2017 H2 Chemistry JC1 & 2 students post your questions here
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Originally posted by greenpika:
Hi, can I ask if you have any really challenging organic chemistry structure elucidation questions to practice?
Just do all the OC deductive elucidation qns from the 2016, 2015, 2014 JC Prelim Papers lor. Anything about those qns u want to ask can post here. -
^_^
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Thanks for the questions. Will appreciate if you take a look.
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Originally posted by greenpika:
Thanks for the questions. Will appreciate if you take a look.
Excellent, you got my 1st 3 questions correct.Are you a JC student? Or a Uni student? Or a private tutor or school teacher? If you're a JC student, are you H2 (only) or H3 or Olympiad?
Take your time with my next 3 questions, if you intend to continue to attempt them.
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Realised I double-posted the same pic in my previous post haha. I've completed the other 3 questions as well do help me take a look! I'm just a normal H2 student but this practice is really good because your questions are challenging and phrased in a novel way. Excellent practice before prelims.
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Originally posted by greenpika:
Realised I double-posted the same pic in my previous post haha. I've completed the other 3 questions as well do help me take a look! I'm just a normal H2 student but this practice is really good because your questions are challenging and phrased in a novel way. Excellent practice before prelims.
Impressive, all correct, you'll be getting an A grade for your H2 Chemistry A level exams for sure!And glad you appreciate my original (and as you say, rather unique) BedokFunland JC questions! :)
If you come across any Prelim Qn that you would like to ask on, feel free to post here to discuss.
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As the following medical study illustrates, the link between Taurine and heart disease is complex. In some cases, heart disease is indicated by unusually high Taurine levels (regardless of supplementation); while in other cases, heart disease is indicated by unusually low Taurine levels (regardless of supplementation).
Medical science is complex, because human biology, human chemistry and human genetics are complex. So while Taurine (or any supplement, for that matter) certainly isn't a magic bullet nor even necessarily helpful (depending on your genetics and exact underlying medical condition, it may or may not be helpful); notwithstanding, self-education is your own responsibility (do your own online research to see if Taurine, or any other supplement for that matter, is worth your trying it out). At the same time, as the adage advises, while knowledge can be empowering, a little knowledge is a dangerous thing. So always proceed in life with sensible caution.
Decreased Myocardial Taurine Levels and Hypertaurinuria in a Kindred with Mitral-Valve Prolapse and Congestive Cardiomyopathy
http://www.nejm.org/doi/full/10.1056/NEJM198101153040301#t=articleTop
Excerpt :
Our study suggests that hypertaurinuria is associated with low levels of taurine in the myocardium, one type of the mitral-valve-prolapse syndrome, and a form of congestive cardiomyopathy. Hypertaurinuria may also account for the relatively rapid development of congestive cardiomyopathy in the two subjects with initially uncomplicated mitral-valve prolapse. It is also not clear whether the depressed myocardial taurine levels are etiologically related to the two heart diseases, whether all three disorders are coincidental genetic accidents, or whether the depressed myocardial taurine concentration is the cause of congestive cardiomyopathy alone and is unrelated to mitral-valve prolapse. The available evidence favors the hypothesis that all three problems are related.
Regardless of the extent of the possible interrelation, one additional point is evident: the syndrome of mitral-valve prolapse, with all its clinical and echocardiographic features, was not caused by mucinous transformation, scalloping of the mitral leaflets, or elongation of the chordae tendineae. Rather, a pathologic process in the papillary muscles seems to be the underlying cause — an interpretation that supports the view that mitral-valve prolapse is a syndrome with diverse causes.
Taurine (2-aminoethanesulfonic acid) is the most abundant free amino acid in the heart, accounting for more than half the total free amino acid pool. Circulating taurine derived from either dietary sources or from biosynthetically active tissues is taken up at various sites, particularly in cardiac and skeletal muscle. The rate of turnover of taurine in normal myocardium is extremely slow, with a half-life of approximately 15 days. Cardiac taurine levels are unchanged by a pyridoxine-deficient diet, fasting, or taurine loading; however, taurine concentrations rise in failing or hypertrophied myocardial tissue.
Loss of cardiac-muscle taurine has been demonstrated in left-ventricular tissue of anesthetized dogs in which ischemia was induced by occlusion of the coronary artery; in the absence of fibrosis, loss occurred as early as four hours after occlusion in one study and at 16 hours in another. In the family members in our study who were patients, however, there was no evidence of extramural or intramural narrowing of the coronary artery in the cardiac tissue in which myocardial taurine levels were depressed. Furthermore, there was no clinical evidence of ischemic heart disease in these patients.
On the other hand, studies in animals and one study of human myocardium at autopsy have both shown moderate to marked elevation of taurine levels in failing or hypertrophied hearts; this elevation was also present in the controls with cardiomyopathy in our study. However, family members with congestive cardiomyopathy had abnormally low levels of myocardial taurine in failing hearts. It therefore appears that at least some of these family members have an unusual combination of features: an absence of myocardial infarction in the presence of myocardial taurine levels that were abnormally low, particularly in comparison with levels found in other studies suggesting that myocardial taurine is elevated in congestive heart failure, perhaps as a compensatory positive inotropic mechanism.
Although a direct causal relation cannot yet be firmly established, it seems likely that in subjects described in this study, clinical and echocardiographic features of mitral-valve prolapse were produced by an early, localized cardiomyopathy in the papillary muscles that was associated with a depressed myocardial taurine concentration and eventual myocardial fibrosis. The congestive cardiomyopathy probably represents an extension of the local process to more or all of the remaining myocardium.
http://www.nejm.org/doi/full/10.1056/NEJM198101153040301#t=articleTop
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[Medicine / Chemistry / Biology ] - You gotta respect the marvelous biochemical-metabolic-genetic design intelligence of the human body*, in this example, using one equilibria system (ie. conjugate acid-base pair of Taurine) to control the pH gradient within mitochondria, in turn to shift the position of equilibrium thermodynamically favorably for a separate biochemical equilibria system : a redox equilibria (since the pH directly affects reduction and oxidation potentials as predicted by Le Chatelier's principle) between the NADH / NAD+ conjugate redox pair and the GSH / GSSG conjugate redox pair (ie. reduced and oxidized forms of the anti-oxidant Glutathione, the functional adequacy of which is in turn correlated with MTHFR gene polymorphisms), for the tricarboxylic acid cycle, the electron transport chain, the proton and electrical gradients and subsequent oxidative phosphorylation and ATP-production by ATP synthase (note : the formation of ATP from ADP and Pi by itself is endergonic, ie. thermodynamically unfeasible with a positive Gibbs free energy change, unless coupled during cellular respiration to the electrochemical gradient created by the difference in proton molarity across the mitochondrial membrane, making the overall coupled reaction exergonic, ie. thermodynamically feasible with a negative Gibbs free energy change.)
* Both the religious-inclined and the atheistic-inclined will no doubt seize upon such examples to egregiously claim rigorous support for each of their own Intelligent-Design-Creator-Creationism and Natural-Selection-Darwinism-Evolution beliefs respectively, but both would be equally inadequate, and would behoove a separate discussion for another day.
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"Taurine, glutathione and bioenergetics" by Hansen SH, Grunnet N.
Biochemistry textbook presentations of bioenergetics and mitochondrial function normally focus on the chemiosmotic theory with introduction of the tricarboxylic acid cycle and the electron transport chain, the proton and electrical gradients and subsequent oxidative phosphorylation and ATP-production by ATP synthase. The compound glutathione (GSH) is often mentioned in relation to mitochondrial function, primarily for a role as redox scavenger. Here we argue that its role as redox pair with oxidised glutathione (GSSG) is pivotal with regard to controlling the electrical or redox gradient across the mitochondrial inner-membrane. The very high concentration of taurine in oxidative tissue has recently led to discussions on the role of taurine in the mitochondria, e.g. with taurine acting as a pH buffer in the mitochondrial matrix. A very important consequence of the slightly alkaline pH is the fact that the NADH/NAD(+) redox pair can be brought in redox equilibrium with the GSH redox pair GSH/GSSG.An additional consequence of having GSH as redox buffer is the fact that from the pH dependence of its redox potential, it becomes possible to explain that the mitochondrial membrane potential has been observed to be independent of the matrix pH. Finally a simplified model for mitochondrial oxidation is presented with introduction of GSH as redox buffer to stabilise the electrical gradient, and taurine as pH buffer stabilising the pH gradient, but simultaneously establishing the equilibrium between the NADH/NAD(+) redox pair and the redox buffer pair GSH/GSSG.
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I've already made 2 posts on Taurine, a cautious case study in which Taurine didn't seem to help an extended family with their heart problems (but that does not mean Taurine wouldn't help other cases of heart disease, and in fact there is medical evidence that Taurine does help in most other cases of heart disease and congestive heart failure), as well as an optimistic case study in which Taurine helped a man with his migraines (when almost nothing else would), and I highlighted that case study as noteworthy because Taurine isn't well-known as a remedy for migraines, so it's certainly worth checking out for migraine sufferers. Most migraines appear to be linked to metabolic energy deficiencies, which is why supplementation of the various B vitamins (required for the various metabolic processes and cycles for energy production) have been medically proven to help migraines, and which is also why it makes sense that Taurine (involved in maintaining the pH and proton gradient in mitochondria for the synthesis of ATP), may also help migraines.
This will likely be my final post on Taurine (unless I've reason to update my views on it). As a concluding overview, the benefits of Taurine seem to far outweigh the cons, because Taurine appears to have a wide-range of health and medical benefits, and medical studies have shown no toxicity risk even from much higher daily dosages of Taurine than what you can get from daily supplementation. And you'll be glad to know Taurine is really cheap, at least compared to other anti-oxidants such as CoQ10 (especially the more expensive reduced Ubiquinol secondary alcohol form, rather than the cheaper oxidized Ubiquinone ketone form), and Glutathione (in which many people suffer from a genetic deficiency of, caused by rather common MTHFR or MethylFolate Reductase gene mutations and polymorphisms). So yeah, Taurine is really cheap, and works synergistically with other anti-oxidants such as vitamin C, CoQ10, Glutathione, etc.
Do your own research on Taurine, and decide for yourself if you want to give it a try. Wide-ranging benefits, with little or no toxicity risk (Taurine is naturally occurring in foods, and is the most abundant amino acid, technically amino-sulfonic acid, found in human body tissues due to it's important metabolic roles). And supplementation is really cheap, too. And if you (or any family or friend) are at risk of more serious (potentially fatal) heart diseases, including mitral valve prolapse, mitral valve regurgitation, congestive heart failure, etc, you'll be desperate to try anything that might help, and cheap Taurine has been medically shown to be safe and non-toxic. Enough said.
Benefits of Taurine :
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As John Tan puts it pithily, "Thousands Of Michigan Kids Poisoned Because They Don't Have PUB And PAP!"
Hundreds of thousands of Americans poisoned with permanent brain damage due to high levels of lead in city's drinking water gone undetected for decades.
https://www.yahoo.com/news/lead-flints-water-linked-decline-birth-rate-study-finds-224123699.html
Did you know... the Mad Hatter character from "Alice In Wonderland" is based on the tragic real-life cases of millions of people gone mad (ie. permanent brain damage) from wearing and/or producing hats, poisoned by mercury used in the manufacturing process of the hats, gone undiagnosed for several centuries!
https://en.wikipedia.org/wiki/Mad_hatter_disease
A BedokFunland JC H2 Chemistry Question :
1. Explain why or how heavy metals cause toxicity in the human body (there are several modalities, use any modality you're familiar with, and/or from the H2 Chemistry and/or H2 Biology syllabus). Include relevant equations and/or diagrams in your answer.
2. State the medical treatment for heavy metal poisoning, eg. lead poisoning, explain why or how this medical treatment works. Include relevant equations and/or diagrams in your answer.
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A BedokFunland JC Original H2 Chemistry Challenge
The thermal decomposition of ammonium sulfate(VI) generates 3 gases as the only products. Draw out the full curved-arrow reaction mechanisms for both the forward and backward reactions. Explain how the changes in enthalpy and entropy pull the reaction into opposite directions (specify the directions), and concordantly, explain how temperature therefore controls the position of equilibrium as predicted by the two relevant Gibbs free energy formulae : one relating Gibbs free energy change to enthalpy and entropy changes, the other relating Gibbs free energy change to equilibrium.
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^_^
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Hey UltimaOnline,
How do you rate PJC's 2017 Chemistry Prelim Paper Difficulty?Is it easy,comparable or slightly difficult as compared to A levels?
I compared my school paper with AJC 2017 Prelim and difficulty is more or less on par.However results wise is drastically different.PJC has 20 students out of 432 attaining As(a dip from 31 in mid years) whereas AJC has only 3 students attaining A(improved from 0As in MYCT) this year.
For me i feel that my school paper is comparable and may be a bit trickier than A levels,otherwise a rather doable paper.Just wanna hear your comments so at least I have a general sensing so at least i know what else to prepare myself for.
P.S. I still got my A for chem,amidst a ton of careless mistakes.
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Actually truth be told, I don't yet have the 2017 Prelim Papers for now, so no comments on the relative difficulties of the PJC and AJC 2017 papers, and/or compared to the expected A level standard.
Congrats on your own A grade (before or after bell-curve moderation, if any?), you're certainly on track to get A grade for A levels.
What are the main reasons, in your opinion, for the dramatic difference between the PJC and AJC students performance (ie. no. of A graders), despite similar Prelim paper difficulties. Do you attribute it mostly to the difference in student cohort competence, or to unreasonable marking by AJC teachers, or to the different bell curves applied, etc?
Originally posted by MapPwner:Hey UltimaOnline,
How do you rate PJC's 2017 Chemistry Prelim Paper Difficulty?Is it easy,comparable or slightly difficult as compared to A levels?
I compared my school paper with AJC 2017 Prelim and difficulty is more or less on par.However results wise is drastically different.PJC has 20 students out of 432 attaining As(a dip from 31 in mid years) whereas AJC has only 3 students attaining A(improved from 0As in MYCT) this year.
For me i feel that my school paper is comparable and may be a bit trickier than A levels,otherwise a rather doable paper.Just wanna hear your comments so at least I have a general sensing so at least i know what else to prepare myself for.
P.S. I still got my A for chem,amidst a ton of careless mistakes.
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Nope no moderations were taken into account for grade determination for both my school and AJC.
My friend messaged me out of nowhere and said that his school paper difficulty were rather comparable to my school,but results show otherwise.Our paper had similar scores in certain areas,such as 28-30/55 being the average score for practical paper in the cohort and other papers too.
So probably maybe AJC teachers marked stricter?I also felt my school teachers marked stricter as i wasn't awarded a mark for expressing +6 Manganese oxidation state as [Ar]3d^1 as i need to write out the 'full' electronic configuration(although qn never implied that).I also questioned the mark scheme on a later question that also just used [Ar] as a short term in electronic configuration to account for differences in ionisation energy between 2 elements,but my teacher just said in this part is not important as the main point is I.E.
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Originally posted by MapPwner:
Nope no moderations were taken into account for grade determination for both my school and AJC.
My friend messaged me out of nowhere and said that his school paper difficulty were rather comparable to my school,but results show otherwise.Our paper had similar scores in certain areas,such as 28-30/55 being the average score for practical paper in the cohort and other papers too.
So probably maybe AJC teachers marked stricter?I also felt my school teachers marked stricter as i wasn't awarded a mark for expressing +6 Manganese oxidation state as [Ar]3d^1 as i need to write out the 'full' electronic configuration(although qn never implied that).I also questioned the mark scheme on a later question that also just used [Ar] as a short term in electronic configuration to account for differences in ionisation energy between 2 elements,but my teacher just said in this part is not important as the main point is I.E.
Yeah, JC teachers are anal like that. Cambridge is more reasonable, and the question would specify 'full' electronic configuration if such was required.If there are any other specific questions (from any JC's 2017 prelim paper) that you would like to share to discuss, eg. if you felt it was particularly challenging, you don't fully agree with the given mark scheme, etc, feel free to post the question and answer here (you'll have to post a photo of the question and mark scheme, because myself and also most JC students wouldn't yet have all the other JCs' 2017 prelim papers at this point in time)..
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It took only a few seconds for 2 drops of dimethylmercury which accidentally fell on her latext gloved hand to be absorbed into her skin, but these 2 drops of dimethylmercury took its time to kill her slowly and painfully over 11 months before she finally died.
https://en.wikipedia.org/wiki/Karen_Wetterhahn#Accident_and_death
https://en.wikipedia.org/wiki/Dimethylmercury
Dimethylmercury is formed by treating sodium amalgam with methyl halides :
Hg + 2 Na + 2 CH3I → Hg(CH3)2 + 2 NaI
Dimethylmercury can also be obtained by alkylation of mercuric chloride with methyllithium :
HgCl2 + 2 LiCH3 → Hg(CH3)2 + 2 LiCl
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A couple of BedokFunland JC Original H2 Chemistry Questions :
Q1. For the two synthesis methods described above, one involves an ionic mechanism, the other a free radical mechanism. Deduce, with reasons, which is which. Draw out the full curved-arrow electron-flow reaction mechanisms for both synthesis methods. In your mechanism structures (for both reactants and products, for both synthesis methods), label the oxidation states for all the Hg and C atoms.
Q2. Write out the full electron configuration of Hg, Hg+ and Hg2+. Mercury is a d-block metal, but is it a transition metal? Explain your answer. Suggest the bond angles and hybridized orbitals (of both the C and Hg atoms) involved in forming each sigma bond in dimethylmercury, and explain your answer.
Q3. "Dimethylmercury is metabolized after several days to methylmercury. Methylmercury crosses the blood–brain barrier easily owing to formation of a complex with cysteine." There are two possible positional isomers (both of which exhibit enantiomerism) for this complex, in which the Hg atom can be either coordinated to the S or to the O atom. Draw the structure of both isomeric complexes (labeling chiral atoms with an asterisk). Suggest which isomer crosses the blood–brain barrier more readily, and explain your answer.
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A BedokFunland JC Original H2 Chemistry Challenge
It can be observed that iron structures rust more rapidly when exposed to sea-spray, ie. iron rusts more rapidly when in contact with salt water, compared to pure water. If you ask around or look this up on the internet, the 'answers' you'll find simply say, "that's because salt water is a better conductor of electricity compared to pure water".
While the statement states the obvious regarding electrical conductivity, it does NOT explain the faster rate of rusting, which principally involves the oxidation of iron and the reduction of oxygen gas (occurring in several steps, involving several different redox equations; and if you research deeper beyond A levels, involves acid-base equilibria, solubility equilibria, coordination complex equilibria, and dehydration equilibria as well).
Fact is, it's a safe bet that almost all of the people on the internet (however well-intended they may be, bless their souls) who gave the abovementioned 'answer' on the internet, that "salt water is a better conductor of electricity compared to pure water", don't actually correctly understand how salt water speeds up rusting. Most 'answers' on the internet give no further elaboration (because they don't actually know the answer and are 'smoking' their way through), while a few imply (erroneously!) either that the salt water itself can help to carry the electrons (from the iron being oxidized to the oxygen gas being reduced), or suggest (erroneously!) that the salt ions present eg. Na+(aq) and Cl-(aq), help to 'temporarily accept and carry' the electrons (from the iron being oxidized to the oxygen gas being reduced), machiam or as if these ions were a chemical catalyst.
Neither of these ideas are correct, since salt water conducts electricity in the form of mobile ions rather than mobile electrons; and based on redox potentials (even considering non-standard molarities in sea water), neither Na+(aq) or Cl-(aq) (or for that matter, almost all of the other ions present in sea water) can be reduced in aqueous conditions to 'temporarily accept and carry' the electrons (from the iron being oxidized to the oxygen gas being reduced).
My BedokFunland JC H2 Chemistry Challenge for you is : Explain the correct mechanism by which salt water speeds up the rusting of iron.
Remember, just writing, "that's because salt water is a better conductor of electricity compared to pure water" in the A level exams should Cambridge ask you this question, will only cause the Cambridge marker to roll eyes and expose your epic-fail attempt at 'smoking' (which is hazardous to your health and grades), and earn you a big fat zero mark.
As with all my BedokFunland JC questions and challenges, I won't reveal the correct answer here. My BedokFunland JC students can ask me during tuition, and all other students can go ask your school teacher or private tutor. Usually I would say, "you can post your attempted answer here, and I'll tell you if you got it correct", but in this case, I will instead say, if you're sure you know the correct answer, DON'T post it here and ruin the fun for others! *insert sadistic laughter*
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A BedokFunland JC Original H2 Chemistry Challenge
Considering only the 1st proton dissociation (ie. regardless of proticity), ie. magnitude of Ka1 value, H2SO4 is a stronger acid compared to H2SO3, just as HNO3 is a stronger acid compared to HNO2, which is indeed expected and concordant to the general trend of acidic strength in any given series of oxoacids. However, bucking the trend are the oxoacids of phosphorus, in which H3PO3 is actually a stronger acid compared to H3PO4. There are actually 2 independent reasons for this unusual behavior, the combined effect of both, outweighs the expected general trend for oxoacid families (I assume you know how to explain the much easier within-H2-Chemistry-syllabus question of why H2SO4 is stronger than H2SO3, and why HNO3 is stronger than HNO2... do you?).
My BedokFunland JC Challenge for you, of course, is : Explain why H3PO3 is a stronger acid compared to H3PO4.
If you can correctly explain just 1 of the 2 reasons, you're already beyond A grade Distinction level (because even 99% of A graders can't solve this challenge question). If you can correctly explain both of the 2 reasons, you're BedokFunland JC level.
As with all my BedokFunland JC challenge questions, I won't reveal the correct answers here. My BedokFunland JC students can ask me during tuition, and all other students can go ask your school teacher or private tutor.
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Can I ask a question regarding the 2017 A level H2 Chemistry Specimen Paper 2 Question 6(i),which involves formation of FAME from reaction between a fatty acid,RCO2H,and diazomethane,CH2N2.
Reaction occurs via two step mechanism:
-The fatty acid reacts with diazomethane to form a carboxylate ion intermediate in the first step.
-N2 is formed in the second step
Suggest the mechanism for this reaction.(4 marks)
Am i right to say that in the first step of the mechanism,CH2N2 deprotonates RCO2H to form RCOO- and CH3N2 respectively?And then subsequently the C-N bond in CH3N2 breaks and the bond pair is donated to positive charged N atom to form N2,before the RCOO- attacks the CH3 thingy to form RCO2CH3?
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Originally posted by MapPwner:
Can I ask a question regarding the 2017 A level H2 Chemistry Specimen Paper 2 Question 6(i),which involves formation of FAME from reaction between a fatty acid,RCO2H,and diazomethane,CH2N2.
Reaction occurs via two step mechanism:
-The fatty acid reacts with diazomethane to form a carboxylate ion intermediate in the first step.
-N2 is formed in the second step
Suggest the mechanism for this reaction.(4 marks)
Am i right to say that in the first step of the mechanism,CH2N2 deprotonates RCO2H to form RCOO- and CH3N2 respectively?And then subsequently the C-N bond in CH3N2 breaks and the bond pair is donated to positive charged N atom to form N2,before the RCOO- attacks the CH3 thingy to form RCO2CH3?
Almost correct, but your described mechanism would be 3 steps, when Cambridge already specified 2 steps. The reason for this is the instability of the methyl carbocation, which is why the next step (after the proton transfer) is SN2, not SN1. Ideally, for the student to demonstrate a correct understanding of this reaction, both resonance contributors of diazomethane should be drawn, with the student showing to Cambridge that he/she knows which resonance contributor more appropriately functions as the Bronsted-Lowry base in the 1st step of the reaction mechanism. -
I love Chem
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Originally posted by UltimaOnline:
Almost correct, but your described mechanism would be 3 steps, when Cambridge already specified 2 steps. The reason for this is the instability of the methyl carbocation, which is why the next step (after the proton transfer) is SN2, not SN1. Ideally, for the student to demonstrate a correct understanding of this reaction, both resonance contributors of diazomethane should be drawn, with the student showing to Cambridge that he/she knows which resonance contributor more appropriately functions as the Bronsted-Lowry base in the 1st step of the reaction mechanism.So first step is correct right?
Yep the 2nd step what u mentioned was what i exactly drawn(if im not wrong),whereby as the carboxylate ion attacks the c bonded to 3 H atoms and positively charged N atom,the C-N positively charged atom also breaks at the same time to eventually give N2 at the end of the step.Maybe what i said may be ambiguous/super unclear,as i said 'before' coo- attacks,meant the bond forming and bond breaking reaction was simultaneous
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Also,with regards to qn 6(h) other question subparts,can i state the following as the answers?:
(i):ICl reacts with alkenes faster as the difference in electronegativites between I and Cl establishes a net dipole moment from I to Cl,resulting in the C=C bond in alkene to break and attack iodine which has a larger partial positive charge.Pure halogens are made up of the same atoms and have no net dipole moment due to same electronegativities.
(ii)Yes,i agree with the student's proposal.
Amt of wijs:0.1x(18/1000)=0.0018mol
Calc of no of C=C bonds in fatty acids:
cervonic:0.0018/ 0.1/328 =5.904 =6 C=C bonds(nearest number)
Stearidonic:0.0018 / 0.1/276=4.968=5 C=C bonds(nearest number)
Likewise for timnodonic too.
Since the calculations show the number of moles of C=C bonds calculated to be near to the actual C=C bonds in the compounds,the student's proposal is valid.
(iii)I didn't really get the purpose of determining molar mass per mole of C=C for fatty acids and unknown,so i merely used my method of determining the no of c=c bonds based on calc for each fatty acid(5.2,4.8,4.4 respectively),before averaging the 3 numbers to get 4.8,which is closest to 5 and thus identifying it as timnodonic acid.Given this was a 3 mark question,how much will i end up getting?
Other parts of the chem p2 specimen paper are considered relatively straightforward and doable for me(even though there may be 1-2 sub qns i cant answer,its because i never revised that particular part present in my notes as i forgotten about it).
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Originally posted by MapPwner:
Also,with regards to qn 6(h) other question subparts,can i state the following as the answers?:
(i):ICl reacts with alkenes faster as the difference in electronegativites between I and Cl establishes a net dipole moment from I to Cl,resulting in the C=C bond in alkene to break and attack iodine which has a larger partial positive charge.Pure halogens are made up of the same atoms and have no net dipole moment due to same electronegativities.
(ii)Yes,i agree with the student's proposal.
Amt of wijs:0.1x(18/1000)=0.0018mol
Calc of no of C=C bonds in fatty acids:
cervonic:0.0018/ 0.1/328 =5.904 =6 C=C bonds(nearest number)
Stearidonic:0.0018 / 0.1/276=4.968=5 C=C bonds(nearest number)
Likewise for timnodonic too.
Since the calculations show the number of moles of C=C bonds calculated to be near to the actual C=C bonds in the compounds,the student's proposal is valid.
(iii)I didn't really get the purpose of determining molar mass per mole of C=C for fatty acids and unknown,so i merely used my method of determining the no of c=c bonds based on calc for each fatty acid(5.2,4.8,4.4 respectively),before averaging the 3 numbers to get 4.8,which is closest to 5 and thus identifying it as timnodonic acid.Given this was a 3 mark question,how much will i end up getting?
Other parts of the chem p2 specimen paper are considered relatively straightforward and doable for me(even though there may be 1-2 sub qns i cant answer,its because i never revised that particular part present in my notes as i forgotten about it).
Um u can ignore my query,as my school already uploaded the chem specimen p2 answers and after checking my answers my doubts are clarified already.
After checking I have lost approximately 12-15 marks total.
The difficulty of the paper is considered normal right?
