This comprehensive pharmacology lecture covers the mechanisms, classifications, and clinical applications of NSAIDs, analgesics, antipyretics, and antigout drugs. Key topics include: (1) Allopurinol as a xanthine oxidase inhibitor for gout treatment; (2) Sulfasalazine as a prodrug activated by intestinal bacterial enzymes for inflammatory bowel disease; (3) Relative nephrotoxicity of NSAIDs (indomethacin > phenoprofen > ibuprofen); (4) Acetaminophen's selective COX-3 inhibition in the CNS with negligible anti-inflammatory effects; (5) TNF blockers (adalimumab, etanercept) for rheumatoid arthritis; (6) Gold compounds for chronic rheumatoid arthritis; (7) Aspirin's irreversible COX inhibition and risks of Reye's syndrome in children; (8) Colchicine for acute gout attacks; (9) Selective COX-2 inhibitors (coxibs) with cardiovascular risks; (10) Secondary gout causes including increased uric acid production, decreased elimination, and enzyme deficiencies.
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Prerequisite Knowledge
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Deep Dive
UPSC Drug Inspector Marathon | Pharmacology- 24: NSAIDs, Analgesics, Antipyretics & Antigout Drugs
Added:Hello dragon inspectors.
Very good evening. How are you? I hope you all are doing good and your preparation is going in full swing. I hope you are not taking rest and you are making the sacrifices yourself and you are giving utmost importance to your preparation.
I hope you already know that you are going to becoming drug inspector that should but for that purpose you require continuous preparation with a discipline as well as focusness and most important thing is you have to manifest yourself in the brain yes I have to make it this at any cost there is a saturations frustrations up and downs whatever it may be but continue preparation continue preparation Your mindset is the key thing. Your mindset is the key thing. So please fix in your brain. Yes, I am going to making this happen. So within soon you'll get the more details regarding the exam date etc etc. But take it as a every day as a final day.
Wake up in the morning going for the preparation revising the topic practicing the MCQs through our GDC English classes madam sessions. You can go for any topic, any subject, you will find MCQs and practice the MCQs and repeat the same thing. Okay? Yes.
Ready? We can start the session. Very good evening. Very good evening. So, please make the energy positive.
Don't think anything in mind in negative form. Do it, study it, make it worth like preparing the arithmetic.
So anyway I hope you already know that so with energy we'll start the session.
Yes. So you already know that today's session on the MCQs from the pharmacology of NSADS antibiotics anesthetics anti-romatide orthodics drugs as well as anti drugs. So start within first MCQ. So what is the first MCQ mentioned here? It is from the UPSCDI 2015. Fabuko stat is favo stat act stat nothing but stops zanthin oxidize inhibit the zanthin oxidize. So zanthin oxidase is one of the enzyme involves in increasing uric acid levels in the blood that may lead to development of that may lead to development of a gout a metabolic disorder. So fabic stat is anticlant antiplatlet zanthan oxidase inhibitor contraceto what is the answer very good you already know the answer so simply fuk stat xo means zanthin oxidate stat means stopping inhibitor fib so stat is option C very good so it is exanthin oxidiz inhibitor non-competitive inhibitor equally or more effective than the alopurol in lowering blood uric cash levels in the patients with hyperin as well as gout. It is rapidly absorbed orally highly plasma oxidized as well as gluconation conjugation. So oxidation is phase one metabolism. Gluconation is a phase 2 metabolism in the liver excited by kidney. Plasma half life is 6 hours.
Plasma halfife is 6 hours. Get ready for the next MCQ.
What is the next one? So regarding the next one sulfa salosyme it is a pro drug that is activated in the intestine by bacterial enzyme. The enzyme is responsible transfer is estate transferase sudo estrase. Sudo estrase there is aolink will be there in the structure. There is aolink will be there that's aolink will undergo reduction under go reduction with help of with help of again option C very good a reductase a reductase and gives two forms gives two forms so sulfas one of the drug preferred in treatment of inflammatory mobile disease like combination of ulcerative qualities as well as chron disease option C is the answer and here it is a discussion sulfin is a pro that is active in the follow by bacterase the colonic bacterond in sulfa salin theorus and produce five amino salicylic acid anti-inflammatory salicylic always having anti-inflammatory property and sulfin having antibacterial property is salonomy here cip 450 not involved in sulfa activation used in liver metabolism of many other drugs so pepidase enzyme that cleepidase a bond asterase breakdown esters not relevant to sulfasel. That is very clear. So remember sulfasin helps in treatment of inflammatory bowel disease.
Next the relative nephrotoxy among the nsid is option a endomethasin greater than fboprofen greater than ibuprofen phenoprofen greater than endomethasin ibuprofen. Ibuprofen greater than endomethasin phenoprofen mephic acid phenoprofen as well as indomeasin. So the relative among nsides. So like these questions you have to think and give your answer.
What is the answer?
Option A. So you are giving the options nothing but answers like skip also. So especially it is indomthasin containing indolin after that phenor after that ibuprofen. So this is a relative nephrotoxin among the nast. So indomethasin. So I fi indopeno as well as ibuprofen. Endometh phenoprofen ibuprofen is order. So the relative nephrotoxity the relative nephrotoxin the order increasing order including penoprofen is a common so that this is order you can go that so penoprofen other discussion you can watch here and moving to the next MCQL is a derative of zanthine napaline and hypoxanthine purol is a derative of what is the Hello is a derative of very simple that is alopol is commonly zanthine derative zanthine derivative even zanthine alkalide zanthine alkides like caffine zanthine alkides like caffeine theophile and theoproin biosynthesis by using zantosintosin is a biosynthetic precursor for zanthan alkides like theo Theopilin, theob broine, caffeine. Okay. And meride test is a chemical test identification test for caffin zanthin alkides.
And hello hypoxanthan analog was censored as a purin antimabate and it is inhibitor of zanthan oxidase enzyme zanthin oxidase enzyme. Okay. Very good.
And moving to the next MCQ. What they given here regarding the next MCQ acetaminophen that is parasittox is characterized by severe abdominal cramping and diarrhea professor conriction and pain central nervous system stimulation and seizures profound liver damage and failure. So estimin nothing but parasitimol and regarding the brand it is also known as tyenol parasitimol or estamino or tyenol acetamino simply acetile amino acetyl amino estamino estamino paracetamol para amino acetyl group. So simply HTML overdose causes liver toxicity. Okay. So liver toxity that's why liver damage as well as a failure. Very good. Keep doing you know the all answers and you know that already. So me toxicity nile par what is the toxicity metabolate? N acetyl parabenzoquin amion nyl parabenzoine amine that is nabqi. So this toxicity can be controlled by antidotes like N estine as well as lionine. Lithionine taken by the world root of administration. Nest taken by the parental root of administration as a antidote for parasitimal overtoxity.
Parasetal overtoxity.
Okay. Next. What is the question here?
Which of the following NSAD is not a propionic acid derivative? Ibuprofen, naproxen, ioprofen, pyro. Very clear. So prop pro uh sorry propionic derivatives pro proyam oicam pyamic anoxicam.
Okay. Very good. Very good. Super so paroxicum is not a propionic acid derative. So again you can observe here clearly. So cell propionic acid derivatives all commonly having propionic acid derives all commonly having a pro propionic acid derives acid mephamic acidic acid pyoxum estic acid that is AC ketoac indomthasamin.
Okay.
Next. So, regarding the next MCQ, which of the following drugs used in romatide arthritis has a mechanism of decreasing tumor necrosis factor? Yes, one of the following drug helps in treatment of rheumatide arthritis having the mechanism of decreasing tumor necrosis factor TNF alpha. So romatide arthritis is one of the autoimmune disease where our own immune system produces antibodies against the cyanob joints causes destruction of syino joints and especially roheide factor RA factor levels higher in the patient suffering from rotatide arthritis. So roicoxip seleto inhibitors cost inhibitor sulfogen a pro drug in treatment of inflammatory bone disease.
Penicellamine penicellamine is a byproduct of peneline. Penelamin is an antidote for Wilson's disease copperation and adonceptor adonceptor like T I T E I what is this nothing but TNF alpha E atept aix map sorry I in so adalum are inhibitors of tissue necrosis factor alpha human necrosis factor alpha helps in treatment of chromatide ar yes clear very good species that's good okay this is a discussion regarding the set how it is showing action especially antibon alpha decreasing activation of macrofasages cells etc and decrease the cell mediated immunity suppress the immune system function in autoimmune disease. Next, what is the question here? Which of the following disease modifying anti-rox can be administered orally? Orally, anarchindra, aptaccept, left at orally. Which of the following disease modifying anti-romatistance administration by using the oral root of administration?
What is your answer?
Generally if you observe this anarchindra inter one antagonist at sept all these are like biologicals means these compounds are prepared based on the biological components involves in the immune system function autoimmune reaction. infection inflammation. So most of these components are preferred not preferred to the world. So leftomide is a common drug one of the drug in treatment of rheumatide are that is it is taken by or of administration left.
So apart from this four drug this is one of the common drug that is taken through the war of administration.
Okay.
Very good.
And this is a classification regarding the drugs for treatment of drugs for treatment of rot. Even in the romide array there's a using of gold compounds aronopin aroalate gold compounds also helps in treatment of romatide arrays. Moving to the next question.
NSADs produces anti-inflammatory and energetistic effects by acting on NSAs produces anti-inflammatory as well as energetic action by acting on tromboxin protocycling prostaglandins all of the above anti-inflammatory energetic controlling the inflammation as well as reducing the pain what is answer these are simple questions I'm waiting for your you are not responding.
So thrombogen generally thrombogen A2 involves in the platelet aggregation clots formation. Protocyc oppose the platelet aggregation and prostaglandins. Prostag glandis produces cox engines and the coxeny are generally involves in the pain as well as inflammation production and here so all of these so all of this means these are controlling the inflammation as well as they're controlling the pain especially all of this is the answer simply so here it is a discussion regarding the different prostins and their respective functions especially prostaglandins so thromboins lucotrins all these are commonly known as all these are commonly known known as ecoenoids. Ecoenoids and I hope you already know that regarding this information. So please practice in the test. Practicing the test is most important to include especially to increase accuracy to give more correct answers. So don't skip practicing test.
Okay. Next. Which type of toxicity?
Which type of toxicity is associated with the ion trapping effects of aspirin? Which type of toxicity associated with the ion topping effects of trapping effects of aspirin? Heptoxy, gastric toxicity, dertoxicity, muscular toxicity. So especially aspirin is interlin with this ion dropping mainly in the gastrointestinal tract because of pH changes aspirin physicochemical properties may be altered that leads to ion trapping that leads to ion trapping and especially this ion trapping is commonly takes place in the g gastrointestinal tract that's why the answer is correct you are telling that so that is simply option B gastric toxicity option be gastric toxicity. So general adverse effects of aspirin like ama salismic ion coupling disagregation rest syndromey noise. So these are the adverse effects of aspirin. Yes you can easily remember this adverse effects of aspirin by using the trigger aspirin itself and I hope you know this we are having many books and especially this is for the Maharash private inspector.
So next one of the interesting question what is this? So let's see which of the following statements about parasetal is correct. Parasetol is correct. Let's see. Parasetol has negligible anti-inflammatory effect. Yes it is having lesser or poor anti-inflammatory.
It is mainly antibiotic in nature. It is a poor inhibitor of proto glandin synthesis in peripheral tissues because paracetimol inhibit coxeny 3 in the CNS and act as a antibiotic. It is more active on the cox in the brain than peripheral. It is a potent anti-inflammatory drug like ibuprofen.
No.
So whichever the following statement about parasol is are correct. I already gave the explanation. I hope you already got your answer and I'm waiting for your answer. So please mention question number along with answer.
Yes, very good. You already given answer option A. Option A is the answer. PQR are correct. S is wrong. It is not an potent anti-inflammator. It is generally analic. Selectively inhibit cox 3 enzyme in the CNS hypothalamic place and help as a antibiotic control the fever. And here it is a discussion regarding parasetal negligible anti-inflammatory poor inhibition of the prostaglandin senses mainly act inhibition of cox in the CNS especially inhibit cox 3 and next. So what is the next question here?
So this is a question already asked in the CZDI 2015.
NSADs can inhibit the production of all except NSAs non-steridal anti-inflammators inhibits the production of all except prostaglandin I2 also known as prostycl inhibit the platelet aggregation cyclic endoparoxide which responsible for production of proto glandins from the PGH2 PG2 thromboxin A2 helps in clot formation Lucot lucotrines produced by P liypoxy enzyme our NSA is inhibit cyclic oxidiz enzyme so that's why your exception will goes to the lucotrines inhibition of cox enzyme inhibit production of prostagland I2 inhibit production of cyclic endoparoxids inhibit production of thrombosin but not lucotrins but not lucotrines okay yes this is a discussion explanation So how all these proto glands are biosynthesis. So especially if you observe COX 1 COX 2 produce PG2.
PG2 further produces PGH2 in of cyclic endoparoxids and PGH2 in of isomease PG2 D2 F2 alpha in thromogen synthes thrombogen B2 in of protocycl synthes PZ2 so procycl produce prostaglandin I2 that's why it is known as procycl produce tromoxin A2 from the A4 but D2 from the A4 and isomearases E2 D2 F2 alpha The two sorry the two is indication of two double bonds. Two is indication of two double bonds and all these are produced by precursor araconic acid containing 20 carbon atoms in a structure.
Okay. Yes. Very good.
Okay. Next question is aspirin intake in pregnancy may lead to premature closure. Aspirin intake in the pregnancy may lead to premature closure of ductus arteriosis veinary artery. So this question is very easy because it is repeating it is repeated many times in the previous question papers. What is the answer?
Some questions you have to give answer immediately because you are studying continuously, you are preparing continuously, you are not relaxing, you are putting your more time for the preparation. So remember only 186 post are there only 186 members are going to selecting and you are one of the person in that selection. So for that purpose continue your preparation self analyze yourself. Yes you are just studying or you are remembering things. So while preparation your all senses should be in coordination. Okay. Parasetal Fox 3 enzyme inhibitor in the hypothalamus parasetyl overdose liver toxity because of depletion of glutathione. So antidote. So like that and you have to study medicine medical chemistic pharmacology in the coordination. For example if you see there isium there is a hroonium regarding hedrophonium. Hedrophonium is a diagnostic agent for the myinadis. So if you observe the structure of hydrophonium e nothing but ethile nothing but hydroxy ph nothing but phenile ethile hydroxy phenile quartinary ammonium oniumary ammonium compounds ammonium compounds are polar nature poor absorption through oral root unable to cross the bed should be taken through parental root. So like that if you observe the structures you can easily remember and even you can like fenolamine fenamine fenamine regarding the phentomine. So phenile to amidoline phenile tooline.
So like that you can observe the names and structures. You can observe the names and structures. So this is the one way to improve your efficacy of the preparation to remember the things easily.
The answer is very clear. Option B is the answer ductus arteriosis. So here it is especially as been contraindicated cancer patients and asthmatic patients due to increased minus like PF LTS PG and contraindicate children suffering from the chickenpox and due to risk of race syndrome and ultimately here also they mentioned clearly so don't take in by the pregnant women don't because of distrogance are interfering with the ductus arteros that is aspirin is responsible for premature closure of ductus arteriosis premature closure of ductus arteriosis Next. Moving to the next. MCQ. This is also very easy. I hope you know the answer already. The metal used in the treatment of chromatide arthus. Silver, gold, copper, SD. So, aronophen, a thiomate are examples of gold salts in treatment of prominent arthritics. Nowadays gold salts are not using because of their toxicity. Generally, gold salts are preferred through the world root of administration also. So AU arament gold answer is very clear very good.
Yes. Gold compounds have been used for the treatment of roots and other autoimmune disease. Arthiomalate aronophin are two formulation used in roots. Gold compounds depress cell mediated immunity that means decrease the T- cells production. Decrease the T- cell production means suppresses cell mediated immunity. Treatment with the gold is associated with several adverse effects like dermatitis, hepattoxy, nephrotoxy, enseitis, perhitis, pulmonary fibrosis, bone marrow suppression. Currently they are not preferred because of all these toxicity and all these drawbacks. Yes.
Next question. What is the next question? Dear drug inspectors, Aspen overdose is characterized by Aspen overdose is characterized by hyperothermia, increased body temperature, metabolicosis, coma, rashes, intestinal nephritis, acute failure, fever, hepatitic dysfunction, encphylopathy, rapid fulminate hepatitic failure. What is your answer? Increase the body temperature, metabolic resis, coma remaining options.
So how many number of options will be there? Whatever it may there first you have to give importance to the metabolicis.
Aspirin is generally acidic in nature.
So accumulation of aspirin may increases metabolic acidosis. So this metabolic acidosis may change oxygen carbon dioxide imbalance that leads to increased carbon dioxide levels in the blood may develop metabolic acidosis may lead to coma also may lead to coma also.
And here it is simply as acute salate poisoning it is more common in the children. Fatal dose in adult is estimated to be 15 to 30 g but it is considerably low in children.
Manifestations. What happen? Cause of aspirin poisoning, warming as well as dehydration, electrolyte imbalance, acidotic breathing, hyper or hypoglycemia, fatial hemorrhages, restlessness, metabolic acidosis, hyper pyroexmia, hyper pyrexia, increased body temperature, convulsions, coma and death due to respiratory failure plus cardiovascular collapse because of metabolic isosis increased carbon dioxide levels in the blindness and treatment symptomatic and supportive treatment, external cooling and IV fluids with sodium, potassium, bicarbonate etc. Glucose according to the need and blood transfusion and vitamin K given if the bleeding occurs in the severe bleeding vitamin K should be there. Vitamin K is a natural co control the bleeding because excess usage of aspirin produce severe bleeding.
Clear?
Yes. Are you there? Are you active? Very good. Next question. What is the next question? Dear drug inspectors, Colchin was used mainly for treating arthritis, gout, diabetes, hypertention.
Colin semiynthetic derivative semiynthetic derivative is thioside.
Thioide generally act as a centrally acting muscle relaxant mainly for treatment of muscle spasms of CNS interiorite addition of extra sulfur.
Colchin naturally from the column belong to the family lia and colin contains circular type of stomata.
Colson commonly helps in treatment of diabetes and chemically it contains propolon ring. Tropolon ring propolon ring but it is also having the ability to produce polyloy poly.
Next question. What is the next question here? Which of the following is TNF blocker?
Tumor necrosis factor blocker. So adol is a beta blocker. sodium chromolin sodium chromolin sodium neocchromal sodium are mashed cell stabilizers as anti-asmatics and previously also I mentioned T I T I T I T means TNF alpha A means aton receptor A means mapal map And I means in click map in the map.
Clear?
Yes. Very good. Keep going. Keep going.
7 + Ci again. The same discussion.
So suppression of T- cells, suppression of T- cells decreases cell immunity.
Suppression of BS cells, Bymphosytes decrease the humoral immunity. Some of the drugs like a thioprine a imunosuppressent suppress both cell mediated as well as the humoral immunity.
So this is regarding the information upcoming one. So in the upcoming Sunday the exciting thing is introduction of code of pharmical ethics pharmacy act 1948 preformulation. So you are going to get online test as immediate discussion.
So don't miss it especially from the jurist students they are asking the more questions. So drug inspector drug inspector follow ethics. So you have to follow ethics means you have to follow friends ultimately you have to follow GDC classics.
Next question. What is the next question? Let's see here which one of the following drug is not commonly combined with without for the treatment of which one of the following drug is not. So please be careful while studying the questions for that purpose you have to practice number of questions number of questions nothing but number of practice test especially more than MCQs you have to go through it. So sulfa leomide aoprine what is the answer? Which one is not generally preferred?
Because if you observe chloropin is an antimal drug and addition of o to the chloropin hydroxychloropin is a antiromatic drug helps in treatment of aopin imosuppressent lephonomide a drug for treatment of sulfagin also helps in treatment of autoimmune disease. So the answer is very clear that is chloroquin.
Chloroquin is not generally combined with methtoid and combination of these two drugs may also increase the risk of toxicity.
So this is regarding the method. Mythot is a folic acid anton also anti-cancer drug especially inhibit dihydropholated enzyme.
And regarding the chloroquin antimal drug inhibit the heolymer enzyme increase the concentration of he in the mal parasite cause the death of malar parasite killing of the mal parasite. So Andra Pradesh DA 2018 so generally maybe it is from the Talangana DA because I am from Andhra Pradesh since 2012 there is a no DA examination I am also waiting but these are the small things. So this is from the most probably from the ibuprofen is a derative of pro ibuprofen keto profici Okay, I hope it is okay regarding my audibility. You are facing any problem.
I hope everything is fine.
I I hope I am going little bit late. I need So this is the classification again based on the chemistry itself.
And next question. Regarding the next question, proinced increases serum levels and prolongs activity of pensin derivatives. Proinced increases serum levels and prolong the activity of pens derivatives by plasma protein binding blocking their glration blocking their tubular secretion blocking their reabsorption. Blocking their reabsorption.
Okay. Thank you.
So we have to go a little bit fast.
I hope you already know that intentionally province combined with pencil because province pencil compete with the excretion at the kidney. So in this combination province going outside of the body through urine pencil is reabsorbing into the body. So reabsorbing of pencil leads to increase in half life of pencil. helps in treatment of especially STD like syphilis as well as geria. So the answer is very clear blocking the reabsorption blocking their reabsorption that proxy is going outside pencil is coming inside.
So simply prolongation of duration of action of pencil because provin is going outside.
Next question. Regarding next question this is from Rice 38. Drugs useful in the chronic chromatide arthritis include drugs used in chronic chromatide arthritis sulfain captopril leisol aopine.
So captopril sulah hydra containing drug captopril AC inhibitor andotensin converting engine inhibitor and CL captopil linopril are not your products remaining all AC inhibitors are products but CL AC inhibitors captopril linopril not produ not drugs and linopril contains a lysin initi structure lysin and captoil contains sulfah hydrol in structure.
So leisol is an imino stimulant as well as antihelmentic.
Levisol is an imunostimulant as well as an anti-helmetic.
Yes, you are correct. The drug in treatment of chronic chromatide arises is sulfagin sulfagin antibacterial as well as anti-inflammatory in nature.
So regarding the sulfen the common adverse effects will be there. It is a sulform. It may produce crystal hyper sensory reactions especially sulform produces Steven Json syndrome a type of group of allergic reactions and penicellin generally produces allergic reactions in the form of jarish hexime allergic reactions of pencil and Steven Johnson syndrome is allergic reactions of sulf moving to the next MCQs the drug which is commonly First choice in DM ADS disease modeling.
First choice. What is the first choice?
Cycllosporin.
First choice. What is the first choice?
Uh of tension. Yes, tension will be there because we are the human beings.
Try to reduce your attention and focus on the things where you are lacking because you have to be sit down and you have to be work simply nothing is there because the combination will be there, difficulty will be there. Focus on your positives.
Try to improve the time of preparation where you are really lacking put the preparation because if you want dragon spectrum means you have to put your efforts you want to put your sweat clear.
Yes, the answer is very clear that is without anti-inflammatory imunosuppressent.
Okay, because of this anticancer anti-inflammatory potent imunosuppressent because of these properties it is preferring as a first choice of drug for treatment of romatide arthritis. First choice of drug for treatment of romatide arthritis but generally common with other drugs along with other drugs. Next question. What is the next question? Which of the following drug is known to cause ray syndrome? Repeated bits. Repeated bits.
This bit is in the 2012 Maharashtra. At the same year in AP also DA notification released till now it is not released.
So rest syndrome race syndrome is commonly because of aspirin. So these are the common MCQs. You know all the concept clearly aspirin. Aspirin produce race syndrome especially in the children. So rare syndrome a rare form of the hepatitic and cyclphopathy seen in the children having viral vicella zost influenza infections.
Nextamino has less or weak anti-inflammatory activity due to estimal having weak or less anti-inflammatory activity due to less effect on the prostaglandin less effect on the cytoines less effect on the pain receptor less effect on the cytoines less effect on the cytoines Thanks.
What is answer?
Yes.
Answer 24 B. Very good. Keep going. Keep going. Suti answer is less effect on cyloin only inhibiting the cox in the CNS but pain inflammation mainly because of cox in the peripheral. So protoag sorry parasetma estaminophen mainly showing action on CNS by inhibiting cox enzyme mainly treatment of fever as a antibiotic.
Next question. So this is question repeated in the HPDI Pradesh DA 2020.
Identify the COX 2 inhibitors. So all COX 2 inhibitors are selective coxips.
Select Cox Cox.
Okay. All these cockips cockips are selective COX two inhibitors. The advantage is no or less risk of peptic. No or less risk of peptic. The drawbacks are cardiovascular toxy as well as nephrotoxy. Severe nephrotoxy, severe cardictoxy are the major drawbacks of coxips and less or very less or no risk of peptic with the cost to inhibits. But the major drawback is nephrotoxic cardiovascular toxin.
Yes.
Next question. What is the next question? Which of the following fox isopform is predominantly found in the brain? Fox on Fox to Fox on this yeah for your information only I'm giving some important things because of that little bit we are going slow but I will make fast don't worry this answer you know that co 3 and J that is a simple so co 3 commonly present in the brain and many reason for the fever increasing body temperature. Next question. The theraputic concentration of estamino in blood theraputic concentration the concentration at which beneficial effects are produced not toxic effect 5 to 10 mg per liter 10 to 20 mg 20 to 30 30 to 40. So like these questions very and we have to pray please give less questions like that like this.
What is the answer? The answer is simply 10 to 20. So the therapeutic concentration will be that 10 to 20 mg per liter at beneficial effects are more compared to side effects. So therapotic index is an indication of safety in a sub. more beneficial effects, lesser side effects. Like you already remember therapotic index equal to LD50 by ED50.
LD50 by ED50.
So this is a discussion regarding explanation.
Next question. What is the next question here? The nonopioid analyica which is a synthetic copy of neuroactive con snail toxin. The nonopiard it is energetic but not like opioids. A synthetic copy of neuroactive corn snail toxin from the natural source. Zonite pentanyl diolac.
is aptic from the natural source. from the nature source. From the nature source gone answer is so the interesting thing is it is it is a nonopidic from the synthetic form of omegaoxin. It is a synthetic form of omega cornoxin and a peptide isolated from the renown of the marine corn snail that is cornus magus cornus magus especially zoned blocks n type gated calcium channels n type voltage gated calcium channels. So can you know which drug block type calcium channels and which drug block n type calcium channel.
So Type calcium channels in the brain blocked by and non selectively also by acid and L type calcium channels are like verab hydro neopen etc. So N type calcium channel blocker zonite T type calcium channel blocker ethosexomide and also valoric acid and L type calcium channel blockers amodipin nodipin dyasm etc. Moving to the next MCQ. Parasetol was detected as a metabolite of parasetal was detected as a metabolite of dopen ibuprofen keboprofen phenetin.
Very good. Ethoseximate selectively block type calcium channels in the hypothalamus and reduce the T type calcium current in the hypothalamus and mainly helps in treatment of absence seizures. Obsent scissors because of over exitation of Type calcium in the hypothalamus. Blocking of Type calcium channels in the hypothalamus helps in treatment of options Caesars.
Answer is phenocetin.
So parasitin have been first discovered as a major active metabolite of phenocetin. Fenacetin metabized to the metabiz in the liver by odilation to the parasit. Finacitin metabolized to parasma through arthodation deilation which produces analyic pain relieving property are nothing but antipoting little bit analyic as well as pain relieving as well as antipotic.
Next the most serious adverse effect of phenile glutazone headache epigastic distress a grand loytosis as well as a blurredness as well as a blurredness.
What is your answer?
Yes, especially because of that reason only phenylone is not using nowadays because of its severe a grandytosis.
Severe a grand low cytosis. Especially if comes under pyroon derivatives.
Answer is option C.
Next question. So select the wrong combination of drugs. Ain plus parasetma pensin plus jeeptoin salicylic plus provin leodopa plus carbidopa.
Wrong combination. What is the wrong combination?
Yes, very good. The answer is simply estic plus propensity. Answer is option C. So why proinc is a urosuric drug used in treatment of chronic aspirin especially in low doses reduce the uric excretion by the kidneys and the uricosuric action of provin making the combination undesirable. So don't combine these two drugs because aspirin opposing the uricosuric action of province and making the uricide present in the blade instead of excretion through the urine.
Okay next which of the following drug is having additional platelet anti-agregatory anti-platelet activity so preosin loart amipin as well as dioxide dioxide. So without the following having additional platelet anti-agregatory.
So opposes platelet aggregation. Opposes platelet aggregation.
What is the answer?
Very good. Very good. Keep going.
Yes. Very good. The answer is low satan.
Lo satan. Candy Sarton LBarton andotensin receptor blocker does not produce dry andotensin converting enzy,000 times more selective for the andotensin one receptor thanotension 2 receptor. So blocking of andotension to produce vasodilation decrease in blood pressure has some platelet anti-agregatory effect. Okay. Mathematica opposes platelet aggregation. So decreasing vaso constriction means decreasing platelet aggregation. If platelet aggregation increasing vaso constriction increases.
Next question. What is the next question? The anti-inflammatory agent which selectively inhibit Cox to zen expression. So anti-inflammatory agent which selectively inhibits cox to gene expression. Trophy dexamethasone insulin answer is very clear. So COX2 enzyme inhibitors COX2 enzyme inhibitors that is sorry and the anti-inflammatory agent which is selectively inhibits COX2 gene expression cox2 gene expression cox to gene expression the question is little bit interesting answer is option B dexamethosone it is a gluccoordicide very important and highly selective gluccocortical S it is also long acting causes marit sepion but fluid retention is a problem edma and hypertension are not a problem it is used for inflammatory and allergic condition 5 to 5 mg per day oral for shock cerebral edma infusion okay let's I have to check once the reason why that is that much important especially opposing the Gene expression of Cox.
Next question. Regarding next question, which statement about cylo oxinous enzyme is incorrect?
Incorrect statement about cyloinous cox enzyme. It is involved in the protoaglandin synthesis. It involves COX 2 expressed constitutively and serves homeostatic function. The products of COX one protocycl have cytorotective functions. NSA induced gastropathy and gastritis occur due to inhibition of cox and synthesis of prostaglandin PZ as well as prostaglandin I2 involves proto gland senses okay products of cox one proto gland have cytoro okay especially products of cox One COX one post gland from the COX one house protective role protect the GI from ulcers. Okay. NSA include gastropathy gastis occur due to inhibition of COX synthesis of prostining PZ to PZ. Yes. Here COX 2 is constituted. No COX 2 is inducible.
Cox 2 levels are increased in the pain as well as inflammation. Cox one is a constitute. Cox one enzyme is a constitute in the g having protective role. Protective role decrease ulcer formation. decrease the ulcers formation.
Cox one is a constitutional house protective homeostasis function in the G decrease the risk of ulcers in the G.
Next question.
An agent that coalently modifies COX by acetalating serin 530 of COX 1 and Sin 516 of COX 2. So an agent that coalently modifies COX by eststeration of serin residue. So serin is amino acid active in the cox enzyme. So estellation of the serin residues in the coxeny making inactivation of coxeny by roof indomeasin aspirin droen. I hope this is clearly mentioned in the rang dish book regarding this information.
So what is your answer?
Yes, very good. Your answer is aspirin because aspirin is a non selective.
Aspirin non selectively irreversibly causes estation of serin residues in the cox phosphoridation of enzyme become active but here estellation of enzyme inactive. So aspirin is a non selective irreversible cox 2 inhibitor by causing estellation of serin residues. Aspirin is the only NSD causes irreversible inhibition of cox cox one cox 2.
Yes.
Next. What is the next question here?
Regarding the next question, nabumeone exerts anti-inflammatory effects mainly by selectively inhibiting CO2 blocking leucotin synthesis dual inhibition of COX one COX 2 direct antism receptor direct antism of opi receptor.
What is the answer?
Dual inhibition of COX one. Cox 2.
Nabbutamine. Nabbutamine is a like preferential drug. So more effect on the Cox and little bit also on COX 2.
Nothing but preferential COX 22 inhibitor. Preferential COX2 inhibitor.
Regarding the navamin it is regarded as a basic NSA and it produce active metabolite sixth mythoxy napile estic acid which inhibit coxone as well as cox effective in treatment of less and all an areic in nature but nabbamin is a basic in nature remember this and producing actamin and acts on both coxone as well as coxin next question region what is assertion pediatric formulation of aspirin are prohibited in India. Reason high dose of aspirin may cause respiratory estosis.
Respiratory. Now this trend is going on especially some formulations are banned because of some adverse effects especially damaging the health of the society.
Yes definitely you can clearly observe pediatric formation of aspirin are prohibited in India. Okay of aspirin may cause respiratory both are correct only but not the correct reason. So simply both A and R but R is not the correct reason. Mark of Jesus.
Next question. Observe carefully. Which of the following statement regarding nephopam? Nepham inhibits proto gland in synthesis contraindicated in peptic disease.
Nonopiodic that does not inhibit the proto gland in synthesis. It is contraindicated in epilepsy. It is an opioid used mainly for the chronic inflammatory.
It is commonly causes respiratory depression as well as constipation like body.
What is your answer?
What is the answer for this MCQ?
Yes, the answer is very clear that is it is a nonvopi analistic that does not inhibit the prostag gland senses. It is contraindicated in the epilepsy. It is contraindicate in the epilepsy. So total 50 questions will be there for our sessions. I hope you know that nephobam it is not it is a nonopioid. It is a parasympathetic action as well as it is having sympathyic action. It is having sympathy action also. So parasympatholytic as well as sympathyic action. So this is the free test and schedule 20 July to 26th July. So please be ready and this is the division like subject time especially all these things.
Okay.
Next question. Regarding the next question, which of the following is a preferential CO2? Preferential COX2 neolic acid, naproxen, diplan.
Which of the following is a preferential COX inhibitor? Preferential CO2 inhibitor. Preferential.
So within 5 minutes we will complete the session. Don't worry. So you have to be be ready, be prepared.
So what is the answer?
So the answer is Nimosite. So Nimslide.
Okay.
So preferential C to inhibitor. And again it is discussion regarding the NLE is concerned preferential C to inhibitor. Next question. Regarding the next question, which of the following is correctly matched with its class under disease modifying anti other biological method to TNF alpha inhibitor to other imuno modulator nonbiological retix map imunosuppressent nonbiological DM?
What is your answer?
Which the following is correctly match.
So if you see atonept atoncept is a TNF alpha anton. So wrong match method decrease T cells not a TNF alitor and retix map is a monoponal antibbody it is not a nonbiological it is a biological and topha other imunomodulator so toa other imomodulator that is non-biological in nature that is non-biological in nature and here it is a discussion non-biological imosent so other immodulators biological so TNF alpha In map andra interaction.
Next question.
Drug causing direct liver damage. Direct liver damage is indomthin drug causing direct liver damage. So is anti drug antipomasin has been considered concern.
So these are the simple questions that is simply from here aspirin is directly causing liver disease especially on high doses or on prolonged usage on prolonged usage and especially in the children causes race syndrome.
Next question. So regarding the next question which of the following statement is correct about tromboxen A2. Tromboxen A2 causes platelet aggregation. Yes.
Tromboxin A2 is metabogen A2 is directly inacted by the aspen binding. Tromboxin A2 is a PZ2.
Which of the following statement is correct?
Thrombogen A2 nothing but thrombogen.
Thrombos is platelet aggregation. It is not metabized to protocin. Not directly by the aspirin binding and it is not a proagland I2. Pro gland in I2 oppose the platelet aggregation. Tromboxen A2 promotes the platelet aggregation.
So thrombogen A2 thrombosis clot formation by promoting the platelet aggregation by promoting the platelet aggregation. So promotes vaso constriction promotes aosclerosis promotes platelet aggregation and may develop strokes vascular disorders myioardial risk.
Next what is the here nothing but all of the following are features of nimolate except less oral absorption vex inhibition high protein binding potent anti-inflammatory all of the following features of are right exception what is the exception what is the exception about saline yes it is a weak oximator generally a preferential oxyin binding potent Anti-inflammatory less oral absorption exception will goes to the less oral absorption option A is the answer. So it is a preferential C to rapidly and well absorbed after oral administration high plasma protein binding potent anti-inflammatory. So excellent absorption is there through the oral.
So also a weak inhibitor of fox enzyme.
Next.
Adali inter one receptor antagonist humannox inhibitor cox selector inhibitor inter one antagonist is an indra.
So generally anomeic carbon first carbon. So interal mumab a monoconal antibbody human monoc and TNF alpha antibody inflict map.
So this is explanation about focus examin.
Next question. Regarding next question, which of the following ensid acts on arachidonic acid? Actonic acid.
Cox enzyme phospholipase lipoxinase.
and lipos.
So answer is very simple. So both coxeny acts on arabomic acid to produce proa glands. Lipoxinness acts on arabomic acid and produces lucotrines.
Answer is option D. Very good. So here it is a clear pathway. So cox to prost gland in first prost gland in G2 PG G2 pro H2 pro H2 again D2 E2 F2 I2 A2. So the the two indicates the two indicates number of double bonds two and here it is a lucot.
Next what is the question here?
The seleto cycllo oxinous 2 inhibitors have been associated with which of the following adverse drug reaction.
Selective COX2 inhibitor Cox silicoxip royoxiptori all select inhibitor the cox 2 they having very less risk of peptic cancer risk of pepicula more with the cox one inhibitance but especially these drugs options like acute liver failure cardiovascular thrombotic events point severe is qualities the major drawback with this selectto inhibitors nephrotoxy as well as cardiovascular is cardiovascular thrombotic events.
Cardiovascular thrombotic events. One of the major problem is the selectto inhibitors that is oxyp.
So selective oxy inhibitors like roic oxipoxip reduce the pro gland I2 production while sparing thrombogen causing an imbalance that promotes plate aggregation and vaso conriction. This increase the risk of cardiovascular thrombotic events like myioardial infection as well as stroke. So prostaglandin I2 decrease the platelet aggregation but here prostaglandin I2 levels are increasing means increase the risk of platelet aggregation increasing the risk of cardiovascular disease like stroke as well myioidal interfaction myioordal interaction is dangerous than the anza where there is a permanent damage of blood vessel adverse effects of default preparation of triumph synolone adverse effect of default preparation of triinolone. So triumpinol one of the gluccocortical like derivative this directly gives to the sino joints. So attopic dermatitis inflammation of dermis layer proximal myopathy vasculitis damage of vascular and atrophic rhinitis atrophic rhinitis.
So trienolone one of the gluccocortical substance helps in treatment of rootadis and triinolone directly inject into the intraarticular into the joints intraarticular into the joints.
Answer is what is answer?
Yes. Very good. Proximal myopathy.
Myopathy muscle pain. So directly the transnolon giving to the joint to intraarticular intraarterial into the arteries.
So trans long acting gluccocortic depart stimulation sorry depart preparation prolong use of cortical can cause steroid injured myopathy and characterized by the proximal muscle weakness difficulty climbing stakes rising from H etc due to protein breakdown and muscle wasting decreasing the strength of muscle protein wasting and sorry protein breakdown leads to muscle wasting decreasing the amin levels also next question what is the next question which of the following drug is used in acute attack of the acute acute colin provinial.
So remember C N G in the acute count the risk of G is less where C will be useful anides will be useful gluccoartic will be useful proced or uricosuric agents increase expression of urication in treatment of chronic yellow inhibitor in treatment of chronic.
So CZN CZN colin lucotic ns whatever it may we can remember G and C what CNG what and this is regarding the discussion especially decrease the movement of inflammatory mediators towards the inflammation decreases movements of inflammatory mediators chemotaxis problem chemotaxis oppose the chemotaxis Next question. So following are the causes of secondary gout except it is caused due to idiopathic reason. Unknown reason. Idiopathic means unknown. It is manifested by the crystization of monos sodium uric acid within the around the joints. It caused due to the known reason of increased uric production. It is caused due to the decreased expression of uric acid.
Following are the causes of secondary except it is caused due to decreased expression. So decreased means increasing uric acid. It is caused due to reason of increased uric acid production. Yes increasing uric production increase level. It is manifested by crystallization of monodium uric crystals within the around the joints. The answer is very clear.
There is no unknown reason. All these are the specific reasons. That's why answer is option A. Idiopathic means unknown reason there is no specific reason but that is a exception option A.
So secondary gout is identified because of disease and drug increase uric acre uric production like leukemia polymia hemother using of anti-cancer drugs decreasing uric acid elimination expression chronic kidney disease diuretics like thidates increase the risk of low dose of aspirin also increase the risk of and we already know that don't compare aspirin with prevention aspirin opposing the prevention anti-code action following are the causes of primary gout except it is associated with the crystization of monos sodium uric crystals in and around joints. It is caused due to known reason of increased uricar production increased uricar senses for theopathic reason. It is caused due to peripheral deficiency of hypoxamin phosphorus transparence. Maybe part 49 question just given in some different manner.
So secondary go we know the specific reasons primary go sometimes it is like idiopathic reason unknown reason idiopathic okay so just reverse things so causes idiopathic increase is most common and partial deficiency of engine partial deficiency of engine okay So engine name is hypoanthine guanine phosphoribos transferase. This hypoanthine sorry hypoanthine guanine phosphor rios transferase is required for metabolism of uric acid but deficiency of this enzyme also develops gout partial deficiency of hgpr causing decreased uric acid. So urine metabolism and ascreased uric acid production.
Okay champions this is regarding today our discussions. So manifest yourself in brain you are going to achieve this. So please please give more time for your preparation. So this is like a lifetime opportunity. 186 post only 186 persons are there. So you are the one person you have to believe in yourself and don't go for the fluctuations. Continue your preparation.
Self analyze your preparation. Thank you. We'll again meet in the upcoming session.
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