 Hello everyone, welcome back to another session in Dentistry Ammo. So we are dealing with some pharmacology sessions. So today's topic is Dreg Anticonism. So Anticonism is something acting against the Dreg. So if we have a Dreg A and it has an effect on the molecule that is normal effect but in presence of another Dreg, this will not be normal under the normal state. So if it is going and reaching the concentration in presence of Dreg A, in presence of this Anticonist, what happens is this will not reach the maximum concentration or it reaches only if there is presence of A in excess amount. So that we will deal later. So this is nothing but a Dreg which inhibits or reduce the action of another Dreg. So that is what we are studying today that is Anticonism. Anticonism is nothing but a molecule which is acting against the Dreg. Okay, so it's a very commonly as short note the Dreg Anticonism and it's very important to understand the mechanism. So which all Dregs not to be given along with another Dreg. So it is not just important for your academic point of view but also for a clinical point of view. So what are the types of Anticonism? So they are broadly classified as physical Anticonism, Chemical Anticonism, Physiological or Functional Anticonism and Pharmacological Anticonism. So these are the various mechanisms. So various mechanisms which interrupts the first trick. So A is our Dreg and B is our Anticonist. So various mechanisms where the Dreg B interferes with the action of the Dreg A. So in physical Anticonism it is nothing but it is based on the physical property, physical property of a Dreg such as the Charcoal which adsorbs the Alkaloid, Charcoal in case of Alkaloid poisoning, Alkaloid Poison. So that is just the physical property. So this Charcoal adds an Anticonist and it reduces the availability of this Alkaloid. So it is actually beneficial sometimes it can be used as an antidote in poisoning cases. This Charcoal will absorb the Alkaloid and reduce the availability of Alkaloid and saves the patient. So physical Anticonism is beneficial in Charcoal and Alkaloid Poison combination where the Charcoal is our Anticonist which is reducing the availability of Alkaloid in the body. So that is the physical Anticonism. Now we have the chemical Anticonism. This is a different mechanism where a Dreg counters the effect of another by simple chemical reaction. So there is chemical reaction happening or neutralization is happening, neutralization or chemical reaction. So this is not like binding to the receptor or such mechanism. So what happens is when calcium, sodium, acetate form insoluble complexes with arsenic or lead. So calcium, sodium which forms insoluble complex with arsenic or lead. So here what happens is there is chemical composition, chemical formation or chemical action is happening. Here it is just a physical absorption happens and reduces the availability. So here there is mechanism of chemical action. So this both campaigns and reduces the availability of one Dreg by the mechanism of chemical action. So this is different, this is different. That is known as neutralization. Next we have the functional Anticonism or physiological Anticonism. This is very simple one just like we know the pancreas has alpha cells and beta cells which produces glucagon and insulin. But in case of Dregs, two Dregs which has got opposite effect. I just said the pancreas example to understand this. We have glucagon which increases the glucose level in body whereas insulin which decreases the glucose level. This is oppressing action and it maintains the blood glucose level in our body. So this is the functional Anticonism or physiological Anticonism. In body we have many types of functional Anticonism. So the common example is a glucagon and insulin which maintains the blood glucose or blood sugar level. Now we have the most important one that is a pharmacological Anticonism. The pharmacological Anticonism the mechanism we need to understand before going into detail that is the common mechanism we have a receptor molecule here okay. So this is our receptor molecule sorry. So this receptor molecule has a binding site okay. So this is our binding site receptor binding site. So this is our receptor. Usually what happens is our agonist molecule will come and attach here and brings out the action okay. So the response will be happening. But what happens is in presence of an Anticonist if we have an Anticonist sometimes instead of agonist there will be Anticonist here. So what happens is there will not be any action taking place because it will not take place any conformational changes. So this receptor will not be active it will be in a passive state there is no change happening so there is no action. So this is what commonly happening. So this is the basic mechanism we have a receptor molecules in and everywhere in the tissue. So there is a receptor binding site where the agonist will bind that is our drug molecule will bind and make out the changes by conformational changes and there will be action happening. So it is a drug who will be dissolution drug dissolution happens and it brings out changes but in case if there is Anticonist present it will bind to the receptor site instead of agonist okay. So this is Anticonist instead of agonist which might be a competitive Anticonism or non-competitive Anticonism that is what we are going to learn now. So this is mechanism you need to understand. So pharmacological we have two classification the first one is competitive and the next one is competitive and the next one is non-competitive. So this is very easy by if you know this mechanism because this competition is happening. So what competition? The competition to bind to the receptor site okay there is a competition between the agonist and Anticonist in competitive Anticonism okay. So competitive again we can classify into as reversible or reversible. So the mechanism is same okay. So Anticonist and the agonist compete to bind to the site okay and sometimes this Anticonist will win the situation and bind to this site and that is known as competitive Anticonism okay. So there is a fight happening between the agonist and Anticonist there is a competition happening. So this will bind to this site and there will not be any action taking place okay. So that is competitive Anticonism. So in case of reversible the binding will be taking place by a weak bone a weak bone is happening but the thing is if we have more and more agonist more and more agonist molecule if we increase the concentration that is the law of mass action. So if we have more and more amount of agonist molecule what happens is eventually this will be reversed that is the action will be taking place because more and more agonist molecule we have it will replace the Anticonist and the action will be taking place because it is a weak bone attached here so it can be easily replaceable okay. So this is basically a concentration dependent more concentration this Anticonist will be replaced from this site by the agonist and the action will takes place okay. But this graph can be represented like this the normal agonist alone without any changes agonist will be like this and the effect on sorry dosage on the x axis and the effect on the y axis this is just with agonist without any Anticonist we need this much of dosage. But what happens is when there is Anticonist this is Anticonist okay when there is Anticonism we need to increase the dosage okay increase the dosage to get the desired response okay. So we need to increase the dosage so the dosage will be increased so this is on x axis this is the dosage okay. So without Anticonist we need only this much dosage okay but in presence of Anticonist we need this much dosage because on the x axis we have dosage to get the effect because on the y axis we have effect okay so to get the effect we need to increase the dosage this is competitive Anticonism okay. So the most common example for competitive Anticonism is a tropin and acetylcholine which compete for the mascarinic R receptor okay. So that is a very common example or the nalexone which is an antidote and morphine compete for the opioid R receptor okay so this is competitive reversible Anticonism. So what happens to this competitive irreversible Anticonist the only change happens is the bond happening here okay. So rest everything is same the bond strength will be different the same mechanism the Anticonist is here so Anticonist is attached here again it is a competition but the bond is very strong the covalent bond okay covalent bond which is very difficult to replace. So in this case that is irreversible Anticonism if we increase our agonist concentration nothing will happen because this is not a weak bond like competitive Anticonism this is very strong covalent bond so this cannot be broken and this will not get into this place by removing it like competitive Anticonism. So this is irreversible competitive Anticonism so this graph will not be like this okay so there will not be any change if it is the agonist alone and if there is Anticonist here so this is our concentration this is Anticonist so ultimately if we add more and more agonist there is no point it will not reach to the effect because this is not moving out of the receptor site that is irreversible competitive Anticonism. So whereas the non-competitive one okay non-competitive mechanism is different because there is no competition we have the receptor here and we have the agonist and we have the Anticonist here but there is no competition is happening what happens is this Anticonist binds to an allosteric allosteric site allosteric site site which is not an active site this is the active site here is a molecule usually binds but in non-competitive there is no competition between the agonist and the Anticonist instead what happens is this Anticonist binds to a allosteric site allosteric site is a site on the molecule which is not an active site okay so once it binds to the site what happens is this process will deactivate okay so once it binds to this molecule this will be deactivated so once it is deactivated there will not be any action taking place so the Anticonism happened so the common example is the common example is the flumazenil flumazenil and the benzodiazepine it's a common example where the flumazenil by binding to this benzodiazepine site which antagonizes the effect of benzodiazepine by preventing the binding of GABA okay GABA to the GABA receptors so there will not be binding of this GABA to the GABA receptors so this is the non-competitive Anticonism so this comes under our pharmacological mechanism before that we learned the functional Anticonism chemical Anticonism and physical Anticonism so that is all about the Drick Anticonism it's a simple one only thing the last part is little trickier that is our pharmacological we need to understand the concept of agonist and antagonist with respect to the receptor site okay so in competitive and non-competitive the agonist and antagonist fight or not fight to get into this active site okay in competitive there is competition and non-competitive there is no competition instead the antagonist cites to the allosteric site and utilizes the molecule hope you understood this concept in pharmacology it is all about the concept and knowing the very core of the concept then you can easily explain it rather than by hearting the topic okay I'll come up with more topics in pharmacology thank you