why does prolonged TPN lead to cholelithiasis

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MudPhud20XX

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I've always wondered this. So why does prolonged TPN make you vulnerable to having gallstone?

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Biliary stasis --> formation of gallstones? I guess that makes sense, so anything that puts your gall bladder inactive will do the same I guess.... Thanks!
 
From UTD:
Conditions that result in bile stasis are associated with a higher prevalence of gallstones. In the normal state, the gallbladder avidly absorbs water from bile. Thus, if bile remains within the gallbladder for a prolonged period, it can become overly concentrated with cholesterol, thereby promoting stone formation. Common examples of this mechanism include spinal cord injuries, prolonged fasting and the use of total parenteral nutrition (both of which prevent the normal enteral stimulation of gallbladder activity), and excess somatostatin.
 
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Without even thinking of the science behind it I'm asking this question.. why couldn't CCK be added to TPN?
 
A good question. It's been studied a lot and is shown that adding CCK either does not prevent parenteral nutrition associated cholestatis or has very little effect.

In these studies was the CCK added enterally or added to the TPN? Usually people are on TPN cause they can't get anything put in their stomach, so giving CCK via NG tube would probably be contraindicated. Adding CCK to the TPN would do nothing as you bypassing the normal enteric route which is the problem to begin with.

I'm too lazy to go look up the studies myself
 
In these studies was the CCK added enterally or added to the TPN? Usually people are on TPN cause they can't get anything put in their stomach, so giving CCK via NG tube would probably be contraindicated. Adding CCK to the TPN would do nothing as you bypassing the normal enteric route which is the problem to begin with.

I'm too lazy to go look up the studies myself
I had this same questions before looking up studies for my last comment!

CCK is an endocrine hormone and is normally secreted into the circulation (not GI tract) by enteroendocrine cells. My understanding is that CCK is added to the TPN and this mimics the normal route of CCK-stimulated gallbladder contraction/increased bile production.
 
I had this same questions before looking up studies for my last comment!

CCK is an endocrine hormone and is normally secreted into the circulation (not GI tract) by enteroendocrine cells. My understanding is that CCK is added to the TPN and this mimics the normal route of CCK-stimulated gallbladder contraction/increased bile production.
ahh yes, but I suppose it could still have a local effect even if secreted into vascular system if only at the duodenal level.

possibly similar to how women still have menstrual cycles after bilateral tubal ligation (Estrogen secreted into circulation locally by the ovary to cause endometrial proliferation, really the same way ovary stimulates endometrium as in normal state w/ the tubes fully intact). Yet systemic estrogen supplements post-menopause don't cause periods...

Or how the excess bHCG secreted from a gestational trophoblastic neoplasm (I assume into systemic circulation) causing effect locally on the ovaries in the way of forming cysts.

I might be thinking too deep here, this is a pretty complex topic probably beyond my level of intelligence
 
also the title of this thread may be wrong. You get acalculous cholecystitis in ICU/critically ill/TPN patients rather than cholelithiasis. Just came across Q on this so be careful of this on the test. RUQ u/s is still the diagnostic test of choice but it will NOT show any gallstones, just inflammation of the gallbladder. Just a warning so you don't get thrown off on test day.

we have the pathophysio correct, gallbladder stasis leads to infection or inflammation and necrosis if bad. This kind of makes sense since a stone takes a long time to form, you wouldn't just be able to make one

Explanation doesn't make any mention of why adding CCK to the TPN doesn't prevent gallbladder stasis though... lol not going that deep!!
 
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