Me UI.

You can use any of these four drugs I just mentioned, but you can also throw in phytonamine to that mix. So again, high yield things you want to keep at the back of your mind. Now, what did they give you a question about a patient, you know, again, maybe they have the amygdda gastroparesis and they've just been started on a new drug, yada yada yada, right? And then they tell you that, oh, this person has like, like they have like these like weird movements of like one part of their face or one outbreak, extremely and it's rigid and all that, right? Under those circumstances, you want to think about acute dystonia, right? Again, acute dystonia happens when you're exposed to antipsychotic and remember it's arising from dysfunction of the migrostriol pathways and extroprimidocenta. And really the way you want to go ahead and treat that is, you want to go ahead and give drugs like, you can give diaphidramine, right? Remember, again, it's an antihistamine that has powerful anticholarity, but another thing you can also give is, you can give, you can give any regular antichrubin, like bench stroking, for example, right? So something to keep at the back of your mind. And then remember that if a person, you know, he started an antipsychotic and then the patient has like, they feel like they can't, they almost feel like they cannot get out of their skin, like they can't sit still, they're like just pacing all over the place.

And under those circumstances, you want to think about a cathedia, right? A cathedia, your drug of choice is a bit of blocker, go ahead and give proprenolol and call it a day and you're good to go. And then remember, right? A person can also have a fucking sentence of right. So they can have all those like, you know, classic issues like, you can tell you that the person has, all your rigidity has trouble like moving, right? So like they are very pretty kinetic and all that stuff. If you see a parking sentence and you know, go ahead and give dopamine agonist, right? So you can give bremocryptin, cabregolin, right? And that should help. You can also give bench stroking, okay? That should help as well. And then if a person has like, targeted dyskinesia, right? So like, it will be something that, oh, they've taken this drug for like a while and then they have like, repetitive movements of like their tongue or whatever. That's targeted dyskinesia, targeted dyskinesia. Go ahead and give those a stop first stop the drug. So if they may try to trick you by saying, I give this new drug or yada yada yada or decrease the dose of the drug or whatever crap, then stop the drug. Whatever a person is having to exist from a drug, the first thing you should always do is stop the drug, okay? I promise you, almost always stop the drug is the right answer. So stop the drug after you stop the drug, then you can go ahead and switch to a different agent, right?

Typically you switch to an atypical anti-psychotic. And then one of the classics in area that we pop up occasionally on test is, let me describe a person that you know has a history of Parkinson's, right? And they tell you that they are cabido, palivo, those, those, you know, bumped recently. And then the person is having like severe side because essentially, you're almost like giving the person dopamine, giving the person dopamine, giving the person dopamine, right? So those things can, those things can cause psychosis, right? A person is getting psychosis from their Parkinson's meds, like the cabido palivo dopa. Your first step in management is to reduce the dose of the cabido palivo dopa. That's the first thing you should always do. But the thing is, many times when a person is taking cabido palivo dopa for Parkinson's, they are depending heavily on that stuff, right? So the thing is, your first step in management will be to lower the dose. But if they don't tolerate the dose reduction, then your next step in management on NV Me exams is to give them with firep, okay? You see, define. The person with Parkinson's giving them an anti-psychotic, I promise you will be the right answer, right? So if dose reduction doesn't work, go ahead and give those people with firep, with firep is a very mild anti-psychotic. I mean, people use it all the time in the ICU for training, like delirium and all that stuff. So you can just something to keep out the back of your mind.

Remember, with firep, remember the big side effect, you can cause cataracts, right? With firep, it causes quarter acts. That's a nice, non-monic that has been thrown around quite a bit. So just again, something to keep out the back of your mind on exams. And then remember your, you know, sympatoma America, like a toxic drum, right? So the person will have like profound hypertension, right? The person may have like a perforation of the nasal septum, especially if they are like cocaine, like users. Well, if a person is like hyperthyroid, that can cause a sympatoma America toxic drum, right? Or if a person is like we're drawing from like alcohol or like sedatives, like benzos, that can also cause, you know, sympathetic like toxic drum. Well, also remember things like, again, cocaine, like I said, and vitamins, like I said, those things can cause a hypertensive of toxic drum. So they'll have like my dry asses, right? They will have like, they can have like, you know, tacky cardia, because again, there's increased speed of conduction now, there are EV nodes, they can have hypertension, and all that stuff, right? So whenever you see all those things, again, think about, think about a sympathetic, a sympathetic, a sympathetic, a sympathetic, a sympathetic toxic drum.

And again, really, what are you trying to do under those circumstances is, essentially, most things you do will be right, especially like the classic poster childhood when it's cocaine toxicity, you can give a benzodiazepine, right? You can give an alpha one blocker, right? You can give an alpha one blocker like, like again, like phantolamine, right? You can give those, you can give an alpha bit of blocker like labetolol, right? The big thing you want to avoid is a pure bit of blocker, like propryonolol, terrible idea, right? You never want to give a bit of blocker in a person that has a cocaine or a toxic drum, because again, they'll have the on-off-post alpha one, they'll have like terrible, terrible, terrible hypertension, and then you throw them into like a hypertensive emergency or something like that, so you don't want that, right? So that's not an ideal thing to have on exams. And then, what do they give you a question about a patient? They'll tell you like it's December, right? Or sometime in the winter, and then this person has like a badlactic acidosis, this person was like found down at home, yada yada yada, if you see that right, I hope you're thinking about like Kaboomonoxide poisoning, right? And obviously, under those circumstances, right, you want to treat with hyperbari oxygen, right? Because again, remember, Kaboomonoxide poisoning very, very, very classically presents in that way, like in the winter, space heaters kind of deal.

And then, right, if a person has, let's see, it's like a person that's going on a missionary trip or a person that's going to like a developing country, right? And you know, they take malaria, prophylaxis or whatever, and then they become like profoundly hypoxic, and they become like super sick, and they tell you that, oh, they have like a central cyanosis, or, you know, they just give you signs and symptoms of hypoxia. I would hope on that those circumstances that you're thinking about methemoglobinemia, right? Remember, whenever you're exposed to an agent that has powerful oxidizing activity, right? So like many of these malaria drugs are like Dapsone, right? Remember, Dapsone uses it classically to treat like Leprosy, or we can also use it for like PCP prophylaxis in HIV patients, or they may give you a question about a patient that is on, like, trimethopermisopharmethoxazole, right? Tremethopermisopharmethoxazole. Again, whenever you see those things, just really, really think about, like methemoglobinemia. And obviously, on the other circumstances, right? You want to go ahead and give the patient a methylene blue, right? Methyline blue, because he methemoglobinemia. The reason you have trouble is that a lot of your fierce irons, Fe2 plus has been converted to ferric iron, Fe3 plus, right? So the patient is in trouble, right? Because again, Fe3 plus hemoglobin that has iron in the Fe3 plus state, cannot carry oxygen, right?

But hemoglobin that has iron in the Fe2 plus state can carry oxygen, right? So, on other circumstances, you go ahead and give the person a methylene blue or increase the production of Fe2 plus. And that can hopefully fix their... Methymo-globinemia. Remember, though, methymo-globinemia is not necessarily a bad thing. You induce methymo-globinemia to treat people that have a toxicity of cyanide, right? Because again, Fe3 plus has a very solid binding affinity, for cyanide. So again, just something. You want to keep on the back of your mind on the exams. Now, what if they give you a question? And in the question, right? You know, this person has a history of like, like, a feb and the utility that they have mitrostinosis. And then, you know, the utility that they iron are today is like a lot. And they have like, they haven't like, bright red bowel movements. Yeah, yeah, yeah, yeah, yeah, yeah. What are you thinking about? Under those circumstances? Well, I would hope you're thinking about like, wafring toxicity, right? So this is a zerozanz wafring toxicity. I remember wafring can cause a lot of bad problems, right? Like, especially like, I don't know if whatever is in your friends at the end being me, they're beginning to like, wafring toxicity. And like, GI bleeds these days. And those GI bleeds, you want to remember them as being from like, do I know him at Thomas or from like, rectus, sheath, hematomas. Those are all classic presentations on the exam.

So that's just again, something I want to sort of kind of want to keep on the back of your mind. But wafring toxicity, for a person who has like, wafring toxicity, right? And they are doing poorly, right? Maybe the tell you that this person is having like a life threatening bleed, like this one, for example. And then they ask for your next best-tempo management. They will try to trick you on your exam into picking a, what's the name of this drug? They will try to trick you into picking a, ffp. Don't pick ffp. For persons having a life threatening, wafring bleed, your, the answer you want to pick on your exam these days is a, four factor PCC. So like a four factor, pro thrombin, complex concentrates. That is now the drug of choice for treating a wafring toxicity. But typically on NV Me exams, if a person is, has a high INR, but they don't have any like symptoms, then typically what you do is you go ahead and stop the wafring again, toxicity, classic thing here, stop the drug. Go ahead and stop the drug. And then you can actually begin to give them like vitamin K. And typically oral vitamin K is preferred over IV vitamin K, right? So that's just something you want to keep at the back of your mind. I mean like as a resident, you have to learn like, oh, if your level is more than, if your INR is more than 20, you do this is between 9 and 20, do this. But that's not something they're going to go after the NV Me exams.

The snares I've just described are really those things you need to know, right? And then what if they give you a question about a patient, you know, try to overdose on something. The person's LF Ts are like super high and the person's creatinine is rising. What are you thinking about, right? Well, this is a set of menophanepoisonin, right? So the menophanepoisonin typically, right? You want to go ahead and give those people an anacetylocysteine, right? Remember, an acetylmenophan, right? Mix this NAPQI, I think is like an acetylope, benzoyquinone, amino, whatever. What napke, NAPQI, you know, screws up your liver, right? You treat that, you prevent that of this thing, like anacetylocysteine. And then if it's like within minutes of the person like consuming the agent, you're going to be going ahead and give activated charcoal, that can bind it up in the GI tract, but usually, you're like far along on MBM exams. So just go ahead and give those people an acetylocysteine and call it a day. And the thing is on MBM exams, right? They may give you, try to be a little nifty. And they may not just give you LFT abnormalities, they may give you other like real things like the person may be hypoglycemic, or the person may have like a metabolic acidosis, the person can have like an anacetylopathy because the urethyclyclo doesn't work so well anymore, right?

And in general, once the person is beginning to have those issues like hypoglycemia telling you that, oh, gluconeogenesis, bye bye, right? Or the person is beginning to have like a metabolic acidosis and like the anaryz bumping up. Those people need to be referred to a transplant center, right? Because those people are beginning to stare down at that door, right? So, yeah, I said, I'm in a friend poisoning again. Most people, you know, are rescued when they come into the ED. But if it progresses along, those people can die relatively rapidly, right? And it's just one of those things you don't want to, if you ever, so if you see like weird and cephalopathy in a patient that tries to commit suicide as a resident, or whatever, I'll strongly strongly encourage you to get an acetylomyne level, right? Just make sure that again, they don't have acetylomyne-phediatoxicity. If you suspect it, go ahead and start the anacetylocysteine and ask questions later, although once you start treating an patient with MAC, you essentially committed to like a fairly long, adverse process of treatment, but again, that will save your lives. Now, what if a person, you know, they give you a question about a person, you know, tried to overdose on something, and then the person's respiratory rate is like 30, right? And this person's PCO3 is like 20, right? And this person's pH is like 7.51, right? And then they have like a bike out of 13, right?

We'll hope you're thinking about like aspirin toxicity, right? So, these people generally have like respiratory alkalosis with a metabolic acidosis. Really, the way you want to treat aspirin toxicity, right? You go ahead and again, if it's within a few minutes, you can give activated charcoal, but that's really the correct answer on exams. Usually the correct answer on NBME exams is to go ahead and give the patient like sodium-point carb, because that will alkalize the urine, right? And when you alkalize the urine, right, you will increase the excretion of the aspirin, right? And again, just again, all weird things you want to give out the back of your mind. But if you don't see alkalizing the urine as an answer choice, and you know, the person's having like severe toxicity, like they have like a perform metabolic acidosis about to die so they're deal. And then one thing you can consider doing is dialysis, right? Quiet and dialize those patients and get rid of all that aspirin. And then remember, if a person you know overdoses on a bit of blocker, right, you want to obviously give those people a look on, I described the mechanism behind that in my biochem video, but that's something I've described in my biochem video. I don't think it's necessary to talk about because I mean, this podcast is really going on for a long time. I really want to try to go ahead and stop soon.

So, bit of blocker, right, to again, consider using a look on, and I mean, obviously, for a person overdoses on a bit of blocker, they'll have like a profound cardiac, they'll have like a hypertension, things of that nature, right? And then if a person overdoses on a calcium channel blocker, right, again, these are not things that people necessarily think about on exams, but if a person overdoses on a calcium channel blocker, right, and they ask for your treatment options, right, you want to go ahead and give those people a calcium chloride, right? Just give them a calcium-based compound, like calcium chloride, calcium gluconeid. Although, remember, right, that calcium business, you can also actually believe that or not, you can use like calcium to reverse some mac toxicity. So, the person has like hypermigrancymia, and they have like severe toxicity with that. You know, go ahead and give them a calcium gluconeid or calcium chloride, just a calcium-based compound. So, the things you can reverse with calcium-based compounds, you can reverse profound hypermigrancymia, you can reverse toxicity of a calcium channel blocker, right? And you can also reverse, you can also treat hyperchillin, at least to stabilize the myocardium, by giving a calcium-based agent. So, that's again something you want to keep at the back of your mind.

Now, if a person has like, you know, they give you a question about a patient that, you know, he's on a lube diuretic, and they also come to the C-chef examination, and then they get a drug, and then they tell you that this person is now having like, a lot of PVC's, like a pre-matrophic and trucolac contraction, all these, like weird, ventricular arrhythmias. I hope, under those circumstances, you're thinking about a D-choxicity, right? So, like, dejuoxentoxicity. Really, for pressing is, has a dejuoxentoxicity, then your drug of choice will be like the anti-dich Fab fragments, right? In the real world, they call it Digibind, but yes, it's a monoclonal antibody against literate dejuoxent. Because remember, the reason I said that the person is on a diuretic, because think about it, for pressing as a C-chef examination, right, what would classically use to treat that? Typically, we treat that by giving lube diuretic, right? We treat that by giving a lube diuretic, so something like, something like, like, if you're a semi-together fluid of, well, what do all diuretics cause? Diuretics in general tend to cause hypochylemia, right? So, the thing is remember, hypochylemia increases your risk of dejuoxentoxicity, right? Because, again, remember that dejuoxent works by inhibiting the sodium potassium eti-p-spump. So, if you inhibits that pump, and then, the thing is, it binds to, like, the potassium site on that pump to do its duties.

So, if a person is hypochylemia, there is, like, more spots open on the sodium potassium eti-p-spump, for dejuoxent to bind to and cause a lot of trouble, right? So, in other circumstances, you give Digibind, or you examine your C-chef, anti-dich Fab fragments. You go ahead and give that, and the patient should be hopefully good to go. And then, remember that if a person is on dejuoxent radios, or you want to just watch out for the toxicities, remember, hypochylemia is a classic side effect of dejuoxent, because, again, if you inhibit the sodium potassium eti-p-spump, remember that the job of that pump is to take three sodiums out of the cell, and two potassiums in, right? So, if it's not working, then potassium can remain outside the cell, and the patient can get a severe hypochylemia and get into trouble on the exams. So, in some of you may be scratching your teeth a bit like this. What is this guy talking about? So, let me clarify this for you, right? Hyperchylemia is a side effect of dejuoxent, but having hypochylemia predisposes you to having dejuoxent toxicity, okay? So, again, just get weird, what high you things you want to keep at the back of your mind on tests. And then one thing I guess I feel to mention, or let me just mention now, so I don't forget, right? If a person has a toxicity from... Dabigatren, remember those anti-besides like warfarin and hipproprineprolycal, you cannot reverse any of these anti-quangolants.

You can actually now reverse a dabigatren, right? There's a monoclonal antibody known as a daracizumab. A daracizumab is a monoclonal against the dabigatren. In the real world, it's called a prox bind, but on the exams you see a daracizumab. So, again, if a person is having like a life-threatening bleeding from dabigatren toxicity, go ahead and give those people a dabigatren, and that will fix whatever is going on, right? And then if a person is having like really bad bleeding and the abitity is elevated, obviously, that person has like a haprin, like a haprin toxicity, go ahead and give programming soft feet. Remember that programming right is used to treat on-frax... like toxicity like bleeding, like toxicity from like unfraxinated haprin, doesn't do squat for low molecular weight haprin, right? So again, just something you want to keep, something you want to keep at the back of your mind on exams. And then, if for example they give you a question about a patient, and a patient has like, again, like a profound hypo glycemia from taking... from taking a... because here's the thing, right? The thing is, the MBM, they may give you a question about a patient that you know is found down, and this patient is not responsive, like these people are very sneaky, right? Found down, not responsive, and they may tell you something about this patient, oh, this patient has a history of type 2 diabetes, and the patient is not being treated with insulin, right?

They will try to give you that, to try to take your mind away from a considering hypo glycemia, as a... as a... as a... thing that may be happening and causing those patient symptoms, you just gotta be careful. Remember, it's not only insulin that can cause hypo glycemia. Remember, those diabetes drugs, right, like those sulfonolureus, those things can also cause hypo glycemia, okay? So if a person, any patient that has a history of diabetes, and they have like altered mental status, and they are not responsive, always think about hypo glycemia, right? And again, like I said, you wanna go ahead and give glucose, if you can, if you... if that's not an answer choice, you can give glucose, glucose is the quickest agent for reason, a person's glucose levels, and really of all the sulfonolureus, really, in fact, of all the... let me put it this way to you. Besides insulin, of all the oral hypo glycine, right? Those oral hypo glycine agents, the one that has the biggest risk of hypo glycemia, is gliburite, okay? Is gliburite, okay? So that's again, one of those weird things you wanna keep at the back of your mind. And again, in general, like I said, you give glucose, or you can give glucose gone, right? But let's assume you get an answer choice, and the answer choice doesn't have glucose, doesn't have glucose gone. One bizarre answer you may want to pick on in exams is octriol type. Octriol type can actually help under those circumstances.

There's a mechanism behind it, but I'm at 15 minutes right now, and I wanna go ahead and end this podcast soon. So I think I'm gonna go ahead and keep going. So again, just again, all hyal things you wanna keep at the back of your mind on exams, right? And then if a person, I'll just rapidly go through a few more quick ones, because I wanna try to hopefully keep this on there an hour. But if a person has... Remember, I was talking about serotonin syndrome. One thing that just dropped in my mind is, remember that this drug, ecstasy, so like MDMA. So MDMA can actually cause many of these problems, right? So you can cause many of these serotonin syndrome-like problems. And if MDMA is one of these drugs, you just wanna know, like the back of your hand on exams, it just shows up too commonly, that you wanna make sure you keep at the back of your mind, right? So like MDMA, for example, can cause rhodomyelosis on MDMA exams, because again, if you dance and dance for hours and hours and hours on end, it's almost like running a marathon, right? We're just doing a different way of dancing. That can cause rhodomyelosis and all the sequelae of rhodomyelosis, like the person can have hyperchylenia, because the muscle cells are dying, the person can have hypocalcemia, the person can have a rising creatinine, right? Because the myoglobin has clunked up their kidneys.

Obviously, under those circumstances, go ahead and give those people like very vigorous hydration and diorosis to flush out those nasty things, right? And then, remember that ecstasy, right, can also cause a serotonin syndrome, like I said. I remember, it can cause a heat exhaustion. Again, you dance, dance, dance, a ton, you wear yourself out, the person can, you know, die from heat exhaustion. And then one other thing you may also see is hypoinitremia. It can present it as a psychogenic polydipsia question in exams, where the person will have a low seroma's molarity and a low urinose molarity after taking like a drug before they go for a dance party, okay? Think about psychogenic polydipsia from like the drinking a ton of water. That's one thing that's MDME, EKE, ecstasy, then cause an MDM Es with people. So again, just something to keep at the back of your mind. So those are all higher things you want to consider with toxicity of ecstasy, right? And then don't forget that, you know, if they give you a question about a patient that's getting surgery, any kind of surgery, right? And then the person becomes like profoundly hypothermic, bababab muscle rigidity. You hopefully are thinking about my lignar hypothermic, one of those circumstances. The presentation is very similar to the presentation of your electric malignant syndrome, but the exposure is different, right?

So things like hollow thing, succinocholine, yada yada yada, those are the things that all cause those toxic drums, or at least of malignant hypothermia, like in yoga and aesthetic kind of business. And your next step in money, then, is to give denturally, right? Denturally, remember denturally is a ryanodine receptor antagonist, okay? They may not even put denturally as an answer choice, and they may put calcium channel blocker, okay? And then, again, it's effectively a calcium channel blocker. This is just, again, simple quick and early way, that game being a mix of this new elliptic malignant, I mean, sorry, malignant hypothermia question harder than it needs to be, right? So, you give denturally, right? Denturally is the drug of choice for treating malignant hypothermia, okay? And again, remember that malignant hypothermia, it's in herithane and an arosomodominant fashion, and arises from mutations in like, the ryanodine receptor mutations, or dihydroperidine receptor mutations, right? And so, the more common receptor mutation that causes malignant hypothermia is, come on, the one thing is, ryanodine receptor mutation. So, again, just big things you want to keep at the back of your mind on tests, and hopefully that, you know, helps you get a lot of questions right on your exam. So, I guess, what are the things that I really want to, you know, walk through real quick?

Again, we can give you a question about a patient, you know, that has pancreatitis, and they've been on a ventilator for a long period of time. Then, I will put on that those circumstances, you think about purple fall, remember purple fall, right? Continues the tone on lipid, right? So, a person can get, you know, can get pancreatitis from hyper-trageless rydemia, when they're on, like, on a long-term, a purple fall infusion. And then, remember that purple fall, right? They may give you, like, a weird contraindication question. This is just me now, just going through things rapid fire at this point. A person can get purple fall toxicity on MIMI exams. I mean, sorry, they may give you a contraindication question on MIMI exams with purple fall, and a patient that has, like, a familial hyperlipidemia. For a person who has, like, a familial hyper-trageless rydemia, then getting purple fall is not a great idea, okay? It's not a great idea because they're really pretty supposed to have in a hyper-trageless rydemia, so you don't want those people getting, like, pancreatitis, or any of those things on an exam. And then, if they give you a question, right, about a patient that, you know, has Parkinson's disease, right, and has serotonin syndrome, like, presentations. Again, don't forget that with, like, your MUB inhibitors.

Like, again, many people are used to, like, oh, your classic MUL Is from psychiatry, your phenylsine, trinealcypromine, isocarboxesate, that, oh, those are the only things that can cause serotonin syndrome with MU Land. The thing is, again, your friends at the MBMID can make things a little unique by giving you, like, cellulogenin and resageling causing those problems, okay? So, again, those are all weird, but high-yield things. You want to keep on the back of your mind. And then, remember, if a person, you know, they give you a question about a patient that is on a cancer drug, and then this patient starts having, like, gross hemat... Like, blood, like, blood plots coming off from your urine. You want to think about hemorrhagiccystitis, like, lymphosphamide. Remember, that is caused by the acrylene and tabolite, and you can prevent that by giving the drug known as a mesda, okay? And then, remember, that, if they give you a question about a patient, you know, that's on a cancer drug, and the acrylene is rising, and you're having, like, hearing difficulty, then all of those circumstances think about cisplatin, okay? cisplatin. Remember, cisplatin is a platymal agent very, very bad toxicity. It's nephrotoxic, and it's odotoxic. Remember, your nephrotoxic drug combinations vancomycin is one of those. If the chronic acid is one of those, cisplatin is one of those, right? So, again, those are all high-yield things. You want to keep... You have amino glycosides as well.

They also have that unique combination of being nephrotanodotoxic, right? And then, remember that if a patient has cisplatin toxicity, right, you can actually prevent the nephrotoxicity of cisplatin with a drug known as imifostate, right? So, AMI, FOS, TIN, okay? So, high-yield things you want to keep at the back of your mind. And then, remember, the irreversible diluted cardiomyopathy that arises with the anthracycline, Dr. Doughsondonorobicin, right? So, they can give you a question about a patient that has, like, a kidney, a propsisimal, mochinoid dyspnea, yada, yada, yada, right? After recently studying, like, a cancer regimen, especially for, like, breast cancer, think about the irreversible diluted cardiomyopathy with your Dr. Doughsondonorobicin. Remember, classically, you can prevent that by giving an ion chelator known as dexerzoxin, because remember that Dr. Doughsondonorobicin, right, the promotes the fainting reaction as a means of causing the diluted cardiomyopathy. Although, also, don't forget, like, you're her two-new receptor, you know, chronic antibody, right? Like, trust us, you're mapp. Remember, that tends to cause a reversible, not irreversible, reversible diluted cardiomyopathy. And then, I know, I talked about, like, chronic alcoholic earlier. Remember that alcoholic strategy? We have, like, the elevated ESD to ALT business, right? Like, two to one, Scotch-Antonic, and the one that you probably remembered. And then, don't forget that alcoholics, right?

Again, like I said, it tends to have, like, a B-worn deficiency, so a thymine deficiency, so transkyrolisols don't work as well, so you can get one in kicker, so a cough. And then remember that alcoholics also tend to get fully deficiency. So if you see a megaloglastic anemia in a patient that has a history of alcoholism, they'll try to trick you on the examine to picking B-12 deficiency. Don't pick B-12 deficiency, pick, fully deficiency, right? So, by the mean B, not by the mean B-12, okay? Again, I believe I described the mechanism behind that in my biochemistry video, right? And, yeah, I think I'm maybe going to go ahead and stop here. I feel like I have, you know, talked about the many of these Ohio toxic drones. So, hopefully you find this to be helpful. If you're taking a side-shelf, right? Or at the end step two, see, or step one, or step three. This is one of those podcasts, right? You definitely want to listen to it, right? If not, you, you know, I mean, you can already just hopefully from listening to this podcast, you can really begin to envision that you're going to get a cup of bunch of questions on this stuff. So, this is of very high yield to know. If you're taking it like an EMET shelf, or you're even an EM resident, and you want to rapidly review like these toxic drones, this podcast should do the trick. So, as I do at the end of every podcast, right? I do offer one of one tutoring for many exams, step one, step two CK, step two CS, step three.

Critical Metz school exams, 30-attractive shelf exams. And then I do this thing called longitudinal tutoring, right? Like if you're a first-second or 30-metre student, I tutor you for like your class blocks, or I tutor you for like your shelf exams. But at the same time, I'm also longitudinally tutoring you for step two, or like step two CK or step one. Basically, you're upcoming a USMLE exam. And again, people have done this with you, been like very successful with this stuff. So, if that's something I'm interested in, reach out to me. And then I also do this USMLE booster course. It's like 10 hours for step two CK and step three, and 20 hours for step one, where again, it's classically good for people that are like at the end of the dedicated periods. Like they just want to put everything together, give themselves like that boost. Basically, in these booster courses, I very rapidly review like an Q&A format, a lot of the high-yield information that's classically tested on these exams. So, if you're feeling good about your knowledge base, or you just want to put everything together for you, just reach out to me. That's something I also offer. And then, if you have like a college buddy that needs to be doing for like Gen CAM, O-CAM Physics, Bio CAM, Physiology, Histology, Alpha Turion for all those things. And then if you're a medicine resident, I need to do it for like the internal medicine, in training exam, or the internal ABI, in internal medicine board exam.

I go for training for those. And some of you may have noticed, I've studied making like pediatric boards material. Again, I just like that stuff. So, again, I'll make as many podcasts as I can for those. And some people have also talked about like, oh, please divine, could you put this on like Spotify or Apple podcasts? Again, I promise I'm working on that. I'm gonna put in more effort when I have more time. It's just things have just been quite easy for me. The last couple of these. So, I wish all the best. Hopefully you got something from this podcast. And again, I also do offer like, you know, one on one coaching for like, if you're a medicine applying to residency, so like an ERAS app, or a medicine applying to a medical school, so an AMCA app, right? So, like, do like coaching or advising for like, at least then. So, like, walking interviews, personal statements, rec letters, editing applications. Again, I've been on the admissions committee of a top two med school for like a year. I've reviewed thousands of high quality applications. So, again, and I've also worked with a lot of people. Even this current ERAS process, I've worked with a ton of people. So, if you need any of those things, I reach out to me. So, have a wonderful rest of your day. God bless you. I'll see you in the next podcast. Hopefully it's not a week from now. I think you'll be a lot sooner than that. Thank you.

Administer IV dextrose solution (Glucose). Never give insulin.

Naloxone. Do not use Flumazenil or Naltrexone.

Hot as a hare (hyperthermia), blind as a bat (mydriasis/dilated pupils), dry as a bone (dry skin/mucous membranes).

Physostigmine. It is an acetylcholinesterase inhibitor that outcompetes the anticholinergic agent at muscarinic receptors.

Hydroxycobalamin. This binds directly to cyanide, forming cyanocobalamin.

Benzodiazepines. Opioids cause miosis; benzodiazepines cause non-specific respiratory depression.

Administer Dantrolene. It is a ryanodine receptor antagonist.

Hot, blind, dry (Hyperthermia, Mydriasis, Dry skin).

Antihistamines (e.g., diphenhydramine), Tricyclic Antidepressants (TC As), and Atropine overdose.

Physostigmine (Acetylcholinesterase inhibitor).

Niacin deficiency, Wernicke-Korsakoff syndrome, and Thiamine deficiency.

Fomepizole (an alcohol dehydrogenase inhibitor).

Daracizumab (a monoclonal antibody against dabigatran).

Phentolamine (an alpha-1 blocker).

Life-threatening bleed requires Four Factor PCC; High INR without symptoms requires stopping warfarin and giving oral Vitamin K.

Folate deficiency. Give Folic Acid/Folinic acid (B9), not necessarily B12.

Hot, blind, dry (Hyperthermia, Mydriasis, Dry skin).

Antihistamines (e.g., diphenhydramine), Tricyclic Antidepressants (TC As), and Atropine overdose.

Physostigmine (Acetylcholinesterase inhibitor).

Niacin deficiency, Wernicke-Korsakoff syndrome, and Thiamine deficiency.

Fomepizole (an alcohol dehydrogenase inhibitor).

Daracizumab (a monoclonal antibody against dabigatran).

Phentolamine (an alpha-1 blocker).

Life-threatening bleed requires Four Factor PCC; High INR without symptoms requires stopping warfarin and giving oral Vitamin K.

Folate deficiency. Give Folic Acid/Folinic acid (B9), not necessarily B12.