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    Bye bye possiblity of revision over Christmas. Hello Minecraft server hosted on my machine.
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    (Original post by Fission_Mailed)
    Bye bye possiblity of revision over Christmas. Hello Minecraft server hosted on my machine.
    amazing!
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    (Original post by John Locke)
    there are certain amino acids which will come up time and time again that you should know the 'pathways' (1 step) of e.g. glutamate, alanine etc for reasons which should be clear once you have done whole organism amino acid metabolism (as AA in particular is impossible to understand based on just the reactions going on in a single cell). also note by intermediates you mean intermediates of the 'final common pathway' yeah?
    Yeah, when I say intermediates I mean bits in the TCR cycle. I've got a picture in my notes of all the different amino acid pathways which I'll learn a couple off.

    okay, it's impossible to understand any of the reactions without understanding their regulation at all so presumably you have done a bit of this at the level of the cell (cf. phosphofructokinase or pyruvate dehydrogenase?) and then there is the additional layer of what happens in a whole person in different tissues under fed conditions for each type of substrate and then the additional additional layer of the whole organism starvation response. okay, proof by counterexample; erythrocytes - how do they produce energy? unfortunately that's a bit of a misunderstanding. in the fed state and during the acute starvation response the brain relies almost exclusively on glucose as a metabolic substrate, it takes a few days for it to be able to switch to utilising ketones after which is can manly, but not exclusively, rely on those as substrate (we're now in the chronic starvation response). if what you were suggesting was the case then why would hypoglycemia, effective or absolute, cause coma? although that said that's a bit more complicated but certainly one way to think about it.
    I've literally done none of the regulation. At least nothing you've mentioned. I've just learnt the pathways as in like Glucose -> G6P via hexakinase etc. You've kind of thrown a curveball into my understanding with the whole coma thing. Why does it take a while to switch to utilising ketones?


    okay, you need to think what questions you need to ask to be able to understand the reason. start with; how do we maintain plasma [glucose] and why is this important? why if i deplete you of almost all of your glycogen stores by making you run a marathon do i still see the ever faithful ~5mM? okay put it this way, cells have a finite possible [ATP] dictating by the amount of A that they create yeah? it may or may not surprise you that actually the cellular [ATP] is almost perfectly constant in all cells regardless of the activity they are producing (cf. resting SkM vs fully active tickets-to-the-gun-show SkM). how? because the metabolic coupling of activity to substrate utilisation is so incredibly good and regulated in a way that amplifies the sensitivity of the system. so there is basically never a capacity for a cell to produce any more ATP than it already has. there are only 2 places that gluconeogenesis can occur in the body (at least of significance) although almost certainly the only one you need to know about is the liver, king/queen of metabolism and as such one of John Locke's top organs. under normal physiological circumstances the liver is a net glucose exporter and once you explain why that is important (cf. above question) you will begin to see why it's such a bloody useful pathway to have, an understanding that will be reenforced when you come to the (hyper) acute and chronic starvation responses. also it brings me back to which 2 tissues actually have the important stores of glycogen? only 1 of them can use GNG so the reason you suggested cannot be true. think about your ketogenesis you learnt, link the livers role there with this and the pieces should start to come together?
    Uh, if you made me run a marathon I'm not entirely sure. Over the first four (I think) hours my glycogen liver stores would keep me going and then would I switch to fat metabolism, the breakdown of glycerol to glucose and fatty acids into acetyl CoA (probably leading to ketogenesis though)?

    I know gluconeogenesis only occures in the liver (it's my standard default organ for anything in metabolism I get stuck on too ). So it stacks up enough ATP for it's own metabolic needs then any extra turns into glucose for other cells? Where would it come from though, excess breakdown of glucose in the first time? Glycerol? Why would it not make it into glycogen? Can only muscle tissues convert glycogen to glucose?

    im not sure how useful i am being, i could just literally tell you the answers but i don't think it would add much to your understanding or make you very likely to retain the, clinically important , information for any length of time. However if you'd rather have short answers do say and i will . bit of a beast to explain here tbh, needs lots of time, paper and proper talking unfortunately! it will make sense at the end though, you need to have covered it all to fit the jigsaw together but it will come promise!
    Bits and bobs. Somethings just confuse me further though. Our metabolism teaching is incredibly poor unfortunately. They don't put lecture slides up either but instead lecture "notes". Learning from somebody elses notes is not useful though.
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    (Original post by RollerBall)
    Yeah, when I say intermediates I mean bits in the TCR cycle. I've got a picture in my notes of all the different amino acid pathways which I'll learn a couple off.



    I've literally done none of the regulation. At least nothing you've mentioned. I've just learnt the pathways as in like Glucose -> G6P via hexakinase etc. You've kind of thrown a curveball into my understanding with the whole coma thing. Why does it take a while to switch to utilising ketones?



    Uh, if you made me run a marathon I'm not entirely sure. Over the first four (I think) hours my glycogen liver stores would keep me going and then would I switch to fat metabolism, the breakdown of glycerol to glucose and fatty acids into acetyl CoA (probably leading to ketogenesis though)?

    I know gluconeogenesis only occures in the liver (it's my standard default organ for anything in metabolism I get stuck on too ). So it stacks up enough ATP for it's own metabolic needs then any extra turns into glucose for other cells? Where would it come from though, excess breakdown of glucose in the first time? Glycerol? Why would it not make it into glycogen? Can only muscle tissues convert glycogen to glucose?



    Bits and bobs. Somethings just confuse me further though. Our metabolism teaching is incredibly poor unfortunately. They don't put lecture slides up either but instead lecture "notes". Learning from somebody elses notes is not useful though.
    I know Im trying to join this way way to late.

    Im assuming you have gone through the regulation of blood glucose as well as the intracellular signaling of insulin and glucagon/Cortisol/adrenaline/Growth Hormone?

    Because trying to understand the pathways without the overall picture or the reasons for its necessity will make them far more confusing.

    I always try to relate the mechanism to hyper or hypoglycemia and then T1/T2 DM, it makes it far easier to remember.
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    (Original post by carcinoma)
    I know Im trying to join this way way to late.

    Im assuming you have gone through the regulation of blood glucose as well as the intracellular signaling of insulin and glucagon/Cortisol/adrenaline/Growth Hormone?

    Because trying to understand the pathways without the overall picture or the reasons for its necessity will make them far more confusing.

    I always try to relate the mechanism to hyper or hypoglycemia and then T1/T2 DM, it makes it far easier to remember.
    Insulin is the next PBL. I know it's breif mechanics though.

    Glucose in the blood enters liver via glut2, leads to glucolysis and rising ATP. ATP closes K+ channels, cell becomes negative, voltage gated channels open and Ca+ moves in. Ca+ leads to exocytosis of insulin. Insulin binds to insulin receptors on muscle and adipose tissues moving glut4 receptors to the surface and increasing uptake of glucose.

    Glycagon causes breakdown of glycogen and fats to bring up blood glucose but my knowledge of that is a lot more sketchy. Have no idea about GH/cotrisol/adrenaline.
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    [QUOTE=RollerBall;35115912]I've literally done none of the regulation. At least nothing you've mentioned. I've just learnt the pathways as in like Glucose -> G6P via hexakinase etc. You've kind of thrown a curveball into my understanding with the whole coma thing. Why does it take a while to switch to utilising ketones?

    i see.. unfortunately learning the pathways in isolation from their regulation is going to make it very challenging for a bit. perhaps go back to each major substrate in turn (mainly glucose and fat) then look at how it's first regulated at a cellular level because otherwise it's going to be hard to build up mechanistic understanding when it comes to complex phenomena like starvation responses. an excellent question, unfortunately not an easy one to answer succinctly. one way to think of it is that the enzymes required to breakdown ketones aren't constitutive and need to be upregulated before they can become serious substrate. in reality everything is complicated by another question you might ask yourself, how exactly are neurones fueled by ketones and what is the role of the neuroglia? this is where we get cutting edge and i can reccomend a few papers but the answer is that we still don't really understand exactly how the brain is using the ketones so can't describe mechanistically in a way that is complete the reason for the delay, just observe the phenomena. whether you find that deeply unsatisfying or good because it's something less to learn depends which side of the fence you sit on .


    (Original post by RollerBall)
    Uh, if you made me run a marathon I'm not entirely sure. Over the first four (I think) hours my glycogen liver stores would keep me going and then would I switch to fat metabolism, the breakdown of glycerol to glucose and fatty acids into acetyl CoA (probably leading to ketogenesis though)?
    bit of a naughty question really as actually you 'hit the barrier' (which probably represents depletion of most glycogen) before the end but ignoring that. you correctly highlight the ketogenesis etc but don't forget you still need a ~5mM plasma glucose or you're dead regardless of how many ketones you churn out so capacity for gluconeogenesis is essential!

    (Original post by RollerBall)
    I know gluconeogenesis only occures in the liver (it's my standard default organ for anything in metabolism I get stuck on too ). So it stacks up enough ATP for it's own metabolic needs then any extra turns into glucose for other cells? Where would it come from though, excess breakdown of glucose in the first time? Glycerol? Why would it not make it into glycogen? Can only muscle tissues convert glycogen to glucose?
    always guess liver! well yes and no, the liver is selfless beyond simply staying alive (so producing enough ATP for that) and what it does is a function of the metabolic requirements of the other organs which is elaborated in the form of hormones and the sympathetic nervous system (not a complete list really there are some fantastic other things but far from medically relevant!). after skeletal muscle, which cheats by its sheer volume, the liver has the largest glycogen stores by a great distance (other cells in the body may have tiny stores as required but these are probably just as hyperacute buffers rather than relevant to starvation responses). don't forget diet and the anatomical relationship of the portal circulation, the liver samples the majority of incoming substrate long before it see's the light of day peripherally and replenishes it's glycogen and synthesises fatty acids and probably the majority of amino acids etc as required and in the absence of substrate also coordinates the starvation response by being the most important gluconeogenic/ketogenic metabolic tissue. basically it doesn't constitutionally produce glucose intrinsically, it is always in response to a requirement but it just so happens to almost always need to be doing it because of the way humans have set out their diet. why not glycogen is partly because there is only so much glycogen each hepatocyte can contain (why? cf. glycogenin etc) and also because of the way glycogen metabolism is regulated which i gather you haven't read about yet. all cells that contain glycogen can convert it back to glucose-6-P but ONLY gluconeogenic tissues have G6Pase which allows export back into the blood. whereas the liver is selfless with its glycogen which exists basically only as a store for the blood, the skeletal muscles etc are greedy.


    (Original post by RollerBall)
    Bits and bobs. Somethings just confuse me further though. Our metabolism teaching is incredibly poor unfortunately. They don't put lecture slides up either but instead lecture "notes". Learning from somebody elses notes is not useful though.
    it doesn't sound very good, how have they set out your course on it? i recommend doing each pathway and its regulation in turn then after that bringing it together and considering how key organs integrate between the pathways then finally how they integrate in complex responses like starvation if you want to understand properly. there is clearly a lot to it and it took me a long time to feel comfortable with how it all comes together in particular so don't worry too much at the moment. Not sure what you need for your exams though?
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    (Original post by RollerBall)
    Insulin is the next PBL. I know it's breif mechanics though.

    Glucose in the blood enters liver via glut2, leads to glucolysis and rising ATP. ATP closes K+ channels, cell becomes negative, voltage gated channels open and Ca+ moves in. Ca+ leads to exocytosis of insulin. Insulin binds to insulin receptors on muscle and adipose tissues moving glut4 receptors to the surface and increasing uptake of glucose.

    Glycagon causes breakdown of glycogen and fats to bring up blood glucose but my knowledge of that is a lot more sketchy. Have no idea about GH/cotrisol/adrenaline.

    Yea you pretty much have insulin down, it does have other effects which are brought about by too many protein kinases.

    Glucagon essentially increases cAMP and thus PKA concentrations, which then goes on to phosphorylate many of the enzymes, regulatory enzymes and proteins involved in glycolysis and gluconeogenesis (where insulin would dephosphorylate some of them)

    Inhibit glucagon synthesis by inhibiting glucokinase (preventing Gluc-6-phos formation) and inhibition of Glycogen synthase.

    Activated glucagon breakdown by activating glycogen phosporylase and G6Pase.

    Inhibits glycolysis through inhibition of glucokinase and phosphofructokinase and pyruvate kinase.

    Boron Medical physiology has a really good explanation with a nice diagram. (attached)


    As for the other hormones they are also secreted at low blood glucose concentrations and have an impact in increasing it.
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    (Original post by John Locke)
    i see.. unfortunately learning the pathways in isolation from their regulation is going to make it very challenging for a bit. perhaps go back to each major substrate in turn (mainly glucose and fat) then look at how it's first regulated at a cellular level because otherwise it's going to be hard to build up mechanistic understanding when it comes to complex phenomena like starvation responses.
    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?
    bit of a naughty question really as actually you 'hit the barrier' (which probably represents depletion of most glycogen) before the end but ignoring that. you correctly highlight the ketogenesis etc but don't forget you still need a ~5mM plasma glucose or you're dead regardless of how many ketones you churn out so capacity for gluconeogenesis is essential!
    Yeah, I had a feeling about the wall as a depletion of glucogen stores.

    always guess liver! well yes and no, the liver is selfless beyond simply staying alive (so producing enough ATP for that) and what it does is a function of the metabolic requirements of the other organs which is elaborated in the form of hormones and the sympathetic nervous system (not a complete list really there are some fantastic other things but far from medically relevant!). after skeletal muscle, which cheats by its sheer volume, the liver has the largest glycogen stores by a great distance (other cells in the body may have tiny stores as required but these are probably just as hyperacute buffers rather than relevant to starvation responses). don't forget diet and the anatomical relationship of the portal circulation, the liver samples the majority of incoming substrate long before it see's the light of day peripherally and replenishes it's glycogen and synthesises fatty acids and probably the majority of amino acids etc as required and in the absence of substrate also coordinates the starvation response by being the most important gluconeogenic/ketogenic metabolic tissue. basically it doesn't constitutionally produce glucose intrinsically, it is always in response to a requirement but it just so happens to almost always need to be doing it because of the way humans have set out their diet. why not glycogen is partly because there is only so much glycogen each hepatocyte can contain (why? cf. glycogenin etc) and also because of the way glycogen metabolism is regulated which i gather you haven't read about yet. all cells that contain glycogen can convert it back to glucose-6-P but ONLY gluconeogenic tissues have G6Pase which allows export back into the blood. whereas the liver is selfless with its glycogen which exists basically only as a store for the blood, the skeletal muscles etc are greedy.
    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.

    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?
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    (Original post by carcinoma)
    Yea you pretty much have insulin down, it does have other effects which are brought about by too many protein kinases.

    Glucagon essentially increases cAMP and thus PKA concentrations, which then goes on to phosphorylate the enzymes involved in glycolysis and gluconeogenesis (where insulin would dephosphorylate them)

    Inhibit glucagon synthesis by inhibiting glucokinase (preventing Gluc-6-phos formation) and inhibition of Glycogen synthase.

    Activated glucagon breakdown by activating glycogen phosporylase and G6Pase.

    Inhibits glycolysis through prosprylation of glucokinase and phosphofructokinase and pyruvate kinase.

    Boron Medical physiology has a really good explanation with a nice diagram. (attached)


    As for the other hormones they are also secreted at low blood glucose concentrations and have an impact in increasing it.
    there are mistakes here but im busy writing an essay so will describe in detail tomorrow evening if we're still on the topic. notable ones are that G6Pase is not regulated by phosphorylation (think of where it is!), insulin doesn't always dephosphorylate (GSK3!), the most important part of insulin signalling is not GLUT4 insertion, otherwise it would be bloody useless in adipose which in humans has virtually no capabilities for lipogenesis so can't do anything with glucose, glucokinase is NOT regulated by phosphorylation directly and neither insulin nor glucagon regulate that particular enzyme - other peripheral hexokinases are not regulated at all etc etc...

    not a criticism!
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    (Original post by John Locke)
    there are mistakes here but im busy writing an essay so will describe in detail tomorrow evening if we're still on the topic. notable ones are that G6Pase is not regulated by phosphorylation (think of where it is!), insulin doesn't always dephosphorylate (GSK3!), the most important part of insulin signalling is not GLUT4 insertion, otherwise it would be bloody useless in adipose which in humans has virtually no capabilities for lipogenesis so can't do anything with glucose, glucokinase is NOT regulated by phosphorylation directly and neither insulin nor glucagon regulate that particular enzyme - other peripheral hexokinases are not regulated at all etc etc...

    not a criticism!
    Agreed! I oversimplified, and while the phosphorylation certainly does not occur directly to the enzymes you have identified.

    However, my understanding was that while the enzymes may have not been directly phsporylated, regulatory enzymes and proteins were being phosphorylated to bring about these effects.

    Mostly from Chapter 51 of MP

    (Original post by Boron -Medical Physiology Chapter 51, Pg 1090)
    Glucagon, Acting Through cAMP, Promotes the Synthesis of Glucose by the Liver

    Glucagon is an important regulator of hepatic glucose production and ketogenesis in the liver. As shown in Figure 51-12, glucagon binds to a receptor that activates the heterotrimeric G protein Gαs, which stimulates membrane-bound adenylyl cyclase (see Chapter 3). The cAMP formed by the cyclase, in turn, activates PKA, which phosphorylates numerous regulatory enzymes and other protein substrates, thus altering glucose and fat metabolism in the liver. Whereas insulin leads to the dephosphorylation of certain key enzymes (i.e., glycogen synthase, acetyl CoA carboxylase, phosphorylase), glucagon leads to their phosphorylation.

    A particularly clear example of the opposing actions of insulin and glucagon involves the activation of glycogenolysis, which is discussed in Chapter 3 (see Fig 3-7). PKA phosphorylates the enzyme phosphorylase kinase (see Fig. 59-8), thus increasing the activity of phosphorylase kinase and allowing it to increase the phosphorylation of its substrate, glycogen phosphorylase b. The addition of a single phosphate residue to phosphorylase b converts it to phosphorylase a. Liver phosphorylase b has little activity in breaking the 1 to 4 glycosidic linkages of glycogen, but phosphorylase a is very active. In addition to converting phosphorylase b to the active phosphorylase a form, PKA also phosphorylates a peptide called inhibitor I. In its phosphorylated form, inhibitor I decreases the activity of protein phosphatase 1 (PP1) that otherwise would dephosphorylate both phosphorylase kinase and phosphorylase a (converting them to their inactive forms). PP1 also activates glycogen synthase. Thus, through inhibitor I, glucagon modulates several of the enzymes involved in hepatic glycogen metabolism to provoke net glycogen breakdown. As a result of similar actions on the pathways of gluconeogenesis and lipid oxidation, glucagon also stimulates these processes. Conversely, glucagon restrains glycogen synthesis, glycolysis, and lipid storage.

    The effects of the glucagon-as well as the effect of glucocorticoids-to enhance gluconeogenesis involve activation of the transcription factor CBP as well as PGC-1 (PPAR-γ coactivator-1), which enhances the transcription factor PPAR-γ (see Chapter 4). The net effect is an increase in the synthesis of such key regulatory enzymes as G6Pase and PEPCK-both of which promote the release of glucose. Insulin restrains the transcription of these two enzymes in two ways, both through the PI3K/protein kinase B pathway (Fig. 51-6). First, insulin increases the release of the transcription factor domain of SREBP-1 (see Chapter 3), which antagonizes the transcription of mRNA encoding the two enzymes. Second, insulin increases the phosphorylation of several transcription factors of the Foxo family, thereby promoting their movement out of the nucleus and preventing them from binding to the promoter regions of the two enzymes.

    These actions of glucagon can be integrated with our understanding of insulin's action on the liver in certain physiological circumstances. For example, after an overnight fast, when insulin concentrations are low, glucagon stimulates the liver to produce the glucose that is required by the brain and other tissues for their ongoing function. With ingestion of a protein meal, absorbed amino acids provoke insulin secretion, which can inhibit hepatic glucose production and promote glucose storage by liver and muscle (see earlier). If the meal lacked carbohydrate, the secreted insulin could cause hypoglycemia. However, glucagon secreted in response to a protein meal balances insulin's action on the liver and thus maintains glucose production and avoids hypoglycemia.
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    (Original post by ThisLittlePiggy)
    A big boy punched me and ran away but then the fuzz caught him and battered him. Instant karma except now I've got a scar on my cheek and I need to go to court as he was so sozzled he probably doesn't remember doing it.
    Are you alright mate?
    I was pretty shaken up when I got assaulted by 8 guys and kinda didn't go back to that road for a year...

    Medic love man x
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    (Original post by carcinoma)
    Agreed! I oversimplified, and while the phosphorylation certainly does not occur directly to the enzymes you have identified.

    However, my understanding was that while the enzymes may have not been directly phsporylated, regulatory enzymes and proteins were being phosphorylated to bring about these effects.

    Mostly from Chapter 51 of MP
    in the case of glycogen signalling that is generally true but it's only acting on hepatocytes which makes it easier for us, insulin signalling however acts far more broadly and is much less linear in terms of mechanism but it is equally important to understand. the B&B section you quote is grossly oversimplified in some bits(e.g. inhibition of PP1)and also there are factual inaccuracies (e.g. phosphorylations of GPase and activities) and plain misleading bits (PPAR gamma coactivator stuff). the metabolic section in boron is not very good at all.
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    (Original post by John Locke)
    in the case of glycogen signalling that is generally true but it's only acting on hepatocytes which makes it easier for us, insulin signalling however acts far more broadly and is much less linear in terms of mechanism but it is equally important to understand. the B&B section you quote is grossly oversimplified in some bits(e.g. inhibition of PP1)and also there are factual inaccuracies (e.g. phosphorylations of GPase and activities) and plain misleading bits (PPAR gamma coactivator stuff). the metabolic section in boron is not very good at all.
    I thought as much about B&B, but I figured that is more than detailed enough for this stage of the course, as we also do the mechanisms, clinical and management side of DM and its complications (DKA, HONK and Hypo's, Microvascular, macrovascular, nephropathy and neuropathy) alongside energy metabolism.

    We return to it later in the year, We only had 2 weeks on all that.


    What would you suggest I use for Carbohydrate and Energy metabolism?
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    For clinical year exams...is it just me or does it always feel like it is impossible to remember everything and no matter how hard you study you know you're going to get your ass kicked by the written papers because they will ask about some obscure scoring system for a specific disease?
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    (Original post by ThisLittlePiggy)
    Just because it's on my face. I quite liked the way my face was before, and as it'll be my second facial scar now.

    Totally knocked my pulling confidence right off.
    **** man, sorry to hear that. I'm sure you'll get to your normal self soon enough, but it's not surprising that it's given you a bit of a knock.
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    (Original post by carcinoma)
    What would you suggest I use for Carbohydrate and Energy metabolism?
    I'm not a metabolism expert, but a book by Frayn called Metabolic Regulation: A Human Perspective I've found to be consistently good.
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    (Original post by Wangers)
    Did some management training recently, among the recognised forms of bad management are 1) the Pidgeon model - fly in, squawk, **** everywhere and leave again; and 2) The Mushroom model - bury in ****, keep in dark. Delightful. The NHS has this in bucketfuls...starting from the health secretary downwards...
    Whilst I've seen some bad managers, I believe the NHS managers do get bad rep on the whole (health secretary notwithstanding). Since I've started as a doctor, I've got nothing but good things to say about the managers I've come into contact with.
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    (Original post by John Locke)
    amazing!
    We did Porphyrias the other week, and glycogen storage diseases. It's like a molecular orgasm...you would have loved it.
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    63 slides on the hostory on blood transfusion and blood groups...
 
 
 
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