Seizure Medications | Antiepileptics

what's up ninja nerds in this video we're going to be talking about the pharmacology of anti-epileptic drugs before we get started if you guys enjoyed this video it helps you it makes sense please continue to support us by hitting that subscribe button hitting the like button and commenting down in the comment section it helps us to continue to keep making free videos for you guys enjoyment all right ninja nerds let's get into it all right engineers so before we start talking about the different types of anti-epileptic drugs their mechanism of action let's briefly and let me briefly go through the pathophysiology of seizures the reason why so we understand the pathophys the mechanism of action will be super easy so first thing we have to understand we talk about seizures is that there's two parts to seizures obviously it's excessive electrical activity that's abnormal it's synchronous that's occurring throughout the central nervous system but what's the trigger for it there's two particular pathways that are involved so one of the pathways is called the gaba pathway and the gaba pathway is an inhibitory pathway so if we actually decrease the activity of an inhibitory pathway that could potentially increase the risk of seizures so there's a decrease in the gaba or we like to say inhibitory pathway and when i say that there's a decrease in the inhibitory pathway the gaba pathway what i really particularly mean is that the gaba a receptors seem to be dysfunctional and you'll see what i'm talking about how this actually can cause this decrease activity really within the gaba pathway the other aspect of the seizures is not just a decrease in the inhibitory pathway but there's an increase in the stimulatory or glutamate pathway so glutamate glutamate is one of the primary like stimulatory neurotransmitters in the central nervous system so if we increase the stimulatory pathway that'll really increase the seizure activity okay and i'll explain to you how that works okay all right so whenever somebody is having these seizures how does this actually work well you know with on here's our glutaminergic neuron right so the red is representing the glutaminergic pathway and this kind of like navy blue is representing the gabaergic pathway when someone is actually going to be exhibiting seizures there is this increase in the action potentials that move down the glutaminergic neurons when these action potentials are increased you know what that happens there's particular ion channels voltage-gated ion channels that are present on the axon of these glutamate neurons glutaminergic neurons these are called sodium channels whenever action potentials travel down the axon they open up these voltage-gated sodium channels and allow sodium ions to flow in to the axon and that makes the inside of the cell nice and nice and positive which is going to increase the depolarization right and if you increase the depolarization of this axon it's going to continue to cause this flow of positive charge to move down the axon if this flow of positive charge continues to move down the axon enough that it stimulates these next channels called voltage-gated calcium channels and those little suckers open they allow for calcium ions to influx into this actual neuron into the axon terminal bulb as calcium ions flood into this axon terminal they love to stimulate these vesicles and when they stimulate the vesicles they stimulate synaptic proteins that cause the fusion of this vesicle with the actual cell membrane and lead to the exocytosis of what what is these little buggers right there glutamate so this little booger here that i'm going to show you is glutamate okay now how does calcium actually do this and how does this vesicle fuse it does it via these little boogers here these things called sv2a proteins they're like synaptic proteins on the vesicle that allow for kind of the fusion of this vesicle with the cell membrane to induce the glutamate release now once glutamate is released guess what happens here's where it gets even better glutamate can act on two different types of receptors one receptor is called an a m p a receptor that's this one here or it can act on a n m d a receptor that's that one there when it acts on these either way the overall consensus is that this causes the flow of cations through both of them right so cations like sodium cations like calcium even magnesium flows through this thing and if you have lots of cations flowing into this neuron what's it going to do it's going to make the neuron super super positive when you make the inside of a neuron positive that's going to trigger depolarization and if you trigger depolarization and you activate or open up specific types of voltage-gated ion channels on the axon of this neuron what would that do that will trigger an increase in action potentials and as you trigger an increase in action potentials that will lead to this excessive abnormal electrical synchronous activity that occurs within the central nervous system that can present as seizures okay so that's one part that's the stimulatory pathway so basically imagine this pathway being increased everything that we just said would be exacerbated more action potentials coming down more sodium rushing in more depolarization more calcium rushing in more fusion of the the synaptic vesicles with the membrane more glutamate release more depolarization and more action potentials all that's increased now think about this for the opposite for the gaba pathway and someone who is having seizures you know um gaba is actually very interestingly you have a molecule and we just talked about glutamate and you know glutamate is kind of a precursor to making gaba and then gaba is actually kind of stored inside of these little vesicles we have here well if there's action potentials that are traveling down this axon in the same kind of manner we just talked about and they stimulate these vesicles that contain gaba to fuse with the cell membrane and release that gaba out into the synaptic cleft where does that gaba go good question the gaba that's being released via this exocytosis mechanism and we're representing like that with these little blue boogers there they come over and they bind onto this little receptor here present on this kind of neuron the same neuron and what is this type of channel this channel is very important this is called your gaba a receptor it's called the gaba a receptor and when they bind onto the gaba a receptor normally what you would want to happen is this would open up that channel and allow chloride ions to flood into the cell chloride is a negative ion right so it's going to make the inside of the cell nice and nice and negative if you make the inside of the cell negative what will that do well that that's called hyper polarization when you make the cell even more negative than its resting membrane potential and that is called again what hyper polarization okay now hyper polarization makes the inside of the cell negative and basically decreases the risk of you actually developing action potentials so it's really going to decrease action potentials at least it should so the the process here is it should decrease firing down this axon and decrease the actual seizure activity right that's kind of the whole thought but remember what i told you in seizures there's a decrease in this gaba pathway what's wrong the gaba a receptors aren't good they're all jacked up they don't want to respond to the gaba so whenever gaba binds here these gaba receptors say hey okay i i hear you you know trying to stimulate me no you know don't be weird i hear you trying to stimulate me but i'm not going to open up i'm not going to allow for chloride ions to flow into me okay and so because of that there will be what if the gaba a receptors are dysfunctional so in this case they are dysfunctional they all jacked up okay there's dysfunction of these gaba a receptors whenever the gaba binds they'll be decreased opening of these chloride channels that means decreased chloride ions enter into this cell if there's decreased chloride ions do you cause hyperpolarization no so there's a decrease in the activity of hyperpolarization if there's less hyperpolarization then what's going to happen then you're going to lead to more action potentials because you're not going to make the cell inside of the cell negative you're actually going to make it a little bit more positive because there's not as many negative ions as you would like coming into that cell if there's less negative ions it won't hyperpolarize instead it'll actually depolarize and that'll trigger an increase in action potentials increase firing of these neurons in an abnormal excessive synchronous way which will present with seizures now after gaba's done exerting its effect naturally what we want to do with that gaba is take and try to recycle it so there's a gaba re-uptake protein that takes the gaba back into the actual synaptic terminal and then once gaba's brought in we kind of want to break it down into an intermediate called succinate semialdehyde and we use an enzyme here called gabaterminase and that basically kind of renders gaba and effective so to summate what happens here is there's an increase in the glutamate pathway that causes increasing action potentials or there's a decrease in the gaba a pathway where is the problem the problem is with the gaba a receptors they don't want to respond to gaba they don't hyperpolarize and because of that they actually depolarize and they trigger increased action potentials now with that being said if somebody is actually developing these seizures right it can develop in two types of ways so one type of way that you can develop a seizure is there can be an abnormal focus there's neurons in this location that are firing and they're staying in this side of the cerebral cortex they're not crossing over to the other hemisphere and that situation this is called a focal seizure and you can have two different types with this you can have it with or without impairment but if you have an actual seizure where there is activity that is spreading throughout the entire cerebral cortex both hemispheres this is actually called a generalized seizure it's called a generalized seizure so i just want you guys to understand the pathophysiology of seizures and the two real types of seizures that you can see now that we understand that we can use particular medications to treat people with focal seizures or generalized seizures what are those medications let's get into it baby all right ninja so now let's talk about the names of these anti-convulsants they're like kind of within their categories and then talk about how they work and this should be super easy we've already built up our foundation now so first ones are your sodium channel blockers so i like to remember these by very problematic two let little phosphonatoin cuddle okay so valproate phenotoine to pyramid lamotrigine lucosamide phosphenetoen and carbamazepine is a big big group of anti-epileptics which are part of the sodium channel blocker group okay so very problematic to let little phosphenotoan cuddle it may not be great but it's it's helpful in some ways right so sodium channel blockers how do they work think about the mechanism before they're going to block or inhibit this channel remember what sodium does sodium is supposed to enter into the cell make the inside of the cell positive and trigger depolarization right now if you block that sodium channel do you allow sodium ions to come in no do you depolarize no if you have decreased depolarization do you have enough positive ions in the cell to open up the calcium channels and allow for calcium ions to flow in no so now there's decreased calcium entry if there's decreased calcium entry can you stimulate the synaptic vesicles to fuse with the cell membrane and release glutamate no and if there is a decrease in glutamate man we're so good at this right now ninjas so this is going to bind onto the ampo receptor bind onto the nmda receptor but there's decreased interaction normally these are supposed to open and allow for cations to inflow but there's going to be decreased numbers of these cations coming in if there's decreased cations coming in that means that there is a decrease in the depolarization and if there's a decrease in the depolarization there is a decrease in the action potentials holy crap look how much sense we just made with all of that we just stopped the seizure by giving sodium channel blockers we're good we're real good all right now here's the next thing i want you guys to think about when we give these drugs obviously we can use them for seizures but you know what else is really interesting and you should be thinking about this making your lives a little bit easier is some of these drugs not only can they help with focal seizures or generalized seizures and some are more preferred in certain situations we're not going to go into that what i want you to remember is valproate can also be used as a mood stabilizer so in patients who have bipolar disorder or certain types of disorders it can be utilized there another thing that can be used for is in a lesser degree is absent seizures okay so it all also can be utilized for absent seizures but there's a particular one that i want you to more particularly associate with that so it can be used as a mood style stabilizer it can be used in focal seizures and generalized seizures another one if you really want to add on what else do we talk about this with headaches it's also used in prophylaxis of migraines and cluster headaches cool right phenotone again focal and particularly even some involvement of generalized seizures to pyramid this one is also used in headaches and it's also you know it's another condition it's actually used as well it's called pseudotumor cerebri or idiopathic intracranial hypertension lamotrigine it's not only important for seizures but it's also a mood stabilizer phosphonitoid lucosa micarbamezapine all interesting but one more and i can't stress enough i don't know how many times they love to throw this on the boards carbamazepine do not forget trigeminal neuralgia they love to throw this one on your board exams okay so that covers a good chunk of those now what's the next one that i want you to think about well think about the next part of the pathway sodium calcium we've already kind of stopped the calcium but we can even think about this more right so calcium channel blockers this category what is this category this is lamotrigine oh i thought lamotrigine was a sodium channel blocker guess what it's also a calcium channel blocker valproate wait how pro it's a sodium channel blocker it's also a calcium channel blocker and the one that i really want you to remember is ethosoxamide how do these work they basically block or inhibit calcium entry into the synaptic terminal they decrease the fusion of the synaptic membrane synaptic vesicle with the membrane decrease glutamate decrease depolarization decrease action potentials decrease seizures and we're good so ethosoxamide is a very very particular one that i want you to remember a very specific type of seizure that it treats and this is called absence seizures okay so absent seizures there is other ones lamotrigine and valproate also treat absence seizures but ethosoxamide i really want you to remember that one okay the other two are technically calcium channel blockers but if we're really really particular there's a little thing called an alpha two gamma sub unit on the calcium channel blocker and these guys like to bind onto that when they do that they basically prevent the calcium from entering in through the calcium channels calcium can't come in can't fuse the synaptic vesicle with the membrane can't make gluta can't release glutamate decrease depolarization decrease action potentials these two drugs are gabapentin and progabaline these are sometimes used in seizures more particularly like maybe long term and focal seizures but other things to remember them for is that they're also used in neuropathic pain so neuropathic pain as well as generalized anxiety disorder and when we talk about neuropathic pain we're talking about like you know different types of diabetic neuropathy but also you know what else it can be used for post-herpetic neuralgia that's another one after someone gets varicella zoster virus shingles all right the next one is your sv2a blocker so now we're just blocking the actual vesicle from fusing with the cell membrane these sv2a blockers which again are going to work here by blocking the synaptic proteins from fusing with the cell membrane is through a particular drug called levatoracetam there's another one called brevityracetam as well it's a newer one still a part of that group though and the same concept you decrease the fusion you decrease glutamate decrease depolarization decrease action potentials you stop the seizures all right we knocked out these let's move on to the next part of the glutamate pathway which is the ampa blockers and the nmda blockers the ampa blockers consist of two particular types now feldbomate is not always mentioned but mate will actually block particularly if we were to show it here without kind of interfering it will inhibit this channel so basically it'll block glutamate from binding onto that receptor and causing cation influx decreasing depolarization decreasing action potentials now felbimate what i want you to remember with this one is that this is used in a very particular type of childhood epilepsy which we call lenox gestat syndrome very sad sad epileptic syndrome but this can be utilized in that condition magnesium also can act in that same fashion what what is a condition we give magnesium for for someone who's a baboo and they got high blood pressure and they're seizing eclampsia so magnesium can also be used for eclampsia there's only one seed in engineers didn't you guys know that only one c all right eclampsia alrighty the next group is the nmda blocker so it's just like the ampas except we're just blocking at this point here we're not letting glutamate bind onto the nmda receptors to pyramid is one of those which we already talked about above okay to pyramid is used not only for focal seizures somewhat in generalized seizures but it's also used as for headache prophylaxis cluster migraine okay and even idiopathic intracranial hypertension but ketamine is a really really good one to not forget ketamine is used in refractory like super refractory status epilepticus right we know that one it's also used in asthma it's also used in depression but particularly whenever someone has tried so many different things like treatment resistant here we'll put we'll abbreviate that treatment resistant asthma treatment resistant depression and it also can be used for procedural sedation so someone comes in with their you know their shoulder all wonky and out of place you can give little bits of ketamine to help for the sedation the analgesic effect and helping to joint red to reduce that joint so that's another benefit of ketamine all right so we talked about the nmda blockers the ampa blockers we covered the glutaminergic pathway and things that we can use to decrease that pathway let's talk about the pathway that we can try to either potentiate or increase gaba all right so the next thing is let's go back to our gaba pathway really quickly you guys remember that glutamate is converted into what it's converted into gaba gaba is kind of incorporated into these vesicles here right now if there's action potentials traveling down the uh the axon it should trigger these vesicles to fuse with the cell membrane and release gaba via exocytosis and then gaba what it'll do is it'll go and bind on to these little receptors what are these receptors here called these are called your gaba a receptors and whenever gaba binds to these it opens up the channel and allows for chloride ions to flood into the cell making the inside of the cell negative that's the goal but in someone who has seizures this gaba a receptors are dysfunctional they just don't want to respond to gaba as well so what we need to do is is increase the concentration of the gaba to just make those receptors say all right fine stop annoying me go ahead and bind to me and i'll open up and i'll let chloride come in so how do we do that well here's one way remember i told you that whenever gaba is done exerting its action we have to take and recycle it back up via this gaba reuptake protein and then what happens is once the gaba gets taken into the cell to the synaptic terminal it'll actually get kind of broken down via this enzyme into what's called succinic semialdehyde which is kind of like a a breakdown product of it what if i inhibited gaba from getting re-uptaken and just keep the gaba in the synapses so there's more gaba in the synapses to stimulate the crap out of these gaba-a receptors that would be cool guess what we got a drug for that baby we can give a gaba reuptake inhibitor like tiago bean which will inhibit this gaba reuptake protein and allow for gaba concentration to be higher boom roasted what else what if i instead of having this gaba that actually we take into the synaptic terminal so let's say that i don't get tiagamine gaba gets taken back up into the axon terminal and instead of it having getting have instead of it being converted into success semialdehyde which is kind of like a breakdown product an intermediate let's say i don't allow for that process to happen and i inhibit this enzyme this gaba transaminase and so i don't convert gaba into succinate semialdehyde and so what happens is the concentration instead of gaba being converted into this gaba just stays gaba it's like i'm gaba baby and they can get incorporated back into these vesicles and if it gets incorporated back into the vesicles more gaba in those vesicles means more gaba getting released more gaba getting released means more concentration of it to bind onto the gaba-a receptors man we're good all right what are those types of drugs which inhibit the gaba transaminases and keep more gaba getting recycled this is valproate and vigabatrin vigabatrine is actually an interesting one that i do want you to remember it can actually be used to treat patients childhood epilepsy syndrome called west syndrome which is generally characterized with these infantile spasms really sad okay so we've got drugs that can increase the concentration of gaba in the synapses by either inhibiting reuptake or inhibiting its conversion into an intermediate and just keeping it concentrated in the vesicles what if what if i give drugs that can act like gaba and bind on to a particular site on the gaba a receptor and increase the channel activity or increase the channel sensitivity to gaba one or the other so either i bind onto a particular site here open up the channel for chloride or i bind onto this site and then make the receptor more sensitive to gaba binding that'd be pretty cool right so we got drugs that can do that what are these drugs we got we're going to call them gaba agonist some of them are direct okay some of them are indirect like benzodiazepine benzodiazepine is one of those that binds to a particular site and causes the channel to be more sensitive to gaba so that more chloride ions inflow if more chloride ions inflow what's the overall result guys if more chloride ions kind of come in here because we have more gaba more negative charges in the cell if there's more negative charges in the cell the cell will not hyperpolarize instead it will depolarize and that'll trigger a decrease in action potentials benzodiazepines are great at this okay what um what are particular there's a bunch of different types of benzodiazepines if you guys really want to remember them the main ones that are used in seizures though is going to be lorazepam diazepam and midazolam these are the main ones now generally what these are used for is they're the first line in status epileptic so when someone comes in with status epileptic is you give this it also can be used for alcohol withdrawal seizures and sometimes if people are taking benzos for a long period of time when they stop taking it they can also develop benzo withdrawal seizures so this is other things that it can be used for as well the next one is propofol now propofol same thing it's going to act as a gaba agonist propofol is great for refractory status epilepticus but it's also just used as an anesthetic so for general anesthesia like whenever you're going to get in an operation right they're cutting open in the knee or something like that phenobarbital also a gaba agonist but great for neonatal seizures so whenever a baby is having a seizure this is also pretty great and it's also good for alcohol withdrawal seizures pentobarbital is actually used in status epilepticus but if you remember it's the last resort for status epilepticus okay and to pyramid we already talked about acting as a sodium channel blocker right so we already know about topiramate as well as being a nmda blocker it's kind of a little bit of everything all right so we covered the different types of drugs their mechanism of action now let's cover their adverse effects all right engineers so now let's talk about the adverse effects so when we talk about the adverse effects there is literally like so many it can be so overwhelming believe me i understand so one of the best ways i think you know it's going to help you to try to remember these better as ones where a lot of them perform the same kind of have the same kind of adverse effect clump those together and try to focus on the ones that are the most kind of like serious it'll also common reactions and the ones that you're probably going to see on the boards so the first one is cardiovascular wise a lot of these for example locosamide phenytoin phosphonatom these are sodium channel blockers so if you have sodium channels on the actual uh particular muscle cells the cardiac muscle cells that are involved in contraction of the heart and that are involved in basically electrical potentials of the heart and you block those you potentially can decrease heart rate and decrease blood pressure so one of the big things here is that you can see patients developing low blood pressure and sometimes lowering of their heart rate okay so it can cause hypotension and potentially arrhythmias propofol actually causes vasodilation so it actually causes vaso dilation so it'll vasodilate which will also decrease systemic vascular resistance and that'll help to decrease blood pressure barbiturates and benzodiazepines they also can work on the heart they can act as cardiac depressants as well decreasing your blood pressure as well as decreasing your heart rate okay but the one that i want you to remember more particularly though is the blood pressure a lot of these drugs can potentially cause hypotension with the risk of arrhythmias sometimes their brady arrhythmias and sometimes they can be tachyrhythmids but most commonly hypotension the next ones is drugs that are going to basically depress the respiratory system you know your respiratory center is located within the brainstem right the pons medulla if you give drugs like benzodiazepines barbiturates propofol these drugs will actually suppress these respiratory centers if you suppress these respiratory centers are you going to be able to breathe no and so this can lead to respiratory depression so that is a very important thing the thing to think about with these particular drugs the next one and i can't stress how important this one is you take a particular type of anti-epileptic it creates an immune reaction that causes uh destruction of the skin and positive nikolsky sign and a really nasty rash it's called stevens johnson syndrome sjs there's very particular drugs that increase the risk of this carbamazepine is a big one ethosamide lamotrigine is a very important one to remember as well as phenotone and phosphoenotone okay the next thing is that these drugs also through again the mechanisms is working particularly on the cytochrome p450 system getting metabolized by the liver putting a lot of stress on the liver a lot of these drugs are metabolized by the liver and so because of that they can actually injure the liver because the liver having to work so hard to metabolize these drugs this can lead to an increase in like your ast an increase in the alt it can lead to an increase in alk foss basically really injuring the liver and so we call this hepatotoxicity and so it's important to monitor lfts on these particular drugs which ones valproate carbamazepine phenytoin phosphonitoid and very important one felbamate okay now what else the other ones that i really need you to remember is these drugs may actually alter the folate absorption so what they may do is they may decrease very specific one though is valproate but some of these other ones may work as well but they may decrease folate or alter the actual neurological development of the neural tube and whenever you don't have folate which is needed for these neural tubes to form this can lead to neural tube defects so this can lead to what's called neural tube defects ntds and so this is a very important thing to remember because these drugs are teratogenic okay so they can cause problems within the developing fetus so big one to remember i can't stress this one enough is valproate very very important one carbamazepine phenotone and phosphonatoin as well but the big one to remember is valproate okay the other thing that you want to do i want you guys to remember is you know there's a structure called the reticular formation within the brain stem you have here what's called the reticular activating system basically any kind of sensory stimulus whether that be a sensory like a somatic sensation whether that be an auditory sensation whether that be a visual stimulation whatever it is has to go to the reticular formation it takes all that information decides what's important tells the thalamus and then says hey thalamus send this to the entire cerebral cortex and let them know about everything that's going on what's the most important thing that i need to alert you of or arouse the actual cerebral cortex of these drugs love to inhibit reticular formation or suppress the reticular formation if you suppress the reticular formation what stimuli should be trying to maybe keep you arouse you or awaken you or make you a little bit more alert will then become depressed and you'll start showing signs of sedation so whenever somebody is taking particular anti-epileptics like these ones over here they may cause sedation by really kind of maybe inhibiting or suppressing that actual reticular formation and these includes benzodiazepines propofol and barbiturates are a very big one valproate to pyramid and ketamine okay so that covers some of these let's move on to some more types of effects that some of these drugs can combine like effect can uh can cause some adverse effects of the next thing is that you can have these drugs that can cause a lot of drug interactions right and so this is a very very important one to remember so a lot of these drugs can act as what's called cyp 450 inducers what i want you to remember with that is that if these are cyp 450s and inducers they decrease the efficacy efficacy of other drugs that's important to remember they decrease the efficacy of other drugs so if you have one of these drugs carbamazepine phenytoin barbiturates what they will do is they will act on the cyp 450 system and increase the activity of the cyp 450 system which will cause them to metabolize and break down more of whatever other drug that they may be taking decreasing the concentration and efficacy of that drug for example why can this be important what if someone has atrial fibrillation and they're taking a warfarin but they're also taking phenetoin for epilepsy if they're taking phenetoin infinitoen is actually an uh incre and increasing the activity of the cyp 450 system it'll break warfarin down more quickly and then decrease the concentration of it so maybe they'll be sub-therapeutic more likely to claw it right so something to think about cyp-450 inhibitors are going to be drugs that are going to inhibit the cyp-450 system and decrease the metabolism of those other drugs and so therefore it'll increase the efficacy or concentration of other drugs why is that important pretend someone's taking valproate and they're also taking apixaban for again their afib if they're taking valproate with the apixaban the valproate will inhibit the cytochrome p450 system which will basically inhibit the breakdown of apixaban into its metabolite now apixaban concentration is higher or super therapeutic now what they're more at risk of bleeding so you can see and understand why these are important things to think about so again cyp450 inducers carbamazepine phenotone barbiturates cyp450 inhibitors remember valproate the other thing to be thinking about is that some of these drugs can also really act on affect your cerebellum they can affect the peduncle system and they can also affect the vestibular system as well and this can lead to ataxia so they can have that wide base gait the loss of coordination what drugs can contribute to this i want you to remember valproate i want you to remember carbamazepine phenytoin phosphonatoin gabapentin and pregabalin these ones here though are really pretty common to cause this kind of effect as well all right the last type of uh adverse effect or scary syndrome that can happen from multiple drugs is a very interesting syndrome called dress syndrome okay so there's another syndrome called dress syndrome and dress syndrome is characterized by someone having a fever it's kind of a reaction basically they have fever they have eosinophilia so increased numbers of eosinophils they have lymphadenopathy swelling of their actual lymph nodes and they also have a really nasty type of rash in this kind of situation you have to remember very particular types of anti-epileptics that can trigger this one and that includes carbamazepine phenetoen phosphonatoin and phenobarbital all right great now that we've talked about some of the big adverse effects that multiple drugs can cause let's talk about some of the very specific ones that you can see with very specific kind of categories let's start with the sodium channel blockers and begin with valproate valproate can actually irritate the pancreas and cause a drug-induced pancreatitis okay so that's an important one to remember it also can decrease the number of white blood cells what is that called it can decrease the number of white blood cells causing leukopenia but it's very specific it actually causes more particularly for the um in a granulocytosis is what it's particularly called it also we already know that it can cause a pathotoxicity but one of the other effects is when you damage the liver it affects their ability to metabolize ammonia and convert it into urea and so these individuals can also develop hyperamminemia or increased ammonia levels and also it can really affect their liver being able to produce thrombopointing and thrombopointing is important for platelets if there's a decrease in thrombopoetin there's going to be a decrease in platelets which is called thrombocytopenia all right so pancreatitis agreeing to cytosis hyper anemia and thrombocytopenia phenetone and phosphonotone a couple of the common things this can cause nystagmus it also is one of the things of the ship mnemonic right so if you guys remember the ship mnemonic it was about hydralazine there was sulfur methyl sulfa drugs there was isoniazid phenytoin and procainamide those were particular drugs that can induce drug induced lupus so it can also cause lupus because it can affect those anti-histone antibodies if you guys remember another super important one that you guys need to remember is that it can also cause gingival hyperplasia can make them gums look all kinds of thick all right the next one that i want you guys to remember to pyramid topiramate can also cause glaucoma okay so it can actually trigger a glaucoma it can also cause kidney stones and it can cause metabolic acidosis so metabolic acidosis lamotrigine this one can produce way to talk about some other stuff that it can cause but it can cause a very rare syndrome called hemophagocytic lymphohistiocytes what it's characterized by a tetrad of fever pancytopenia pancytopenia is basically whenever you have a low white blood cells red blood cells and platelets it also increases the risk of neurological dysfunction and one of the most common things is seizure so you're like wait i'm trying to treat seizures and i cause seizures it's rare but again this is a thing to think about and also hepato splenomegaly all right carbamazepine it also can suppress your bone marrow and actually cause aplastic anemia but particularly of all cell lines you're going to drop so it's going to lead to low white blood cells red blood cells platelets called pancytopenia you know what else it does it triggers the posterior pituitary to make lots of adh when you act have lots of adh acting on the kidneys it actually increases the water reabsorption and causes a drop in your actual sodium concentration in the blood what is this condition called when you make too much adh an inappropriate amount syndrome of inappropriate adhc creation it can cause that as well boom roasted let's move on to the calcium channel blockers all right just kidding we're going to cover calcium channel blockers what i forgot we got to hit this little guy here hidden in here sv2a blockers love it terazetan to be honest with you it's a nice drug there's not many side effects from this one thankfully one of the few and it's been reported more particularly with like younger individuals is it can cause kind of like maybe aggression uh or kind of like agitation really so maybe some neuropsychiatric or you know behaviors all right so calcium channel blockers so what do i want you guys to remember about these so we've talked about a lot of these but ethosoxamide is actually a pretty simple one we already talked about its effect particularly on sjs but the other one that i want you to remember is that it can also cause myopia and then the other ones which we kind of talked about as kind of acting as calcium channel blockers but if we really want to be particular they're son of a gun they're called alpha two gamma subunit blockers okay and this was your gabapentin and then your pregabalin but they're technically under the calcium channel blocker category these can also cause nausea and vomiting the gaba transaminase inhibitors this one i really want you to remember these can affect the eyeballs man and they can lead to bilateral blindness you're like holy crap i'm never taken by gabatran you need to make sure that you take into consideration this is a potential side effect okay ketamine ketamine is super cool and the reason why is it actually increases the sympathetic nervous system activity and so if you increase the sympathetic nervous system on the heart what is that going to do that's going to increase blood pressure that's also going to increase heart rate it also acts on the salivary glands and increases salivary secretion so it's going to cause what's called hyper salivation and you know what else is very interesting with this drug it's been known to cause more like psychometric effects potentially hallucinations so sometimes whenever people are on this drug it can induce these hallucinations or psychomymetic effects so something to think about with this drug all right last group is the gaba agonist what are some particular or specific side effects that i need you guys to remember well benzodiazepines we already talked about a ton of them really we hit most of them the only one that i want you guys to add on besides the hypotension the respiratory depression the sedative effect things like that i also want you to remember that this has a high risk of dependence and so with that if people kind of increasingly use this and it leads to an increased risk of an overdose you should know and this is going to be asked on your exams what is the drug that you give to reverse a benzodiazepine overdose and this drug is called flumazinil okay the other thing is that if you abruptly stop benzos and you've been taking them for a while this can induce a benzo withdrawal which can induce seizures how do you treat benzo withdrawal we already said give them the benzos back all right so that's something to think about all right propofol hmm propofol this one we already talked about i wouldn't cause hypotension respiratory depression sedation and we talked about a bunch of stuff like that one other thing that i need you guys to remember because they like to ask this as well is called propofol infusion syndrome propofol infusion syndrome this is characterized by a very specific set of signs one is propofol will actually kind of inhibit uh kind of the conversion of pyruvate into acetyl coa and what happens is it leads to an increased production of lactate and you know when i have an increased production of lactate or lactic acid this can lead to what's called lactic acidosis this is a very specific type of lactic acidosis it's actually called type b the other thing it can do is it can actually really particularly do what it can cause vasodilation and so this can lower your blood pressure and cause hypotension it can also really affect the kidneys because of the perfusion to the kidneys as well as direct effect on the kidneys this can lead to renal failure so acute renal failure it can also affect the muscles and cause spilling of ck out of the muscles and this is called rhabdomyolysis and also it can cause triglycerides to spill out of the adipose tissue and if you have lots of triglycerides that spill out of the adipose tissue and into the blood what does this call when you have lots of triglycerides in the blood hypertriglyceridemia so this is called propofol infusion syndrome when someone develops a lactic acidosis this is a metabolic acidosis anion gap this is a hypotension renal failure rhabdo and hypertriglyceridemia is characterized as propofol infusion syndrome the last one is pentobarb pentobarbitol can actually depress your immune system so it can cause immunosuppression lowering your white blood cells it also can really kind of shut down your body's metabolic activity and lead to hypothermia it can increase the risk of what's called dvt's deep vein thrombosis and it can really shut down the activity okay the contractility of the gut leading to a pattern called ileus okay which is a non-mechanical obstruction of the gi tract these are big things to remember as potential adverse effects of anti-epileptics iron engineers in this video we talk about the pharmacology of anti-epileptic drugs i hope it made sense i hope that you guys enjoyed it as always ninja nerds until next time [Music] you

Channel: Ninja Nerd

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Keywords: Ninja Nerd Lectures, Ninja Nerd, Ninja Nerd Science, education, whiteboard lectures, medicine, science

Id: 7nJner7LP9Y

Length: 49min 25sec (2965 seconds)

Published: Thu Aug 05 2021