Pharmacology - Antiepileptics

epilepsy is a disease characterized by seizures epilepsy there are different types there's seizures that are well localized in the brain or that spread out throughout the whole brain in this video we're only going to focus on the pharmacology of epilepsy so here I'm drawing the brain and the brain is made up of cells known as neurons in epilepsy you have episodic high frequency discharge of impulses by a group of neurons in the brain it can be in one part of the brain so localized this is known this will create what's known as a partial seizure or it can start local and then spread throughout the brain or through a part of the brain and this is known as generalized seizure now before we go into the pharmacology of epilepsy I think it's important to watch a video on how the neurons send send signals to one another and have a video on that which I'll provide the link so again epilepsy is a is characterized by seizures and it's where the neurons are excited they just send all these impulses all the time so therefore drugs to treat epilepsy can be divided into three types one drugs that modulate voltage-gated ion channels responsible for the propagation of the impulse two drugs that enhance basically synaptic inhibition so stopping the impulses and or three drugs that stop or inhibit a synaptic excitement so drugs that modulate voltage-gated ion channels are drugs that target the sodium and calcium channels and these and they will inhibit these channels drugs that enhance synaptic inhibition arm will cause increase in gaba activity which is the inhibitory neurotransmitter in the CNS and then drugs that want to inhibit synaptic excitement will essentially decrease gluten glutamate activity so again to recap in the central nervous system you have our two main neurotransmitters that sort of counteract one another these are glutamate which are excitatory neurotransmitters and then you have gaba which are inhibitory neurotransmitters so this cell here let's just say is a glutamate glutaminergic neuron and they will you know excite the brain and they will send impulses and stuff like that and then and of course it will it will stimulate the this postsynaptic neuron and this you know if this happens it will result if it hits a threshold it will result in a seizure and then you have this other neuron here in blue which is inhibitory neuron and these inhibitory neurons release gaba gaba again is an inhibitory neurotransmitter and again this neuron that releases glutamate is a excitatory neuron so let us zoom in here we're all these synapse is are occurring and then learn a bit more about the physiology and then the pharmacology so here I'm drawing the glutamatergic neurons a terminal bulb and then here we have the post synaptic neuron and then the blue here is the gabaergic neuron so when an action potential comes down again it essentially causes an influx of sodium via the voltage-gated sodium channels and then once it hits the terminal this will cause the voltage calcium channels to open up resulting in calcium to come in and this will then lead to depolarization more you know more positive resulting in the vesicles in the terminal bub to release glutamate in this case glutamate will bind on to receptors or channels in the postsynaptic neuron in this case the glutamate neurotransmitters are binding onto the am PA and n NMDA channels resulting in the influx of sodium and calcium from outside which will then lead to depolarization reaching a threshold which will result in an action potential so this is creating impulses you know it's stimulating the neurons in the area and if this happens like a lot or cons like consecutively this will result in what's known as a seizure so I hope that part of the story made sense and how that's like exciting you know the neurons are exciting each other and then here in blue we have the gabaergic neuron with gaba in the terminal bulb gaba is actually made from glutamate but anyway this neuron can release GABA right and the gaba can then bind onto its own receptors on the postsynaptic neuron here which are in this case gaba-a receptors when gaba binds onto this receptor it will actually cause an influx of chloride ions which are negatively charged and though it's and so it sort of counteracts the depolarization so it inhibits this process from happening once gaba you know finishes its job it gets taken back up to this terminal bulb and then it gets converted to ssa through gaba transaminase so that was sort of so as you can see we have you know a glutamate neuron and your transmitters which you know explore exciting the cells and then you have GABAergic neurons which releases gaba and GABA are the ones that inhibit sort of suppress neuronal activity so this is regulated normally but again in epilepsy you have more excitement so now let's talk about the pharmacology the drugs used to treat epilepsy let's begin with the drugs that modulate voltage-gated ion channels and these drugs include car car carbamazepine side effects here in the sad face include water retention sedation ataxia and mental disturbances phenytoin is another drug and side effects include confusion gum hyperplasia skin rash anemia and it's also teratogenic so it's not good for pregnancy you have Ethos amide side effects include nausea and anorexia and finally in this group we have lamotrigine then you have the other class of anti-politics that want to stimulate gap activity and these drugs include benzodiazepines v gaba Trin and TIA Gabon I hope I pronounced those right so if we were looked we were to draw those drugs up in respect this diagram we have carbamazepine phenytoin lamotrigine which will inhibit the sodium voltage channels here so thus inhibiting depolarization and then we have lamotrigine and ether Samad which will inhibit the calcium voltage-gated channels and also inhibiting depolarization so stopping the glutamate activity essentially or excitement of the neuronal excitement then we have the benzodiazepine which will stimulate essentially this receptor activity this channel activity here resulting in more gaba gaba activity resulting which will inhibit the depolarization the excitement tyaga bond will inhibit the reuptake of gaba resulting in more gab activity in the synaptic cleft then you have the of the gaba v GABA Trin which will inhibit the gaba transaminase enzyme here which will obviously result in more gaba being available in the synaptic cleft then you have another anti EV electric drug which I actually have an introduced which is sodium valproate and it's quite a common drug for for epilepsy and it does actually a lot of these things which I just mentioned so it can it can target the voltage channels and it can stimulate the gab activity so I didn't group it into a particular class of anti-politics but it's important some important things to realize is that in pregnancy anti anti-epileptics are not very safe so consideration so in pregnancy we have teratogenic antiepileptic drugs and these include Finn at Owen and lamotrigine and valproate however it's been shown that lamotrigine is probably the most safest out of the lot you can say the best out of the lot for for for people who are pregnant so I hope you enjoyed this video on the pharmacology of epilepsy thank you for watching you

Channel: Armando Hasudungan

Views: 357,508

Rating: 4.9112206 out of 5

Keywords: epilepsy medication, antiepilepsy, treatment for epilepsy, seizure medication, seizure drugs, pharmacology epilepsy, seizure management, sodium valproate, lamotrgine, classes, pharmacy, mechanism of action of antiepileptics, summary, lecture, antiseizure, medicine, science, armando, pathophysiology, simple and complex seizures

Id: c-Cf1xkKofg

Length: 9min 23sec (563 seconds)

Published: Wed Apr 27 2016