dangit

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Okay, if someone could please help me out, I'll be so grateful.. maybe even take you out to lunch ;)

anyway, I'm trying to answer question #15 on page 211.

However, on page 173, 4c says that:
"impaired protein synthesis prevents assembly and secretion of VLDL..."
This statement is in regards to chronic alcoholism and basically, I interpret this as having low VLDL due to chronic alcoholism.

I'm really confused because the question says that the man is a chronic alcoholic and that he has high levels of VLDL...

am i not getting something or is there something wrong with the questions in RR because i've been looking at just this one question for the last hour.. very frustrated right now
 

turkeyjerky

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So, if you have alcoholic cirrhosis liver function is gonna be impaired and you'll have low cholesterol levels because of the reduced liver functions (just like a low BUN, and clotting factors and albumin).

But the question isn't asking about that, it's asking about the mechanism of increased VLDL in someone who chronically drinks alcohol (which is a cause of increased VLDL). Just cause you're a chronic alcoholic doesn't mean you have hepatic insufficiency, in fact most do not.
 

dangit

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okay, so chronic alcoholism leads to increase in VLDL...

can you explain the mechanism?
i'm really confused because p.173 4c says "impaired protein synthesis prevents assembly and secretion of VLDL..."

Doesn't that statement means that you should have low VLDL in chronic alcoholics?
 

FutureDoc4

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You have to seperate this into two patients:

Patient A) Alcoholic but NO cirrhosis. That means protein synthesis in the liver is in tact. They have increased glycerol-3-phosphate produced (due to increased NADH) and that will combine with FA to form TAG. The TAG will be packed with PROTEIN (which is in abundance) into VLDL and released by the liver (increased VLDL).

Patient B) Alcoholic but CIRRHOSIS. Impaired protein synthesis. They also have increased glycerol-3-phosphate produced (due to increased NADH) and that will combine with FA to form TAG. The TAG CANNOT be packed into VLDL particle because VLDL requires certain proteins and protein synthesis in the liver is impaired.

Overall: Patient A: increased VLDL and Patient B: Decreased VLDL

Hopefully that clears things up.
 

dangit

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thanks for the reply!

i don't see in RR anything about cirrhosis... could you point me to where i can read about cirrhosis impairing protein synth

in other words, how was i supposed to know that from RR? is this something i was supposed to learn in class?
 

FutureDoc4

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You should of learned in class that the liver has certain functions such as creating clotting factors, estrogen metabolism, albumin and protein synthesis:

Hence, with cirrhosis you get symptoms such as prolonged PT, interstitial (pitting edema-due to decreased albumin), hyperestrogenism--spider angiomas etc, and decreased protein synthesis and tons more.
 

dangit

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are you on a systems based curriculum?

we're on a traditional based curriculum and i'm a first year....i'm asking because i'm preparing for the biochem shelf

also, i found my notes for biochem and it says that a high ratio of NADH/NAD+ causes FA synth and thus increase of VLDL. so i guess as long as you don't have cirrhosis, you can make VLDL....

so basically:
cirrhosis -> no VLDL
no cirrhosis -> increased VLDL

is this correct?
 

FutureDoc4

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This is probably something you will learn about more about during second year than. I wouldn't worry about it to much.
 

dangit

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well, i still need to prepare for the shelf, but i wanted to thank you regardless. :)