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    99 slides on fractures and their fixation yesterday :drool: I'm sure FFCrusader can attest to the fact that I was more than a little bit excited
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    Found out my SSC choices today: Accelerated learning and human dissection: limbs

    I get to power nap and cut up dead people :awesome:


    Also I told myself that now FunMed is gone forever (or until next year? :afraid:) that I would actually pay attention in lectures and make notes.

    Day two of CR and already fallen asleep with a massive hangover (I'm old now :sigh:) but at least I turned up to PBL :king1:
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    (Original post by Penguinsaysquack)
    Day two of CR and already fallen asleep with a massive hangover (I'm old now :sigh:) but at least I turned up to PBL :king1:
    Hahaha, well done!

    We have exams in like 2 week's time and whenever I think about how much I have to learn by then I feel a bit sick. Overwhelmed is not the word. Arrrrgggghhhhh.
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    (Original post by DexterM)
    Hahaha, well done!

    We have exams in like 2 week's time and whenever I think about how much I have to learn by then I feel a bit sick. Overwhelmed is not the word. Arrrrgggghhhhh.
    My end of semester exams and OSCEs aren't until after christmas. We've had a few formatives so far though.

    Plus side, more time to revise. Downside, revising over christmas.
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    (Original post by DexterM)
    Hahaha, well done!

    We have exams in like 2 week's time and whenever I think about how much I have to learn by then I feel a bit sick. Overwhelmed is not the word. Arrrrgggghhhhh.
    Where do you study again?

    You'll be fine though, good luck for then
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    (Original post by Wangers)
    We did Porphyrias the other week, and glycogen storage diseases. It's like a molecular orgasm...you would have loved it.
    sounds good, all nice conditions scientifically as well as clinically, i bet i would haha.

    righty ho, essay all packaged off so time for a bit of metabolism haha.

    (Original post by RollerBall)
    Is regulation not going to be something fairly simple? As in glucose is high so you release insulin which encourages glucose into the cells to become fat in fats or glycogen in the liver/muscles? Then when blood glucose is the low the opposite happens with glycagon? When you've depleted glycogen stores then you start to break down fatty acids into ketogenesis using glycerol to make glucose to maintain blood glucose levels?
    regulation is by far the most complex and important aspect of understanding metabolism. Individual reactions are meaningless, if all you know are the regulated steps and how they are regulated then you've got all that's important (medically) out of it. insulin does indeed promote conversion of glucose into fatty acids in liver and glycogen in the various tissues with capacity for synthesis but it is also important in it's other growth/mitotic signalling which all occurs in the context of its role in metabolic regulation. Insulin is the only hormone in the body that signals 'times of plenty' vs the myriad of others that signal the opposite such as the glucocorticoids, catecholamines etc. okay regarding the 'opposite' happening that just isn't the case. insulin acts on all tissues to promote different things but the only human tissue with metabolically significant quantities of the glucagon receptor is hepatocytes (some more than others) so the effects are much more concentrated. ketogenesis kicks up as soon as gluconeogensis does (you can explain mechanistically), liver stores of glycogen last literally a few hours then its all gone so it's only useful during hyperacute starvation responses. i am unsure of your love of glycerol, it's actually not a very significant gluconeogenic substrate whatever anyone else may say, by far the most important are alanine (generated by the glucose-alanine cycle) and lactate (generated by the Cori cycle) which will become much more obvious when you start linking different fuels and tissues together. if you consider the rate of fat breakdown vs. the rate of glucose turnover by active muscles the difference should become apparent. that said it probably does play a slightly bigger role during chronic starvation but the odd-chain fatty acids (terminating in propanoyl-CoA) also provide an even larger GNG substrate.

    (Original post by RollerBall)
    My basic understanding of it is as follows:

    Blood glucose is high so enters cells via insulin release I outlined before. Cells use glucose to maintain ATP via glycolysis/TCA/ETC/O.P, excess is turned into glycogen via glycogenisis. Blood glucose is also uptaken by adipocytes and made into fatty acids via glycolysis to produce acetyl CoA then making that into fatty acids.
    via insulin mediated GLUT4 insertion you mean? okay, we did plants in a previous exchange now we're onto rat biochemistry - quite the tour of biology! In man adipocytes are not significant synthetic organs of fatty acids, it's almost all done by the liver.

    (Original post by RollerBall)
    When blood glucose goes low you first use glucose in the blood until it reaches a level when glycogen stores are used up. First in the local area and then glycogen stores are broken down by the liver and glucose is released into the blood to be used by other cells. When glycogen stores are used up gluconeogenesis is intitated by the liver to make amino acids into glucose and glycerol. Fatty acids are also broken down to produce acetyl CoA and further fuel TCA cycle. However, acetyl CoA cannot undergo glyconeogenesis as it's gone past the pyruvate stage. Therefore eventually you start to really run your glucose stores down low and you start to use mass amounts of fatty acids/amino acids to fuel tissues leading to breaking down of fat stores and muscle. This overloads the TCA cycle (particually with oxoacatate being used in glyconeogensis to maintain brain etc) and leads to ketogenesis to.

    How am I doing?
    err getting there. blood glucose remains virtually constant (unless concurrent pathology) all the time, if what you put there were the case there would presumably be some point between glycogen stores finishing and GNG kicking in fully that would kill you. glycogen release occurs very quickly but fat breakdown, GNG and ketogenesis (which happen at the same time) rolls into action simultaneously with only a very short latency. presuming you havent just eaten the use of amino acids as GNG substrate is not general acutely, only certain amino acids (e.g. alanine) are key substrate until chronic starvation in which muscle begins to break down and unleash more of the others. don't forget some tissues can never use some fuels so there is a requirement for glucose (e.g. RBCs) and fatty acids (e.g. cardiac myocytes) at all times so it is essential to produce both fat breakdown and GNG. fat breakdown occurs far earlier than muscle breakdown and this is reflected in the mechanisms by which hormone cause them to happen (which hormones?). as far as you need to worry the OAA thing is only in the liver which is the primary ketogenic organ. ketones are essential to happen simultaneously with GNG as they allow tissues which cannot normally use fatty acids (such as the brain) to use a simpler 'prepackaged' fatty fuel which partly relieves the drain on blood glucose depletion which even maximum GNG would be unable to maintain without the aid of glycogen (which is rapidly lost) hence why individuals with IEMs of ketogenesis or fatty acid breakdown are so stuffed and love to hypo and die.
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    (Original post by John Locke)
    regulation is by far the most complex and important aspect of understanding metabolism. Individual reactions are meaningless, if all you know are the regulated steps and how they are regulated then you've got all that's important (medically) out of it. insulin does indeed promote conversion of glucose into fatty acids in liver and glycogen in the various tissues with capacity for synthesis but it is also important in it's other growth/mitotic signalling which all occurs in the context of its role in metabolic regulation. Insulin is the only hormone in the body that signals 'times of plenty' vs the myriad of others that signal the opposite such as the glucocorticoids, catecholamines etc. okay regarding the 'opposite' happening that just isn't the case. insulin acts on all tissues to promote different things but the only human tissue with metabolically significant quantities of the glucagon receptor is hepatocytes (some more than others) so the effects are much more concentrated. ketogenesis kicks up as soon as gluconeogensis does (you can explain mechanistically), liver stores of glycogen last literally a few hours then its all gone so it's only useful during hyperacute starvation responses. i am unsure of your love of glycerol, it's actually not a very significant gluconeogenic substrate whatever anyone else may say, by far the most important are alanine (generated by the glucose-alanine cycle) and lactate (generated by the Cori cycle) which will become much more obvious when you start linking different fuels and tissues together. if you consider the rate of fat breakdown vs. the rate of glucose turnover by active muscles the difference should become apparent. that said it probably does play a slightly bigger role during chronic starvation but the odd-chain fatty acids (terminating in propanoyl-CoA) also provide an even larger GNG substrate.
    I have another PBL on the action of insulin based on a diabetic ketoacidosis. I've also got a lecture handout to go through.

    via insulin mediated GLUT4 insertion you mean? okay, we did plants in a previous exchange now we're onto rat biochemistry - quite the tour of biology! In man adipocytes are not significant synthetic organs of fatty acids, it's almost all done by the liver.
    We've been taught that glucose is taken up into muscles and fat cells via insulin mediated GLUT4 . I always thought it was a bit random though as I wasn't exaclty sure what they would do with it. The only logical explanation I could think of was convert it to acetyl CoA via glucolysis and then convert it to fatty acids via lipidgenesis but it seemed a bit odd.

    [/quote]
    err getting there. blood glucose remains virtually constant (unless concurrent pathology) all the time, if what you put there were the case there would presumably be some point between glycogen stores finishing and GNG kicking in fully that would kill you. glycogen release occurs very quickly but fat breakdown, GNG and ketogenesis (which happen at the same time) rolls into action simultaneously with only a very short latency. presuming you havent just eaten the use of amino acids as GNG substrate is not general acutely, only certain amino acids (e.g. alanine) are key substrate until chronic starvation in which muscle begins to break down and unleash more of the others. don't forget some tissues can never use some fuels so there is a requirement for glucose (e.g. RBCs) and fatty acids (e.g. cardiac myocytes) at all times so it is essential to produce both fat breakdown and GNG. fat breakdown occurs far earlier than muscle breakdown and this is reflected in the mechanisms by which hormone cause them to happen (which hormones?). as far as you need to worry the OAA thing is only in the liver which is the primary ketogenic organ. ketones are essential to happen simultaneously with GNG as they allow tissues which cannot normally use fatty acids (such as the brain) to use a simpler 'prepackaged' fatty fuel which partly relieves the drain on blood glucose depletion which even maximum GNG would be unable to maintain without the aid of glycogen (which is rapidly lost) hence why individuals with IEMs of ketogenesis or fatty acid breakdown are so stuffed and love to hypo and die.[/QUOTE]

    Okay, so replace high and low with slight increases or decreases in blood glucose

    So it goes more like:
    1. Glucose after a meal
    2. Glycogen stores break down
    3. GNG (Odd chain fatty acid breakdown, alanine, glycerol), fatty acid break down (Acetyl CoA + glycerol) and ketogenesis (due to excess acetyl CoA from fatty acid breakdown)
    4. Amino acid break down from muscles


    This would be sort of a timeline of starvation?

    Not sure where the lactate is coming from, why would you undergo anaerobic respiration in hunger?
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    (Original post by Becca-Sarah)
    99 slides on fractures and their fixation yesterday :drool: I'm sure FFCrusader can attest to the fact that I was more than a little bit excited
    It was like Christmas for you, but better. :p:

    :ahee:

    Please rate some other members before rating this member again.
    :bebored:
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    (Original post by Penguinsaysquack)
    Also I told myself that now FunMed is gone forever (or until next year? :afraid:) that I would actually pay attention in lectures and make notes.

    Day two of CR and already fallen asleep with a massive hangover (I'm old now :sigh:) but at least I turned up to PBL :king1:
    Until May exams
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    (Original post by Becca-Sarah)
    99 slides on fractures and their fixation yesterday :drool: I'm sure FFCrusader can attest to the fact that I was more than a little bit excited
    Did they have to mop the floor afterwards?
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    On the plus side, this strike gives me a day off tomorrow i.e. a night out tonight :yy:
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    (Original post by lekky)
    On the plus side, this strike gives me a day off i.e. a night out tonight :yy:
    Jealousy. :unimpressed:
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    (Original post by Penguinsaysquack)
    Found out my SSC choices today: Accelerated learning and human dissection: limbs
    Problem being limbs are the most dull, tedious, monotonous things to learn about ever.
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    (Original post by Kinkerz)
    Problem being limbs are the most dull, tedious, monotonous things to learn about ever.
    Oh :sad:
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    Just got introduced to SSC today. Posters and cutting out paper and crayons and group-gluing.

    I thought I escaped that when I left school. :lolwut:
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    Got my next SSC last week. Analysis of drug adverts
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    Lecture today on the realities of choosing a specialty. **** how soon we have to decide. I want te old system where you could postpone a little longer.

    I also rather disliked the Realities of the improving quality paperwork and that soft stuff which I apparently have to do a report on next term (debating how much fun I can have by finding something totally trivial to report on)

    Seriously trying to work out if it is feasible to escape this by leaving the sodding country.
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    (Original post by RollerBall)
    I have another PBL on the action of insulin based on a diabetic ketoacidosis. I've also got a lecture handout to go through.
    okay, very jealous as discussing insulin signalling is a fantastic way to spend an hour haha!



    (Original post by RollerBall)
    We've been taught that glucose is taken up into muscles and fat cells via insulin mediated GLUT4 . I always thought it was a bit random though as I wasn't exaclty sure what they would do with it. The only logical explanation I could think of was convert it to acetyl CoA via glucolysis and then convert it to fatty acids via lipidgenesis but it seemed a bit odd.
    it probably does but it's not significant, in rats though it is one of the main ways they de novo synthesise FAs/TAGs and if you're taught by pure biochemists they might not make such a clarification.


    (Original post by RollerBall)
    Okay, so replace high and low with slight increases or decreases in blood glucose

    So it goes more like:
    1. Glucose after a meal
    2. Glycogen stores break down
    3. GNG (Odd chain fatty acid breakdown, alanine, glycerol), fatty acid break down (Acetyl CoA + glycerol) and ketogenesis (due to excess acetyl CoA from fatty acid breakdown)
    4. Amino acid break down from muscles


    This would be sort of a timeline of starvation?

    Not sure where the lactate is coming from, why would you undergo anaerobic respiration in hunger?
    fatty acid breakdown in adipose into non-esterified (free) fatty acids and glycerol into the blood. otherwise that is generally a fair list, although it's a continuum and never happens so discretely of course. now you can strive to explain on a neuro-hormonal and cellular level why and how each of those occur .

    lactate is more important in excersise.
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    (Original post by Oggz)
    ...
    Why do you keep spending your worthless neg rep on me? 3 times now in 4 months? That must take effort to be regularly dishing out the rep to do that but you don't even get to write a fun mean comment with it anymore & I have no idea who you are. :bird:
    Are you trying to provoke people to neg you back to be ‘cool’ collecting red gems?
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    (Original post by Elles)
    Why do you keep spending your worthless neg rep on me? 3 times now in 4 months? That must take effort to be regularly dishing out the rep to do that but you don't even get to write a fun mean comment with it anymore & I have no idea who you are. :bird:
    Are you trying to provoke people to neg you back to be ‘cool’ collecting red gems?
    He just did the exact same thing to me :rolleyes:
 
 
 
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