Biochemistry Rapid Revision || Dr Priyansh Jain || FMGe July 2024 🧬🧬🧬

e e e e okay so good evening good evening good evening sorry uh for the mic was closed and now I think uh I'm am audible visible is everything is fine now yeah yes okay so I was also so very much eagerly waiting to see you all and uh very happy to see the enthusiasm that you are having I I hope that uh you are all keeping with your nerves and uh the things this this very crucial time these last 10 15 days towards any exam becomes very important and uh both Sara we feel a lot of time that it's uh we are not able to keep up with the same momentum it is very much normal don't worry in the exam also if sometime we don't know any answers maybe continuously 3 four five question there's no need to worry there are easy questions are there and you will have to make sure that the easy questions you are marking right right uh the the exam when the exam will be and all these things let's keep it very simple let's it it be on the 6th of July we are going to prepare like this only and uh will not take your much time time it is going to be a very crisp session as we did also the last time so I will tell you the buzzword that if that is there the most likely answer will be this one so starting with the first one don't worry guys uh uh I'm not able to read the chat box very frequently as I'm not very acclimatized to the system but uh let's get started when it comes to the classification of amino acid there are three four important questions from classif ification one that they will say that there is uh there is amino acid we we keep the amino acid in the sunlight and they will give you some UV rays uh they will not write the UV ray word but they will say that uh they will say about uh this thing the light frequency they will tell you that we are having a certain light frequency we are putting some amino acid which one is going to absorb that light maximum the moment you see that thing the light Ray is there and they are saying that who is going to absorb the maximum basically they are talking about the UV ray absorption and the maximum UV R absorption it is in trypt ofen so UV R they will give you the frequency maximum UV R absorption tript ofen the second thing to be remembered is the most glucogenic amino acid the most glucogenic amino acid among all of them it is LIN glucon Genesis there are two important question one which is the most uh common source for glucono Genesis it is LIN and which is not a source of glucono Genesis not a source not a source of gluconeogenesis the answer is going to be atile Co so these are the two important question I will share the PDF uh I will share the PDF with you that is uh fine and that will come to you so you don't have to write anything just be with me for next one one and a half hour and we'll take care you of majority of the part of your biochemistry the second is the relation of sgot sgbt clinical relation of sgot sgpt see these are the lver enzymes and we always see whenever there is any liver damage whether it is because of alcohol or it is because of other than alcohol whether it is alcoholic or non-alcoholic the sgot sgbt is going to increase so we have to see that which enzyme has increased more if s has increased more means the ratio of s sgpt is more than two that is alcoholic liver disease so keep it simple sgot if it is twice higher it is going towards alcoholic but if the sgpt is more it is non-alcoholic such as hepatitis hepatitis A d s it is found at three places atot is found at three places lver SE sceletal muscle and cardiac muscle that is why in the myidal infection also the SG is going to increase so if they ask that which enzyme is going to increase in myoid infection that is troponine is there the LDH is there and one more you need to remember is s right let's go to the next one when it comes to Ura cycle what what what is happening is in our body when whatever amount of protein we are having we are metabolizing the protein and we are making the ammonia we are making the ammonia this ammonia is very toxic so it is supposed to be converted into UA and then this UA will be excreted out so this conversion of ammonia to UA it is mainly occurring in the lever so we can see like that the factory of converting the ammonia into UA is in the lever so how this ammonia is getting converted it is taking to Total five steps there are three questions to be remembered there are total five steps the first question the conversion of ammonia to Ura which is called as the UA cycle it occurs where it is mainly occurring in the liver this is the first thing the second is there are total five reaction out of five reaction you can see first two reaction in the mitochondria and the remaining three reaction in the cytoplasm so there are total five reactions means there are total five enzymes will be there so here you can see the first enzyme is the cps1 in the mitochondria the second enzyme is Oran trans carbom Myas in the mitochondria the remaining three enzyme the arinos suin synthet Argos suxin lias and Argin hydras that is there in the mitochondria cytoplasm so what they ask is all of the following enzyme of UA cycle is found in the mitochondria except so we should know that which one is mitochondrial which one is cytoplasmic how we are going to remember the enzyme which is starting with alphabet a these are cytoplasmic these are cytoplasmic remaining is the mitochondrial whatever starts with the a that is cytoplasmic remaining is mitochondrial the third and last question the rate limiting enzyme is cps1 but it is not activ it to activate it we require a molecule called as nag an atile glutamate so they ask this question who is the sixth enzyme of Ura cycle there are only five reaction but who is the sixth enzyme the sixth enzyme is n so there are three questions to be remembered Ura cycle occurs where liver total how many reactions five reaction two in the mitochondria three in the cytoplasm and cytoplasmic enzymes Alpha starts with the alphabet a what is the name of the sixth enzyme the name of the sixth enzyme is actually is the activator of the CPS one that is nag nag is considered as the sixth enzyme and aile glutamate is considered as the sixth enzyme okay let's move forward the next is the concept of the the Phile Ketone UA we know that Phile alinin converts into tyrosin and from tyrosin we can make melanin to convert the phy into tyrosin we require the phy alanin hydroxy sometimes in some children this enzyme is not there if this enzyme is not there the reaction will not occur properly if this reaction will not occur the phileine will start accumulating and the thyrosin will be depleted if the tyrosin will be depleted the melanin will not be synthesized and the child will have relatively Fair complexion now there is increase in the fil Phile alinin that is going to trigger alternate pathway and it will convert into the Ketone body of the Phile alinin these are called as the Phile acetate Phile pyate Phile lactate and they will start coming in the urine and because the Phile Ketone bodies are coming in the urine so this disease is called as Phile Ketone Uria and interestingly when Ketone body is Phile acetate it has a very bad smell it smells like Mouse so this child urine will have the mousy smell what are the three symptoms to be remembered is see nowadays they have stopped saying the word mousy smell they will use the alternate thing one thing they will say that the mother is saying that whenever the mother is changing the diaper the diaper is having a very bad smell instead of mousy smell they will say very bad smell this child will have a decreased IQ also also and a relatively Fair complexion than other family members so these are the three things to be remembered mousy smell instead of that there's a bad smell but bad smell the bad smell is due to Phile acetate so bad smell is because of Phile acetate IQ is less Fair complexion it is Phile Ketone UA one more thing Phile Ketone UA symptoms are not there on the day one of Life they will come after 3 to 4 days so sometimes they can say Phile Ketone UA child is absolutely normal at Birth yes the child is absolutely normal at Birth the symptoms are not going to be there on the on the day one of the life because the maternal enzymes are there they can do the task but uh let's don't go into the concept of that but keep it simple if these are the three things Fair complexion decrease IQ me bad smell it is final Ketone Ura the child will have no problem on day one of life and we do one test called as gu test to diagnose this okay very good the next is the next is the question on the tyrosinemia it's a very hot favorite topic see how the thyrosin is getting metabolized thyrosin say we are having three molecules melanin thyroid hormone and kacise cacam means the norepinephrine epinephrine dopamin we are making from tyrosin so these are the three important molecules this is itself McQ that tyrosin is made from which amino acid melanin when the thyrosin is extra that thyrosin has to be cut down and how we we are going to cut down the tyrosin is like this we'll break the tyrosin by this pathway if by any chance if any enzyme is not there in the pathway the thyrosin will not cut down and the thyrosin will accumulate and that is called as tyrosinemia for example in this list if you look at this enzyme fa hydris if it is not there the reaction will not happen and ultimately ultimately the tyrosin is going to accumulate ultimately the thyrosin is going to accumulate so that is uh that is going to be called as the the the tymia that is going to be called as tymia in fact if any enzyme is not there that will be called as a tymia so we should know that what are the various tymas and what are the various what are the various tymas plus uh we should also know that what enzyme deficiency they are carrying see here it is very simple to remember if they say thymia type 1 is due to deficiency of what tyrosa type 1 that is going to start with the letter f f a hydris thos type instead of one you can remember is first thymia type first is due to the enzyme which is starting with the letter F thymia type two it is due to deficiency of tyrosin trans aminase so it is called as T2 Ty one is first starting with the letter F type two is T2 and type three type three is going to be four hydroxy Phile pyate deoxy so we can remember 3 4 34 so one is starting with the letter F two is T2 and three is 4 but here is now there is a tricky part the tricky part is sometimes instead of tyrosin trans amines everyone pay attention here sometimes instead of this enzyme tyrosin trans aminase they can use the word tyrosin Amino transferase they can use the word aminot transf but the the thing is simple instead of trans aminase they're using the word aminot transf that is more or less the same right so that you have to keep in mind while using this pneumonic very good the next is the concept of alpon UA there are three things again to remember in alpon UA what we do is actually whenever we see the dark urine we jump to the alpon UA that should not be the right approach the problem with the dark urine is the moment you see dark urine you jump on alpona always you have to see the associated symptom is it associated with the joint joint pain is it associated with abdominal pain or is it associated with muscular pain so dark urine can be seen in three condition if they say dark urine with joint pain they are talking about alpon UA if they say dark urine with abdominal pain then they are talking about acute intermittent Poria if they say dark urine with muscle pain severe muscle pain followed by dark urine they are talking about mardal disease so dark urine alpt UA don't jump on alpon UA see any of the three can be there plus now let's look at the name of the enzymes also here alpon UA is due to deficiency of homogenic acid oxidase deficiency deficiency of HG oxidase acute intermittent P firea it is due to deficiency of PBG Damas PBG Damas deficiency mardal disease it is due to deficiency of muscle glycogen phosphor muscle glycogen phosphor deficiency so dark urine joint pepton UA abdominal pain acute intermittent Poria and muscle pain meal disease now let's uh focus on eltone UA part as of now sometimes when the tyrosin metabolism is happening we generate this homogenic acid that is supposed to be metabolized by this HG oxidase if it is not there the hga is going to increase homogenic acid is going to increase and that is going to make a molecule called as benzon acetate that will start coming in the urine that will make the urine dark and that is going to deposit in the cartilage and that is going to destroy the cartilage called as OSIS in this entire disease there is no mental retardation it's a very important McQ what they will say is all of the following are the symptom of alapon Uria except mental retardation is not a symptom in alpon UA we don't have mental retardation we don't have mental retardation two very important McQ in alpon UA we don't have mental retardation Plus for the treatment of alpon UA we give a drug that is niol the treatment of alpona the drug that we are using is nion very good the next is from the tryptophan we are making several special products from dpen the special products that we are making is such as vitamin B3 nasin we are making serotonin and we are making melatonin this is itself is a McQ that serotonin is made up of What vitamin B3 is made from what melatonin is made from what they are made from tryptophan now when the tryptophan is I'm saying that from tryptophan we can make nasin as well as from tryptophan we can make the serotonin from tryptophan to serotonin it occurs in the arenta seals sometimes there is a tumor of the arenta Cs that is called as arenta phenoma or also called as carcinoid tumor in that case all the majority of the tryptophan will be diverted towards this part because the arenta F seals are working more and if all these will be shifting towards this side a very less this tryptophan will go towards the nasin synthesis so this patient will have the nasin deficiency that is pelra like symptoms one more thing that is going to happen is because all the tryptophan has been diverted this side so a lot of Serotonin will be made and because of increas in the serotonin the patient is going to have the facial flushing means there is going to the face will turn red there's going to be increase in the intestinal motility that is diarrhea plus it can lead to bronos spasm so in any McQ if you see there is facial flushing face the patient is having continuous diarrhea and the Broncos SP then they are talking about the carcinoid you remember like this flushing with diarrhea flushing diarrhea flushing diarrhea flushing means face turns red that is Flushing flushing diara flushing diarhea it is carcinoid it is carcinoid and this patient will also have the symptoms of pelra like symptoms pelra like symptoms like dermititis dementia that can also be there one more thing to be remembered in carcinoid what we have discussed is that in carcinoid there is excess serotonin excess serotonin converts into excess amount of five hydroxy indol atic acid a lot of five hydroxy indol acetic acid will be formed and that will come in the urine so whenever we are suspecting carcinoid we check the level of 5 hiia this is again McQ that how to confirm the carcinoid we are going to check the five hydroxy endol atic acid level we are going to check the five hydroxy indolic acid level very good the next is the hyper homos symia increased level of homoy is called as hyperosmia what are the points to be remembered is one is what is the most common cause the most common cause is deficiency of this enzyme cion beta synthes if there's deficiency of Cy beta synthes this is the most common cause of hyper homocystinemia the most common cause the second point to be remembered is ke if there is increase in the homoy how we are going to make a diagnosis see one thing is the patient body features will be like this the fingers will be long the arm length will be more there will be ectopia lenes these things will be there that is called as marfanoid diabetus so if the homos is more the patient will have the body features looks like Marin syndrome but homos sytin also increases the the thickness of the blood there is increase in the coagulability of the blood so that can lead to deep vein thrombosis if you look at these two parameters marfanoid habit plus defen thrombosis marfanoid habitus plus DBT then it is going towards hyperosmia hyper homos so if there is increase in the uh uh there are two questions to be remembered again I'm repeating two questions very important everyone remember here itself they will say the most common cause of hyperosmia the most common cause is deficiency of cathine beta synthes second how to make a diagnosis that homos is more the body feature will be like Maran syndrome and along with that they will give you the the history of the pain in the Cal muscle that is DBT in fact in any McQ of biochemistry any McQ of biochemistry they talk about DBT they talk about the calf pain they are talking about basically is the homos symia homos symia very good now coming to the protein this is all about from the first major unit that is amino acid now coming to the second one protein protein May two three points only one if you are having two proteins let's say there is one protein in the secondary structure another protein in the secondary structure and we want to join them so you are either you will take a short chain of amino acid to join them or you can take a long chain of amino acid to join them if you are taking a short chain of amino acid to join the proteins it's called as turn and bend and if you are taking a long chain if you're taking a long chain it's called as Loop so the question that will come to your exam will be turn and bend we understand it's a short chain of amino acid they will say that it is made up of which amino acid what are the amino acids here in turn and bend the turn and bend the amino acids are Proline and Glycine and interestingly both will be there in the choice so you have to select croline the question will be like this turn and bends are made up of what they are made up of Proline keep it very simple turn and bends are made up of what they are made up of Proline done okay the next is the collagen disorders if the type 1 collagen is defective type one is making the bones Scara so if the type one is defective the bones will be defective the child will have recurrent fractures that is called as osteogenesis imperfecta so the child will have multiple fractures is Scara will be very thin so on the back side of the Scara we have the Venus plexus that will be visible that is called as the blue Scara so multiple flexures the Scara will turn blue because the Scara is very thin and the child may have the hearing loss also so this is the Triad that we see in oogenesis imperfecta multiple fracture blue Scara and hearing loss coming to the type two if the type two is defective type two is there in the cartilage if the cartilage uh is defective it is called as condro displasia condro displasia the type four the type four is defective type four is there in the basement membrane it is itself is a McQ that type four collagen it is found where it is found in the basement membrane if the type four is defected it will lead to elport syndrome and the classical Triad of elport syndrome huria snhl and anterior lenticonus there's going to be hematuria as and anti loners there's one more condition which is very similar if they say a patient is coming to us and he's having hematuria with hopis hematuria with hopis then what is happening is there is no problem with the typ for collagen actually there is a wrong antibody against the typ for collagen so that that is autoimmune destruction of the type four Collision autoimmune destruction of the type four collision and that is called as the yes very good that is called as utar good pasture syndrome so good pure syndrome and elport syndrome they are they are quite similar the difference is in elport syndrome the typ for colision itself is deflective and in good pure the type four was normal but there was a wrong antibody that is destroying the Ty for collagen antibody Ty for collagen that is good pure and that that way we are going to have the huria with hopis okay very important isomerism it's a very important topic isomerism what is isomerism is basically there is going to be uh same molecule with different different structures and that is they making the different different molecules formula is same formula is say for example glucose formula is C6 h206 from the same formula we can make the different different molecules that is called as isomerism I want you to remember one example if you can remember all the example very good if not remember glucose and Menos they are isomers they are which type of isomers epimers so glucose and Menos they are epimers and how the glucose and Menos are different you just have to rotate the HOH at which carbon if it is the glucose molecule and you if here is the H here is the O if you just rotate the H at the carbon number two the molecule that will be formed is called as menos so glucose and Menos they are epimers they are epimers at which carbon carbon number two so the the language of the question will be what is the relation between glucose and Menos they are carbon 2 epimers Carbon 2 epimers one more what is the relation between glucose and galactose they are carbon four epimers if you rotate the HOH at Carbon number four if you rotate the HOH at the carbon number four of glucose the molecule that you are going to get is galactose so glucose and Menos they are they are epimer at Carbon number two and glucose and galactose they are epimer at Carbon number four carbon number four right to be remembered very good let's go next the various types of gag glucosa Amino glycin keep it very simple which gag does not contain Hy onic acid which gag does not contain uronic acid glucuronic acid which gag does not contain acid the gag which is found in your cornea does not contain acid the answer is keratan sulfate carrot means cornea I will take tell you two questions super important one which gag does not contain acid keratan sulfate it is found in cornea and what it is doing it is maintaining the coral transparency it helps in maintaining the coral transp transy the cornea is transparent because of keraton sulfate so two points which gag does not contain acid the gag which is found in the I that is keraton sulfate plus the which gag helps in maintaining the coral transplant Coral transpl again is the keratan sulfate very good let's move forward the glycolysis when it comes to glycolysis they ask this question that when we do the sugar estimation if we want to check the blood sugar let's say here is the blood sample and I want to check that how much glucose is there in this blood sample how much glucose is there then when we want to estimate the glucose in the blood sample we don't want the glycolysis to occur in the blood sample because if the glycolysis will occur the glucose will will go down right and we will not get the correct value so in in all the blood samples we want to stop the glycolysis and to stop the glycolysis we add one toxin that is called as the fluides sodium fluoride they don't write the word sodium fluoride they just write the word fluides so for the correct glucose estimation which toxin is in which toxin is added in the blood sample fluides and fluides inhibit which enzyme of the glycolysis inol so two question from fluide fluide is used for the correct glucose estimation for the glucose estimation we use the fluide and in the test tube we are reading this chloride that is going to inhibit which cycle of the glycolysis it is enol very good in the glycolysis the total amount of ATP that is generated is seven and in glycolysis we are cutting the glucose what do you think can you tell me in the chat box okay this is the first question from my side in your chat box that which uh sorry in the glycolysis what will be the effect of insulin the insulin is going to stimulate or it is going to inhibit insulin is going to stimulate the glycolysis or inhibit the glycolysis insulin is going to stimulate or inhibit yes write down in the chat box insulin is going to stimulate the glycolysis or inhibit the glycolysis it is going to yes it is going to stimulate the gly yes it's going to stimulate it's going to stimulate beta see in any pathway if you are cutting the glucose see insulin insulin wants to decrease the glucose level insulin wants to decrease the glucose level so in glycolysis what you are doing you are cutting the glucose insulin wants the same right so insulin is going to stimulate all such processes insulin wants to stimulate all such processes where you are cutting the glucose wherever you are cutting the glucose insulin is going to stimulate so question see here they will ask either for glycolysis or they will ask for gluconeogenesis that what will be the effect of insulin in glycolysis basically we are doing is we are cutting the glucose and we are making pyu it so insulin insulin wants to cut the glucose so insulin should stimulate such process insulin should stimulate such process but when we talk about gluconeogenesis in glucon jesis what is happening from elenin let's say you are making glucose insulin never wants the glucose to be made so what is going to happen with the effect of insulin on gluconeogenesis inate in all the reaction where the product is glucose insulin will stop such process and in all the reaction where you are cutting the glucose insulin very good and the opposite of insulin is glucagon the opposite of insulin is glucagon right okay very good the next thing uh very good the next is the the crab cycle in the crab cycle there are some toxins to be remembered first thing first from the crab cycle we are going to generate 10 atps from one crab cycle we generate 10 atps and the craft cycle occurs in the mitochondria there are various toxins which can inhibit the craft cycle but the most important for us the most important for us is the melate the melate inhibites the succinate dehydrogenase enzyme melate inhibit the succinate de hydrogenous I will tell you three questions from Craft Cycle One how much ATP stand atps where it is uring is the crab cycle crab cycle is occuring in the mitochondria and we are getting the 10 atps second melon inhibites which enzyme succinate dehydrogen third question see in our in our Cycles we are generating the energy either in the form of ATP nadh or fadh so they ask this question in which uh whenever we we either we generate the energy in the form of ATP nadh or fadh but whenever we are generating the energy directly in the form of ATP such reactions are called as substrate level phosphorilation whenever you make ADP that is called as SLP substate level phosphorization and in the crab cycle the substate level phosphorization is only occurring once only occurring once so they ask that what is the name of the enzyme and what is the name of substrate when when we are doing the substrate level phosphorization the name of the enzyme is suil thinas and the name of the substrate is suil COA remember it if you can't remember both remember the language will be like this which of the following is a substrate for substrate level phosphorilation in crab cycle what is the name of the substate for substate level phosphorilation suin co suxin co Su go remember it very good the next is they will give you the the reaction where we are converting the pyu into atile that is going to be a structure based question they will give you a carbon structure molecule three carbon structure and from that you are making the two carbon structure there will be a different complex carbon carbon carbons will be there and multiple structures will be there what they will ask is there are three enzymes which are doing this reaction E2 e E1 E2 E3 and they will ask you what is the name of E1 what is the name of e3 the name of the E1 to be remembered that is there in their question Bank it is pyu dehyd renous and E3 is De hydrogenous dihydro lioil dihydro lioil in fact I will tell you the easy way to solve this question if this question comes they are giving you a three carbon structure from that you are making two carbon structure and they will say what is the name of enzyme E1 and E3 just remember the option which is saying the dehydrogenase E1 also contain dehydrogenase E3 also contain dehydrogenase there is only one option in their Q Bank where the E1 and E3 both means there is only one option which is having dehydrogenase two times so you will select the option where where you are having the dehydrogen dehydrogen that is going to be the answer the next is the W disease the clinical questions will be like this they will not ask you the diagnosis of w they will give you a clinical scenario and they will ask you that which of the following statement is not true for one grk disease they will give you the the clinical scenario they will give you the diagnosis also and then they will ask which of the following is not correct for WK see what is the meaning of wer is they will give you a child and they will say that whenever the mother forgets to give a male the child goes into hypoglycemia if a child is going into hypoglycemia the answer is going to be wer disease now V disease what are the points to be remember it only affects lever it does not affect muscle the first thing it only affects lever second in the W disease there's increase in the lipid there's increase in the uric acid there's decrease in the glucose hyper lipidemia hyper urmia but there is Hypoglycemia the glucose is less in W disease lipid is more uric acid is more but the glucose is going to be less this child will have decrease in the growth the growth will be less so these are the points to be remembered they will they will ask you all except question that all of the following are true except there's going to be increase in the lipid there's going to be increase in the lipid increase in the uric acid but the blood glucose will be less blood glucose will be less in fact in any McQ of biochemistry a child is going into hypoglycemia it's one grk it's due to deficiency of glucose 6 phosphate dehydrogenase the glucose 6 it is due to glucose 6 phosphates due to glucose 6 phosphates the glucose 6 phosphate is unable to convert into glucose as I told you right now about the glucose 6 phosphate dehydrogenase that is a different one that is used in the HM patient that you have discussed in the your pathology also that is referred as G6PD so we all know that if there's a deficiency of G6PD the patient develops anemia that is the hemolytic anemia there are two questions from this particular statement they will give they will they will tell you like this the hint in the McQ will be like this they will say that the patient has started on a particular drug and after starting the drug the patient has developed anemia after starting a drug the patient is developing anemia and generally that drug is going to be primar for malaria we started primacin next day the patient was having anemia because the G6PD was not there and it is a xlink recessive disorder super important what is the inheritance pattern of G6PD it is xlink recessive it's xlink recessive disorder it's only going to affect males very good the next is the mardal dis dis although I have told you three points already about the mardal disease that whenever they say the patient is doing some physical exertion if they say the patient is doing the hint will be like this the patient is doing some physical exertion either the patient is going into gym or going in the staircase physical exertion followed by muscle pain followed by dark urine physical extion followed by muscle pain followed by dark urine it is mardal disase physical extion followed by muscle pain followed by dark color urine it is mardles and mardles is due to deficiency of muscle glycogen phosphor muscle glycogen phospholes in fact they can ask you the treatment of this disease also for the treatment of this we try with the vitamin B6 we we give vitamin B6 if that works very good if not then the enzyme replacement therapy initially we are going to give vitamin B6 if that works if not we are going to give the enzyme replacement therapy let's move forward the next is galactosemia galactosemia they will give you a clinical scenario like this the whenever the breastfeed is given to the child the child is having vomiting breastfeed followed by vomiting it is galactosemia and we have remembered a pneumonic if remember in the class Fab gut galactosemia it is due to deficiency of galactosemia is due to deficiency of Ural trans phace so the breast feed followed by vomiting the answer is going to be galactosemia but definitely they will not ask you the diagnosis but they will go forward galactosemia it is due to deficiency of Ural transf there is increased risk of eoli infection there is oil drop C it's going to be all drop C and that is due to deposition of gdol guess it it all so I want you to remember these three four points one it's due to efficiency of V transfers there's increased risk of ecoli infection and the child will develop the oil drop CCT there's going to be mental retardation these things will be there because nowadays they have stopped asking the the question like this they they will give you more of such questions listen to the words the question language will be like this you most of the questions will not be the oneliner type of pattern the questions will be maybe like this all of the following are true about this disease except so you should be knowing the three facts the fourth one is going to the answer so you have to apply the concept you have to apply the things then only we are going to crack the things if you know the core Crux so these are the important points to be remembered from the galactosemia part if they say this is galactosemia breastfeed followed by vomiting but if they say fruit juice followed by abdominal pain then this is fructose intolerance and fructose intolerance is due to deficiency of eldes b eles b the pneumonic we have discussed was Fab gut fructose intolerance is due to eldes B deficiency galactosemia is due to Ural transas deficiency galactosemia is due to Ural transfers deficiency fructose intolerance UL B deficiency right okay let's move forward the next is the Goucher disease and Feb disease I will I will not go to see it's the reason I'm going fast the reason I'm just focusing on the keywords because I don't want you to lose and invest your precious time in these things I want to keep the things very straightforward if this thing will come that is going to be the answer if this thing will come that will be going to the answer it's not a class to learn the concept right we will not dig down the things in this short session so uh that is why U I am compiled to do the things in this way and if you are not uh able to write down the things nothing to worry the file will be shared with you in a while just after the session Plus I want one thing from you is when you are there with me for next uh this 1 hour try to get involved and try to remember the words what I am saying if this will be there the answer is this right and try to remember that as much as possible so the next is going to be a 8-year-old child the hemoglobin will be 6.5 the exact values are there 8 year old hemoglobin is less and hosal 8year old child hemoglobin is less hosal the bone Maro biopsy was done and there was a special sail that is there the image is not like this there is a slightly different image but it is going to be there it is even I will tell you the it is going to be like this and uh they will ask you that we understand that in the child anemia hpos the bone marrow is showing this crumbled tissue paper appearance it is going towards the gaer disease but what they going to ask is not the diagnosis they will say that it is due to which enzyme deficiency it is due to deficiency of beta glucose cerebrosides and this is the exact name of the enzyme that is there deficiency leads to Goucher but in their question Bank the beta word is missing the answer is going to be glucose cerebros cides glucosides if it is there if the beta glucosides is there that is the best answer but in that the beta word will not be there the beta word will be there but the name of the enzyme after the beta word will be different say for example one option will be beta galactosides and one option will be glucos cerebrosides these two options will be there beta Galo and glucos iotis then you are going to select glucosides because the answer is beta glucosides although the beta word is not there okay then we we will select the P we'll select the glucos citis we will not select galao any any day we are not going to select galao okay very good in any McQ if they use the word enoc keratoma the moment you see the enera the answer is febri disease and it is due to deficiency of alpha galactosides febri alpha FAA fa febri fa Alpha febri Eno and it is xlink recessive disorder in Biochemistry there are only few disorders which are xlink recessive and we have already discussed two out of them one is G6PD and second is Feb disease second is Feb disease let's move forward okay see normally the fatty acids are metabolized in the mitochondria normally the fatty acids are metabolized in the mitochondria but to enter inside the mitochondria we require a transporter and the name of this transporter which is there on the mitochondrial membrane in the mitochondrial membrane this is cat can an a transporter so there is a cat who is sitting there to transport the fatty acid from the cytoplast to mitochondria so one question who transports fatty acid from the cytoplasm to mitochondria the answer is cat the full form of cat it is cartin and asile transporter remember this image this IM this image will help you cartin asile transporter can't e an asil transporter cat now what happens is if the fatty acid is very big the cat cannot transfer the fatty acid in the mitochondria if the fatty acid is very big that is called as a very long chain fatty acid if the fatty acid is very big if we have the very long chain fatty acid then that cannot enter in the mitochondria then it has to go in the peroxy so one question will be like this very long chain fatty acid metabolism occurs where it is occurring in the peroxisome so two question who transport the fatty acid from the cytoplast to mitochondria C but it cannot transport a big fatty acid so the big fatty acids they will go where they will go in the peroxy they will go in the peroxy very good the next is in any McQ if they say Coral transparency okay I will use the word coral clouding if they use the coral clouding word you have to see whether it is present or absent if the coral clouding is absent the answer is Hunter disease and if the coral clouding is present the answer is hler disease in the McQ if the options are saying hunter or hler search for Coral clouding if the coral clouding is present it's hler and if it's not there it's Hunter because you understand a hunter always has to have a very good eyesight then only he can be Hunter so Hunter has a very good cornea the corneal clouding is not there the cornea is clear in a hunter and Hunter is xlink recessive so this is the third disorder in the biochemistry for us xlink recessive is Hunter and Hunter no Cal clouding if the Cal clouding is there it's h very good the next is the HG prts deficiency if there's deficiency of HG prts the patient will have a significant mental retardation and self mutilation the child will eat out its own finger the child will eat out its own finger it's Les neon syndrome the moment you see self mutilation in Biochemistry is Les neon syndrome it's due to efficiency of GPRS and interestingly this is the xlink recessive disorder there's none another xlink recessive disorder if there's deficiency of adenosin Damas it lead to severe combined immuno deficiency disease skid severe combined why it is combined because the T C and the b c both are affected so it's a combined immun deficiency so two questions from purine catabolism if the hgp prts deficiency is there it's lesan syndrome adinos damin deficiency it is Sever combined immun deficiency adinos dous deficiency leads to skin we all know that the DNA is there in the nucleus right now how this DNA get fit into the nucleus we take the DNA we turn around the hisone and then we fit in the nucleus so DNA and hisone they are in very close proximity DNA andone they are very closely related because DNA we turn the DNA around the stone so DNA Stone very good relationship in fact if you want to do anything on the DNA you have to take the permission from his stone for example from DNA you want to make RNA that is transcription if you want to do transcription you have to take the permission from the his Stone you have to take the permission of his Stone means if you want to do activate the transcription you have to do the acylation of a stone if you want to stop the transcription you need to do the methylation of a stone so acation remember everyone a ilation a ilation leads to activation of transcription if do the acylation of a stone if you give a lot of atile group on the stone the transcription will happen if you want to stop it methylation methylation is not important for your exam they will say which process will activate the transcription it is a ilation which process will activate the transcription acid delation very good the next is the DNA repair disorders DNA repair disorders if there is a mismatch if there is a a mismatch means normally what happens is the d uh in the DNA in the DNA a clubs with the T and G clubs with C this is normal a clubs with t g clubs with C but by any chance if there is a mismatch and that has not been corrected the patient will develop something called as the hnpcc hory non polyposis colon cancer if there's a mismatch repair def if there's a mismatch the patient will develop the hnpcc herit non polyposis colon cancer also called as the Lynch syndrome mismatch repair effect leads to colon cancer leads to colon cancer uh in their Q Bank the answer is like this they will say there's a mismatch repair effect it will lead to what and the option is hnpcc hnpcc CC stands for colon cancer mismatch effect will lead to hnpcc for colum cancer there are two three points to be remembered further one is from the medicine that colon cancer is the most common cancer of acromegaly in a patient of acromegaly the most common cancer is colon cancer and in the colon cancer we have the apple core sign on the Radiology we have the apple core sign the most common cancer in acral is colon cancer the mismatch def effect also leads to colon cancer the next is if there is defect in the nucleotide oxygen repair if there's a nucleotide oygen repair rep effect if there's a nucleotide oxygen repair effect when this patient is going to go in the sunlight see in our skin there is some part of the DNA which is having multiple 80 base pairs a lot of 80 base pairs are there in some part of a DNA so when we go in the sunlight the sunlight will fall on this DNA and by chance by mistake the T molecules will club together and they will make the thymidine diers we don't want these thyine diers so in you and me these thyine diers are and we don't have any problem but in some patients these thyine diers nucleotides are not excised and if the oygen will not occur the patient will develop the dry and pigmented skin dry and pigmented skin that is called as the zerod Derma Pigmentosa so zero derap Pigmentosa two question to remember it is due to Persistence of the thymidine diers and there is the nucleotide oxygen repaired effect nucleotide oxygen repaired effect and there's a formation of the thymidine diers where very good the next is the msense mutation the example of missense mutation is the CLE cell anemia in CLE cell anemia in our hemoglobin we have total four chains of protein two alpha chains and two beta chains we have total four chains 2 Alpha and 2 Beta sometimes in the hemoglobin in the beta chain at sixth position the glutamic acid is replaced by veine if the glutamic acid is replaced by veine the rbcs are going to change the shape and the shape of the RBC will like this the Cent shape RBC the Cent shape of RBC and the RBC becomes very sticky this is called as CLE emia the CLE emia also called as hand foot syndrome also called as hand foot syndrome CLE cell anemia is also called as hand foot syndrome very good the next is a question from the electron transport chain in the electron transport chain there are three gos first it occurs on the inner mitochondrial membrane we all know what is happening in the electron transport chain the basic concept is we want to convert the nadh fadh into atps we want to convert the nadh fadh into ATP that is called as electron transport chain the first question is in the electron transport chain there are five complex enzymes and they ask that they are pumping how many hydrogens they are pumping how many electrons so the pneumonic is 40 42 40 42 the complex one pumps four hydrogen complex 2 pumps zero hydrogen then four then two so 40 42 4042 electron transport chain the second question 4042 how many electrons to be pumped by each complex 4042 the third is who is going to inhibit the electron transport chain what are the name of the Inhibitors such as the renon is going to inhibit the complex one the melonade can inhibit the complex two Bal antimycin can inhibit the complex 3 cide carbon mono carbon dioxide carbon monoxide hydrogen sulfide can inhibit the complex for so they ask this who is going to inhibit the complex the pneumonic is Bak ma balak ma renon melonade Bal animy K cyanate carbon monoxide but I want to add here everyone remember right now here itself in this session carboxin inhibites which complex carboxin inhibites complex 2 carboxin inhibites complex 2 remember right now itself carboxin inhibites complex 2 complex 2 the last question in the electron transport chain see normally nadh fadh converts into ATP via electron transport chain sometimes the nadh fadh converts into heat in the electron transport chain and this process is called as uncoupling this process is called as uncoupling so they ask that who is promoting this uncoupling who can promote this uncoupling there are many uncouplers such as the thyroid hormone thyroxin and the important is 24 d nitrophenol 24 D nitrophenol that is uncoupler 24 D nitrophenol that converts the nadh fadh into heat so they will ask that which of the following is a pathological uncoupler the answer is 24 D nitrophenol so three questions electron transport chain occuring on the inner mital membrane the how many hydrogens are ped 4042 where comes to uncoupling the uncoupler example the pathological uncoupler is 24 D nitrophenol 24 d phol the carox yes there are many others yes rightly said esin saki esin it is there but right now we are just keeping the things to the point the next is the various coenzymes and co-actor coenzymes and co-actor among this list the important is the trans keto the coenzyme is vitamin B1 trans Amin the coenzyme is vitamin B6 and methy melony Co mutas is vitamin B12 why these three are very important the reason is if you want to check someone is having the vitamin B1 or not you are going to check the activity of transis transis if you want to check vitamin B12 is there or not you will check the activity of methy melany Co mutas and if you want to check whether the B6 is adequately there or not you can check trans amines so these three are the very important ones that and among them also these two are very important if we want to check vitamin B1 is there or not we check the activ of transas if we want to check vitamin B12 is there or not we check the activity of methy melany Co mutas and for vitamin B6 we check the activity of trans amines when it comes to the co-actors among the co-actor the important is this one zenin Ides zenin oxidase the co-actor is mum for zenin oxidase the co-actor is midam and for suin dehydrogenase the co-actor is IR these two go factors important to be remembered suin dehydrogen is the co-actor is iron and Zen oxid the caor is mum very good the next is the vitamin A now coming to the vitamins vitamin A deficiency vitamin A deficiency can lead to several thing one is the night blindness second is the follicular hyper keratosis the hair follicles there will be a lot of keratin deposition can happen that is follicular hyper cardosis that is seen with vitamin A deficiency and third is vitamin A deficiency can also lead to the dryness in the eye that is the bitot spot bitot spot so vitamin A deficiency is night blindness bot spot follicular hyper cardosis that can be there x1b this is the wh classification for vitamin A deficiency x1b stands for the Beto spot X2 stands for the coral xerosis vitamin B2 deficiency vitamin B2 deficiency vitamin B2 is also called as the riboflavin the active form of riboflavin is Flavin adinin dinucleotide Flavin adinin dinucleotide if there is deficiency of vitamin B2 if there is a deficiency of vitamin B2 it will lead to glossitis it can lead to choisis and the important is the new blood vessel formation that is coral neovascularization Coral neovascular vitamin B2 deficiency leads to Coral neovascularization V uh next is the vitamin B3 vitamin B3 is nasin that is made from typen if there's deficiency it can lead to pelra and from typen when we make the nasin the name of the pathway is kenin pathway from typen when we make the nasin the name of the pathway is kin pathway the next is selenium deficiency selenium deficiency leads to kesan disease they ask that which vitamin contains Cobalt which vitamin contains Cobalt it is vitamin B12 because the name of the vitamin B12 is CYO cobalamine cobalamine because it contains the Cobalt so selenium deficiency leads to Quan disease which vitamin contains Cobalt Calamine interestingly in the exam if a McQ is there and you are unable to get any clue out of that McQ one of the alternate that you can use is try to search for some alternative names sometimes the answer can be there in the alternative names so we'll try to search for the alternative name and that might give you some hint right because see what is happening is earlier you have seen the earlier pattern that was there was 150 mcqs were there in the first half 150 in the second half so there were two advantage that was there when the exam was happening in two slots one because you were having the access to 150 questions so sometime for example the question number 22 you were confused between two option and when you reached at the question number 141 you got a hint about the question number 22 it was possible sometime we get the hint of one McQ in other McQ and that way you could have came here easily and can access it and can can mark it correct so that was the additional Advantage earlier the second additional advantage that was there was earlier because the exam closing time was here and here so we were getting little anxious or some anxiety in just before the last few minutes particularly in the second half we were getting little anxious right towards the end because the second half was little lengthy and we can get a Time crunch in the second half but now as the things has changed there are going to be six such slots so we are going to get anxious for six times and one more thing that is going to be there is if this question is here and one more question is related to this disease is here you can't come back you can't you can't get the access to that so these are the two losses that we are going to have but as we change the things we don't have much things and uh much thing that we can do about this but what we can do is the practice so now what I want is for the last these 10 12 14 15 days whatever is left try to solve everyday 50 McQ slot not I'm saying 50 McQ I'm using the word 50 McQ slot because I want your mental frame to be the same the way it is going to be asked in the exam means in the morning say for example 9:00 a.m. you are starting doing the McQ you give yourself the time of 50 minutes and give you 50 minutes whichever McQ you want to do maybe from a single subject maybe from mixed bag whatever it is whichever McQ you want to solve today do it in a 50 McQ slot don't look at the answer immediately after finishing each question first complete the slot and see that how much time it is consuming and then you see the answers so that every day if you are going to do this you are going to do the 15 14 slots now 14 days are left to the exam 13 14 days so you'll do 14 slots in your exam there will be six slots right 50/50 question six slots are there if you do 14 slots basically it is equal to two GTS it is equal to two grand test so without investing a single day we are practicing for two GTS the see now many of you are asking that ke should we give any one more GT why we asking this question is because in the last GT many of us may have not get a very good score maybe maybe 148 maybe 150 maybe 160 and we just want to reach to that 180 score in the GT so we go to the exam with that confidence oh 180 GT so now I'm going to pass only see the GT score is not going to make us pass what is going to make us pass is the knowledge is the is the practice of the MCU how we are going to implement it right and that way we have to prepare we are not preparing to get a good score in GT we are preparing to get a good score in the real exam right and what we are doing is we just want to get a good score in GT so confidence idea should not be like this the why we are giving the G is to get acclimatized to the system that has to be the idea see recently I have told in the class also that however hard paper they want to make see we can't stop them we can't control them but you will find at least 100 120 easy questions 120 125 easy question in out of these 300 mcqs there will be somewhere in between those McQ you have to control your nerves and you have to wait for those easy questions the moment easy question give more attention give more attention and make sure that you are making it correct and if you get the maximum out of this no one can stop you in clearing the exam because you can see that out of 200 question it can't be zero you will get something out of this and that will be enough to clear the exam if you if you just Mark that easy questions correct but what happens is it's a human tendency that if we don't know continuously five question even the six seventh question is from your notes which you were knowing we get anxious what is going to happen the things are getting very worse this time the exam is very difficult the the reason we feel the exam difficul is for two reason one the language is slightly changed not difficult slightly changed the words here and there here and there so we we kind of get worried you have studed everything you just have to recollect the thoughts just try to rephrase uh the statement what they want to ask try to find that the simple words that and then you can recollect the things and you can easily get the answer I'm not saying that uh difficult questions will not be there difficult questions will be there there are easy questions are there I just want to pick those easy question I have to make sure that I'm making it correct why I'm saying is because you are having the 50 questions slot because there are only 50 minutes and if you are if you are doing the McQ like this that whatever answer is there for question number one first I will take it then I will go to the second then I will go to the third then it might be there question number let's say 5 11 12 13 they were very lengthy and you have invested so much time in that said you are left with only 3 minute for last 10 questions and out of 10 questions they were very easy questions were there where you could have scored very well so we have lost that chance right so what we are going to do is when we are having the 50 slots the first idea is out of 50 questions at least there will be 17 20 easy questions will be there and I have to mark it correct just imagine out of 50 question can't we make 17 or 20 questions correct we can't we can easily do that 50 out of 50 17 question is not a big deal right there will be there will be easy 17 18 20 question that we can Mark right and first say for example the question number one was very difficult two was very difficult I will just smile we'll go away I just have to find the easy questions which I know I will take them and then I will Rec and then I will do these difficult questions also so in that way at least I'm sure thatas question second thing don't change your answer whatever comes as the first take that don't overthink don't overthink he wants to twist the things don't worry right see these they were also made the paper and uh the easy questions are easy only keep the things straight keep your mental frame very stable in the examination Hall don't get distracted from the difficult question they are bound to be there they are just to test your temperament they are not going to decide the result listen in the words they are not going to decide the result the result will be decided by these 180 120 125 easy questions how you are making them correct just imagine that if someone makes maximum out of them correct out of 125 easy questions maximum is correct then what is the difficult task that out of 200 question to get 50 50 60 70 marks it's not difficult the reason why we are not able to crack the exam with a very good high pass percentage because most of us get breakdown the nervous breakdown that happens in the exam because of this anxiety that question I have prepared Fara very well I have prepared B very well and five questions continuously I was not knowing right and six question we lose the temperament we lose the control on our nerves and we start making the mistake right the same thing happens in the cricket also you give continuous dot balls to a very good Bassment on the next ball he is going to make the mistake right so you just have to wait wait wait my dear friends and the the things will start coming to you and definitely you are going to make it see for last 5 months and uh these 10 15 days we can't just let it go like this my sincere suggestion to you is flip the pages as much as you can flip the pages very quickly don't give the time to your brain to think the random things the random thoughts because the moment you stuck somewhere on some pages your mind will start deting he will tell you no your notes are gold stuck to that if some pages where you are not able to overcome the things it's taking a lot of time don't worry with that topic just whatever the teacher has told just focus on that and move to the next page that flipping pages is going to release a lot of dopamine in your brain and you will be so much indulged that the random thoughts will not come to your mind and that way these 13 14 days we are going to utilize to the best don't run here and there here and there stick to your notes and you are going to make it happen see you are just not doing this thing for you you the the entire family is waiting for that one result that one day that they are patiently waiting for last 6 years 7even years right they have invested everything and we can't just let it happen for 14 days it's like a war situation for us right just imagine that if someone has going to a war right 300 400 500 right at that time if the war is going on is there any thought that came to their mind take a it such breaks never happens right if it is a war war nothing comes to the mind and this is the war time that such no thing should come to your mind if it is coming to your mind means we have to correct our mental frame come the chai Bey everything will will be secondary right everything is secondary everything will be just flip the pages and if you do the that thing you can till from today onwards if you start flipping the pages continuously you might flip your entire syus maybe for two times three times but if you stuck if you are thinking that three times if it is coming to your in front of your eyes in the last 14 days how how it is possible that you will not remember that in the exam it is going to be there so don't have to worry for problem that that is one thing that you have to overcome I have to this that I have to do that also is nothing like that don't worry these notes are more than enough to clear to exam the the the things even right now today if someone gives you that 300 McQ right now right you will be you will be easily able to crack the exam right now this much amount of enough is because right now you don't have the nervousness you give the exam you clear it but in the real exam those 300 McQ you might not score that good the score that actually you get is minus 20 if your real score is 170 then you are getting 150 only because you are having the knowledge to get at least 150 as 170 plus but we are just getting 150 plus the reason being the nervousness that pressure force you to do the mistakes and we are not let it happen because we are going to practice in this way so every day do 50 McQ and a slot right will not take much your time time guys and uh it was a very short and a crisp session that I want to have with you and uh I was thinking that it would have taken maybe 2 hours but we have just completed in 1 hour 15 minutes but uh most of the things we have tried to cover from all the major units why it has not taken much time although we have covered so many topics because we have just kept to the point we don't have went into the concept right into the concept but we just went to the clue words so that it has not taken much time so and don't overthink about the exam dates just keep it simple yes it is going to happen on 6th of July why we are Rand see why our brain gives you that random ideas because we just want to escape the things right so in most of the situation it is going to happen on the 6th of July only let's keep that thing let's work hard for you for your family and definitely you are going to make it happen the the the almighty is looking at you the hard work that you have did in the last four five month the justice is going to happen the hard work is going to be paid off it is not never going to be in vain right so wish you all the very best keep this hard work going and we will be in touch if anything you can write me down and I'm very sure sorry that if I will not able to answer you just write it down again and I will try to answer you and uh if not you can call any time right and we'll discuss the things on the phone no need to write in the uh WhatsApp that when I can call you you can call anytime you call any time we'll try to answer but the whole and sole agenda is the exam has to be cleared in this attempt only this is the whole and sole agenda you and me both we are having and a lot of family members are waiting back right and you you are definitely is going to make it happen okay my dear friends so we'll finish the session here thank you and we'll we we will be sharing the PDF with you a while thank you guys e e e e

Channel: Dr.G Bhanu Prakash Animated Medical Videos

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Keywords: biochemistry rapid revision, biochem rapid revision fmge, biochemistry rapid revision fmge, biochemistry rapid revision neet pg, rapid revision biochemistry, biochemistry rapid revision series, biochemistry last minute revision, fmge biochemistry rapid revision, biochemistry fmge rapid revision, rapid revision biochemistry fmge, biochemistry fmge pyq revision, dr priyansh jain, fmge rapid revision, rapid revision of biochemistry, biochemistry revision neet pg, usmle step 1, fmge

Id: ugQIKthktjo

Length: 77min 44sec (4664 seconds)

Published: Sun Jun 23 2024